asmbs guidelines asmbs allied health nutritional ... · ness for change, realistic goal setting,...

36
ASMBS Guidelines ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient Allied Health Sciences Section Ad Hoc Nutrition Committee: Linda Aills, R.D. (Chair) a , Jeanne Blankenship, M.S., R.D. b , Cynthia Buffington, Ph.D. c , Margaret Furtado, M.S., R.D. d , Julie Parrott, M.S., R.D. e, * a Private practice, Reston, Virginia b University of California, Davis Medical Center, Sacramento, California c Florida Hospital Celebration Health, Celebration, Florida d Johns Hopkins Bayview Medical Center, Baltimore, Maryland e Private practice, Fort Worth, Texas Received March 11, 2008; accepted March 12, 2008 This document is intended to provide an overview of the elements that are important to the nutritional care of the bariatric patient. It is not intended to serve as training, a statement of standardization, or scientific consensus. It should be viewed as an educational tool to increase aware- ness among medical professionals of the potential risk of nutritional deficiencies common to bariatric surgery pa- tients. The goal of this document is to provide suggestions for conducting a nutrition assessment, education, supplementa- tion, and follow-up care. These suggestions are not man- dates and should be treated with common sense. When needed, exceptions should be made according to individual variations and the evaluation findings. It is intended to present a reasonable approach to patient nutrition care and at the same time allow for flexibility among individual practice-based protocols, procedures, and policies. Amend- ments to this document are anticipated as more research, scientific evidence, resources, and information become available. Nutrition care The Dietitian’s role is a vital component of the bariatric surgery process. Nutrition assessment and dietary manage- ment in surgical weight loss have been shown to be an important correlate with success [1,2]. A comprehensive nutrition assessment should be conducted preoperatively by a dietitian, physician, and/or well-informed, qualified mul- tidisciplinary team to identify the patient’s nutritional and educational needs. It is essential to determine any pre- existing nutritional deficiencies, develop appropriate dietary interventions for correction, and create a plan for postoper- ative dietary intake that will enhance the likelihood of success. The management of postoperative nutrition begins pre- operatively with a thorough assessment of nutrient status, a strong educational program, and follow-up to reinforce im- portant principals associated with long-term weight loss maintenance. A comprehensive nutrition evaluation goes far beyond assessing the actual dietary intake of the bariatric patient. It takes into account the whole person, encompass- ing several multidisciplinary facets. Not only should the practitioner review the standard assessment components (i.e., medical co-morbidities, weight history, laboratory val- ues, and nutritional intake), it is also important to evaluate other issues that could affect nutrient status, including readi- ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic issues. The role of nutrition education and medical nutrition therapy in bariatric surgery will continue to grow as tools to enhance surgical outcome and long-term weight loss maintenance are explored further and identified. The fol- lowing tables suggest the possible components of bariat- ric nutrition care: Table 1: Suggested preoperative nutrition assessment Table 2: Suggested preoperative nutrition education *Reprint requests: American Society for Metabolic and Bariatric Sur- gery, 100 SW 75th Street, Suite 201, Gainesville, FL 32607. E-mail: [email protected] Surgery for Obesity and Related Diseases 4 (2008) S73-S108 1550-7289/08/$ – see front matter © 2008 American Society for Metabolic and Bariatric Surgery. All rights reserved. doi:10.1016/j.soard.2008.03.002

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Page 1: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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ASMBS Guidelines

ASMBS Allied Health Nutritional Guidelines for the Surgical WeightLoss Patient

Allied Health Sciences Section Ad Hoc Nutrition CommitteeLinda Aills RD (Chair)a Jeanne Blankenship MS RDb Cynthia Buffington PhDc

Margaret Furtado MS RDd Julie Parrott MS RDeaPrivate practice Reston Virginia

bUniversity of California Davis Medical Center Sacramento CaliforniacFlorida Hospital Celebration Health Celebration Florida

dJohns Hopkins Bayview Medical Center Baltimore MarylandePrivate practice Fort Worth Texas

Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Received March 11 2008 accepted March 12 2008

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This document is intended to provide an overview of thelements that are important to the nutritional care of theariatric patient It is not intended to serve as training atatement of standardization or scientific consensus Ithould be viewed as an educational tool to increase aware-ess among medical professionals of the potential risk ofutritional deficiencies common to bariatric surgery pa-ients

The goal of this document is to provide suggestions foronducting a nutrition assessment education supplementa-ion and follow-up care These suggestions are not man-ates and should be treated with common sense Wheneeded exceptions should be made according to individualariations and the evaluation findings It is intended toresent a reasonable approach to patient nutrition care andt the same time allow for flexibility among individualractice-based protocols procedures and policies Amend-ents to this document are anticipated as more research

cientific evidence resources and information becomevailable

utrition care

The Dietitianrsquos role is a vital component of the bariatricurgery process Nutrition assessment and dietary manage-ent in surgical weight loss have been shown to be an

mportant correlate with success [12] A comprehensive

Reprint requests American Society for Metabolic and Bariatric Sur-ery 100 SW 75th Street Suite 201 Gainesville FL 32607

E-mail infoasmbsorg

550-728908$ ndash see front matter copy 2008 American Society for Metabolic and Boi101016jsoard200803002

utrition assessment should be conducted preoperatively bydietitian physician andor well-informed qualified mul-

idisciplinary team to identify the patientrsquos nutritional andducational needs It is essential to determine any pre-xisting nutritional deficiencies develop appropriate dietarynterventions for correction and create a plan for postoper-tive dietary intake that will enhance the likelihood ofuccess

The management of postoperative nutrition begins pre-peratively with a thorough assessment of nutrient status atrong educational program and follow-up to reinforce im-ortant principals associated with long-term weight lossaintenance A comprehensive nutrition evaluation goes far

eyond assessing the actual dietary intake of the bariatricatient It takes into account the whole person encompass-ng several multidisciplinary facets Not only should theractitioner review the standard assessment componentsie medical co-morbidities weight history laboratory val-es and nutritional intake) it is also important to evaluatether issues that could affect nutrient status including readi-ess for change realistic goal setting general nutritionnowledge as well as behavioral cultural psychosocialnd economic issues

The role of nutrition education and medical nutritionherapy in bariatric surgery will continue to grow as toolso enhance surgical outcome and long-term weight lossaintenance are explored further and identified The fol-

owing tables suggest the possible components of bariat-ic nutrition care

Table 1 Suggested preoperative nutrition assessment

Table 2 Suggested preoperative nutrition education

ariatric Surgery All rights reserved

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S74 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able 1uggested Preoperative Nutrition Assessment

ecommended Suggested Other considerations

nthropometricsAge sex race accurate height and weight BMI excess body weight Visual inspection of hair

skin and nailsWaist circumferenceOther body measurements

eight historyFailed weight loss attemptsRecent preoperative weight loss attempt (if required by program)

Life events that may havecaused weight change

Personal weight loss goals

edical historyCurrent co-morbiditiesCurrent medicationsVitaminmineralherbal supplementsFood allergiesintolerances

Past medical historyIf available body fat using

bioelectrical impedanceresting metabolic rate(volume of oxygen uptake)respiratory quotient

Observation of body fatdistribution

Consideration of patients whoare athletic or muscular andBMI classifications

vailable laboratory values

sychological historyHistory of eating disorderCurrentpast psychiatric diagnosis

therAlcoholtobaccodrug useProblems with eyesightProblems with dentitionLiteracy levelLanguage barrier

ietary intake foodfluid24-hr recall (weekdayweekend)Food frequency record orFood mood and activity log (helps identify food group omission or

dietary practices that increase nutritional risk)Restaurant meal intakeDisordered eating patterns

Cultural diet influencesReligious diet restrictionsMeal preparation skill levelCravingtrigger foodsEats while engaged in other

activities

Computerized nutrient analysis(if available)

Food preferencesAttitudes toward food

hysical activityPhysical conditions limiting activityCurrent level of activity

Types of activities enjoyed inthe past

Amount of time spent indaily sedentary activities

Activity preference for the futureAttitude toward physical activity

sychosocialMotivationreasons for seeking surgical interventionReadiness to make behavioral diet exercise and lifestyle changesPrevious application of above principles listed to demonstrate ability to

make lifestyle changeWillingness to comply with program protocolEmotional connection with foodStress level and coping mechanismsIdentify personal barriers to postoperative success

Confidence to maintainweight loss

Anticipated life changesMarital statuschildrenSupport systemWork scheduleFinancial constraintsReferral to appropriate

professionals forspecialized physicalactivity instruction andormental health evaluation

Attitude toward lifestyle changeAttitude toward taking life-long

vitamin supplementation

BMI body mass index

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S75L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Table 3 Suggested postoperative follow-upTable 4 Suggested biochemical monitoring tools for

nutrition statusTable 5 Suggested postoperative vitamin supplemen-

tation

These suggestions included in Tables 1-5 have beenased on committee consensus and current research that hasocumented the pre- and postoperative likelihood of nutri-ion deficiency [1ndash18]

iochemical monitoring for nutrition status (Table 4)

Deficiencies of single vitamins are less often encounteredhan those of multiple vitamins Although proteinndashcalorie un-ernutrition can result in concurrent vitamin deficiency mosteficiencies are associated with malabsorption andor incom-lete digestion related to negligible gastric acid and pepsinlcoholism medications hemodialysis total parenteral nutri-ion food faddism or inborn errors of metabolism Bariatricurgery procedures specifically alter the absorption pathwaysndor dietary intake Symptoms of vitamin deficiency areommonly nonspecific and physical examination might not beeliable for early diagnosis without laboratory confirmation

ost characteristic physical findings are seen late in the coursef nutrient deficiency [17]

Laboratory markers are considered imperative forompleting the initial nutrition assessment and follow-upor surgical weight loss patients Established baselinealues are important when trying to distinguish betweenostoperative complications deficiencies related to sur-

able 2uggested Preoperative Nutrition Education

ecommended Su

iscussincludeImportance of taking personal responsibility for self-

care and lifestyle choicesTechniques for self-monitoring and keeping daily food

journalPreoperative diet preparation (if required by program)

ReBe

ostoperative intake CoAdequate hydrationTexture progressionVitaminmineral supplementsProtein supplementsMeal planning and spacingAppropriate carbohydrate protein and fat intake and

foodfluid choices to maximize safe weight lossnutrient intake and tolerance

Concepts of intuitive eatingTechniques and tips to maximize food and fluid

tolerancePossibility of nutrient malabsorption and importance of

supplement compliancePossibility of weight regain

DNAEfReStDReCoDFlLaA

ery noncompliance with recommended nutrient supple- c

entation or nutritional complications arising from pre-xisting deficiencies Additional laboratory measuresight be required and are defined by the presence of the

xisting individual co-morbid conditions They are notncluded in Table 4 Table 4 is a sample of laboratoryeasures that programs might consider using to compre-

ensively monitor patientsrsquo nutrition status It is not aandate or guideline for laboratory testing

itamin supplementation (Table 5)

Table 5 is an example of a supplementation regimens advances are made in the field of bariatrics andutrition updates regarding supplementation suggestionsre expected This information is intended for life-longaily supplementation for routine postoperative patientsnd is not intended to treat deficiencies Information onreating deficiencies can be found in the Appendix ldquoIden-ifying and Treating Micronutrient Deficienciesrdquo A pa-ientrsquos individual co-morbid conditions or changes inealth status might require adjustments to this regimen

ationale for recommendations

mportance of multivitamin and mineral supplementation

It is common knowledge that a comprehensive bariatricrogram includes nutritional supplementation guidanceoutine monitoring of the patientrsquos physicalmental well-eing laboratory values and frequent counseling to rein-orce nutrition education behavior modification and prin-

d Other considerations

goal settingf physical activity

Appropriate monitoring of weight loss

complaints Long-term maintenanceionomiting

ketosishungerstruction from foodsyndrome

hypoglycemiaionsteatorrheaebowel soundsntolerance

Self-monitoringNutrient dense food choices for

disease preventionRestaurantsLabel readingHealthy cooking techniquesRelapse management

ggeste

alisticnefits o

mmonehydratauseavnorexiafects ofturn of

omal obumpingactivenstipat

iarrheaatulencctose i

lopecia

iples of responsible self-care As the popularity of surgical

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S76 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nterventions for morbid obesity continues to grow concerns increasing regarding the long-term effects of nutritionaleficiencies Nutritional complications that remain undiag-osed and untreated can lead to adverse health conse-uences and loss of productivity The benefits of weight lossurgery must be balanced against the risk of developingutritional deficiencies to provide appropriate identificationreatment and prevention

Vitamins and minerals are essential factors and co-fac-ors in numerous biological processes that regulate bodyize They include appetite hunger nutrient absorptionetabolic rate fat and sugar metabolism thyroid and adre-

al function energy storage glucose homeostasis neuralctivities and others Thus micronutrient ldquorepletionrdquomeaning the body has sufficient amounts of vitamins andinerals to perform these functions) is not only important

or good health but also for maximal weight loss successnd long-term weight maintenance

Obtaining micronutrients from food is the most desirableay to ensure the body has sufficient amounts of vitamins

nd minerals However some experts have suggested that

able 3uggested Postoperative Nutrition Follow-up

ecommended Sugge

nthropometricCurrent and accurate height weight BMI and

percentage of excess body weightOvera

iochemical ActiviReview laboratory findings when available Amou

freq

edication reviewEncourage patients to follow-up with PCP regarding

medications that treat rapidly resolving co-morbidities (eg hypertension diabetes mellitus)

itaminmineral supplementsAdherence to protocol

ietary intakeUsual or actual daily intakeProtein intakeFluid intakeAssess intake of anti-obesity foodsFood texture complianceFood tolerance issues (eg nauseavomiting

ldquodumpingrdquo)Appropriate diet advanceAddress individual patient complaintsAddress lifestyle and educational needs for long

term weight loss maintenance

Estimaactu

Reinfoimp

Appro

BMI body mass index PCP primary care physician

ost individuals in our ldquofast-paced eat-outrdquo society fail to a

onsume sufficient amounts of unprocessed foods that areigh in vitamins and minerals such as fruits and vegetablessh and other protein sources dairy products whole grainsuts and legumes Poor dietary selection and habits coupledith the reduced vitamin and mineral content of foods can

ead to micronutrient deficiencies among the general publichat interfere with body weight control increasing the riskf weight gain and obesity Therefore a daily vitamin andineral supplement is likely to be of value in ensuring

dequate intake of micronutrients for maximal functioningf those processes that help to regulate appropriate bodyeightTaking daily micronutrient supplements and eating foods

igh in vitamins and minerals are important aspects of anyuccessful weight loss program For the morbidly obeseaking vitamin and mineral supplements is essential forppropriate micronutrient repletion both before and afterariatric surgery Studies have found that 60ndash80 of mor-idly obese preoperative candidates have defects in vitamin

[19ndash22] Such defects would reduce dietary calcium

Other considerations

of well-being Use of contraception to avoidpregnancy

Psychosocial intensity andf activity

Changing relationship with foodChanges in support systemStress managementBody image

oric intake of usual oreitive eating style to

od toleranceeal planning

Promote anti-obesity foodscontaining

Omega-3 fatty acidsHigh fiberLean quality protein sourcesWhole fruits and vegetablesFoods rich in phytochemicals and

antioxidantsLow-fat dairy (calcium)Discourage pro-obesity processed

foods containingRefined carbohydratesTrans and saturated fatty acids

sted

ll sense

ty levelnt typeuency o

ted calal intakrce inturove fopriate m

bsorption and increase a substance known as calcitriol

Table 4Suggested Biochemical Monitoring Tools for Nutrition Status

Vitaminmineral Screening Normal range Additional laboratoryindexes

Critical range Preoperative deficiency Postoperativedeficiency

Comments

B1 (thiamin) Serum thiamin 10ndash64 ngmL 2RBC transketolase1Pyruvate

Transketolase activity20

Pyruvate 1 mgdL

15ndash29 more common inAfrican Americans andHispanics oftenassociated with poorhydration

Rare but occurs withRYGB AGB andBPDDS

Serum thiamin responds todietary supplementationbut is poor indicator oftotal body stores

B6 (pyridoxine) PLP 5ndash24 ngmL RBC glutamic pyruvateOxaloacetic

PLP 3 ngmL Unknown Rare Consider with unresolvedanemia diabetes couldinfluence valuestransaminase

B12 (cobalamin) Serum B12 200ndash1000 pgmL 1Serum and urinaryMMA

1Serum tHcy

Serum B12

200 pgmL deficiency400 pgmL

suboptimalsMMA 0376 molLMMA 36 mol

mmol CRTtHcy 132 molL

10ndash13 may occur witholder patients and thosetaking H2 blockers andPPIs

Common withRYGB in absenceofsupplementation12ndash33

When symptoms arepresent and B12 200ndash250 pgmL MMA andtHcy are useful serumB12 may miss 25ndash30of deficiency cases

Folate RBC folate 280ndash791 ngmL Urinary FIGLUNormal serum andurinary MMA1Serum tHcy

RBC folate305 nmolL

deficiency227 nmolL anemia

Uncommon Uncommon Serum folate reflectsrecent dietary intakerather than folate statusRBC folate is a moresensitive marker

Excessive supplementationcan mask B12 deficiencyin CBC neurologicsymptoms will persist

Iron Ferritin Males15ndash200 ngmLFemales12ndash150 ngmL

2Serum iron1TIBC

Ferritin 20 ngmLSerum iron 50 gdLTIBC 450 gdL

9ndash16 of adult women ingeneral population aredeficient

20ndash49 of patientscommon withRYGB formenstruatingwomen (51) andpatients with superobesity (49ndash52)

Low Hgb and Hct areconsistent with irondeficiency anemia instage 3 or stage 4anemia ferritin is anacute phase reactant andwill be elevated withillness andorinflammation oralcontraceptives reduceblood loss formenstruating females

Vitamin A Plasma retinol 20ndash80 gdL RBP Plasma retinol 10gdL

Uncommon up to 7 insome studies

Common (50) withBPDDS after 1 yrup to 70 at 4 yrmay occur withRYGBAGB

Ocular finding maysuggest diagnosis

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Table 4Continued

Vitaminmineral Screening Normal range Additional laboratoryindexes

Critical range Preoperative deficiency Postoperativedeficiency

Comments

Vitamin D 25(OH)D 25ndash40 ngmL 2Serum phosphorus1Alkaline phosphatase1Serum PTH2Urinary calcium

Serum 25(OH)D 20ngmL suggestsdeficiency 20ndash30 ngmL suggestsinsufficiency

Common 60ndash70 Common with BPDDS after 1 yr mayoccur with RYGBprevalenceunknown

With deficiency serumcalcium may be low ornormal serumphosphorus maydecrease serum alkalinephosphatase increasesPTH elevated

Vitamin E Plasma alphatocopherol

5ndash20 gmL Plasma lipids 5 gmL Uncommon Uncommon Low plasma alphatocopherol to plasmalipids (08 mgg totallipid) should be usedwith hyperlipidemia

Vitamin K PT 10ndash13 seconds 1DCP 2Plasmaphylloquinone

Variable Uncommon Common with BPDDS after 1 yr

PT is not a sensitivemeasure of vitamin Kstatus

Zinc Plasma zinc 60ndash130 gdL 2RBC zinc Plasma zinc 70 gdL Uncommon but increasedrisk of low levelsassociated with obesity

Common with BPDDS after 1 yr mayoccur with RYGB

Monitor albumin levelsand interpret zincaccordingly albumin isprimary binding proteinfor zinc no reliablemethod of determiningzinc status is availableplasma zinc is methodgenerally used studiescited in this report didnot adequately describemethods of zinc analysis

Protein Serum albuminSerum totalprotein

4ndash6 gdL6ndash8 gdL

2Serum prealbumin(transthyretin)

Albumin 30 gdLPrealbumin 20 mgdL

Uncommon Rare but can occurwith RYGB AGBand BPDDS ifprotein intake islow in total intakeor indispensableamino acids

Half-life for prealbumin is2ndash4 d and reflectschanges in nutritionalstatus sooner thanalbumin a nonspecificprotein carrier with ahalf-life of 22 d

RYGB Roux-en-Y gastric bypass AGB adjustable gastric banding BPDDS biliopancreatic diversionduodenal switch PLP pyridoxal-5rsquo-phosphate RBC red blood cell MMA methylmalonic acid tHcy total homocysteine CRT creatinine PPIs protein pump inhibitors FIGLU formiminogluatmic acid CBC complete blood count TIBC total iron binding capacityHgb hemoglobin Hct hematocrit RPB retinol binding protein PTH parathyroid hormone 25(OH)D 25-hydroxyvitamin D PT prothrombin time DCP des-gamma-carboxypromthrom-bin

In general laboratory values should be reviewed annually or as indicated by clinical presentation Laboratory normal values vary among laboratory settings and are method dependent This chart providesa brief summary of monitoring tools See the Appendix for additional detail and diagnostic tools

copy Jeanne Blankenship MS RD Used with permission

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S79L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able 5uggested Postoperative Vitamin Supplementation

upplement AGB RYGB BPDDS Comment

ultivitamin-mineral supplementA high-potency vitamin containing 100 of daily value for

at least 23 of nutrients100 of daily

value

200 of dailyvalue

200 of daily value Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to whole tabletcapsule as toleratedAvoid time-released supplementsAvoid enteric coatingChoose a complete formula with at least 18 mg iron 400

g folic acid and containing selenium and zinc in eachserving

Avoid childrenrsquos formulas that are incompleteMay improve gastrointestinal tolerance when taken close to

food intakeMay separate dosageDo not mix multivitamin containing iron with calcium

supplement take at least 2 hr apartIndividual brands should be reviewed for absorption rate and

bioavailabilitySpecialized bariatric formulations are available

dditional cobalamin (B12)Available forms include sublingual tablets liquid drops

mouth spray or nasal gelsprayIntramuscular injection mdash 1000 gmo mdash Begin 0ndash3 mo after

surgeryOral tablet (crystalline form) mdash 350ndash500 gd mdashSupplementation after AGB and BPDDS may be required

dditional elemental calciumChoose a brand that contains calcium citrate and vitamin D3

Begin with chewable or liquidProgress to whole tabletcapsule as tolerated

1500 mgd 1500ndash 2000 mgd 1800ndash 2400 mgd May begin on day 1after hospitaldischarge orwithin 1 mo aftersurgery

Split into 500ndash600 mg doses be mindful of serving size onsupplement label

Space doses evenly throughout daySuggest a brand that contains magnesium especially for

BPDDSDo not combine calcium with iron containing supplements

To maximize absorptionTo minimize gastrointestinal intoleranceWait 2 h after taking multivitamin or iron supplement

Promote intake of dairy beverages andor foods that aresignificant sources of dietary calcium in addition torecommended supplements up to 3 servings daily

Combined dietary and supplemental calcium intake 1700mgd may be required to prevent bone loss during rapidweight loss

dditional elemental iron (above that provided by mvi)Recommended for menstruating women and those at risk of

anemia (total goal intake 50-100 mg elemental irond)

mdash Add a minimumof 18ndash27 mgdelemental

Add a minimum of18ndash27 mgdelemental

Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to tablet as toleratedDosage may need to be adjusted based on biochemical

markersNo enteric coatingDo not mix iron and calcium supplements take 2 h apartAvoid excessive intake of tea due to tannin interactionEncourage foods rich in heme iron

Vitamin C may enhance absorption of non-heme iron sources

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S80 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hich in turn causes metabolic changes that favor fatccumulation [23ndash25]

Several of the B-complex vitamins important for appro-riate metabolism of carbohydrate and neural functions thategulate appetite have been found to be deficient in someatients with morbid obesity [212627] Iron deficiencieshich would significantly hinder energy use have been

eported in nearly 50 of morbidly obese preoperativeandidates [21] Zinc and selenium deficits have been re-orted as well as deficits in vitamins A E and C allmportant antioxidants helpful in regulating energy produc-ion and various other processes of body weight manage-ent [1926ndash28]The risk of micronutrient depletion continues to be quite

igh particularly after surgeries that affect the digestion andbsorption of nutrients such as Roux-en-Y gastric bypassRYGB) and biliopancreatic diversion with or without du-denal switch (BPDDS) RYGB increases the risk of vita-in B12 and other B vitamin deficits in addition to iron and

alcium BPDDS procedures may also cause an increasedisk of iron and calcium deficits along with significant

able 5ontinued

upplement AGB

at-soluble vitaminsWith all procedures higher maintenance doses may be

required for those with a history of deficiencyWater-soluble preparations of fat-soluble vitamins are

availableRetinol sources of vitamin A should be used to calculatedosageMost supplements contain a high percentage of beta

carotene which does not contribute to vitamin A toxicityIntake of 2000 IU Vitamin D3 may be achieved with careful

selection of multivitamin and calcium supplementsNo toxic effect known for vitamin K1 phytonadione

(phyloquinone)

mdash

mdash

mdash

Vitamin K requirement varies with dietary sources andcolonic production

Caution with vitamin K supplementation for patientsreceiving coagulation therapy

Vitamin E deficiency has been suggested but is notprevalent in published studies

ptional B complexB-50 dosageLiquid form is available

1 servi

Avoid time released tabletsNo known risk of toxicityMay provide additional prophylaxis against B-vitamin

deficiencies including thiamin especially for BPDDSprocedures as water-soluble vitamins are absorbed in theproximal jejunum

Note 1000 mg of supplemental folic acid provided incombination with multivitamins could mask B12

deficiency

Abbreviations as in Table 4

eficiencies in the fat-soluble vitamins A D E and K d

hich are important for driving many of the biologicalrocesses that help to regulate body size [29ndash31] As theate of noncompliance with prophylactic multivitamin sup-lementation increases the rate of postoperative deficiencyay increase almost twofold [32]In the past it has been thought that the specific nutri-

ional deficiencies commonly seen among malabsorptiverocedures would not be present in patients choosing aurely restrictive surgery such as the adjustable gastric bandAGB) However poor eating behavior low nutrient-denseood choices food intolerance and a restricted portion sizean contribute to potential nutrient deficiencies in theseatients as well Although the incidence of nutritional com-lications may be less frequent in this patient population itould be detrimental to assume that they do not existIt is important for the bariatric patient to take vitamin and

ineral supplements not only to prevent adverse healthonditions that can arise after surgery but because someutrients such as calcium can enhance weight loss and helprevent weight regain The nutrient deficiency might beroportional to the length of the absorptive area bypassed

RYGB BPDDS Comment

mdash

mdash

mdash

10000 IU of vitamin A

2000 IU of vitamin D

300 g of vitamin K

May begin 2ndash4weeks aftersurgery

1 servingd 1 servingd May begin on day 1after hospitaldischarge

ngd

uring surgical procedures and to a lesser extent to the

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S81L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ercentage of weight lost Iron vitamin B12 and vitamin Deficiencies along with changes in calcium metabolism areommon after RYGB Protein fat-soluble vitamin andther micronutrient deficiencies as well as altered calciumetabolism are most notably found after BPDDS Folate

eficiency has been reported after AGB [33] Thiamin de-ciency is common among all surgical patients with fre-uent vomiting regardless of the type of procedure per-ormed Because many nutritional deficiencies progressith time patients should be monitored frequently and

egularly to prevent malnutrition [29] Reinforcement ofupplement compliance at each patient follow-up is alsomportant in the fight to enhance nutrition status and preventutritional complications

eight loss and nutrient deficits restrictionersus malabsorption

Malabsorptive procedures such as the BPDDS arehought to cause weight loss primarily through the malab-orption of macronutrients with as much as 25 of proteinnd 72 of fat malabsorbed Such primary malabsorptionesults in concomitant malabsorption of micronutrients3435] Vitamins and minerals relying on fat metabolismncluding vitamins D A E K and zinc may be affectedhen absorption is impaired [36] The decrease in gastro-

ntestinal transit time may also result in secondary malab-orption of a wide range of micronutrients related to by-assing the duodenum and jejunum or limited contact withhe brush border secondary to a short common limb Othericronutrient deficiency concerns reported for patients

hoosing a procedure with malabsorptive features includeron calcium vitamin B12 and folate

Nutrient deficiencies after RYGB can result from eitherrimary or secondary malabsorption or from inadequateietary intake A minimal amount of macronutrient malab-orption is thought to occur However specific micronutri-nts appear to be malabsorbed postoperatively and presents deficiencies without adequate vitamin and mineral sup-lementation Retrospective analyses of patients who havendergone gastric bypass have revealed predictable micro-utrient deficiencies including iron vitamin B12 and folate2627ndash39] Case reports have also shown that thiamin de-ciency can develop especially when persistent postopera-

ive vomiting occurs [40ndash43]Few studies that measure absorption after measured and

uantified intake have been published It can be hypothe-ized that the bypassed duodenum and proximal jejunumegatively affect nutrient assimilation Bradley et al [44]tudied patients who had undergone total gastrectomy therocedure from which the RYGB evolved The researchersound that most nutritional status changes in patients wereost likely due to changes in intake versus malabsorptionhese balance studies were conducted in a controlled re-

earch setting however they did not measure pre- and c

ostoperative changes nor include radioisotope labeling toeasure absorption of key nutrients and the subjects had

ndergone the procedure for reasons other than weight lossIt is unclear whether intestinal adaptation occurs after

ombination procedures and to what degree it affects long-erm weight maintenance and nutrition status Adaptation iscompensatory response that follows an abrupt decrease inucosal surface area and has been well studied in short-

owel patients who require bowel resection [45] The pro-ess includes both anatomic and functional changes thatncrease the gutrsquos digestive and absorptive capacity Al-hough these changes begin to take place in the early post-perative period total adaptation may take up to three yearso complete Adaptation in gastric bypass has not beenonsidered in absorption or metabolic studies This consid-ration could be important even when determining early andate macro- and micronutrient intake recommendations Theffect of pancreatic enzyme replacement therapy on vitaminnd mineral absorption in this population is also unknown

Purely restrictive procedures such as the AGB can resultn micronutrient deficiencies related to changes in dietaryntake It is commonly accepted that because no alteration isade in the absorptive pathway malabsorption does not

ccur as a result of AGB procedures However nutrienteficits would be likely to occur because of the low nutrientntake and avoidance of nutrient-rich foods in the earlyonths postoperatively and later possibly as a result of

xcessive band restriction Food with high nutritional valueuch as meat and fibrous fresh fruits and vegetables mighte poorly tolerated

Literature has been published that addresses the effect ofalabsorptive restrictive and combination surgical proce-

ures on acute and long-term nutritional status These stud-es have attempted for the most part to indirectly determinehe surgical impact on nutrition status by the evaluation ofetabolic and laboratory markers Although some studies

ave included certain aspects of absorption few have in-luded the necessary components to evaluate absorption ofprescribed andor monitored diet in a controlled metabolic

ettingThe following sections examine the pre- and postopera-

ive risks for nutritional deficiencies associated with RYGBPDDS and AGB It is important for all members of theedical team to increase their awareness of the nutritional

omplications and challenges that lie ahead for the patientontinued review of current research by the medical team

egarding advances in nutrition science beyond the bound-ries of the present report cannot be emphasized enough

hiamin (vitamin B1)

Beriberi is a thiamin deficiency that can affect variousrgan systems including the heart gastrointestinal tractnd peripheral and central nervous systems Although the

ondition is generally considered rare a number of reported

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S82 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nd possibly a much greater number of unreported or un-iagnosed cases of beriberi have occurred among individ-als who have undergone surgery for morbid obesity Earlyetection and prompt treatment of thiamin deficits in thesendividuals can help to prevent serious health consequencesf beriberi is misdiagnosed or goes undetected for even ahort period the bariatric patient can develop irreversibleeuromuscular disorders permanent defects in learning andhort-term memory coma and even death Because of theife-altering and potentially life-threatening nature of a thi-min deficiency it is important that healthcare professionalsn the field of bariatric surgery have knowledge of thetiology of the condition and its signs and symptomsreatment and prevention

tiology of potential deficiency Thiamin is a water-solubleitamin that is absorbed in the proximal jejunum by anctive (saturable high-affinity) transport system [4647] Inhe body thiamin is found in high concentrations in therain heart muscle liver and kidneys However withoutegular and sufficient intake these tissues become rapidlyevoid of thiamin [4647] The total amount of thiamin inhe body of an adult is approximately 30 mg with a half-lifef only 9ndash18 days Persistent vomiting a diet deficient inhe vitamin or the bodyrsquos excessive utilization of thiaminse can result in a severe state of thiamin depletion withinnly a short period producing symptoms of beriberi46ndash48]

Bariatric surgery increases the risk of beriberi through ex-cerbation of pre-existing thiamin deficits low nutrient intakealabsorption and episodes of nausea and vomiting [49ndash51]hronic or acute thiamin deficiencies in bariatric patients oftenresent with symptoms of peripheral neuropathy or Wer-ickersquos encephalopathy and Korsakoffrsquos psychoses [2148ndash4] Early diagnosis of the signs and symptoms of these con-itions is extremely important to prevent serious adverse healthonsequences Even if treatment is initiated recovery can bencomplete with cognitive andor neuromuscular impairmentsersisting long term or permanently

igns symptoms and treatment of deficiency (seeppendix Table A1)

reoperative risk The risk of the development of beriberifter bariatric surgery is far greater for individuals present-ng for surgery with low thiamin levels Investigators at theleveland Clinic of Florida reported that 15 of their pre-perative bariatric patients had deficiencies in thiamin be-ore surgery [52] A study by Flancbaum et al [21] similarlyound that 29 of their preoperative patients had low thia-in levels Data obtained by that study also showed a

ignificant difference between ethnicity and preoperativehiamin levels Although only 67 of whites presentedith thiamin deficiencies before surgery nearly one third

31) of African Americans and almost one half (47) of

ispanics had thiamin deficits The results of these studies S

uggested a need for preoperative thiamin testing as well ashiamin repletion by diet or supplementation to reduce theisk of ldquobariatricrdquo beriberi postoperatively

ostoperative risk Beriberi has been observed after gastricestrictive and malabsorptive procedures A number of casesf Wernicke-Korsakoff syndrome (WKS) as well as periph-ral neuropathy have been reported for patients havingndergone vertical banded gastroplasty [53ndash61] A fewncidences of WKS have also been reported after AGB436263] Additionally reports of thiamin deficiencies and

KS after RYGB [404164ndash73] and several cases of WKSnd neuropathy in patients who had undergone BPD [74]ave been published Many more cases of WKS are be-ieved to have occurred with bariatric procedures that haveither not been reported or have been misdiagnosed becausef limited knowledge regarding the signs and symptoms ofcute or severe thiamin deficits Because many foods areortified with thiamin beriberi has been nearly eradicatedhroughout the world except for patients with severe alco-olism severe vomiting during pregnancy (hyperemesisravidarium) or those malnourished and starved For thiseason few healthcare professionals until recently havead a patient present with beriberi

According to the published reports of thiamin deficitsfter bariatric procedures most patients develop such defi-iencies in the early postoperative months after an episodef intractable vomiting Nausea and vomiting are relativelyommon after all bariatric procedures early in the postop-rative period Thiamin stores in the body are small andaintenance of appropriate thiamin levels requires daily

eplenishment A deficiency of thiamin for only a couple ofeeks or less caused by persistent vomiting can deplete

hiamin stores Symptoms of WKS were reported in aYGB patient after only two weeks of persistent vomiting

67]Bariatric beriberi can also develop in postoperative patients

ho are given infusate containing dextrose without thiaminnd other vitamins which is often the case for patients inritical care units postoperative patients with complicationsnterfering with the ingestion of food or patients dehydratedrom persistent vomiting Malnutrition caused by a lack ofppetite and dietary intake postoperatively also contributes toariatric beriberi as does noncompliance in taking postopera-ive vitamin supplements

Although most cases of beriberi occur in the early post-perative periods cases of patients with severe thiamineficiency more than one year after surgery have beeneported One study reported WKS in association with al-ohol abuse 13 years after RYGB [75] Other conditionsontributing to late cases of bariatric beriberi include ahiamin-poor diet a diet high in carbohydrates anorexiand bulimia [46ndash48]

uggested supplementation Because of the greater likeli-

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S83L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ood of low dietary thiamin intake patients should be sup-lemented with thiamin This is usually accomplishedhrough daily intake of a multivitamin Most multivitaminsontain thiamin at 100 of the daily value Patients havingpisodes of nausea and vomiting and those who are anorec-ic might require sublingual intramuscular or intravenoushiamin to avoid depletion of thiamin stores and beriberiaution should be used when infusing bariatric patientsith solutions containing dextrose without additional vita-ins and thiamin because an increase in glucose utilizationithout additional thiamin can deplete thiamin stores [76]Thiamin deficiency in bariatric patients is treated with

hiamin together with other B-complex vitamins and mag-esium for maximal thiamin absorption and appropriateeurologic function [46 ndash 48] Early symptoms of neuropa-hy can often be resolved by providing the patient with oralhiamin doses of 20ndash30 mgd until symptoms disappear Forore advanced signs of neuropathy or for individuals with

rotracted vomiting 50ndash100 mgd of intravenous or intra-uscular thiamin may be necessary for resolution or im-

rovement of symptoms or for the prevention of suchatients with WKS generally require 100 mg thiamindministered intravenously for several days or longer fol-owed by intramuscular thiamin or high oral doses untilymptoms have resolved or significantly improved This canequire months to years Some patients might have to takehiamin for life to prevent the reoccurrence of neuropathy

itamin B12 and folate

Vitamin B12 (cobalamin) and folate (folic acid) are bothnvolved in the maturation of red blood cells and are com-only discussed in the literature together Over time a

eficiency in either vitamin B12 or folate can lead to mac-ocytic anemia a condition characterized by the productionf fewer but larger red blood cells and a decreased abilityo carry oxygen Most (95) cases of megaloblastic anemiacharacterized by large immature abnormal undifferenti-ted red blood cells in bone marrow) are attributed toitamin B12 or folate deficiency [77]

itamin B12

tiology of potential deficiency RYGB patients have bothncomplete digestion and release of vitamin B12 from pro-ein foods With a significant decrease in hydrochloric acidepsinogen is not converted into pepsin which is necessaryor the release of vitamin B12 from protein [78] BecauseGB patients have an artificial restriction yet complete usef the stomach and BPD patients do not have as great aestriction in stomach capacity and parietal cells as RYGBatients the reduction in hydrochloric acid and subsequentitamin B12 deficiency is not as prevalent with these tworocedures

Intrinsic factor (IF) is produced by the parietal cells of

he stomach and in certain conditions (eg atrophic gastri- a

is resected small bowel elderly patients) can be impairedausing an IF deficiency Subsequent vitamin B12 deficiencypernicious anemia) occurs without IF production or useecause IF is needed to absorb vitamin B12 in the terminalleum [77] Factors that increase the risk of vitamin B12

eficiency relevant to bariatric surgery include the follow-ng

An inability to release protein-bound vitamin B12

from food particularly in hypochlorhydria andatrophic gastritis

Malabsorption due to inadequate IF in perniciousanemia

Gastrectomy and gastric bypassResection or disease of terminal ileumLong-term vegan dietMedications such as neomycin metformin colch-

icines medications used in the management ofbowel inflammation and gastroesophageal refluxand ulcers (eg proton pump inhibitors) and anti-convulsant agents [79]

Cobalamin stores are known to exist for long periods3ndash5 yr) and are dependent on dietary repletion and dailyepletion However gastric bypass patients have both aecreased production of stomach acid and a decreased avail-bility of IF thus a vitamin B12 deficiency could developithout appropriate supplementation Because the typical

bsorption pathway cannot be relied on the surgical weightoss patient must rely on passive absorption of B12 whichccurs independent of IF

igns symptoms and treatment of deficiency (seeppendix Table A3)

reoperative risk Several medications common to preop-rative bariatric patients have been noted to affect preoper-tive vitamin B12 absorption and stores Of patients takingetformin 10ndash30 present with reduced vitamin B12 ab-

orption [80] Additionally patients with obesity have aigh incidence of gastroesophageal reflux disease for whichhey take proton pump inhibitors thus increasing the poten-ial to develop a vitamin B12 deficiency

Flancbaum et al [21] conducted a retrospective study of79 (320 women and 59 men) pre-operative patients Vita-in B12 deficiency was reported as negative in all patients

f various ethnic backgrounds [21] No clinical criteria orymptoms for vitamin B12 deficiency were noted In theeneral population 5ndash10 present with neurologic symp-oms with vitamin B12 levels of 200ndash400 pgmL Amongreoperative gastric bypass patients Madan et al [27] foundhat 13 (n 59) of patients were deficient in vitamin B12n a comparison of patients presenting for either RYGB orPD Skroubis et al [81] recently reported that preoperativeitamin B12 levels were low-normal in both groups Itould be prudent to screen for and treat IF deficiency

ndor vitamin B12 deficiency in all patients preoperatively

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S84 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ut it is essential for RYGB patients so as not to hasten theevelopment of a potential postoperative deficiency

ostoperative risk Vitamin B12 deficiency has been fre-uently reported after RYGB Schilling et al [82] estimatedhe prevalence of vitamin B12 deficiency to be 12ndash33ther researchers have suggested a much greater prevalencef B12 deficiency in up to 75 of postoperative RYGBatients however most reports have cited approximately5 of postoperative RYGB patients as vitamin B12 defi-ient [82ndash87] Brolin et al [87] reported that low levels ofitamin B12 might be seen as soon as six months afterariatric surgery but most often occurring more than oneear postoperatively as liver stores become depleted Sk-oubis et al [88] predicted that the deficiency will mostikely occur 7 months after RYGB and 79 months afterPDDS although their research did not consider compro-ised preoperative status and its correlation to postopera-

ive deficiency After the first postoperative year the prev-lence of vitamin B12 deficiency appears to increase yearlyn RYGB patients [89]

Although the bodyrsquos storage of vitamin B12 is significant2000 g) compared with daily needs (24 gd) thisarticular deficiency has been found within 1ndash9 years ofastric bypass surgery [29] Brolin et al [84] reported thatne third of RYGB patients are deficient at four yearsostoperatively However non-surgical variables were notxplored and many patients might have had preoperativealues near the lower end of the normal range Ocon Bretont al [90] compared micronutrient deficiencies among two-ear postoperative BPDDS and RYGB patients and foundhat all nutritional deficiencies were more common amongPDDS patients except for vitamin B12 for which theeficiency was more common among the RYGB patientstudied A lack of B12 deficiency among BPDDS patientsight result from a better tolerance of animal proteins in a

arger pouch greater pepsingastric acid production to re-ease protein-bound B12 and increased availability and in-eraction of IF with the pouch contents

Experts have noted the significance of subclinical defi-iency in the low-normal cobalamin range in nongastricypass patients who do not exhibit clinical evidence ofeficiency The methylmalonic acid (MMA) assay is thereferred marker of B12 status because metabolic changesften precede low B12 levels in the progression to defi-iency Serum B12 assays may miss as much as 25ndash30 of

12 deficiencies making them less reliable than the MMAssay [91] It has been suggested that early signs of vitamin

12 deficiency can be detected if the serum levels of bothMA and homocysteine are measured [91] Vitamin B12

eficiency after RYGB has been associated with megalo-lastic anemia [92] Some vitamin B12-deficient patientsevelop significant symptoms such as polyneuropathy par-

sthesia and permanent neural impairment On occasion

ome patients may experience extreme delusions halluci-ations and even overt psychosis [93]

uggested supplementation Because of the frequent lack ofymptoms of vitamin B12 deficiency the suggested dili-ence in following up or treating these values among thosesymptomatic patients has been questioned The decisionot to supplement or routinely screen patients for B12 defi-iency should be examined very carefully given the risk ofrreversible neurologic damage if vitamin B12 goes un-reated for long periods At least one case report has beenublished of an exclusively breastfed infant with vitamin

12 deficiency who was born of an asymptomatic motherho had undergone gastric bypass surgery [94]Deficiency of vitamin B12 is typically defined at levels

200 pgmL However about 50 of patients with obviousigns and symptoms of deficiency have normal vitamin B12

evels [31] Kaplan et al [95] reported that vitamin B12

eficiency usually resolves after several weeks of treatmentith 700ndash2000 gwk Rhode et al [96] found that aosage of 350ndash600 gd of oral B12 prevented vitamin B12

eficiency in 95 of patients and an oral dose of 500 gdas sufficient to overcome an existing deficiency as re-orted by Brolin et al [87] in a similar study Thereforeupplementation of RYGB patients with 350ndash500 gd mayrevent most postoperative vitamin B12 deficiency

While most vitamin B12 in normal adults is absorbed inhe ileum in the presence of IF approximately 1 of sup-lemented B12 will be absorbed passively (by diffusion)long the entire length of the (non-bypassed) intestine byurgical weight loss patients given a high-dose oral supple-ent [97] Thus the consumption of 350ndash500 g yields a

5ndash50-g absorption which is greater than the daily re-uirement Although the use of monthly intramuscular in-ections or a weekly oral dose of vitamin B12 is commonmong practices it relies on patient compliance Practitio-ers should assess the patientrsquos preference and the potentialor compliance when considering a daily weekly oronthly regimen of B12 supplementation In addition to oral

upplements or intramuscular injections nasal sprays andublingual sources of vitamin B12 are also available Pa-ients should be monitored closely for their lifetime becauseevere anemia can develop with or without supplementation98]

olate

tiology of potential deficiency Factors that increase theisk of folic acid deficiency relevant to bariatric surgerynclude the following

Inadequate dietary intakeNoncompliance with multivitamin supplementationMalabsorptionMedications (anticonvulsants oral contraceptives

and cancer treating agents) [79]

pmo

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S85L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Folic acid stores can be depleted within a few monthsostoperatively unless replenished by a multivitamin supple-ent and dietary sources (ie green leafy vegetables fruits

rgan meats liver dried yeast and fortified grain products)

igns symptoms and treatment of deficiency (seeppendix Table A4)

reoperative risk The goals of the 1998 Food and Drugdministration policy requiring all enriched grain products

o be fortified with folate included increasing the averagemerican diet by 100 g folate daily and decreasing the

ate of neural tube defects in childbearing women [99]entley et al [100] reported that the proportion of womenged 15ndash44 years old (in the general population) who meethe recommended dietary intake of 400 gd folate variesetween 23 and 33 With the increasing popularity ofigh proteinlow carbohydrate diets one cannot assume thatreoperative patients consume dietary sources of folatehrough fortified grain products fruits and vegetables Boy-an et al [26] found folate deficiencies preoperatively in6 of RYGB patients studied

ostoperative risk Although it has been observed that fo-ate deficiency after RYGB surgery is less common than B12

eficiency and is thought to occur because of decreasedietary or multivitamin supplement intake low serum folateevels have been cited from 6 to 65 among RYGBatients [2686101] Additionally folate deficiencies haveccurred postoperatively even with supplementation Boy-an et al [26] found that 47 (n 17) of RYGB patientsad low folate levels six months postoperatively and 41n 17) had low levels at one year This deficiency oc-urred despite patient adherence to taking a multivitaminupplement that contained at least the daily value for folate00 g [26] Postoperative bariatric patients with rapideight loss might have an increased risk of micronutrienteficiencies MacLean et al [86] reported that 65 ofostoperative patients had low folate levels These sameatients exhibited additional B vitamin deficiencies 24itamin B12 and 50 thiamin [86] An increased risk ofeficiency has also been noted among AGB patients pos-ibly because of decreased folate intake Gasteyger et al33] found a significant decrease in serum folate levels441) between the baseline and 24-month postoperativeeasurementsDixon and OrsquoBrien [101] reported elevated serum ho-

ocysteine levels in patients after bariatric surgery regard-ess of the type of procedure (restrictive or malabsorptive)levated homocysteine levels can indicate not only low

olate levels and a greater risk of neural tube defects but canlso be indicative of an independent risk factor for heartisease andor oxidative stress in the nonbariatric popula-ion [102] However unlike iron and vitamin B12 the folate

ontained in the multivitamin supplementation essentially e

orrects the deficiency in the vast majority of postoperativeariatric patients [103] Therefore persistent folate defi-iency might indicate a patientrsquos lack of compliance withhe prescribed vitamin protocol [32]

It is common knowledge that folic acid deficiency amongregnant women has been associated with a greater risk ofeural tube defects in newborns Consistent supplementa-ion and monitoring among women of child-bearing agencluding pre- and postoperative bariatric patients is vital inn effort to prevent the possibility of neural tube defects inhe developing fetus

Because folate does not affect the myelin of nerveseurologic damage is not as common with folate such as ishe case for vitamin B12 deficiency In contrast patientsith folate deficiency often present with forgetfulness irri-

ability hostility and even paranoid behaviors [29] Similaro that evidenced with vitamin B12 most postoperativeYGB patients who are folate deficient are asymptomatic orave subclinical symptoms therefore these deficient statesay not be easily identified

uggested supplementation Even though folate absorptionccurs preferentially in the proximal portion of the smallntestine it can occur along the entire length of the small bowelith postoperative adaptation Therefore it is generally agreed

hat folate deficiency is corrected with 1000 mgd folic acid32] and is preventable with supplementation that provides00 of the daily value (800 g) This level can also benefithe fetus in a female patient unaware of her postoperativeregnancy Folate supplementation 1000 mgd has noteen recommended because of the potential for maskingitamin B12 deficiency Carmel et al [104] suggested thatomocysteine is the most sensitive marker of folic acidtatus in conjunction with erythrocyte folate Althougholic acid deficiency could potentially occur among post-perative bariatric surgery patients it has not been seenidely in recent studies especially when patients haveeen compliant with postoperative multivitamin supple-entation Therefore it is imperative to closely follow

olic acid both pre- and postoperatively especially inhose patients suspected to be noncompliant with theirultivitamin supplementation

ron

Much of the iron and surgical weight loss research con-ucted to date has been generated from a limited number ofurgeons and scientists however the data have consistentlyointed toward the risk of iron deficiency and anemia afterariatric procedures Iron deficiency is defined as a decreasen the total iron body content Iron deficiency anemia occurshen erythropoiesis is impaired as a result of the lack of

ron stores In the absence of anemia iron deficiency issually asymptomatic Fatigue and a diminished capacity to

xercise however are common symptoms of anemia

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S86 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

tsmp

lsnfwTlopaechc

Rtbwdsaar

fdaiwiiedasdt

Stbadtbpcwl

mccmacdrrT

C

EeamadmsDfd

dbdh7DtnDcwsh

SA

Pcptt[hmtlcgc

S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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S89L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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S90 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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S91L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

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hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

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S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

ratbrdd

aebaaa

apcptaasosdbc

afciitdmptpcrsPEv

TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

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[

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[

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[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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T

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F

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A

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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c

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S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

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T

T

V

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EA

D

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S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

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S

D

T

T

T

V

DFFS

D

T

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S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

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DFF

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S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 2: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S74 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able 1uggested Preoperative Nutrition Assessment

ecommended Suggested Other considerations

nthropometricsAge sex race accurate height and weight BMI excess body weight Visual inspection of hair

skin and nailsWaist circumferenceOther body measurements

eight historyFailed weight loss attemptsRecent preoperative weight loss attempt (if required by program)

Life events that may havecaused weight change

Personal weight loss goals

edical historyCurrent co-morbiditiesCurrent medicationsVitaminmineralherbal supplementsFood allergiesintolerances

Past medical historyIf available body fat using

bioelectrical impedanceresting metabolic rate(volume of oxygen uptake)respiratory quotient

Observation of body fatdistribution

Consideration of patients whoare athletic or muscular andBMI classifications

vailable laboratory values

sychological historyHistory of eating disorderCurrentpast psychiatric diagnosis

therAlcoholtobaccodrug useProblems with eyesightProblems with dentitionLiteracy levelLanguage barrier

ietary intake foodfluid24-hr recall (weekdayweekend)Food frequency record orFood mood and activity log (helps identify food group omission or

dietary practices that increase nutritional risk)Restaurant meal intakeDisordered eating patterns

Cultural diet influencesReligious diet restrictionsMeal preparation skill levelCravingtrigger foodsEats while engaged in other

activities

Computerized nutrient analysis(if available)

Food preferencesAttitudes toward food

hysical activityPhysical conditions limiting activityCurrent level of activity

Types of activities enjoyed inthe past

Amount of time spent indaily sedentary activities

Activity preference for the futureAttitude toward physical activity

sychosocialMotivationreasons for seeking surgical interventionReadiness to make behavioral diet exercise and lifestyle changesPrevious application of above principles listed to demonstrate ability to

make lifestyle changeWillingness to comply with program protocolEmotional connection with foodStress level and coping mechanismsIdentify personal barriers to postoperative success

Confidence to maintainweight loss

Anticipated life changesMarital statuschildrenSupport systemWork scheduleFinancial constraintsReferral to appropriate

professionals forspecialized physicalactivity instruction andormental health evaluation

Attitude toward lifestyle changeAttitude toward taking life-long

vitamin supplementation

BMI body mass index

bdt

B

tddpatsacrMo

cfvpg

memeimhm

V

Anadattth

R

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S75L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Table 3 Suggested postoperative follow-upTable 4 Suggested biochemical monitoring tools for

nutrition statusTable 5 Suggested postoperative vitamin supplemen-

tation

These suggestions included in Tables 1-5 have beenased on committee consensus and current research that hasocumented the pre- and postoperative likelihood of nutri-ion deficiency [1ndash18]

iochemical monitoring for nutrition status (Table 4)

Deficiencies of single vitamins are less often encounteredhan those of multiple vitamins Although proteinndashcalorie un-ernutrition can result in concurrent vitamin deficiency mosteficiencies are associated with malabsorption andor incom-lete digestion related to negligible gastric acid and pepsinlcoholism medications hemodialysis total parenteral nutri-ion food faddism or inborn errors of metabolism Bariatricurgery procedures specifically alter the absorption pathwaysndor dietary intake Symptoms of vitamin deficiency areommonly nonspecific and physical examination might not beeliable for early diagnosis without laboratory confirmation

ost characteristic physical findings are seen late in the coursef nutrient deficiency [17]

Laboratory markers are considered imperative forompleting the initial nutrition assessment and follow-upor surgical weight loss patients Established baselinealues are important when trying to distinguish betweenostoperative complications deficiencies related to sur-

able 2uggested Preoperative Nutrition Education

ecommended Su

iscussincludeImportance of taking personal responsibility for self-

care and lifestyle choicesTechniques for self-monitoring and keeping daily food

journalPreoperative diet preparation (if required by program)

ReBe

ostoperative intake CoAdequate hydrationTexture progressionVitaminmineral supplementsProtein supplementsMeal planning and spacingAppropriate carbohydrate protein and fat intake and

foodfluid choices to maximize safe weight lossnutrient intake and tolerance

Concepts of intuitive eatingTechniques and tips to maximize food and fluid

tolerancePossibility of nutrient malabsorption and importance of

supplement compliancePossibility of weight regain

DNAEfReStDReCoDFlLaA

ery noncompliance with recommended nutrient supple- c

entation or nutritional complications arising from pre-xisting deficiencies Additional laboratory measuresight be required and are defined by the presence of the

xisting individual co-morbid conditions They are notncluded in Table 4 Table 4 is a sample of laboratoryeasures that programs might consider using to compre-

ensively monitor patientsrsquo nutrition status It is not aandate or guideline for laboratory testing

itamin supplementation (Table 5)

Table 5 is an example of a supplementation regimens advances are made in the field of bariatrics andutrition updates regarding supplementation suggestionsre expected This information is intended for life-longaily supplementation for routine postoperative patientsnd is not intended to treat deficiencies Information onreating deficiencies can be found in the Appendix ldquoIden-ifying and Treating Micronutrient Deficienciesrdquo A pa-ientrsquos individual co-morbid conditions or changes inealth status might require adjustments to this regimen

ationale for recommendations

mportance of multivitamin and mineral supplementation

It is common knowledge that a comprehensive bariatricrogram includes nutritional supplementation guidanceoutine monitoring of the patientrsquos physicalmental well-eing laboratory values and frequent counseling to rein-orce nutrition education behavior modification and prin-

d Other considerations

goal settingf physical activity

Appropriate monitoring of weight loss

complaints Long-term maintenanceionomiting

ketosishungerstruction from foodsyndrome

hypoglycemiaionsteatorrheaebowel soundsntolerance

Self-monitoringNutrient dense food choices for

disease preventionRestaurantsLabel readingHealthy cooking techniquesRelapse management

ggeste

alisticnefits o

mmonehydratauseavnorexiafects ofturn of

omal obumpingactivenstipat

iarrheaatulencctose i

lopecia

iples of responsible self-care As the popularity of surgical

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S76 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nterventions for morbid obesity continues to grow concerns increasing regarding the long-term effects of nutritionaleficiencies Nutritional complications that remain undiag-osed and untreated can lead to adverse health conse-uences and loss of productivity The benefits of weight lossurgery must be balanced against the risk of developingutritional deficiencies to provide appropriate identificationreatment and prevention

Vitamins and minerals are essential factors and co-fac-ors in numerous biological processes that regulate bodyize They include appetite hunger nutrient absorptionetabolic rate fat and sugar metabolism thyroid and adre-

al function energy storage glucose homeostasis neuralctivities and others Thus micronutrient ldquorepletionrdquomeaning the body has sufficient amounts of vitamins andinerals to perform these functions) is not only important

or good health but also for maximal weight loss successnd long-term weight maintenance

Obtaining micronutrients from food is the most desirableay to ensure the body has sufficient amounts of vitamins

nd minerals However some experts have suggested that

able 3uggested Postoperative Nutrition Follow-up

ecommended Sugge

nthropometricCurrent and accurate height weight BMI and

percentage of excess body weightOvera

iochemical ActiviReview laboratory findings when available Amou

freq

edication reviewEncourage patients to follow-up with PCP regarding

medications that treat rapidly resolving co-morbidities (eg hypertension diabetes mellitus)

itaminmineral supplementsAdherence to protocol

ietary intakeUsual or actual daily intakeProtein intakeFluid intakeAssess intake of anti-obesity foodsFood texture complianceFood tolerance issues (eg nauseavomiting

ldquodumpingrdquo)Appropriate diet advanceAddress individual patient complaintsAddress lifestyle and educational needs for long

term weight loss maintenance

Estimaactu

Reinfoimp

Appro

BMI body mass index PCP primary care physician

ost individuals in our ldquofast-paced eat-outrdquo society fail to a

onsume sufficient amounts of unprocessed foods that areigh in vitamins and minerals such as fruits and vegetablessh and other protein sources dairy products whole grainsuts and legumes Poor dietary selection and habits coupledith the reduced vitamin and mineral content of foods can

ead to micronutrient deficiencies among the general publichat interfere with body weight control increasing the riskf weight gain and obesity Therefore a daily vitamin andineral supplement is likely to be of value in ensuring

dequate intake of micronutrients for maximal functioningf those processes that help to regulate appropriate bodyeightTaking daily micronutrient supplements and eating foods

igh in vitamins and minerals are important aspects of anyuccessful weight loss program For the morbidly obeseaking vitamin and mineral supplements is essential forppropriate micronutrient repletion both before and afterariatric surgery Studies have found that 60ndash80 of mor-idly obese preoperative candidates have defects in vitamin

[19ndash22] Such defects would reduce dietary calcium

Other considerations

of well-being Use of contraception to avoidpregnancy

Psychosocial intensity andf activity

Changing relationship with foodChanges in support systemStress managementBody image

oric intake of usual oreitive eating style to

od toleranceeal planning

Promote anti-obesity foodscontaining

Omega-3 fatty acidsHigh fiberLean quality protein sourcesWhole fruits and vegetablesFoods rich in phytochemicals and

antioxidantsLow-fat dairy (calcium)Discourage pro-obesity processed

foods containingRefined carbohydratesTrans and saturated fatty acids

sted

ll sense

ty levelnt typeuency o

ted calal intakrce inturove fopriate m

bsorption and increase a substance known as calcitriol

Table 4Suggested Biochemical Monitoring Tools for Nutrition Status

Vitaminmineral Screening Normal range Additional laboratoryindexes

Critical range Preoperative deficiency Postoperativedeficiency

Comments

B1 (thiamin) Serum thiamin 10ndash64 ngmL 2RBC transketolase1Pyruvate

Transketolase activity20

Pyruvate 1 mgdL

15ndash29 more common inAfrican Americans andHispanics oftenassociated with poorhydration

Rare but occurs withRYGB AGB andBPDDS

Serum thiamin responds todietary supplementationbut is poor indicator oftotal body stores

B6 (pyridoxine) PLP 5ndash24 ngmL RBC glutamic pyruvateOxaloacetic

PLP 3 ngmL Unknown Rare Consider with unresolvedanemia diabetes couldinfluence valuestransaminase

B12 (cobalamin) Serum B12 200ndash1000 pgmL 1Serum and urinaryMMA

1Serum tHcy

Serum B12

200 pgmL deficiency400 pgmL

suboptimalsMMA 0376 molLMMA 36 mol

mmol CRTtHcy 132 molL

10ndash13 may occur witholder patients and thosetaking H2 blockers andPPIs

Common withRYGB in absenceofsupplementation12ndash33

When symptoms arepresent and B12 200ndash250 pgmL MMA andtHcy are useful serumB12 may miss 25ndash30of deficiency cases

Folate RBC folate 280ndash791 ngmL Urinary FIGLUNormal serum andurinary MMA1Serum tHcy

RBC folate305 nmolL

deficiency227 nmolL anemia

Uncommon Uncommon Serum folate reflectsrecent dietary intakerather than folate statusRBC folate is a moresensitive marker

Excessive supplementationcan mask B12 deficiencyin CBC neurologicsymptoms will persist

Iron Ferritin Males15ndash200 ngmLFemales12ndash150 ngmL

2Serum iron1TIBC

Ferritin 20 ngmLSerum iron 50 gdLTIBC 450 gdL

9ndash16 of adult women ingeneral population aredeficient

20ndash49 of patientscommon withRYGB formenstruatingwomen (51) andpatients with superobesity (49ndash52)

Low Hgb and Hct areconsistent with irondeficiency anemia instage 3 or stage 4anemia ferritin is anacute phase reactant andwill be elevated withillness andorinflammation oralcontraceptives reduceblood loss formenstruating females

Vitamin A Plasma retinol 20ndash80 gdL RBP Plasma retinol 10gdL

Uncommon up to 7 insome studies

Common (50) withBPDDS after 1 yrup to 70 at 4 yrmay occur withRYGBAGB

Ocular finding maysuggest diagnosis

S77L

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Table 4Continued

Vitaminmineral Screening Normal range Additional laboratoryindexes

Critical range Preoperative deficiency Postoperativedeficiency

Comments

Vitamin D 25(OH)D 25ndash40 ngmL 2Serum phosphorus1Alkaline phosphatase1Serum PTH2Urinary calcium

Serum 25(OH)D 20ngmL suggestsdeficiency 20ndash30 ngmL suggestsinsufficiency

Common 60ndash70 Common with BPDDS after 1 yr mayoccur with RYGBprevalenceunknown

With deficiency serumcalcium may be low ornormal serumphosphorus maydecrease serum alkalinephosphatase increasesPTH elevated

Vitamin E Plasma alphatocopherol

5ndash20 gmL Plasma lipids 5 gmL Uncommon Uncommon Low plasma alphatocopherol to plasmalipids (08 mgg totallipid) should be usedwith hyperlipidemia

Vitamin K PT 10ndash13 seconds 1DCP 2Plasmaphylloquinone

Variable Uncommon Common with BPDDS after 1 yr

PT is not a sensitivemeasure of vitamin Kstatus

Zinc Plasma zinc 60ndash130 gdL 2RBC zinc Plasma zinc 70 gdL Uncommon but increasedrisk of low levelsassociated with obesity

Common with BPDDS after 1 yr mayoccur with RYGB

Monitor albumin levelsand interpret zincaccordingly albumin isprimary binding proteinfor zinc no reliablemethod of determiningzinc status is availableplasma zinc is methodgenerally used studiescited in this report didnot adequately describemethods of zinc analysis

Protein Serum albuminSerum totalprotein

4ndash6 gdL6ndash8 gdL

2Serum prealbumin(transthyretin)

Albumin 30 gdLPrealbumin 20 mgdL

Uncommon Rare but can occurwith RYGB AGBand BPDDS ifprotein intake islow in total intakeor indispensableamino acids

Half-life for prealbumin is2ndash4 d and reflectschanges in nutritionalstatus sooner thanalbumin a nonspecificprotein carrier with ahalf-life of 22 d

RYGB Roux-en-Y gastric bypass AGB adjustable gastric banding BPDDS biliopancreatic diversionduodenal switch PLP pyridoxal-5rsquo-phosphate RBC red blood cell MMA methylmalonic acid tHcy total homocysteine CRT creatinine PPIs protein pump inhibitors FIGLU formiminogluatmic acid CBC complete blood count TIBC total iron binding capacityHgb hemoglobin Hct hematocrit RPB retinol binding protein PTH parathyroid hormone 25(OH)D 25-hydroxyvitamin D PT prothrombin time DCP des-gamma-carboxypromthrom-bin

In general laboratory values should be reviewed annually or as indicated by clinical presentation Laboratory normal values vary among laboratory settings and are method dependent This chart providesa brief summary of monitoring tools See the Appendix for additional detail and diagnostic tools

copy Jeanne Blankenship MS RD Used with permission

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S79L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able 5uggested Postoperative Vitamin Supplementation

upplement AGB RYGB BPDDS Comment

ultivitamin-mineral supplementA high-potency vitamin containing 100 of daily value for

at least 23 of nutrients100 of daily

value

200 of dailyvalue

200 of daily value Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to whole tabletcapsule as toleratedAvoid time-released supplementsAvoid enteric coatingChoose a complete formula with at least 18 mg iron 400

g folic acid and containing selenium and zinc in eachserving

Avoid childrenrsquos formulas that are incompleteMay improve gastrointestinal tolerance when taken close to

food intakeMay separate dosageDo not mix multivitamin containing iron with calcium

supplement take at least 2 hr apartIndividual brands should be reviewed for absorption rate and

bioavailabilitySpecialized bariatric formulations are available

dditional cobalamin (B12)Available forms include sublingual tablets liquid drops

mouth spray or nasal gelsprayIntramuscular injection mdash 1000 gmo mdash Begin 0ndash3 mo after

surgeryOral tablet (crystalline form) mdash 350ndash500 gd mdashSupplementation after AGB and BPDDS may be required

dditional elemental calciumChoose a brand that contains calcium citrate and vitamin D3

Begin with chewable or liquidProgress to whole tabletcapsule as tolerated

1500 mgd 1500ndash 2000 mgd 1800ndash 2400 mgd May begin on day 1after hospitaldischarge orwithin 1 mo aftersurgery

Split into 500ndash600 mg doses be mindful of serving size onsupplement label

Space doses evenly throughout daySuggest a brand that contains magnesium especially for

BPDDSDo not combine calcium with iron containing supplements

To maximize absorptionTo minimize gastrointestinal intoleranceWait 2 h after taking multivitamin or iron supplement

Promote intake of dairy beverages andor foods that aresignificant sources of dietary calcium in addition torecommended supplements up to 3 servings daily

Combined dietary and supplemental calcium intake 1700mgd may be required to prevent bone loss during rapidweight loss

dditional elemental iron (above that provided by mvi)Recommended for menstruating women and those at risk of

anemia (total goal intake 50-100 mg elemental irond)

mdash Add a minimumof 18ndash27 mgdelemental

Add a minimum of18ndash27 mgdelemental

Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to tablet as toleratedDosage may need to be adjusted based on biochemical

markersNo enteric coatingDo not mix iron and calcium supplements take 2 h apartAvoid excessive intake of tea due to tannin interactionEncourage foods rich in heme iron

Vitamin C may enhance absorption of non-heme iron sources

wa

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S80 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hich in turn causes metabolic changes that favor fatccumulation [23ndash25]

Several of the B-complex vitamins important for appro-riate metabolism of carbohydrate and neural functions thategulate appetite have been found to be deficient in someatients with morbid obesity [212627] Iron deficiencieshich would significantly hinder energy use have been

eported in nearly 50 of morbidly obese preoperativeandidates [21] Zinc and selenium deficits have been re-orted as well as deficits in vitamins A E and C allmportant antioxidants helpful in regulating energy produc-ion and various other processes of body weight manage-ent [1926ndash28]The risk of micronutrient depletion continues to be quite

igh particularly after surgeries that affect the digestion andbsorption of nutrients such as Roux-en-Y gastric bypassRYGB) and biliopancreatic diversion with or without du-denal switch (BPDDS) RYGB increases the risk of vita-in B12 and other B vitamin deficits in addition to iron and

alcium BPDDS procedures may also cause an increasedisk of iron and calcium deficits along with significant

able 5ontinued

upplement AGB

at-soluble vitaminsWith all procedures higher maintenance doses may be

required for those with a history of deficiencyWater-soluble preparations of fat-soluble vitamins are

availableRetinol sources of vitamin A should be used to calculatedosageMost supplements contain a high percentage of beta

carotene which does not contribute to vitamin A toxicityIntake of 2000 IU Vitamin D3 may be achieved with careful

selection of multivitamin and calcium supplementsNo toxic effect known for vitamin K1 phytonadione

(phyloquinone)

mdash

mdash

mdash

Vitamin K requirement varies with dietary sources andcolonic production

Caution with vitamin K supplementation for patientsreceiving coagulation therapy

Vitamin E deficiency has been suggested but is notprevalent in published studies

ptional B complexB-50 dosageLiquid form is available

1 servi

Avoid time released tabletsNo known risk of toxicityMay provide additional prophylaxis against B-vitamin

deficiencies including thiamin especially for BPDDSprocedures as water-soluble vitamins are absorbed in theproximal jejunum

Note 1000 mg of supplemental folic acid provided incombination with multivitamins could mask B12

deficiency

Abbreviations as in Table 4

eficiencies in the fat-soluble vitamins A D E and K d

hich are important for driving many of the biologicalrocesses that help to regulate body size [29ndash31] As theate of noncompliance with prophylactic multivitamin sup-lementation increases the rate of postoperative deficiencyay increase almost twofold [32]In the past it has been thought that the specific nutri-

ional deficiencies commonly seen among malabsorptiverocedures would not be present in patients choosing aurely restrictive surgery such as the adjustable gastric bandAGB) However poor eating behavior low nutrient-denseood choices food intolerance and a restricted portion sizean contribute to potential nutrient deficiencies in theseatients as well Although the incidence of nutritional com-lications may be less frequent in this patient population itould be detrimental to assume that they do not existIt is important for the bariatric patient to take vitamin and

ineral supplements not only to prevent adverse healthonditions that can arise after surgery but because someutrients such as calcium can enhance weight loss and helprevent weight regain The nutrient deficiency might beroportional to the length of the absorptive area bypassed

RYGB BPDDS Comment

mdash

mdash

mdash

10000 IU of vitamin A

2000 IU of vitamin D

300 g of vitamin K

May begin 2ndash4weeks aftersurgery

1 servingd 1 servingd May begin on day 1after hospitaldischarge

ngd

uring surgical procedures and to a lesser extent to the

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S81L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ercentage of weight lost Iron vitamin B12 and vitamin Deficiencies along with changes in calcium metabolism areommon after RYGB Protein fat-soluble vitamin andther micronutrient deficiencies as well as altered calciumetabolism are most notably found after BPDDS Folate

eficiency has been reported after AGB [33] Thiamin de-ciency is common among all surgical patients with fre-uent vomiting regardless of the type of procedure per-ormed Because many nutritional deficiencies progressith time patients should be monitored frequently and

egularly to prevent malnutrition [29] Reinforcement ofupplement compliance at each patient follow-up is alsomportant in the fight to enhance nutrition status and preventutritional complications

eight loss and nutrient deficits restrictionersus malabsorption

Malabsorptive procedures such as the BPDDS arehought to cause weight loss primarily through the malab-orption of macronutrients with as much as 25 of proteinnd 72 of fat malabsorbed Such primary malabsorptionesults in concomitant malabsorption of micronutrients3435] Vitamins and minerals relying on fat metabolismncluding vitamins D A E K and zinc may be affectedhen absorption is impaired [36] The decrease in gastro-

ntestinal transit time may also result in secondary malab-orption of a wide range of micronutrients related to by-assing the duodenum and jejunum or limited contact withhe brush border secondary to a short common limb Othericronutrient deficiency concerns reported for patients

hoosing a procedure with malabsorptive features includeron calcium vitamin B12 and folate

Nutrient deficiencies after RYGB can result from eitherrimary or secondary malabsorption or from inadequateietary intake A minimal amount of macronutrient malab-orption is thought to occur However specific micronutri-nts appear to be malabsorbed postoperatively and presents deficiencies without adequate vitamin and mineral sup-lementation Retrospective analyses of patients who havendergone gastric bypass have revealed predictable micro-utrient deficiencies including iron vitamin B12 and folate2627ndash39] Case reports have also shown that thiamin de-ciency can develop especially when persistent postopera-

ive vomiting occurs [40ndash43]Few studies that measure absorption after measured and

uantified intake have been published It can be hypothe-ized that the bypassed duodenum and proximal jejunumegatively affect nutrient assimilation Bradley et al [44]tudied patients who had undergone total gastrectomy therocedure from which the RYGB evolved The researchersound that most nutritional status changes in patients wereost likely due to changes in intake versus malabsorptionhese balance studies were conducted in a controlled re-

earch setting however they did not measure pre- and c

ostoperative changes nor include radioisotope labeling toeasure absorption of key nutrients and the subjects had

ndergone the procedure for reasons other than weight lossIt is unclear whether intestinal adaptation occurs after

ombination procedures and to what degree it affects long-erm weight maintenance and nutrition status Adaptation iscompensatory response that follows an abrupt decrease inucosal surface area and has been well studied in short-

owel patients who require bowel resection [45] The pro-ess includes both anatomic and functional changes thatncrease the gutrsquos digestive and absorptive capacity Al-hough these changes begin to take place in the early post-perative period total adaptation may take up to three yearso complete Adaptation in gastric bypass has not beenonsidered in absorption or metabolic studies This consid-ration could be important even when determining early andate macro- and micronutrient intake recommendations Theffect of pancreatic enzyme replacement therapy on vitaminnd mineral absorption in this population is also unknown

Purely restrictive procedures such as the AGB can resultn micronutrient deficiencies related to changes in dietaryntake It is commonly accepted that because no alteration isade in the absorptive pathway malabsorption does not

ccur as a result of AGB procedures However nutrienteficits would be likely to occur because of the low nutrientntake and avoidance of nutrient-rich foods in the earlyonths postoperatively and later possibly as a result of

xcessive band restriction Food with high nutritional valueuch as meat and fibrous fresh fruits and vegetables mighte poorly tolerated

Literature has been published that addresses the effect ofalabsorptive restrictive and combination surgical proce-

ures on acute and long-term nutritional status These stud-es have attempted for the most part to indirectly determinehe surgical impact on nutrition status by the evaluation ofetabolic and laboratory markers Although some studies

ave included certain aspects of absorption few have in-luded the necessary components to evaluate absorption ofprescribed andor monitored diet in a controlled metabolic

ettingThe following sections examine the pre- and postopera-

ive risks for nutritional deficiencies associated with RYGBPDDS and AGB It is important for all members of theedical team to increase their awareness of the nutritional

omplications and challenges that lie ahead for the patientontinued review of current research by the medical team

egarding advances in nutrition science beyond the bound-ries of the present report cannot be emphasized enough

hiamin (vitamin B1)

Beriberi is a thiamin deficiency that can affect variousrgan systems including the heart gastrointestinal tractnd peripheral and central nervous systems Although the

ondition is generally considered rare a number of reported

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S82 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nd possibly a much greater number of unreported or un-iagnosed cases of beriberi have occurred among individ-als who have undergone surgery for morbid obesity Earlyetection and prompt treatment of thiamin deficits in thesendividuals can help to prevent serious health consequencesf beriberi is misdiagnosed or goes undetected for even ahort period the bariatric patient can develop irreversibleeuromuscular disorders permanent defects in learning andhort-term memory coma and even death Because of theife-altering and potentially life-threatening nature of a thi-min deficiency it is important that healthcare professionalsn the field of bariatric surgery have knowledge of thetiology of the condition and its signs and symptomsreatment and prevention

tiology of potential deficiency Thiamin is a water-solubleitamin that is absorbed in the proximal jejunum by anctive (saturable high-affinity) transport system [4647] Inhe body thiamin is found in high concentrations in therain heart muscle liver and kidneys However withoutegular and sufficient intake these tissues become rapidlyevoid of thiamin [4647] The total amount of thiamin inhe body of an adult is approximately 30 mg with a half-lifef only 9ndash18 days Persistent vomiting a diet deficient inhe vitamin or the bodyrsquos excessive utilization of thiaminse can result in a severe state of thiamin depletion withinnly a short period producing symptoms of beriberi46ndash48]

Bariatric surgery increases the risk of beriberi through ex-cerbation of pre-existing thiamin deficits low nutrient intakealabsorption and episodes of nausea and vomiting [49ndash51]hronic or acute thiamin deficiencies in bariatric patients oftenresent with symptoms of peripheral neuropathy or Wer-ickersquos encephalopathy and Korsakoffrsquos psychoses [2148ndash4] Early diagnosis of the signs and symptoms of these con-itions is extremely important to prevent serious adverse healthonsequences Even if treatment is initiated recovery can bencomplete with cognitive andor neuromuscular impairmentsersisting long term or permanently

igns symptoms and treatment of deficiency (seeppendix Table A1)

reoperative risk The risk of the development of beriberifter bariatric surgery is far greater for individuals present-ng for surgery with low thiamin levels Investigators at theleveland Clinic of Florida reported that 15 of their pre-perative bariatric patients had deficiencies in thiamin be-ore surgery [52] A study by Flancbaum et al [21] similarlyound that 29 of their preoperative patients had low thia-in levels Data obtained by that study also showed a

ignificant difference between ethnicity and preoperativehiamin levels Although only 67 of whites presentedith thiamin deficiencies before surgery nearly one third

31) of African Americans and almost one half (47) of

ispanics had thiamin deficits The results of these studies S

uggested a need for preoperative thiamin testing as well ashiamin repletion by diet or supplementation to reduce theisk of ldquobariatricrdquo beriberi postoperatively

ostoperative risk Beriberi has been observed after gastricestrictive and malabsorptive procedures A number of casesf Wernicke-Korsakoff syndrome (WKS) as well as periph-ral neuropathy have been reported for patients havingndergone vertical banded gastroplasty [53ndash61] A fewncidences of WKS have also been reported after AGB436263] Additionally reports of thiamin deficiencies and

KS after RYGB [404164ndash73] and several cases of WKSnd neuropathy in patients who had undergone BPD [74]ave been published Many more cases of WKS are be-ieved to have occurred with bariatric procedures that haveither not been reported or have been misdiagnosed becausef limited knowledge regarding the signs and symptoms ofcute or severe thiamin deficits Because many foods areortified with thiamin beriberi has been nearly eradicatedhroughout the world except for patients with severe alco-olism severe vomiting during pregnancy (hyperemesisravidarium) or those malnourished and starved For thiseason few healthcare professionals until recently havead a patient present with beriberi

According to the published reports of thiamin deficitsfter bariatric procedures most patients develop such defi-iencies in the early postoperative months after an episodef intractable vomiting Nausea and vomiting are relativelyommon after all bariatric procedures early in the postop-rative period Thiamin stores in the body are small andaintenance of appropriate thiamin levels requires daily

eplenishment A deficiency of thiamin for only a couple ofeeks or less caused by persistent vomiting can deplete

hiamin stores Symptoms of WKS were reported in aYGB patient after only two weeks of persistent vomiting

67]Bariatric beriberi can also develop in postoperative patients

ho are given infusate containing dextrose without thiaminnd other vitamins which is often the case for patients inritical care units postoperative patients with complicationsnterfering with the ingestion of food or patients dehydratedrom persistent vomiting Malnutrition caused by a lack ofppetite and dietary intake postoperatively also contributes toariatric beriberi as does noncompliance in taking postopera-ive vitamin supplements

Although most cases of beriberi occur in the early post-perative periods cases of patients with severe thiamineficiency more than one year after surgery have beeneported One study reported WKS in association with al-ohol abuse 13 years after RYGB [75] Other conditionsontributing to late cases of bariatric beriberi include ahiamin-poor diet a diet high in carbohydrates anorexiand bulimia [46ndash48]

uggested supplementation Because of the greater likeli-

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S83L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ood of low dietary thiamin intake patients should be sup-lemented with thiamin This is usually accomplishedhrough daily intake of a multivitamin Most multivitaminsontain thiamin at 100 of the daily value Patients havingpisodes of nausea and vomiting and those who are anorec-ic might require sublingual intramuscular or intravenoushiamin to avoid depletion of thiamin stores and beriberiaution should be used when infusing bariatric patientsith solutions containing dextrose without additional vita-ins and thiamin because an increase in glucose utilizationithout additional thiamin can deplete thiamin stores [76]Thiamin deficiency in bariatric patients is treated with

hiamin together with other B-complex vitamins and mag-esium for maximal thiamin absorption and appropriateeurologic function [46 ndash 48] Early symptoms of neuropa-hy can often be resolved by providing the patient with oralhiamin doses of 20ndash30 mgd until symptoms disappear Forore advanced signs of neuropathy or for individuals with

rotracted vomiting 50ndash100 mgd of intravenous or intra-uscular thiamin may be necessary for resolution or im-

rovement of symptoms or for the prevention of suchatients with WKS generally require 100 mg thiamindministered intravenously for several days or longer fol-owed by intramuscular thiamin or high oral doses untilymptoms have resolved or significantly improved This canequire months to years Some patients might have to takehiamin for life to prevent the reoccurrence of neuropathy

itamin B12 and folate

Vitamin B12 (cobalamin) and folate (folic acid) are bothnvolved in the maturation of red blood cells and are com-only discussed in the literature together Over time a

eficiency in either vitamin B12 or folate can lead to mac-ocytic anemia a condition characterized by the productionf fewer but larger red blood cells and a decreased abilityo carry oxygen Most (95) cases of megaloblastic anemiacharacterized by large immature abnormal undifferenti-ted red blood cells in bone marrow) are attributed toitamin B12 or folate deficiency [77]

itamin B12

tiology of potential deficiency RYGB patients have bothncomplete digestion and release of vitamin B12 from pro-ein foods With a significant decrease in hydrochloric acidepsinogen is not converted into pepsin which is necessaryor the release of vitamin B12 from protein [78] BecauseGB patients have an artificial restriction yet complete usef the stomach and BPD patients do not have as great aestriction in stomach capacity and parietal cells as RYGBatients the reduction in hydrochloric acid and subsequentitamin B12 deficiency is not as prevalent with these tworocedures

Intrinsic factor (IF) is produced by the parietal cells of

he stomach and in certain conditions (eg atrophic gastri- a

is resected small bowel elderly patients) can be impairedausing an IF deficiency Subsequent vitamin B12 deficiencypernicious anemia) occurs without IF production or useecause IF is needed to absorb vitamin B12 in the terminalleum [77] Factors that increase the risk of vitamin B12

eficiency relevant to bariatric surgery include the follow-ng

An inability to release protein-bound vitamin B12

from food particularly in hypochlorhydria andatrophic gastritis

Malabsorption due to inadequate IF in perniciousanemia

Gastrectomy and gastric bypassResection or disease of terminal ileumLong-term vegan dietMedications such as neomycin metformin colch-

icines medications used in the management ofbowel inflammation and gastroesophageal refluxand ulcers (eg proton pump inhibitors) and anti-convulsant agents [79]

Cobalamin stores are known to exist for long periods3ndash5 yr) and are dependent on dietary repletion and dailyepletion However gastric bypass patients have both aecreased production of stomach acid and a decreased avail-bility of IF thus a vitamin B12 deficiency could developithout appropriate supplementation Because the typical

bsorption pathway cannot be relied on the surgical weightoss patient must rely on passive absorption of B12 whichccurs independent of IF

igns symptoms and treatment of deficiency (seeppendix Table A3)

reoperative risk Several medications common to preop-rative bariatric patients have been noted to affect preoper-tive vitamin B12 absorption and stores Of patients takingetformin 10ndash30 present with reduced vitamin B12 ab-

orption [80] Additionally patients with obesity have aigh incidence of gastroesophageal reflux disease for whichhey take proton pump inhibitors thus increasing the poten-ial to develop a vitamin B12 deficiency

Flancbaum et al [21] conducted a retrospective study of79 (320 women and 59 men) pre-operative patients Vita-in B12 deficiency was reported as negative in all patients

f various ethnic backgrounds [21] No clinical criteria orymptoms for vitamin B12 deficiency were noted In theeneral population 5ndash10 present with neurologic symp-oms with vitamin B12 levels of 200ndash400 pgmL Amongreoperative gastric bypass patients Madan et al [27] foundhat 13 (n 59) of patients were deficient in vitamin B12n a comparison of patients presenting for either RYGB orPD Skroubis et al [81] recently reported that preoperativeitamin B12 levels were low-normal in both groups Itould be prudent to screen for and treat IF deficiency

ndor vitamin B12 deficiency in all patients preoperatively

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S84 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ut it is essential for RYGB patients so as not to hasten theevelopment of a potential postoperative deficiency

ostoperative risk Vitamin B12 deficiency has been fre-uently reported after RYGB Schilling et al [82] estimatedhe prevalence of vitamin B12 deficiency to be 12ndash33ther researchers have suggested a much greater prevalencef B12 deficiency in up to 75 of postoperative RYGBatients however most reports have cited approximately5 of postoperative RYGB patients as vitamin B12 defi-ient [82ndash87] Brolin et al [87] reported that low levels ofitamin B12 might be seen as soon as six months afterariatric surgery but most often occurring more than oneear postoperatively as liver stores become depleted Sk-oubis et al [88] predicted that the deficiency will mostikely occur 7 months after RYGB and 79 months afterPDDS although their research did not consider compro-ised preoperative status and its correlation to postopera-

ive deficiency After the first postoperative year the prev-lence of vitamin B12 deficiency appears to increase yearlyn RYGB patients [89]

Although the bodyrsquos storage of vitamin B12 is significant2000 g) compared with daily needs (24 gd) thisarticular deficiency has been found within 1ndash9 years ofastric bypass surgery [29] Brolin et al [84] reported thatne third of RYGB patients are deficient at four yearsostoperatively However non-surgical variables were notxplored and many patients might have had preoperativealues near the lower end of the normal range Ocon Bretont al [90] compared micronutrient deficiencies among two-ear postoperative BPDDS and RYGB patients and foundhat all nutritional deficiencies were more common amongPDDS patients except for vitamin B12 for which theeficiency was more common among the RYGB patientstudied A lack of B12 deficiency among BPDDS patientsight result from a better tolerance of animal proteins in a

arger pouch greater pepsingastric acid production to re-ease protein-bound B12 and increased availability and in-eraction of IF with the pouch contents

Experts have noted the significance of subclinical defi-iency in the low-normal cobalamin range in nongastricypass patients who do not exhibit clinical evidence ofeficiency The methylmalonic acid (MMA) assay is thereferred marker of B12 status because metabolic changesften precede low B12 levels in the progression to defi-iency Serum B12 assays may miss as much as 25ndash30 of

12 deficiencies making them less reliable than the MMAssay [91] It has been suggested that early signs of vitamin

12 deficiency can be detected if the serum levels of bothMA and homocysteine are measured [91] Vitamin B12

eficiency after RYGB has been associated with megalo-lastic anemia [92] Some vitamin B12-deficient patientsevelop significant symptoms such as polyneuropathy par-

sthesia and permanent neural impairment On occasion

ome patients may experience extreme delusions halluci-ations and even overt psychosis [93]

uggested supplementation Because of the frequent lack ofymptoms of vitamin B12 deficiency the suggested dili-ence in following up or treating these values among thosesymptomatic patients has been questioned The decisionot to supplement or routinely screen patients for B12 defi-iency should be examined very carefully given the risk ofrreversible neurologic damage if vitamin B12 goes un-reated for long periods At least one case report has beenublished of an exclusively breastfed infant with vitamin

12 deficiency who was born of an asymptomatic motherho had undergone gastric bypass surgery [94]Deficiency of vitamin B12 is typically defined at levels

200 pgmL However about 50 of patients with obviousigns and symptoms of deficiency have normal vitamin B12

evels [31] Kaplan et al [95] reported that vitamin B12

eficiency usually resolves after several weeks of treatmentith 700ndash2000 gwk Rhode et al [96] found that aosage of 350ndash600 gd of oral B12 prevented vitamin B12

eficiency in 95 of patients and an oral dose of 500 gdas sufficient to overcome an existing deficiency as re-orted by Brolin et al [87] in a similar study Thereforeupplementation of RYGB patients with 350ndash500 gd mayrevent most postoperative vitamin B12 deficiency

While most vitamin B12 in normal adults is absorbed inhe ileum in the presence of IF approximately 1 of sup-lemented B12 will be absorbed passively (by diffusion)long the entire length of the (non-bypassed) intestine byurgical weight loss patients given a high-dose oral supple-ent [97] Thus the consumption of 350ndash500 g yields a

5ndash50-g absorption which is greater than the daily re-uirement Although the use of monthly intramuscular in-ections or a weekly oral dose of vitamin B12 is commonmong practices it relies on patient compliance Practitio-ers should assess the patientrsquos preference and the potentialor compliance when considering a daily weekly oronthly regimen of B12 supplementation In addition to oral

upplements or intramuscular injections nasal sprays andublingual sources of vitamin B12 are also available Pa-ients should be monitored closely for their lifetime becauseevere anemia can develop with or without supplementation98]

olate

tiology of potential deficiency Factors that increase theisk of folic acid deficiency relevant to bariatric surgerynclude the following

Inadequate dietary intakeNoncompliance with multivitamin supplementationMalabsorptionMedications (anticonvulsants oral contraceptives

and cancer treating agents) [79]

pmo

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S85L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Folic acid stores can be depleted within a few monthsostoperatively unless replenished by a multivitamin supple-ent and dietary sources (ie green leafy vegetables fruits

rgan meats liver dried yeast and fortified grain products)

igns symptoms and treatment of deficiency (seeppendix Table A4)

reoperative risk The goals of the 1998 Food and Drugdministration policy requiring all enriched grain products

o be fortified with folate included increasing the averagemerican diet by 100 g folate daily and decreasing the

ate of neural tube defects in childbearing women [99]entley et al [100] reported that the proportion of womenged 15ndash44 years old (in the general population) who meethe recommended dietary intake of 400 gd folate variesetween 23 and 33 With the increasing popularity ofigh proteinlow carbohydrate diets one cannot assume thatreoperative patients consume dietary sources of folatehrough fortified grain products fruits and vegetables Boy-an et al [26] found folate deficiencies preoperatively in6 of RYGB patients studied

ostoperative risk Although it has been observed that fo-ate deficiency after RYGB surgery is less common than B12

eficiency and is thought to occur because of decreasedietary or multivitamin supplement intake low serum folateevels have been cited from 6 to 65 among RYGBatients [2686101] Additionally folate deficiencies haveccurred postoperatively even with supplementation Boy-an et al [26] found that 47 (n 17) of RYGB patientsad low folate levels six months postoperatively and 41n 17) had low levels at one year This deficiency oc-urred despite patient adherence to taking a multivitaminupplement that contained at least the daily value for folate00 g [26] Postoperative bariatric patients with rapideight loss might have an increased risk of micronutrienteficiencies MacLean et al [86] reported that 65 ofostoperative patients had low folate levels These sameatients exhibited additional B vitamin deficiencies 24itamin B12 and 50 thiamin [86] An increased risk ofeficiency has also been noted among AGB patients pos-ibly because of decreased folate intake Gasteyger et al33] found a significant decrease in serum folate levels441) between the baseline and 24-month postoperativeeasurementsDixon and OrsquoBrien [101] reported elevated serum ho-

ocysteine levels in patients after bariatric surgery regard-ess of the type of procedure (restrictive or malabsorptive)levated homocysteine levels can indicate not only low

olate levels and a greater risk of neural tube defects but canlso be indicative of an independent risk factor for heartisease andor oxidative stress in the nonbariatric popula-ion [102] However unlike iron and vitamin B12 the folate

ontained in the multivitamin supplementation essentially e

orrects the deficiency in the vast majority of postoperativeariatric patients [103] Therefore persistent folate defi-iency might indicate a patientrsquos lack of compliance withhe prescribed vitamin protocol [32]

It is common knowledge that folic acid deficiency amongregnant women has been associated with a greater risk ofeural tube defects in newborns Consistent supplementa-ion and monitoring among women of child-bearing agencluding pre- and postoperative bariatric patients is vital inn effort to prevent the possibility of neural tube defects inhe developing fetus

Because folate does not affect the myelin of nerveseurologic damage is not as common with folate such as ishe case for vitamin B12 deficiency In contrast patientsith folate deficiency often present with forgetfulness irri-

ability hostility and even paranoid behaviors [29] Similaro that evidenced with vitamin B12 most postoperativeYGB patients who are folate deficient are asymptomatic orave subclinical symptoms therefore these deficient statesay not be easily identified

uggested supplementation Even though folate absorptionccurs preferentially in the proximal portion of the smallntestine it can occur along the entire length of the small bowelith postoperative adaptation Therefore it is generally agreed

hat folate deficiency is corrected with 1000 mgd folic acid32] and is preventable with supplementation that provides00 of the daily value (800 g) This level can also benefithe fetus in a female patient unaware of her postoperativeregnancy Folate supplementation 1000 mgd has noteen recommended because of the potential for maskingitamin B12 deficiency Carmel et al [104] suggested thatomocysteine is the most sensitive marker of folic acidtatus in conjunction with erythrocyte folate Althougholic acid deficiency could potentially occur among post-perative bariatric surgery patients it has not been seenidely in recent studies especially when patients haveeen compliant with postoperative multivitamin supple-entation Therefore it is imperative to closely follow

olic acid both pre- and postoperatively especially inhose patients suspected to be noncompliant with theirultivitamin supplementation

ron

Much of the iron and surgical weight loss research con-ucted to date has been generated from a limited number ofurgeons and scientists however the data have consistentlyointed toward the risk of iron deficiency and anemia afterariatric procedures Iron deficiency is defined as a decreasen the total iron body content Iron deficiency anemia occurshen erythropoiesis is impaired as a result of the lack of

ron stores In the absence of anemia iron deficiency issually asymptomatic Fatigue and a diminished capacity to

xercise however are common symptoms of anemia

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S86 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

tsmp

lsnfwTlopaechc

Rtbwdsaar

fdaiwiiedasdt

Stbadtbpcwl

mccmacdrrT

C

EeamadmsDfd

dbdh7DtnDcwsh

SA

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S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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S88 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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S89L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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S91L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

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S93L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

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S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

ratbrdd

aebaaa

apcptaasosdbc

afciitdmptpcrsPEv

TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

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[

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[

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[

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[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

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S

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T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

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S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

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D

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S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 3: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S75L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Table 3 Suggested postoperative follow-upTable 4 Suggested biochemical monitoring tools for

nutrition statusTable 5 Suggested postoperative vitamin supplemen-

tation

These suggestions included in Tables 1-5 have beenased on committee consensus and current research that hasocumented the pre- and postoperative likelihood of nutri-ion deficiency [1ndash18]

iochemical monitoring for nutrition status (Table 4)

Deficiencies of single vitamins are less often encounteredhan those of multiple vitamins Although proteinndashcalorie un-ernutrition can result in concurrent vitamin deficiency mosteficiencies are associated with malabsorption andor incom-lete digestion related to negligible gastric acid and pepsinlcoholism medications hemodialysis total parenteral nutri-ion food faddism or inborn errors of metabolism Bariatricurgery procedures specifically alter the absorption pathwaysndor dietary intake Symptoms of vitamin deficiency areommonly nonspecific and physical examination might not beeliable for early diagnosis without laboratory confirmation

ost characteristic physical findings are seen late in the coursef nutrient deficiency [17]

Laboratory markers are considered imperative forompleting the initial nutrition assessment and follow-upor surgical weight loss patients Established baselinealues are important when trying to distinguish betweenostoperative complications deficiencies related to sur-

able 2uggested Preoperative Nutrition Education

ecommended Su

iscussincludeImportance of taking personal responsibility for self-

care and lifestyle choicesTechniques for self-monitoring and keeping daily food

journalPreoperative diet preparation (if required by program)

ReBe

ostoperative intake CoAdequate hydrationTexture progressionVitaminmineral supplementsProtein supplementsMeal planning and spacingAppropriate carbohydrate protein and fat intake and

foodfluid choices to maximize safe weight lossnutrient intake and tolerance

Concepts of intuitive eatingTechniques and tips to maximize food and fluid

tolerancePossibility of nutrient malabsorption and importance of

supplement compliancePossibility of weight regain

DNAEfReStDReCoDFlLaA

ery noncompliance with recommended nutrient supple- c

entation or nutritional complications arising from pre-xisting deficiencies Additional laboratory measuresight be required and are defined by the presence of the

xisting individual co-morbid conditions They are notncluded in Table 4 Table 4 is a sample of laboratoryeasures that programs might consider using to compre-

ensively monitor patientsrsquo nutrition status It is not aandate or guideline for laboratory testing

itamin supplementation (Table 5)

Table 5 is an example of a supplementation regimens advances are made in the field of bariatrics andutrition updates regarding supplementation suggestionsre expected This information is intended for life-longaily supplementation for routine postoperative patientsnd is not intended to treat deficiencies Information onreating deficiencies can be found in the Appendix ldquoIden-ifying and Treating Micronutrient Deficienciesrdquo A pa-ientrsquos individual co-morbid conditions or changes inealth status might require adjustments to this regimen

ationale for recommendations

mportance of multivitamin and mineral supplementation

It is common knowledge that a comprehensive bariatricrogram includes nutritional supplementation guidanceoutine monitoring of the patientrsquos physicalmental well-eing laboratory values and frequent counseling to rein-orce nutrition education behavior modification and prin-

d Other considerations

goal settingf physical activity

Appropriate monitoring of weight loss

complaints Long-term maintenanceionomiting

ketosishungerstruction from foodsyndrome

hypoglycemiaionsteatorrheaebowel soundsntolerance

Self-monitoringNutrient dense food choices for

disease preventionRestaurantsLabel readingHealthy cooking techniquesRelapse management

ggeste

alisticnefits o

mmonehydratauseavnorexiafects ofturn of

omal obumpingactivenstipat

iarrheaatulencctose i

lopecia

iples of responsible self-care As the popularity of surgical

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S76 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nterventions for morbid obesity continues to grow concerns increasing regarding the long-term effects of nutritionaleficiencies Nutritional complications that remain undiag-osed and untreated can lead to adverse health conse-uences and loss of productivity The benefits of weight lossurgery must be balanced against the risk of developingutritional deficiencies to provide appropriate identificationreatment and prevention

Vitamins and minerals are essential factors and co-fac-ors in numerous biological processes that regulate bodyize They include appetite hunger nutrient absorptionetabolic rate fat and sugar metabolism thyroid and adre-

al function energy storage glucose homeostasis neuralctivities and others Thus micronutrient ldquorepletionrdquomeaning the body has sufficient amounts of vitamins andinerals to perform these functions) is not only important

or good health but also for maximal weight loss successnd long-term weight maintenance

Obtaining micronutrients from food is the most desirableay to ensure the body has sufficient amounts of vitamins

nd minerals However some experts have suggested that

able 3uggested Postoperative Nutrition Follow-up

ecommended Sugge

nthropometricCurrent and accurate height weight BMI and

percentage of excess body weightOvera

iochemical ActiviReview laboratory findings when available Amou

freq

edication reviewEncourage patients to follow-up with PCP regarding

medications that treat rapidly resolving co-morbidities (eg hypertension diabetes mellitus)

itaminmineral supplementsAdherence to protocol

ietary intakeUsual or actual daily intakeProtein intakeFluid intakeAssess intake of anti-obesity foodsFood texture complianceFood tolerance issues (eg nauseavomiting

ldquodumpingrdquo)Appropriate diet advanceAddress individual patient complaintsAddress lifestyle and educational needs for long

term weight loss maintenance

Estimaactu

Reinfoimp

Appro

BMI body mass index PCP primary care physician

ost individuals in our ldquofast-paced eat-outrdquo society fail to a

onsume sufficient amounts of unprocessed foods that areigh in vitamins and minerals such as fruits and vegetablessh and other protein sources dairy products whole grainsuts and legumes Poor dietary selection and habits coupledith the reduced vitamin and mineral content of foods can

ead to micronutrient deficiencies among the general publichat interfere with body weight control increasing the riskf weight gain and obesity Therefore a daily vitamin andineral supplement is likely to be of value in ensuring

dequate intake of micronutrients for maximal functioningf those processes that help to regulate appropriate bodyeightTaking daily micronutrient supplements and eating foods

igh in vitamins and minerals are important aspects of anyuccessful weight loss program For the morbidly obeseaking vitamin and mineral supplements is essential forppropriate micronutrient repletion both before and afterariatric surgery Studies have found that 60ndash80 of mor-idly obese preoperative candidates have defects in vitamin

[19ndash22] Such defects would reduce dietary calcium

Other considerations

of well-being Use of contraception to avoidpregnancy

Psychosocial intensity andf activity

Changing relationship with foodChanges in support systemStress managementBody image

oric intake of usual oreitive eating style to

od toleranceeal planning

Promote anti-obesity foodscontaining

Omega-3 fatty acidsHigh fiberLean quality protein sourcesWhole fruits and vegetablesFoods rich in phytochemicals and

antioxidantsLow-fat dairy (calcium)Discourage pro-obesity processed

foods containingRefined carbohydratesTrans and saturated fatty acids

sted

ll sense

ty levelnt typeuency o

ted calal intakrce inturove fopriate m

bsorption and increase a substance known as calcitriol

Table 4Suggested Biochemical Monitoring Tools for Nutrition Status

Vitaminmineral Screening Normal range Additional laboratoryindexes

Critical range Preoperative deficiency Postoperativedeficiency

Comments

B1 (thiamin) Serum thiamin 10ndash64 ngmL 2RBC transketolase1Pyruvate

Transketolase activity20

Pyruvate 1 mgdL

15ndash29 more common inAfrican Americans andHispanics oftenassociated with poorhydration

Rare but occurs withRYGB AGB andBPDDS

Serum thiamin responds todietary supplementationbut is poor indicator oftotal body stores

B6 (pyridoxine) PLP 5ndash24 ngmL RBC glutamic pyruvateOxaloacetic

PLP 3 ngmL Unknown Rare Consider with unresolvedanemia diabetes couldinfluence valuestransaminase

B12 (cobalamin) Serum B12 200ndash1000 pgmL 1Serum and urinaryMMA

1Serum tHcy

Serum B12

200 pgmL deficiency400 pgmL

suboptimalsMMA 0376 molLMMA 36 mol

mmol CRTtHcy 132 molL

10ndash13 may occur witholder patients and thosetaking H2 blockers andPPIs

Common withRYGB in absenceofsupplementation12ndash33

When symptoms arepresent and B12 200ndash250 pgmL MMA andtHcy are useful serumB12 may miss 25ndash30of deficiency cases

Folate RBC folate 280ndash791 ngmL Urinary FIGLUNormal serum andurinary MMA1Serum tHcy

RBC folate305 nmolL

deficiency227 nmolL anemia

Uncommon Uncommon Serum folate reflectsrecent dietary intakerather than folate statusRBC folate is a moresensitive marker

Excessive supplementationcan mask B12 deficiencyin CBC neurologicsymptoms will persist

Iron Ferritin Males15ndash200 ngmLFemales12ndash150 ngmL

2Serum iron1TIBC

Ferritin 20 ngmLSerum iron 50 gdLTIBC 450 gdL

9ndash16 of adult women ingeneral population aredeficient

20ndash49 of patientscommon withRYGB formenstruatingwomen (51) andpatients with superobesity (49ndash52)

Low Hgb and Hct areconsistent with irondeficiency anemia instage 3 or stage 4anemia ferritin is anacute phase reactant andwill be elevated withillness andorinflammation oralcontraceptives reduceblood loss formenstruating females

Vitamin A Plasma retinol 20ndash80 gdL RBP Plasma retinol 10gdL

Uncommon up to 7 insome studies

Common (50) withBPDDS after 1 yrup to 70 at 4 yrmay occur withRYGBAGB

Ocular finding maysuggest diagnosis

S77L

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iseases4

(2008)S73-S108

Table 4Continued

Vitaminmineral Screening Normal range Additional laboratoryindexes

Critical range Preoperative deficiency Postoperativedeficiency

Comments

Vitamin D 25(OH)D 25ndash40 ngmL 2Serum phosphorus1Alkaline phosphatase1Serum PTH2Urinary calcium

Serum 25(OH)D 20ngmL suggestsdeficiency 20ndash30 ngmL suggestsinsufficiency

Common 60ndash70 Common with BPDDS after 1 yr mayoccur with RYGBprevalenceunknown

With deficiency serumcalcium may be low ornormal serumphosphorus maydecrease serum alkalinephosphatase increasesPTH elevated

Vitamin E Plasma alphatocopherol

5ndash20 gmL Plasma lipids 5 gmL Uncommon Uncommon Low plasma alphatocopherol to plasmalipids (08 mgg totallipid) should be usedwith hyperlipidemia

Vitamin K PT 10ndash13 seconds 1DCP 2Plasmaphylloquinone

Variable Uncommon Common with BPDDS after 1 yr

PT is not a sensitivemeasure of vitamin Kstatus

Zinc Plasma zinc 60ndash130 gdL 2RBC zinc Plasma zinc 70 gdL Uncommon but increasedrisk of low levelsassociated with obesity

Common with BPDDS after 1 yr mayoccur with RYGB

Monitor albumin levelsand interpret zincaccordingly albumin isprimary binding proteinfor zinc no reliablemethod of determiningzinc status is availableplasma zinc is methodgenerally used studiescited in this report didnot adequately describemethods of zinc analysis

Protein Serum albuminSerum totalprotein

4ndash6 gdL6ndash8 gdL

2Serum prealbumin(transthyretin)

Albumin 30 gdLPrealbumin 20 mgdL

Uncommon Rare but can occurwith RYGB AGBand BPDDS ifprotein intake islow in total intakeor indispensableamino acids

Half-life for prealbumin is2ndash4 d and reflectschanges in nutritionalstatus sooner thanalbumin a nonspecificprotein carrier with ahalf-life of 22 d

RYGB Roux-en-Y gastric bypass AGB adjustable gastric banding BPDDS biliopancreatic diversionduodenal switch PLP pyridoxal-5rsquo-phosphate RBC red blood cell MMA methylmalonic acid tHcy total homocysteine CRT creatinine PPIs protein pump inhibitors FIGLU formiminogluatmic acid CBC complete blood count TIBC total iron binding capacityHgb hemoglobin Hct hematocrit RPB retinol binding protein PTH parathyroid hormone 25(OH)D 25-hydroxyvitamin D PT prothrombin time DCP des-gamma-carboxypromthrom-bin

In general laboratory values should be reviewed annually or as indicated by clinical presentation Laboratory normal values vary among laboratory settings and are method dependent This chart providesa brief summary of monitoring tools See the Appendix for additional detail and diagnostic tools

copy Jeanne Blankenship MS RD Used with permission

S78L

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andR

elatedD

iseases4

(2008)S73-S108

TS

S

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S79L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able 5uggested Postoperative Vitamin Supplementation

upplement AGB RYGB BPDDS Comment

ultivitamin-mineral supplementA high-potency vitamin containing 100 of daily value for

at least 23 of nutrients100 of daily

value

200 of dailyvalue

200 of daily value Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to whole tabletcapsule as toleratedAvoid time-released supplementsAvoid enteric coatingChoose a complete formula with at least 18 mg iron 400

g folic acid and containing selenium and zinc in eachserving

Avoid childrenrsquos formulas that are incompleteMay improve gastrointestinal tolerance when taken close to

food intakeMay separate dosageDo not mix multivitamin containing iron with calcium

supplement take at least 2 hr apartIndividual brands should be reviewed for absorption rate and

bioavailabilitySpecialized bariatric formulations are available

dditional cobalamin (B12)Available forms include sublingual tablets liquid drops

mouth spray or nasal gelsprayIntramuscular injection mdash 1000 gmo mdash Begin 0ndash3 mo after

surgeryOral tablet (crystalline form) mdash 350ndash500 gd mdashSupplementation after AGB and BPDDS may be required

dditional elemental calciumChoose a brand that contains calcium citrate and vitamin D3

Begin with chewable or liquidProgress to whole tabletcapsule as tolerated

1500 mgd 1500ndash 2000 mgd 1800ndash 2400 mgd May begin on day 1after hospitaldischarge orwithin 1 mo aftersurgery

Split into 500ndash600 mg doses be mindful of serving size onsupplement label

Space doses evenly throughout daySuggest a brand that contains magnesium especially for

BPDDSDo not combine calcium with iron containing supplements

To maximize absorptionTo minimize gastrointestinal intoleranceWait 2 h after taking multivitamin or iron supplement

Promote intake of dairy beverages andor foods that aresignificant sources of dietary calcium in addition torecommended supplements up to 3 servings daily

Combined dietary and supplemental calcium intake 1700mgd may be required to prevent bone loss during rapidweight loss

dditional elemental iron (above that provided by mvi)Recommended for menstruating women and those at risk of

anemia (total goal intake 50-100 mg elemental irond)

mdash Add a minimumof 18ndash27 mgdelemental

Add a minimum of18ndash27 mgdelemental

Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to tablet as toleratedDosage may need to be adjusted based on biochemical

markersNo enteric coatingDo not mix iron and calcium supplements take 2 h apartAvoid excessive intake of tea due to tannin interactionEncourage foods rich in heme iron

Vitamin C may enhance absorption of non-heme iron sources

wa

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S80 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hich in turn causes metabolic changes that favor fatccumulation [23ndash25]

Several of the B-complex vitamins important for appro-riate metabolism of carbohydrate and neural functions thategulate appetite have been found to be deficient in someatients with morbid obesity [212627] Iron deficiencieshich would significantly hinder energy use have been

eported in nearly 50 of morbidly obese preoperativeandidates [21] Zinc and selenium deficits have been re-orted as well as deficits in vitamins A E and C allmportant antioxidants helpful in regulating energy produc-ion and various other processes of body weight manage-ent [1926ndash28]The risk of micronutrient depletion continues to be quite

igh particularly after surgeries that affect the digestion andbsorption of nutrients such as Roux-en-Y gastric bypassRYGB) and biliopancreatic diversion with or without du-denal switch (BPDDS) RYGB increases the risk of vita-in B12 and other B vitamin deficits in addition to iron and

alcium BPDDS procedures may also cause an increasedisk of iron and calcium deficits along with significant

able 5ontinued

upplement AGB

at-soluble vitaminsWith all procedures higher maintenance doses may be

required for those with a history of deficiencyWater-soluble preparations of fat-soluble vitamins are

availableRetinol sources of vitamin A should be used to calculatedosageMost supplements contain a high percentage of beta

carotene which does not contribute to vitamin A toxicityIntake of 2000 IU Vitamin D3 may be achieved with careful

selection of multivitamin and calcium supplementsNo toxic effect known for vitamin K1 phytonadione

(phyloquinone)

mdash

mdash

mdash

Vitamin K requirement varies with dietary sources andcolonic production

Caution with vitamin K supplementation for patientsreceiving coagulation therapy

Vitamin E deficiency has been suggested but is notprevalent in published studies

ptional B complexB-50 dosageLiquid form is available

1 servi

Avoid time released tabletsNo known risk of toxicityMay provide additional prophylaxis against B-vitamin

deficiencies including thiamin especially for BPDDSprocedures as water-soluble vitamins are absorbed in theproximal jejunum

Note 1000 mg of supplemental folic acid provided incombination with multivitamins could mask B12

deficiency

Abbreviations as in Table 4

eficiencies in the fat-soluble vitamins A D E and K d

hich are important for driving many of the biologicalrocesses that help to regulate body size [29ndash31] As theate of noncompliance with prophylactic multivitamin sup-lementation increases the rate of postoperative deficiencyay increase almost twofold [32]In the past it has been thought that the specific nutri-

ional deficiencies commonly seen among malabsorptiverocedures would not be present in patients choosing aurely restrictive surgery such as the adjustable gastric bandAGB) However poor eating behavior low nutrient-denseood choices food intolerance and a restricted portion sizean contribute to potential nutrient deficiencies in theseatients as well Although the incidence of nutritional com-lications may be less frequent in this patient population itould be detrimental to assume that they do not existIt is important for the bariatric patient to take vitamin and

ineral supplements not only to prevent adverse healthonditions that can arise after surgery but because someutrients such as calcium can enhance weight loss and helprevent weight regain The nutrient deficiency might beroportional to the length of the absorptive area bypassed

RYGB BPDDS Comment

mdash

mdash

mdash

10000 IU of vitamin A

2000 IU of vitamin D

300 g of vitamin K

May begin 2ndash4weeks aftersurgery

1 servingd 1 servingd May begin on day 1after hospitaldischarge

ngd

uring surgical procedures and to a lesser extent to the

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oa

S81L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ercentage of weight lost Iron vitamin B12 and vitamin Deficiencies along with changes in calcium metabolism areommon after RYGB Protein fat-soluble vitamin andther micronutrient deficiencies as well as altered calciumetabolism are most notably found after BPDDS Folate

eficiency has been reported after AGB [33] Thiamin de-ciency is common among all surgical patients with fre-uent vomiting regardless of the type of procedure per-ormed Because many nutritional deficiencies progressith time patients should be monitored frequently and

egularly to prevent malnutrition [29] Reinforcement ofupplement compliance at each patient follow-up is alsomportant in the fight to enhance nutrition status and preventutritional complications

eight loss and nutrient deficits restrictionersus malabsorption

Malabsorptive procedures such as the BPDDS arehought to cause weight loss primarily through the malab-orption of macronutrients with as much as 25 of proteinnd 72 of fat malabsorbed Such primary malabsorptionesults in concomitant malabsorption of micronutrients3435] Vitamins and minerals relying on fat metabolismncluding vitamins D A E K and zinc may be affectedhen absorption is impaired [36] The decrease in gastro-

ntestinal transit time may also result in secondary malab-orption of a wide range of micronutrients related to by-assing the duodenum and jejunum or limited contact withhe brush border secondary to a short common limb Othericronutrient deficiency concerns reported for patients

hoosing a procedure with malabsorptive features includeron calcium vitamin B12 and folate

Nutrient deficiencies after RYGB can result from eitherrimary or secondary malabsorption or from inadequateietary intake A minimal amount of macronutrient malab-orption is thought to occur However specific micronutri-nts appear to be malabsorbed postoperatively and presents deficiencies without adequate vitamin and mineral sup-lementation Retrospective analyses of patients who havendergone gastric bypass have revealed predictable micro-utrient deficiencies including iron vitamin B12 and folate2627ndash39] Case reports have also shown that thiamin de-ciency can develop especially when persistent postopera-

ive vomiting occurs [40ndash43]Few studies that measure absorption after measured and

uantified intake have been published It can be hypothe-ized that the bypassed duodenum and proximal jejunumegatively affect nutrient assimilation Bradley et al [44]tudied patients who had undergone total gastrectomy therocedure from which the RYGB evolved The researchersound that most nutritional status changes in patients wereost likely due to changes in intake versus malabsorptionhese balance studies were conducted in a controlled re-

earch setting however they did not measure pre- and c

ostoperative changes nor include radioisotope labeling toeasure absorption of key nutrients and the subjects had

ndergone the procedure for reasons other than weight lossIt is unclear whether intestinal adaptation occurs after

ombination procedures and to what degree it affects long-erm weight maintenance and nutrition status Adaptation iscompensatory response that follows an abrupt decrease inucosal surface area and has been well studied in short-

owel patients who require bowel resection [45] The pro-ess includes both anatomic and functional changes thatncrease the gutrsquos digestive and absorptive capacity Al-hough these changes begin to take place in the early post-perative period total adaptation may take up to three yearso complete Adaptation in gastric bypass has not beenonsidered in absorption or metabolic studies This consid-ration could be important even when determining early andate macro- and micronutrient intake recommendations Theffect of pancreatic enzyme replacement therapy on vitaminnd mineral absorption in this population is also unknown

Purely restrictive procedures such as the AGB can resultn micronutrient deficiencies related to changes in dietaryntake It is commonly accepted that because no alteration isade in the absorptive pathway malabsorption does not

ccur as a result of AGB procedures However nutrienteficits would be likely to occur because of the low nutrientntake and avoidance of nutrient-rich foods in the earlyonths postoperatively and later possibly as a result of

xcessive band restriction Food with high nutritional valueuch as meat and fibrous fresh fruits and vegetables mighte poorly tolerated

Literature has been published that addresses the effect ofalabsorptive restrictive and combination surgical proce-

ures on acute and long-term nutritional status These stud-es have attempted for the most part to indirectly determinehe surgical impact on nutrition status by the evaluation ofetabolic and laboratory markers Although some studies

ave included certain aspects of absorption few have in-luded the necessary components to evaluate absorption ofprescribed andor monitored diet in a controlled metabolic

ettingThe following sections examine the pre- and postopera-

ive risks for nutritional deficiencies associated with RYGBPDDS and AGB It is important for all members of theedical team to increase their awareness of the nutritional

omplications and challenges that lie ahead for the patientontinued review of current research by the medical team

egarding advances in nutrition science beyond the bound-ries of the present report cannot be emphasized enough

hiamin (vitamin B1)

Beriberi is a thiamin deficiency that can affect variousrgan systems including the heart gastrointestinal tractnd peripheral and central nervous systems Although the

ondition is generally considered rare a number of reported

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S82 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nd possibly a much greater number of unreported or un-iagnosed cases of beriberi have occurred among individ-als who have undergone surgery for morbid obesity Earlyetection and prompt treatment of thiamin deficits in thesendividuals can help to prevent serious health consequencesf beriberi is misdiagnosed or goes undetected for even ahort period the bariatric patient can develop irreversibleeuromuscular disorders permanent defects in learning andhort-term memory coma and even death Because of theife-altering and potentially life-threatening nature of a thi-min deficiency it is important that healthcare professionalsn the field of bariatric surgery have knowledge of thetiology of the condition and its signs and symptomsreatment and prevention

tiology of potential deficiency Thiamin is a water-solubleitamin that is absorbed in the proximal jejunum by anctive (saturable high-affinity) transport system [4647] Inhe body thiamin is found in high concentrations in therain heart muscle liver and kidneys However withoutegular and sufficient intake these tissues become rapidlyevoid of thiamin [4647] The total amount of thiamin inhe body of an adult is approximately 30 mg with a half-lifef only 9ndash18 days Persistent vomiting a diet deficient inhe vitamin or the bodyrsquos excessive utilization of thiaminse can result in a severe state of thiamin depletion withinnly a short period producing symptoms of beriberi46ndash48]

Bariatric surgery increases the risk of beriberi through ex-cerbation of pre-existing thiamin deficits low nutrient intakealabsorption and episodes of nausea and vomiting [49ndash51]hronic or acute thiamin deficiencies in bariatric patients oftenresent with symptoms of peripheral neuropathy or Wer-ickersquos encephalopathy and Korsakoffrsquos psychoses [2148ndash4] Early diagnosis of the signs and symptoms of these con-itions is extremely important to prevent serious adverse healthonsequences Even if treatment is initiated recovery can bencomplete with cognitive andor neuromuscular impairmentsersisting long term or permanently

igns symptoms and treatment of deficiency (seeppendix Table A1)

reoperative risk The risk of the development of beriberifter bariatric surgery is far greater for individuals present-ng for surgery with low thiamin levels Investigators at theleveland Clinic of Florida reported that 15 of their pre-perative bariatric patients had deficiencies in thiamin be-ore surgery [52] A study by Flancbaum et al [21] similarlyound that 29 of their preoperative patients had low thia-in levels Data obtained by that study also showed a

ignificant difference between ethnicity and preoperativehiamin levels Although only 67 of whites presentedith thiamin deficiencies before surgery nearly one third

31) of African Americans and almost one half (47) of

ispanics had thiamin deficits The results of these studies S

uggested a need for preoperative thiamin testing as well ashiamin repletion by diet or supplementation to reduce theisk of ldquobariatricrdquo beriberi postoperatively

ostoperative risk Beriberi has been observed after gastricestrictive and malabsorptive procedures A number of casesf Wernicke-Korsakoff syndrome (WKS) as well as periph-ral neuropathy have been reported for patients havingndergone vertical banded gastroplasty [53ndash61] A fewncidences of WKS have also been reported after AGB436263] Additionally reports of thiamin deficiencies and

KS after RYGB [404164ndash73] and several cases of WKSnd neuropathy in patients who had undergone BPD [74]ave been published Many more cases of WKS are be-ieved to have occurred with bariatric procedures that haveither not been reported or have been misdiagnosed becausef limited knowledge regarding the signs and symptoms ofcute or severe thiamin deficits Because many foods areortified with thiamin beriberi has been nearly eradicatedhroughout the world except for patients with severe alco-olism severe vomiting during pregnancy (hyperemesisravidarium) or those malnourished and starved For thiseason few healthcare professionals until recently havead a patient present with beriberi

According to the published reports of thiamin deficitsfter bariatric procedures most patients develop such defi-iencies in the early postoperative months after an episodef intractable vomiting Nausea and vomiting are relativelyommon after all bariatric procedures early in the postop-rative period Thiamin stores in the body are small andaintenance of appropriate thiamin levels requires daily

eplenishment A deficiency of thiamin for only a couple ofeeks or less caused by persistent vomiting can deplete

hiamin stores Symptoms of WKS were reported in aYGB patient after only two weeks of persistent vomiting

67]Bariatric beriberi can also develop in postoperative patients

ho are given infusate containing dextrose without thiaminnd other vitamins which is often the case for patients inritical care units postoperative patients with complicationsnterfering with the ingestion of food or patients dehydratedrom persistent vomiting Malnutrition caused by a lack ofppetite and dietary intake postoperatively also contributes toariatric beriberi as does noncompliance in taking postopera-ive vitamin supplements

Although most cases of beriberi occur in the early post-perative periods cases of patients with severe thiamineficiency more than one year after surgery have beeneported One study reported WKS in association with al-ohol abuse 13 years after RYGB [75] Other conditionsontributing to late cases of bariatric beriberi include ahiamin-poor diet a diet high in carbohydrates anorexiand bulimia [46ndash48]

uggested supplementation Because of the greater likeli-

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imdrot(av

V

EitpfAorpvp

t

tc(bidi

(ddawalo

SA

Peamshtt

3mosgtptIBvw

S83L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ood of low dietary thiamin intake patients should be sup-lemented with thiamin This is usually accomplishedhrough daily intake of a multivitamin Most multivitaminsontain thiamin at 100 of the daily value Patients havingpisodes of nausea and vomiting and those who are anorec-ic might require sublingual intramuscular or intravenoushiamin to avoid depletion of thiamin stores and beriberiaution should be used when infusing bariatric patientsith solutions containing dextrose without additional vita-ins and thiamin because an increase in glucose utilizationithout additional thiamin can deplete thiamin stores [76]Thiamin deficiency in bariatric patients is treated with

hiamin together with other B-complex vitamins and mag-esium for maximal thiamin absorption and appropriateeurologic function [46 ndash 48] Early symptoms of neuropa-hy can often be resolved by providing the patient with oralhiamin doses of 20ndash30 mgd until symptoms disappear Forore advanced signs of neuropathy or for individuals with

rotracted vomiting 50ndash100 mgd of intravenous or intra-uscular thiamin may be necessary for resolution or im-

rovement of symptoms or for the prevention of suchatients with WKS generally require 100 mg thiamindministered intravenously for several days or longer fol-owed by intramuscular thiamin or high oral doses untilymptoms have resolved or significantly improved This canequire months to years Some patients might have to takehiamin for life to prevent the reoccurrence of neuropathy

itamin B12 and folate

Vitamin B12 (cobalamin) and folate (folic acid) are bothnvolved in the maturation of red blood cells and are com-only discussed in the literature together Over time a

eficiency in either vitamin B12 or folate can lead to mac-ocytic anemia a condition characterized by the productionf fewer but larger red blood cells and a decreased abilityo carry oxygen Most (95) cases of megaloblastic anemiacharacterized by large immature abnormal undifferenti-ted red blood cells in bone marrow) are attributed toitamin B12 or folate deficiency [77]

itamin B12

tiology of potential deficiency RYGB patients have bothncomplete digestion and release of vitamin B12 from pro-ein foods With a significant decrease in hydrochloric acidepsinogen is not converted into pepsin which is necessaryor the release of vitamin B12 from protein [78] BecauseGB patients have an artificial restriction yet complete usef the stomach and BPD patients do not have as great aestriction in stomach capacity and parietal cells as RYGBatients the reduction in hydrochloric acid and subsequentitamin B12 deficiency is not as prevalent with these tworocedures

Intrinsic factor (IF) is produced by the parietal cells of

he stomach and in certain conditions (eg atrophic gastri- a

is resected small bowel elderly patients) can be impairedausing an IF deficiency Subsequent vitamin B12 deficiencypernicious anemia) occurs without IF production or useecause IF is needed to absorb vitamin B12 in the terminalleum [77] Factors that increase the risk of vitamin B12

eficiency relevant to bariatric surgery include the follow-ng

An inability to release protein-bound vitamin B12

from food particularly in hypochlorhydria andatrophic gastritis

Malabsorption due to inadequate IF in perniciousanemia

Gastrectomy and gastric bypassResection or disease of terminal ileumLong-term vegan dietMedications such as neomycin metformin colch-

icines medications used in the management ofbowel inflammation and gastroesophageal refluxand ulcers (eg proton pump inhibitors) and anti-convulsant agents [79]

Cobalamin stores are known to exist for long periods3ndash5 yr) and are dependent on dietary repletion and dailyepletion However gastric bypass patients have both aecreased production of stomach acid and a decreased avail-bility of IF thus a vitamin B12 deficiency could developithout appropriate supplementation Because the typical

bsorption pathway cannot be relied on the surgical weightoss patient must rely on passive absorption of B12 whichccurs independent of IF

igns symptoms and treatment of deficiency (seeppendix Table A3)

reoperative risk Several medications common to preop-rative bariatric patients have been noted to affect preoper-tive vitamin B12 absorption and stores Of patients takingetformin 10ndash30 present with reduced vitamin B12 ab-

orption [80] Additionally patients with obesity have aigh incidence of gastroesophageal reflux disease for whichhey take proton pump inhibitors thus increasing the poten-ial to develop a vitamin B12 deficiency

Flancbaum et al [21] conducted a retrospective study of79 (320 women and 59 men) pre-operative patients Vita-in B12 deficiency was reported as negative in all patients

f various ethnic backgrounds [21] No clinical criteria orymptoms for vitamin B12 deficiency were noted In theeneral population 5ndash10 present with neurologic symp-oms with vitamin B12 levels of 200ndash400 pgmL Amongreoperative gastric bypass patients Madan et al [27] foundhat 13 (n 59) of patients were deficient in vitamin B12n a comparison of patients presenting for either RYGB orPD Skroubis et al [81] recently reported that preoperativeitamin B12 levels were low-normal in both groups Itould be prudent to screen for and treat IF deficiency

ndor vitamin B12 deficiency in all patients preoperatively

bd

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Eri

S84 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ut it is essential for RYGB patients so as not to hasten theevelopment of a potential postoperative deficiency

ostoperative risk Vitamin B12 deficiency has been fre-uently reported after RYGB Schilling et al [82] estimatedhe prevalence of vitamin B12 deficiency to be 12ndash33ther researchers have suggested a much greater prevalencef B12 deficiency in up to 75 of postoperative RYGBatients however most reports have cited approximately5 of postoperative RYGB patients as vitamin B12 defi-ient [82ndash87] Brolin et al [87] reported that low levels ofitamin B12 might be seen as soon as six months afterariatric surgery but most often occurring more than oneear postoperatively as liver stores become depleted Sk-oubis et al [88] predicted that the deficiency will mostikely occur 7 months after RYGB and 79 months afterPDDS although their research did not consider compro-ised preoperative status and its correlation to postopera-

ive deficiency After the first postoperative year the prev-lence of vitamin B12 deficiency appears to increase yearlyn RYGB patients [89]

Although the bodyrsquos storage of vitamin B12 is significant2000 g) compared with daily needs (24 gd) thisarticular deficiency has been found within 1ndash9 years ofastric bypass surgery [29] Brolin et al [84] reported thatne third of RYGB patients are deficient at four yearsostoperatively However non-surgical variables were notxplored and many patients might have had preoperativealues near the lower end of the normal range Ocon Bretont al [90] compared micronutrient deficiencies among two-ear postoperative BPDDS and RYGB patients and foundhat all nutritional deficiencies were more common amongPDDS patients except for vitamin B12 for which theeficiency was more common among the RYGB patientstudied A lack of B12 deficiency among BPDDS patientsight result from a better tolerance of animal proteins in a

arger pouch greater pepsingastric acid production to re-ease protein-bound B12 and increased availability and in-eraction of IF with the pouch contents

Experts have noted the significance of subclinical defi-iency in the low-normal cobalamin range in nongastricypass patients who do not exhibit clinical evidence ofeficiency The methylmalonic acid (MMA) assay is thereferred marker of B12 status because metabolic changesften precede low B12 levels in the progression to defi-iency Serum B12 assays may miss as much as 25ndash30 of

12 deficiencies making them less reliable than the MMAssay [91] It has been suggested that early signs of vitamin

12 deficiency can be detected if the serum levels of bothMA and homocysteine are measured [91] Vitamin B12

eficiency after RYGB has been associated with megalo-lastic anemia [92] Some vitamin B12-deficient patientsevelop significant symptoms such as polyneuropathy par-

sthesia and permanent neural impairment On occasion

ome patients may experience extreme delusions halluci-ations and even overt psychosis [93]

uggested supplementation Because of the frequent lack ofymptoms of vitamin B12 deficiency the suggested dili-ence in following up or treating these values among thosesymptomatic patients has been questioned The decisionot to supplement or routinely screen patients for B12 defi-iency should be examined very carefully given the risk ofrreversible neurologic damage if vitamin B12 goes un-reated for long periods At least one case report has beenublished of an exclusively breastfed infant with vitamin

12 deficiency who was born of an asymptomatic motherho had undergone gastric bypass surgery [94]Deficiency of vitamin B12 is typically defined at levels

200 pgmL However about 50 of patients with obviousigns and symptoms of deficiency have normal vitamin B12

evels [31] Kaplan et al [95] reported that vitamin B12

eficiency usually resolves after several weeks of treatmentith 700ndash2000 gwk Rhode et al [96] found that aosage of 350ndash600 gd of oral B12 prevented vitamin B12

eficiency in 95 of patients and an oral dose of 500 gdas sufficient to overcome an existing deficiency as re-orted by Brolin et al [87] in a similar study Thereforeupplementation of RYGB patients with 350ndash500 gd mayrevent most postoperative vitamin B12 deficiency

While most vitamin B12 in normal adults is absorbed inhe ileum in the presence of IF approximately 1 of sup-lemented B12 will be absorbed passively (by diffusion)long the entire length of the (non-bypassed) intestine byurgical weight loss patients given a high-dose oral supple-ent [97] Thus the consumption of 350ndash500 g yields a

5ndash50-g absorption which is greater than the daily re-uirement Although the use of monthly intramuscular in-ections or a weekly oral dose of vitamin B12 is commonmong practices it relies on patient compliance Practitio-ers should assess the patientrsquos preference and the potentialor compliance when considering a daily weekly oronthly regimen of B12 supplementation In addition to oral

upplements or intramuscular injections nasal sprays andublingual sources of vitamin B12 are also available Pa-ients should be monitored closely for their lifetime becauseevere anemia can develop with or without supplementation98]

olate

tiology of potential deficiency Factors that increase theisk of folic acid deficiency relevant to bariatric surgerynclude the following

Inadequate dietary intakeNoncompliance with multivitamin supplementationMalabsorptionMedications (anticonvulsants oral contraceptives

and cancer treating agents) [79]

pmo

SA

PAtArBatbhptl5

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pntiat

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Soiwt[2tpbvhsfowbmftm

I

dspbiwiu

S85L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Folic acid stores can be depleted within a few monthsostoperatively unless replenished by a multivitamin supple-ent and dietary sources (ie green leafy vegetables fruits

rgan meats liver dried yeast and fortified grain products)

igns symptoms and treatment of deficiency (seeppendix Table A4)

reoperative risk The goals of the 1998 Food and Drugdministration policy requiring all enriched grain products

o be fortified with folate included increasing the averagemerican diet by 100 g folate daily and decreasing the

ate of neural tube defects in childbearing women [99]entley et al [100] reported that the proportion of womenged 15ndash44 years old (in the general population) who meethe recommended dietary intake of 400 gd folate variesetween 23 and 33 With the increasing popularity ofigh proteinlow carbohydrate diets one cannot assume thatreoperative patients consume dietary sources of folatehrough fortified grain products fruits and vegetables Boy-an et al [26] found folate deficiencies preoperatively in6 of RYGB patients studied

ostoperative risk Although it has been observed that fo-ate deficiency after RYGB surgery is less common than B12

eficiency and is thought to occur because of decreasedietary or multivitamin supplement intake low serum folateevels have been cited from 6 to 65 among RYGBatients [2686101] Additionally folate deficiencies haveccurred postoperatively even with supplementation Boy-an et al [26] found that 47 (n 17) of RYGB patientsad low folate levels six months postoperatively and 41n 17) had low levels at one year This deficiency oc-urred despite patient adherence to taking a multivitaminupplement that contained at least the daily value for folate00 g [26] Postoperative bariatric patients with rapideight loss might have an increased risk of micronutrienteficiencies MacLean et al [86] reported that 65 ofostoperative patients had low folate levels These sameatients exhibited additional B vitamin deficiencies 24itamin B12 and 50 thiamin [86] An increased risk ofeficiency has also been noted among AGB patients pos-ibly because of decreased folate intake Gasteyger et al33] found a significant decrease in serum folate levels441) between the baseline and 24-month postoperativeeasurementsDixon and OrsquoBrien [101] reported elevated serum ho-

ocysteine levels in patients after bariatric surgery regard-ess of the type of procedure (restrictive or malabsorptive)levated homocysteine levels can indicate not only low

olate levels and a greater risk of neural tube defects but canlso be indicative of an independent risk factor for heartisease andor oxidative stress in the nonbariatric popula-ion [102] However unlike iron and vitamin B12 the folate

ontained in the multivitamin supplementation essentially e

orrects the deficiency in the vast majority of postoperativeariatric patients [103] Therefore persistent folate defi-iency might indicate a patientrsquos lack of compliance withhe prescribed vitamin protocol [32]

It is common knowledge that folic acid deficiency amongregnant women has been associated with a greater risk ofeural tube defects in newborns Consistent supplementa-ion and monitoring among women of child-bearing agencluding pre- and postoperative bariatric patients is vital inn effort to prevent the possibility of neural tube defects inhe developing fetus

Because folate does not affect the myelin of nerveseurologic damage is not as common with folate such as ishe case for vitamin B12 deficiency In contrast patientsith folate deficiency often present with forgetfulness irri-

ability hostility and even paranoid behaviors [29] Similaro that evidenced with vitamin B12 most postoperativeYGB patients who are folate deficient are asymptomatic orave subclinical symptoms therefore these deficient statesay not be easily identified

uggested supplementation Even though folate absorptionccurs preferentially in the proximal portion of the smallntestine it can occur along the entire length of the small bowelith postoperative adaptation Therefore it is generally agreed

hat folate deficiency is corrected with 1000 mgd folic acid32] and is preventable with supplementation that provides00 of the daily value (800 g) This level can also benefithe fetus in a female patient unaware of her postoperativeregnancy Folate supplementation 1000 mgd has noteen recommended because of the potential for maskingitamin B12 deficiency Carmel et al [104] suggested thatomocysteine is the most sensitive marker of folic acidtatus in conjunction with erythrocyte folate Althougholic acid deficiency could potentially occur among post-perative bariatric surgery patients it has not been seenidely in recent studies especially when patients haveeen compliant with postoperative multivitamin supple-entation Therefore it is imperative to closely follow

olic acid both pre- and postoperatively especially inhose patients suspected to be noncompliant with theirultivitamin supplementation

ron

Much of the iron and surgical weight loss research con-ucted to date has been generated from a limited number ofurgeons and scientists however the data have consistentlyointed toward the risk of iron deficiency and anemia afterariatric procedures Iron deficiency is defined as a decreasen the total iron body content Iron deficiency anemia occurshen erythropoiesis is impaired as a result of the lack of

ron stores In the absence of anemia iron deficiency issually asymptomatic Fatigue and a diminished capacity to

xercise however are common symptoms of anemia

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ifftBibfagowtimiB

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S86 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

tsmp

lsnfwTlopaechc

Rtbwdsaar

fdaiwiiedasdt

Stbadtbpcwl

mccmacdrrT

C

EeamadmsDfd

dbdh7DtnDcwsh

SA

Pcptt[hmtlcgc

S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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S88 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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S89L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

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hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

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S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

ratbrdd

aebaaa

apcptaasosdbc

afciitdmptpcrsPEv

TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

[

[

[

[

[

[

[

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[

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[

[

[

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[

[

[

[

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[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

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S

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T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

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S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

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S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

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S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 4: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S76 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nterventions for morbid obesity continues to grow concerns increasing regarding the long-term effects of nutritionaleficiencies Nutritional complications that remain undiag-osed and untreated can lead to adverse health conse-uences and loss of productivity The benefits of weight lossurgery must be balanced against the risk of developingutritional deficiencies to provide appropriate identificationreatment and prevention

Vitamins and minerals are essential factors and co-fac-ors in numerous biological processes that regulate bodyize They include appetite hunger nutrient absorptionetabolic rate fat and sugar metabolism thyroid and adre-

al function energy storage glucose homeostasis neuralctivities and others Thus micronutrient ldquorepletionrdquomeaning the body has sufficient amounts of vitamins andinerals to perform these functions) is not only important

or good health but also for maximal weight loss successnd long-term weight maintenance

Obtaining micronutrients from food is the most desirableay to ensure the body has sufficient amounts of vitamins

nd minerals However some experts have suggested that

able 3uggested Postoperative Nutrition Follow-up

ecommended Sugge

nthropometricCurrent and accurate height weight BMI and

percentage of excess body weightOvera

iochemical ActiviReview laboratory findings when available Amou

freq

edication reviewEncourage patients to follow-up with PCP regarding

medications that treat rapidly resolving co-morbidities (eg hypertension diabetes mellitus)

itaminmineral supplementsAdherence to protocol

ietary intakeUsual or actual daily intakeProtein intakeFluid intakeAssess intake of anti-obesity foodsFood texture complianceFood tolerance issues (eg nauseavomiting

ldquodumpingrdquo)Appropriate diet advanceAddress individual patient complaintsAddress lifestyle and educational needs for long

term weight loss maintenance

Estimaactu

Reinfoimp

Appro

BMI body mass index PCP primary care physician

ost individuals in our ldquofast-paced eat-outrdquo society fail to a

onsume sufficient amounts of unprocessed foods that areigh in vitamins and minerals such as fruits and vegetablessh and other protein sources dairy products whole grainsuts and legumes Poor dietary selection and habits coupledith the reduced vitamin and mineral content of foods can

ead to micronutrient deficiencies among the general publichat interfere with body weight control increasing the riskf weight gain and obesity Therefore a daily vitamin andineral supplement is likely to be of value in ensuring

dequate intake of micronutrients for maximal functioningf those processes that help to regulate appropriate bodyeightTaking daily micronutrient supplements and eating foods

igh in vitamins and minerals are important aspects of anyuccessful weight loss program For the morbidly obeseaking vitamin and mineral supplements is essential forppropriate micronutrient repletion both before and afterariatric surgery Studies have found that 60ndash80 of mor-idly obese preoperative candidates have defects in vitamin

[19ndash22] Such defects would reduce dietary calcium

Other considerations

of well-being Use of contraception to avoidpregnancy

Psychosocial intensity andf activity

Changing relationship with foodChanges in support systemStress managementBody image

oric intake of usual oreitive eating style to

od toleranceeal planning

Promote anti-obesity foodscontaining

Omega-3 fatty acidsHigh fiberLean quality protein sourcesWhole fruits and vegetablesFoods rich in phytochemicals and

antioxidantsLow-fat dairy (calcium)Discourage pro-obesity processed

foods containingRefined carbohydratesTrans and saturated fatty acids

sted

ll sense

ty levelnt typeuency o

ted calal intakrce inturove fopriate m

bsorption and increase a substance known as calcitriol

Table 4Suggested Biochemical Monitoring Tools for Nutrition Status

Vitaminmineral Screening Normal range Additional laboratoryindexes

Critical range Preoperative deficiency Postoperativedeficiency

Comments

B1 (thiamin) Serum thiamin 10ndash64 ngmL 2RBC transketolase1Pyruvate

Transketolase activity20

Pyruvate 1 mgdL

15ndash29 more common inAfrican Americans andHispanics oftenassociated with poorhydration

Rare but occurs withRYGB AGB andBPDDS

Serum thiamin responds todietary supplementationbut is poor indicator oftotal body stores

B6 (pyridoxine) PLP 5ndash24 ngmL RBC glutamic pyruvateOxaloacetic

PLP 3 ngmL Unknown Rare Consider with unresolvedanemia diabetes couldinfluence valuestransaminase

B12 (cobalamin) Serum B12 200ndash1000 pgmL 1Serum and urinaryMMA

1Serum tHcy

Serum B12

200 pgmL deficiency400 pgmL

suboptimalsMMA 0376 molLMMA 36 mol

mmol CRTtHcy 132 molL

10ndash13 may occur witholder patients and thosetaking H2 blockers andPPIs

Common withRYGB in absenceofsupplementation12ndash33

When symptoms arepresent and B12 200ndash250 pgmL MMA andtHcy are useful serumB12 may miss 25ndash30of deficiency cases

Folate RBC folate 280ndash791 ngmL Urinary FIGLUNormal serum andurinary MMA1Serum tHcy

RBC folate305 nmolL

deficiency227 nmolL anemia

Uncommon Uncommon Serum folate reflectsrecent dietary intakerather than folate statusRBC folate is a moresensitive marker

Excessive supplementationcan mask B12 deficiencyin CBC neurologicsymptoms will persist

Iron Ferritin Males15ndash200 ngmLFemales12ndash150 ngmL

2Serum iron1TIBC

Ferritin 20 ngmLSerum iron 50 gdLTIBC 450 gdL

9ndash16 of adult women ingeneral population aredeficient

20ndash49 of patientscommon withRYGB formenstruatingwomen (51) andpatients with superobesity (49ndash52)

Low Hgb and Hct areconsistent with irondeficiency anemia instage 3 or stage 4anemia ferritin is anacute phase reactant andwill be elevated withillness andorinflammation oralcontraceptives reduceblood loss formenstruating females

Vitamin A Plasma retinol 20ndash80 gdL RBP Plasma retinol 10gdL

Uncommon up to 7 insome studies

Common (50) withBPDDS after 1 yrup to 70 at 4 yrmay occur withRYGBAGB

Ocular finding maysuggest diagnosis

S77L

A

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Obesity

andR

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iseases4

(2008)S73-S108

Table 4Continued

Vitaminmineral Screening Normal range Additional laboratoryindexes

Critical range Preoperative deficiency Postoperativedeficiency

Comments

Vitamin D 25(OH)D 25ndash40 ngmL 2Serum phosphorus1Alkaline phosphatase1Serum PTH2Urinary calcium

Serum 25(OH)D 20ngmL suggestsdeficiency 20ndash30 ngmL suggestsinsufficiency

Common 60ndash70 Common with BPDDS after 1 yr mayoccur with RYGBprevalenceunknown

With deficiency serumcalcium may be low ornormal serumphosphorus maydecrease serum alkalinephosphatase increasesPTH elevated

Vitamin E Plasma alphatocopherol

5ndash20 gmL Plasma lipids 5 gmL Uncommon Uncommon Low plasma alphatocopherol to plasmalipids (08 mgg totallipid) should be usedwith hyperlipidemia

Vitamin K PT 10ndash13 seconds 1DCP 2Plasmaphylloquinone

Variable Uncommon Common with BPDDS after 1 yr

PT is not a sensitivemeasure of vitamin Kstatus

Zinc Plasma zinc 60ndash130 gdL 2RBC zinc Plasma zinc 70 gdL Uncommon but increasedrisk of low levelsassociated with obesity

Common with BPDDS after 1 yr mayoccur with RYGB

Monitor albumin levelsand interpret zincaccordingly albumin isprimary binding proteinfor zinc no reliablemethod of determiningzinc status is availableplasma zinc is methodgenerally used studiescited in this report didnot adequately describemethods of zinc analysis

Protein Serum albuminSerum totalprotein

4ndash6 gdL6ndash8 gdL

2Serum prealbumin(transthyretin)

Albumin 30 gdLPrealbumin 20 mgdL

Uncommon Rare but can occurwith RYGB AGBand BPDDS ifprotein intake islow in total intakeor indispensableamino acids

Half-life for prealbumin is2ndash4 d and reflectschanges in nutritionalstatus sooner thanalbumin a nonspecificprotein carrier with ahalf-life of 22 d

RYGB Roux-en-Y gastric bypass AGB adjustable gastric banding BPDDS biliopancreatic diversionduodenal switch PLP pyridoxal-5rsquo-phosphate RBC red blood cell MMA methylmalonic acid tHcy total homocysteine CRT creatinine PPIs protein pump inhibitors FIGLU formiminogluatmic acid CBC complete blood count TIBC total iron binding capacityHgb hemoglobin Hct hematocrit RPB retinol binding protein PTH parathyroid hormone 25(OH)D 25-hydroxyvitamin D PT prothrombin time DCP des-gamma-carboxypromthrom-bin

In general laboratory values should be reviewed annually or as indicated by clinical presentation Laboratory normal values vary among laboratory settings and are method dependent This chart providesa brief summary of monitoring tools See the Appendix for additional detail and diagnostic tools

copy Jeanne Blankenship MS RD Used with permission

S78L

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andR

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(2008)S73-S108

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S

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S79L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able 5uggested Postoperative Vitamin Supplementation

upplement AGB RYGB BPDDS Comment

ultivitamin-mineral supplementA high-potency vitamin containing 100 of daily value for

at least 23 of nutrients100 of daily

value

200 of dailyvalue

200 of daily value Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to whole tabletcapsule as toleratedAvoid time-released supplementsAvoid enteric coatingChoose a complete formula with at least 18 mg iron 400

g folic acid and containing selenium and zinc in eachserving

Avoid childrenrsquos formulas that are incompleteMay improve gastrointestinal tolerance when taken close to

food intakeMay separate dosageDo not mix multivitamin containing iron with calcium

supplement take at least 2 hr apartIndividual brands should be reviewed for absorption rate and

bioavailabilitySpecialized bariatric formulations are available

dditional cobalamin (B12)Available forms include sublingual tablets liquid drops

mouth spray or nasal gelsprayIntramuscular injection mdash 1000 gmo mdash Begin 0ndash3 mo after

surgeryOral tablet (crystalline form) mdash 350ndash500 gd mdashSupplementation after AGB and BPDDS may be required

dditional elemental calciumChoose a brand that contains calcium citrate and vitamin D3

Begin with chewable or liquidProgress to whole tabletcapsule as tolerated

1500 mgd 1500ndash 2000 mgd 1800ndash 2400 mgd May begin on day 1after hospitaldischarge orwithin 1 mo aftersurgery

Split into 500ndash600 mg doses be mindful of serving size onsupplement label

Space doses evenly throughout daySuggest a brand that contains magnesium especially for

BPDDSDo not combine calcium with iron containing supplements

To maximize absorptionTo minimize gastrointestinal intoleranceWait 2 h after taking multivitamin or iron supplement

Promote intake of dairy beverages andor foods that aresignificant sources of dietary calcium in addition torecommended supplements up to 3 servings daily

Combined dietary and supplemental calcium intake 1700mgd may be required to prevent bone loss during rapidweight loss

dditional elemental iron (above that provided by mvi)Recommended for menstruating women and those at risk of

anemia (total goal intake 50-100 mg elemental irond)

mdash Add a minimumof 18ndash27 mgdelemental

Add a minimum of18ndash27 mgdelemental

Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to tablet as toleratedDosage may need to be adjusted based on biochemical

markersNo enteric coatingDo not mix iron and calcium supplements take 2 h apartAvoid excessive intake of tea due to tannin interactionEncourage foods rich in heme iron

Vitamin C may enhance absorption of non-heme iron sources

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S80 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hich in turn causes metabolic changes that favor fatccumulation [23ndash25]

Several of the B-complex vitamins important for appro-riate metabolism of carbohydrate and neural functions thategulate appetite have been found to be deficient in someatients with morbid obesity [212627] Iron deficiencieshich would significantly hinder energy use have been

eported in nearly 50 of morbidly obese preoperativeandidates [21] Zinc and selenium deficits have been re-orted as well as deficits in vitamins A E and C allmportant antioxidants helpful in regulating energy produc-ion and various other processes of body weight manage-ent [1926ndash28]The risk of micronutrient depletion continues to be quite

igh particularly after surgeries that affect the digestion andbsorption of nutrients such as Roux-en-Y gastric bypassRYGB) and biliopancreatic diversion with or without du-denal switch (BPDDS) RYGB increases the risk of vita-in B12 and other B vitamin deficits in addition to iron and

alcium BPDDS procedures may also cause an increasedisk of iron and calcium deficits along with significant

able 5ontinued

upplement AGB

at-soluble vitaminsWith all procedures higher maintenance doses may be

required for those with a history of deficiencyWater-soluble preparations of fat-soluble vitamins are

availableRetinol sources of vitamin A should be used to calculatedosageMost supplements contain a high percentage of beta

carotene which does not contribute to vitamin A toxicityIntake of 2000 IU Vitamin D3 may be achieved with careful

selection of multivitamin and calcium supplementsNo toxic effect known for vitamin K1 phytonadione

(phyloquinone)

mdash

mdash

mdash

Vitamin K requirement varies with dietary sources andcolonic production

Caution with vitamin K supplementation for patientsreceiving coagulation therapy

Vitamin E deficiency has been suggested but is notprevalent in published studies

ptional B complexB-50 dosageLiquid form is available

1 servi

Avoid time released tabletsNo known risk of toxicityMay provide additional prophylaxis against B-vitamin

deficiencies including thiamin especially for BPDDSprocedures as water-soluble vitamins are absorbed in theproximal jejunum

Note 1000 mg of supplemental folic acid provided incombination with multivitamins could mask B12

deficiency

Abbreviations as in Table 4

eficiencies in the fat-soluble vitamins A D E and K d

hich are important for driving many of the biologicalrocesses that help to regulate body size [29ndash31] As theate of noncompliance with prophylactic multivitamin sup-lementation increases the rate of postoperative deficiencyay increase almost twofold [32]In the past it has been thought that the specific nutri-

ional deficiencies commonly seen among malabsorptiverocedures would not be present in patients choosing aurely restrictive surgery such as the adjustable gastric bandAGB) However poor eating behavior low nutrient-denseood choices food intolerance and a restricted portion sizean contribute to potential nutrient deficiencies in theseatients as well Although the incidence of nutritional com-lications may be less frequent in this patient population itould be detrimental to assume that they do not existIt is important for the bariatric patient to take vitamin and

ineral supplements not only to prevent adverse healthonditions that can arise after surgery but because someutrients such as calcium can enhance weight loss and helprevent weight regain The nutrient deficiency might beroportional to the length of the absorptive area bypassed

RYGB BPDDS Comment

mdash

mdash

mdash

10000 IU of vitamin A

2000 IU of vitamin D

300 g of vitamin K

May begin 2ndash4weeks aftersurgery

1 servingd 1 servingd May begin on day 1after hospitaldischarge

ngd

uring surgical procedures and to a lesser extent to the

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S81L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ercentage of weight lost Iron vitamin B12 and vitamin Deficiencies along with changes in calcium metabolism areommon after RYGB Protein fat-soluble vitamin andther micronutrient deficiencies as well as altered calciumetabolism are most notably found after BPDDS Folate

eficiency has been reported after AGB [33] Thiamin de-ciency is common among all surgical patients with fre-uent vomiting regardless of the type of procedure per-ormed Because many nutritional deficiencies progressith time patients should be monitored frequently and

egularly to prevent malnutrition [29] Reinforcement ofupplement compliance at each patient follow-up is alsomportant in the fight to enhance nutrition status and preventutritional complications

eight loss and nutrient deficits restrictionersus malabsorption

Malabsorptive procedures such as the BPDDS arehought to cause weight loss primarily through the malab-orption of macronutrients with as much as 25 of proteinnd 72 of fat malabsorbed Such primary malabsorptionesults in concomitant malabsorption of micronutrients3435] Vitamins and minerals relying on fat metabolismncluding vitamins D A E K and zinc may be affectedhen absorption is impaired [36] The decrease in gastro-

ntestinal transit time may also result in secondary malab-orption of a wide range of micronutrients related to by-assing the duodenum and jejunum or limited contact withhe brush border secondary to a short common limb Othericronutrient deficiency concerns reported for patients

hoosing a procedure with malabsorptive features includeron calcium vitamin B12 and folate

Nutrient deficiencies after RYGB can result from eitherrimary or secondary malabsorption or from inadequateietary intake A minimal amount of macronutrient malab-orption is thought to occur However specific micronutri-nts appear to be malabsorbed postoperatively and presents deficiencies without adequate vitamin and mineral sup-lementation Retrospective analyses of patients who havendergone gastric bypass have revealed predictable micro-utrient deficiencies including iron vitamin B12 and folate2627ndash39] Case reports have also shown that thiamin de-ciency can develop especially when persistent postopera-

ive vomiting occurs [40ndash43]Few studies that measure absorption after measured and

uantified intake have been published It can be hypothe-ized that the bypassed duodenum and proximal jejunumegatively affect nutrient assimilation Bradley et al [44]tudied patients who had undergone total gastrectomy therocedure from which the RYGB evolved The researchersound that most nutritional status changes in patients wereost likely due to changes in intake versus malabsorptionhese balance studies were conducted in a controlled re-

earch setting however they did not measure pre- and c

ostoperative changes nor include radioisotope labeling toeasure absorption of key nutrients and the subjects had

ndergone the procedure for reasons other than weight lossIt is unclear whether intestinal adaptation occurs after

ombination procedures and to what degree it affects long-erm weight maintenance and nutrition status Adaptation iscompensatory response that follows an abrupt decrease inucosal surface area and has been well studied in short-

owel patients who require bowel resection [45] The pro-ess includes both anatomic and functional changes thatncrease the gutrsquos digestive and absorptive capacity Al-hough these changes begin to take place in the early post-perative period total adaptation may take up to three yearso complete Adaptation in gastric bypass has not beenonsidered in absorption or metabolic studies This consid-ration could be important even when determining early andate macro- and micronutrient intake recommendations Theffect of pancreatic enzyme replacement therapy on vitaminnd mineral absorption in this population is also unknown

Purely restrictive procedures such as the AGB can resultn micronutrient deficiencies related to changes in dietaryntake It is commonly accepted that because no alteration isade in the absorptive pathway malabsorption does not

ccur as a result of AGB procedures However nutrienteficits would be likely to occur because of the low nutrientntake and avoidance of nutrient-rich foods in the earlyonths postoperatively and later possibly as a result of

xcessive band restriction Food with high nutritional valueuch as meat and fibrous fresh fruits and vegetables mighte poorly tolerated

Literature has been published that addresses the effect ofalabsorptive restrictive and combination surgical proce-

ures on acute and long-term nutritional status These stud-es have attempted for the most part to indirectly determinehe surgical impact on nutrition status by the evaluation ofetabolic and laboratory markers Although some studies

ave included certain aspects of absorption few have in-luded the necessary components to evaluate absorption ofprescribed andor monitored diet in a controlled metabolic

ettingThe following sections examine the pre- and postopera-

ive risks for nutritional deficiencies associated with RYGBPDDS and AGB It is important for all members of theedical team to increase their awareness of the nutritional

omplications and challenges that lie ahead for the patientontinued review of current research by the medical team

egarding advances in nutrition science beyond the bound-ries of the present report cannot be emphasized enough

hiamin (vitamin B1)

Beriberi is a thiamin deficiency that can affect variousrgan systems including the heart gastrointestinal tractnd peripheral and central nervous systems Although the

ondition is generally considered rare a number of reported

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S82 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nd possibly a much greater number of unreported or un-iagnosed cases of beriberi have occurred among individ-als who have undergone surgery for morbid obesity Earlyetection and prompt treatment of thiamin deficits in thesendividuals can help to prevent serious health consequencesf beriberi is misdiagnosed or goes undetected for even ahort period the bariatric patient can develop irreversibleeuromuscular disorders permanent defects in learning andhort-term memory coma and even death Because of theife-altering and potentially life-threatening nature of a thi-min deficiency it is important that healthcare professionalsn the field of bariatric surgery have knowledge of thetiology of the condition and its signs and symptomsreatment and prevention

tiology of potential deficiency Thiamin is a water-solubleitamin that is absorbed in the proximal jejunum by anctive (saturable high-affinity) transport system [4647] Inhe body thiamin is found in high concentrations in therain heart muscle liver and kidneys However withoutegular and sufficient intake these tissues become rapidlyevoid of thiamin [4647] The total amount of thiamin inhe body of an adult is approximately 30 mg with a half-lifef only 9ndash18 days Persistent vomiting a diet deficient inhe vitamin or the bodyrsquos excessive utilization of thiaminse can result in a severe state of thiamin depletion withinnly a short period producing symptoms of beriberi46ndash48]

Bariatric surgery increases the risk of beriberi through ex-cerbation of pre-existing thiamin deficits low nutrient intakealabsorption and episodes of nausea and vomiting [49ndash51]hronic or acute thiamin deficiencies in bariatric patients oftenresent with symptoms of peripheral neuropathy or Wer-ickersquos encephalopathy and Korsakoffrsquos psychoses [2148ndash4] Early diagnosis of the signs and symptoms of these con-itions is extremely important to prevent serious adverse healthonsequences Even if treatment is initiated recovery can bencomplete with cognitive andor neuromuscular impairmentsersisting long term or permanently

igns symptoms and treatment of deficiency (seeppendix Table A1)

reoperative risk The risk of the development of beriberifter bariatric surgery is far greater for individuals present-ng for surgery with low thiamin levels Investigators at theleveland Clinic of Florida reported that 15 of their pre-perative bariatric patients had deficiencies in thiamin be-ore surgery [52] A study by Flancbaum et al [21] similarlyound that 29 of their preoperative patients had low thia-in levels Data obtained by that study also showed a

ignificant difference between ethnicity and preoperativehiamin levels Although only 67 of whites presentedith thiamin deficiencies before surgery nearly one third

31) of African Americans and almost one half (47) of

ispanics had thiamin deficits The results of these studies S

uggested a need for preoperative thiamin testing as well ashiamin repletion by diet or supplementation to reduce theisk of ldquobariatricrdquo beriberi postoperatively

ostoperative risk Beriberi has been observed after gastricestrictive and malabsorptive procedures A number of casesf Wernicke-Korsakoff syndrome (WKS) as well as periph-ral neuropathy have been reported for patients havingndergone vertical banded gastroplasty [53ndash61] A fewncidences of WKS have also been reported after AGB436263] Additionally reports of thiamin deficiencies and

KS after RYGB [404164ndash73] and several cases of WKSnd neuropathy in patients who had undergone BPD [74]ave been published Many more cases of WKS are be-ieved to have occurred with bariatric procedures that haveither not been reported or have been misdiagnosed becausef limited knowledge regarding the signs and symptoms ofcute or severe thiamin deficits Because many foods areortified with thiamin beriberi has been nearly eradicatedhroughout the world except for patients with severe alco-olism severe vomiting during pregnancy (hyperemesisravidarium) or those malnourished and starved For thiseason few healthcare professionals until recently havead a patient present with beriberi

According to the published reports of thiamin deficitsfter bariatric procedures most patients develop such defi-iencies in the early postoperative months after an episodef intractable vomiting Nausea and vomiting are relativelyommon after all bariatric procedures early in the postop-rative period Thiamin stores in the body are small andaintenance of appropriate thiamin levels requires daily

eplenishment A deficiency of thiamin for only a couple ofeeks or less caused by persistent vomiting can deplete

hiamin stores Symptoms of WKS were reported in aYGB patient after only two weeks of persistent vomiting

67]Bariatric beriberi can also develop in postoperative patients

ho are given infusate containing dextrose without thiaminnd other vitamins which is often the case for patients inritical care units postoperative patients with complicationsnterfering with the ingestion of food or patients dehydratedrom persistent vomiting Malnutrition caused by a lack ofppetite and dietary intake postoperatively also contributes toariatric beriberi as does noncompliance in taking postopera-ive vitamin supplements

Although most cases of beriberi occur in the early post-perative periods cases of patients with severe thiamineficiency more than one year after surgery have beeneported One study reported WKS in association with al-ohol abuse 13 years after RYGB [75] Other conditionsontributing to late cases of bariatric beriberi include ahiamin-poor diet a diet high in carbohydrates anorexiand bulimia [46ndash48]

uggested supplementation Because of the greater likeli-

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S83L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ood of low dietary thiamin intake patients should be sup-lemented with thiamin This is usually accomplishedhrough daily intake of a multivitamin Most multivitaminsontain thiamin at 100 of the daily value Patients havingpisodes of nausea and vomiting and those who are anorec-ic might require sublingual intramuscular or intravenoushiamin to avoid depletion of thiamin stores and beriberiaution should be used when infusing bariatric patientsith solutions containing dextrose without additional vita-ins and thiamin because an increase in glucose utilizationithout additional thiamin can deplete thiamin stores [76]Thiamin deficiency in bariatric patients is treated with

hiamin together with other B-complex vitamins and mag-esium for maximal thiamin absorption and appropriateeurologic function [46 ndash 48] Early symptoms of neuropa-hy can often be resolved by providing the patient with oralhiamin doses of 20ndash30 mgd until symptoms disappear Forore advanced signs of neuropathy or for individuals with

rotracted vomiting 50ndash100 mgd of intravenous or intra-uscular thiamin may be necessary for resolution or im-

rovement of symptoms or for the prevention of suchatients with WKS generally require 100 mg thiamindministered intravenously for several days or longer fol-owed by intramuscular thiamin or high oral doses untilymptoms have resolved or significantly improved This canequire months to years Some patients might have to takehiamin for life to prevent the reoccurrence of neuropathy

itamin B12 and folate

Vitamin B12 (cobalamin) and folate (folic acid) are bothnvolved in the maturation of red blood cells and are com-only discussed in the literature together Over time a

eficiency in either vitamin B12 or folate can lead to mac-ocytic anemia a condition characterized by the productionf fewer but larger red blood cells and a decreased abilityo carry oxygen Most (95) cases of megaloblastic anemiacharacterized by large immature abnormal undifferenti-ted red blood cells in bone marrow) are attributed toitamin B12 or folate deficiency [77]

itamin B12

tiology of potential deficiency RYGB patients have bothncomplete digestion and release of vitamin B12 from pro-ein foods With a significant decrease in hydrochloric acidepsinogen is not converted into pepsin which is necessaryor the release of vitamin B12 from protein [78] BecauseGB patients have an artificial restriction yet complete usef the stomach and BPD patients do not have as great aestriction in stomach capacity and parietal cells as RYGBatients the reduction in hydrochloric acid and subsequentitamin B12 deficiency is not as prevalent with these tworocedures

Intrinsic factor (IF) is produced by the parietal cells of

he stomach and in certain conditions (eg atrophic gastri- a

is resected small bowel elderly patients) can be impairedausing an IF deficiency Subsequent vitamin B12 deficiencypernicious anemia) occurs without IF production or useecause IF is needed to absorb vitamin B12 in the terminalleum [77] Factors that increase the risk of vitamin B12

eficiency relevant to bariatric surgery include the follow-ng

An inability to release protein-bound vitamin B12

from food particularly in hypochlorhydria andatrophic gastritis

Malabsorption due to inadequate IF in perniciousanemia

Gastrectomy and gastric bypassResection or disease of terminal ileumLong-term vegan dietMedications such as neomycin metformin colch-

icines medications used in the management ofbowel inflammation and gastroesophageal refluxand ulcers (eg proton pump inhibitors) and anti-convulsant agents [79]

Cobalamin stores are known to exist for long periods3ndash5 yr) and are dependent on dietary repletion and dailyepletion However gastric bypass patients have both aecreased production of stomach acid and a decreased avail-bility of IF thus a vitamin B12 deficiency could developithout appropriate supplementation Because the typical

bsorption pathway cannot be relied on the surgical weightoss patient must rely on passive absorption of B12 whichccurs independent of IF

igns symptoms and treatment of deficiency (seeppendix Table A3)

reoperative risk Several medications common to preop-rative bariatric patients have been noted to affect preoper-tive vitamin B12 absorption and stores Of patients takingetformin 10ndash30 present with reduced vitamin B12 ab-

orption [80] Additionally patients with obesity have aigh incidence of gastroesophageal reflux disease for whichhey take proton pump inhibitors thus increasing the poten-ial to develop a vitamin B12 deficiency

Flancbaum et al [21] conducted a retrospective study of79 (320 women and 59 men) pre-operative patients Vita-in B12 deficiency was reported as negative in all patients

f various ethnic backgrounds [21] No clinical criteria orymptoms for vitamin B12 deficiency were noted In theeneral population 5ndash10 present with neurologic symp-oms with vitamin B12 levels of 200ndash400 pgmL Amongreoperative gastric bypass patients Madan et al [27] foundhat 13 (n 59) of patients were deficient in vitamin B12n a comparison of patients presenting for either RYGB orPD Skroubis et al [81] recently reported that preoperativeitamin B12 levels were low-normal in both groups Itould be prudent to screen for and treat IF deficiency

ndor vitamin B12 deficiency in all patients preoperatively

bd

PqtOop3cvbyrlBmtai

(pgopeveytBdsmllt

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sldwddwpsp

tpasm3qjanfmssts[

F

Eri

S84 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ut it is essential for RYGB patients so as not to hasten theevelopment of a potential postoperative deficiency

ostoperative risk Vitamin B12 deficiency has been fre-uently reported after RYGB Schilling et al [82] estimatedhe prevalence of vitamin B12 deficiency to be 12ndash33ther researchers have suggested a much greater prevalencef B12 deficiency in up to 75 of postoperative RYGBatients however most reports have cited approximately5 of postoperative RYGB patients as vitamin B12 defi-ient [82ndash87] Brolin et al [87] reported that low levels ofitamin B12 might be seen as soon as six months afterariatric surgery but most often occurring more than oneear postoperatively as liver stores become depleted Sk-oubis et al [88] predicted that the deficiency will mostikely occur 7 months after RYGB and 79 months afterPDDS although their research did not consider compro-ised preoperative status and its correlation to postopera-

ive deficiency After the first postoperative year the prev-lence of vitamin B12 deficiency appears to increase yearlyn RYGB patients [89]

Although the bodyrsquos storage of vitamin B12 is significant2000 g) compared with daily needs (24 gd) thisarticular deficiency has been found within 1ndash9 years ofastric bypass surgery [29] Brolin et al [84] reported thatne third of RYGB patients are deficient at four yearsostoperatively However non-surgical variables were notxplored and many patients might have had preoperativealues near the lower end of the normal range Ocon Bretont al [90] compared micronutrient deficiencies among two-ear postoperative BPDDS and RYGB patients and foundhat all nutritional deficiencies were more common amongPDDS patients except for vitamin B12 for which theeficiency was more common among the RYGB patientstudied A lack of B12 deficiency among BPDDS patientsight result from a better tolerance of animal proteins in a

arger pouch greater pepsingastric acid production to re-ease protein-bound B12 and increased availability and in-eraction of IF with the pouch contents

Experts have noted the significance of subclinical defi-iency in the low-normal cobalamin range in nongastricypass patients who do not exhibit clinical evidence ofeficiency The methylmalonic acid (MMA) assay is thereferred marker of B12 status because metabolic changesften precede low B12 levels in the progression to defi-iency Serum B12 assays may miss as much as 25ndash30 of

12 deficiencies making them less reliable than the MMAssay [91] It has been suggested that early signs of vitamin

12 deficiency can be detected if the serum levels of bothMA and homocysteine are measured [91] Vitamin B12

eficiency after RYGB has been associated with megalo-lastic anemia [92] Some vitamin B12-deficient patientsevelop significant symptoms such as polyneuropathy par-

sthesia and permanent neural impairment On occasion

ome patients may experience extreme delusions halluci-ations and even overt psychosis [93]

uggested supplementation Because of the frequent lack ofymptoms of vitamin B12 deficiency the suggested dili-ence in following up or treating these values among thosesymptomatic patients has been questioned The decisionot to supplement or routinely screen patients for B12 defi-iency should be examined very carefully given the risk ofrreversible neurologic damage if vitamin B12 goes un-reated for long periods At least one case report has beenublished of an exclusively breastfed infant with vitamin

12 deficiency who was born of an asymptomatic motherho had undergone gastric bypass surgery [94]Deficiency of vitamin B12 is typically defined at levels

200 pgmL However about 50 of patients with obviousigns and symptoms of deficiency have normal vitamin B12

evels [31] Kaplan et al [95] reported that vitamin B12

eficiency usually resolves after several weeks of treatmentith 700ndash2000 gwk Rhode et al [96] found that aosage of 350ndash600 gd of oral B12 prevented vitamin B12

eficiency in 95 of patients and an oral dose of 500 gdas sufficient to overcome an existing deficiency as re-orted by Brolin et al [87] in a similar study Thereforeupplementation of RYGB patients with 350ndash500 gd mayrevent most postoperative vitamin B12 deficiency

While most vitamin B12 in normal adults is absorbed inhe ileum in the presence of IF approximately 1 of sup-lemented B12 will be absorbed passively (by diffusion)long the entire length of the (non-bypassed) intestine byurgical weight loss patients given a high-dose oral supple-ent [97] Thus the consumption of 350ndash500 g yields a

5ndash50-g absorption which is greater than the daily re-uirement Although the use of monthly intramuscular in-ections or a weekly oral dose of vitamin B12 is commonmong practices it relies on patient compliance Practitio-ers should assess the patientrsquos preference and the potentialor compliance when considering a daily weekly oronthly regimen of B12 supplementation In addition to oral

upplements or intramuscular injections nasal sprays andublingual sources of vitamin B12 are also available Pa-ients should be monitored closely for their lifetime becauseevere anemia can develop with or without supplementation98]

olate

tiology of potential deficiency Factors that increase theisk of folic acid deficiency relevant to bariatric surgerynclude the following

Inadequate dietary intakeNoncompliance with multivitamin supplementationMalabsorptionMedications (anticonvulsants oral contraceptives

and cancer treating agents) [79]

pmo

SA

PAtArBatbhptl5

Plddlpolh(cs4wdppvds[(m

mlEfadtc

cbct

pntiat

ntwttRhm

Soiwt[2tpbvhsfowbmftm

I

dspbiwiu

S85L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Folic acid stores can be depleted within a few monthsostoperatively unless replenished by a multivitamin supple-ent and dietary sources (ie green leafy vegetables fruits

rgan meats liver dried yeast and fortified grain products)

igns symptoms and treatment of deficiency (seeppendix Table A4)

reoperative risk The goals of the 1998 Food and Drugdministration policy requiring all enriched grain products

o be fortified with folate included increasing the averagemerican diet by 100 g folate daily and decreasing the

ate of neural tube defects in childbearing women [99]entley et al [100] reported that the proportion of womenged 15ndash44 years old (in the general population) who meethe recommended dietary intake of 400 gd folate variesetween 23 and 33 With the increasing popularity ofigh proteinlow carbohydrate diets one cannot assume thatreoperative patients consume dietary sources of folatehrough fortified grain products fruits and vegetables Boy-an et al [26] found folate deficiencies preoperatively in6 of RYGB patients studied

ostoperative risk Although it has been observed that fo-ate deficiency after RYGB surgery is less common than B12

eficiency and is thought to occur because of decreasedietary or multivitamin supplement intake low serum folateevels have been cited from 6 to 65 among RYGBatients [2686101] Additionally folate deficiencies haveccurred postoperatively even with supplementation Boy-an et al [26] found that 47 (n 17) of RYGB patientsad low folate levels six months postoperatively and 41n 17) had low levels at one year This deficiency oc-urred despite patient adherence to taking a multivitaminupplement that contained at least the daily value for folate00 g [26] Postoperative bariatric patients with rapideight loss might have an increased risk of micronutrienteficiencies MacLean et al [86] reported that 65 ofostoperative patients had low folate levels These sameatients exhibited additional B vitamin deficiencies 24itamin B12 and 50 thiamin [86] An increased risk ofeficiency has also been noted among AGB patients pos-ibly because of decreased folate intake Gasteyger et al33] found a significant decrease in serum folate levels441) between the baseline and 24-month postoperativeeasurementsDixon and OrsquoBrien [101] reported elevated serum ho-

ocysteine levels in patients after bariatric surgery regard-ess of the type of procedure (restrictive or malabsorptive)levated homocysteine levels can indicate not only low

olate levels and a greater risk of neural tube defects but canlso be indicative of an independent risk factor for heartisease andor oxidative stress in the nonbariatric popula-ion [102] However unlike iron and vitamin B12 the folate

ontained in the multivitamin supplementation essentially e

orrects the deficiency in the vast majority of postoperativeariatric patients [103] Therefore persistent folate defi-iency might indicate a patientrsquos lack of compliance withhe prescribed vitamin protocol [32]

It is common knowledge that folic acid deficiency amongregnant women has been associated with a greater risk ofeural tube defects in newborns Consistent supplementa-ion and monitoring among women of child-bearing agencluding pre- and postoperative bariatric patients is vital inn effort to prevent the possibility of neural tube defects inhe developing fetus

Because folate does not affect the myelin of nerveseurologic damage is not as common with folate such as ishe case for vitamin B12 deficiency In contrast patientsith folate deficiency often present with forgetfulness irri-

ability hostility and even paranoid behaviors [29] Similaro that evidenced with vitamin B12 most postoperativeYGB patients who are folate deficient are asymptomatic orave subclinical symptoms therefore these deficient statesay not be easily identified

uggested supplementation Even though folate absorptionccurs preferentially in the proximal portion of the smallntestine it can occur along the entire length of the small bowelith postoperative adaptation Therefore it is generally agreed

hat folate deficiency is corrected with 1000 mgd folic acid32] and is preventable with supplementation that provides00 of the daily value (800 g) This level can also benefithe fetus in a female patient unaware of her postoperativeregnancy Folate supplementation 1000 mgd has noteen recommended because of the potential for maskingitamin B12 deficiency Carmel et al [104] suggested thatomocysteine is the most sensitive marker of folic acidtatus in conjunction with erythrocyte folate Althougholic acid deficiency could potentially occur among post-perative bariatric surgery patients it has not been seenidely in recent studies especially when patients haveeen compliant with postoperative multivitamin supple-entation Therefore it is imperative to closely follow

olic acid both pre- and postoperatively especially inhose patients suspected to be noncompliant with theirultivitamin supplementation

ron

Much of the iron and surgical weight loss research con-ucted to date has been generated from a limited number ofurgeons and scientists however the data have consistentlyointed toward the risk of iron deficiency and anemia afterariatric procedures Iron deficiency is defined as a decreasen the total iron body content Iron deficiency anemia occurshen erythropoiesis is impaired as a result of the lack of

ron stores In the absence of anemia iron deficiency issually asymptomatic Fatigue and a diminished capacity to

xercise however are common symptoms of anemia

Emspwabiebteiitaiccdpdgedatlrccaiam

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Pb4stdbu

ifftBibfagowtimiB

rsttdttpft

S86 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

tsmp

lsnfwTlopaechc

Rtbwdsaar

fdaiwiiedasdt

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mccmacdrrT

C

EeamadmsDfd

dbdh7DtnDcwsh

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Pcptt[hmtlcgc

S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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cpbaesrct

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S88 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

tmcbettb

gtctp

SoscvrwaDomi

tmprwoinc[vbnabc(prsdhp

ch

wpbcfbacat

V

Etva3dg5natshRh

sfeAilgt

SA

V

sttab

ceAwg5

S89L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

ww

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S90 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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O

VcslwAwvIvmtbrvsee

S91L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

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S93L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

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S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

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S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

s

aildquo

T

T

DFF

F

E

A

D

T

T

P

DFF

S

D

T

S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

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S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

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S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 5: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

Table 4Suggested Biochemical Monitoring Tools for Nutrition Status

Vitaminmineral Screening Normal range Additional laboratoryindexes

Critical range Preoperative deficiency Postoperativedeficiency

Comments

B1 (thiamin) Serum thiamin 10ndash64 ngmL 2RBC transketolase1Pyruvate

Transketolase activity20

Pyruvate 1 mgdL

15ndash29 more common inAfrican Americans andHispanics oftenassociated with poorhydration

Rare but occurs withRYGB AGB andBPDDS

Serum thiamin responds todietary supplementationbut is poor indicator oftotal body stores

B6 (pyridoxine) PLP 5ndash24 ngmL RBC glutamic pyruvateOxaloacetic

PLP 3 ngmL Unknown Rare Consider with unresolvedanemia diabetes couldinfluence valuestransaminase

B12 (cobalamin) Serum B12 200ndash1000 pgmL 1Serum and urinaryMMA

1Serum tHcy

Serum B12

200 pgmL deficiency400 pgmL

suboptimalsMMA 0376 molLMMA 36 mol

mmol CRTtHcy 132 molL

10ndash13 may occur witholder patients and thosetaking H2 blockers andPPIs

Common withRYGB in absenceofsupplementation12ndash33

When symptoms arepresent and B12 200ndash250 pgmL MMA andtHcy are useful serumB12 may miss 25ndash30of deficiency cases

Folate RBC folate 280ndash791 ngmL Urinary FIGLUNormal serum andurinary MMA1Serum tHcy

RBC folate305 nmolL

deficiency227 nmolL anemia

Uncommon Uncommon Serum folate reflectsrecent dietary intakerather than folate statusRBC folate is a moresensitive marker

Excessive supplementationcan mask B12 deficiencyin CBC neurologicsymptoms will persist

Iron Ferritin Males15ndash200 ngmLFemales12ndash150 ngmL

2Serum iron1TIBC

Ferritin 20 ngmLSerum iron 50 gdLTIBC 450 gdL

9ndash16 of adult women ingeneral population aredeficient

20ndash49 of patientscommon withRYGB formenstruatingwomen (51) andpatients with superobesity (49ndash52)

Low Hgb and Hct areconsistent with irondeficiency anemia instage 3 or stage 4anemia ferritin is anacute phase reactant andwill be elevated withillness andorinflammation oralcontraceptives reduceblood loss formenstruating females

Vitamin A Plasma retinol 20ndash80 gdL RBP Plasma retinol 10gdL

Uncommon up to 7 insome studies

Common (50) withBPDDS after 1 yrup to 70 at 4 yrmay occur withRYGBAGB

Ocular finding maysuggest diagnosis

S77L

A

illset

al

Surgeryfor

Obesity

andR

elatedD

iseases4

(2008)S73-S108

Table 4Continued

Vitaminmineral Screening Normal range Additional laboratoryindexes

Critical range Preoperative deficiency Postoperativedeficiency

Comments

Vitamin D 25(OH)D 25ndash40 ngmL 2Serum phosphorus1Alkaline phosphatase1Serum PTH2Urinary calcium

Serum 25(OH)D 20ngmL suggestsdeficiency 20ndash30 ngmL suggestsinsufficiency

Common 60ndash70 Common with BPDDS after 1 yr mayoccur with RYGBprevalenceunknown

With deficiency serumcalcium may be low ornormal serumphosphorus maydecrease serum alkalinephosphatase increasesPTH elevated

Vitamin E Plasma alphatocopherol

5ndash20 gmL Plasma lipids 5 gmL Uncommon Uncommon Low plasma alphatocopherol to plasmalipids (08 mgg totallipid) should be usedwith hyperlipidemia

Vitamin K PT 10ndash13 seconds 1DCP 2Plasmaphylloquinone

Variable Uncommon Common with BPDDS after 1 yr

PT is not a sensitivemeasure of vitamin Kstatus

Zinc Plasma zinc 60ndash130 gdL 2RBC zinc Plasma zinc 70 gdL Uncommon but increasedrisk of low levelsassociated with obesity

Common with BPDDS after 1 yr mayoccur with RYGB

Monitor albumin levelsand interpret zincaccordingly albumin isprimary binding proteinfor zinc no reliablemethod of determiningzinc status is availableplasma zinc is methodgenerally used studiescited in this report didnot adequately describemethods of zinc analysis

Protein Serum albuminSerum totalprotein

4ndash6 gdL6ndash8 gdL

2Serum prealbumin(transthyretin)

Albumin 30 gdLPrealbumin 20 mgdL

Uncommon Rare but can occurwith RYGB AGBand BPDDS ifprotein intake islow in total intakeor indispensableamino acids

Half-life for prealbumin is2ndash4 d and reflectschanges in nutritionalstatus sooner thanalbumin a nonspecificprotein carrier with ahalf-life of 22 d

RYGB Roux-en-Y gastric bypass AGB adjustable gastric banding BPDDS biliopancreatic diversionduodenal switch PLP pyridoxal-5rsquo-phosphate RBC red blood cell MMA methylmalonic acid tHcy total homocysteine CRT creatinine PPIs protein pump inhibitors FIGLU formiminogluatmic acid CBC complete blood count TIBC total iron binding capacityHgb hemoglobin Hct hematocrit RPB retinol binding protein PTH parathyroid hormone 25(OH)D 25-hydroxyvitamin D PT prothrombin time DCP des-gamma-carboxypromthrom-bin

In general laboratory values should be reviewed annually or as indicated by clinical presentation Laboratory normal values vary among laboratory settings and are method dependent This chart providesa brief summary of monitoring tools See the Appendix for additional detail and diagnostic tools

copy Jeanne Blankenship MS RD Used with permission

S78L

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illset

al

Surgeryfor

Obesity

andR

elatedD

iseases4

(2008)S73-S108

TS

S

M

A

A

A

S79L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able 5uggested Postoperative Vitamin Supplementation

upplement AGB RYGB BPDDS Comment

ultivitamin-mineral supplementA high-potency vitamin containing 100 of daily value for

at least 23 of nutrients100 of daily

value

200 of dailyvalue

200 of daily value Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to whole tabletcapsule as toleratedAvoid time-released supplementsAvoid enteric coatingChoose a complete formula with at least 18 mg iron 400

g folic acid and containing selenium and zinc in eachserving

Avoid childrenrsquos formulas that are incompleteMay improve gastrointestinal tolerance when taken close to

food intakeMay separate dosageDo not mix multivitamin containing iron with calcium

supplement take at least 2 hr apartIndividual brands should be reviewed for absorption rate and

bioavailabilitySpecialized bariatric formulations are available

dditional cobalamin (B12)Available forms include sublingual tablets liquid drops

mouth spray or nasal gelsprayIntramuscular injection mdash 1000 gmo mdash Begin 0ndash3 mo after

surgeryOral tablet (crystalline form) mdash 350ndash500 gd mdashSupplementation after AGB and BPDDS may be required

dditional elemental calciumChoose a brand that contains calcium citrate and vitamin D3

Begin with chewable or liquidProgress to whole tabletcapsule as tolerated

1500 mgd 1500ndash 2000 mgd 1800ndash 2400 mgd May begin on day 1after hospitaldischarge orwithin 1 mo aftersurgery

Split into 500ndash600 mg doses be mindful of serving size onsupplement label

Space doses evenly throughout daySuggest a brand that contains magnesium especially for

BPDDSDo not combine calcium with iron containing supplements

To maximize absorptionTo minimize gastrointestinal intoleranceWait 2 h after taking multivitamin or iron supplement

Promote intake of dairy beverages andor foods that aresignificant sources of dietary calcium in addition torecommended supplements up to 3 servings daily

Combined dietary and supplemental calcium intake 1700mgd may be required to prevent bone loss during rapidweight loss

dditional elemental iron (above that provided by mvi)Recommended for menstruating women and those at risk of

anemia (total goal intake 50-100 mg elemental irond)

mdash Add a minimumof 18ndash27 mgdelemental

Add a minimum of18ndash27 mgdelemental

Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to tablet as toleratedDosage may need to be adjusted based on biochemical

markersNo enteric coatingDo not mix iron and calcium supplements take 2 h apartAvoid excessive intake of tea due to tannin interactionEncourage foods rich in heme iron

Vitamin C may enhance absorption of non-heme iron sources

wa

prpwrcpitm

ha(omcrd

wprpm

tpp(fcppw

mcnpp

TC

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F

O

S80 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hich in turn causes metabolic changes that favor fatccumulation [23ndash25]

Several of the B-complex vitamins important for appro-riate metabolism of carbohydrate and neural functions thategulate appetite have been found to be deficient in someatients with morbid obesity [212627] Iron deficiencieshich would significantly hinder energy use have been

eported in nearly 50 of morbidly obese preoperativeandidates [21] Zinc and selenium deficits have been re-orted as well as deficits in vitamins A E and C allmportant antioxidants helpful in regulating energy produc-ion and various other processes of body weight manage-ent [1926ndash28]The risk of micronutrient depletion continues to be quite

igh particularly after surgeries that affect the digestion andbsorption of nutrients such as Roux-en-Y gastric bypassRYGB) and biliopancreatic diversion with or without du-denal switch (BPDDS) RYGB increases the risk of vita-in B12 and other B vitamin deficits in addition to iron and

alcium BPDDS procedures may also cause an increasedisk of iron and calcium deficits along with significant

able 5ontinued

upplement AGB

at-soluble vitaminsWith all procedures higher maintenance doses may be

required for those with a history of deficiencyWater-soluble preparations of fat-soluble vitamins are

availableRetinol sources of vitamin A should be used to calculatedosageMost supplements contain a high percentage of beta

carotene which does not contribute to vitamin A toxicityIntake of 2000 IU Vitamin D3 may be achieved with careful

selection of multivitamin and calcium supplementsNo toxic effect known for vitamin K1 phytonadione

(phyloquinone)

mdash

mdash

mdash

Vitamin K requirement varies with dietary sources andcolonic production

Caution with vitamin K supplementation for patientsreceiving coagulation therapy

Vitamin E deficiency has been suggested but is notprevalent in published studies

ptional B complexB-50 dosageLiquid form is available

1 servi

Avoid time released tabletsNo known risk of toxicityMay provide additional prophylaxis against B-vitamin

deficiencies including thiamin especially for BPDDSprocedures as water-soluble vitamins are absorbed in theproximal jejunum

Note 1000 mg of supplemental folic acid provided incombination with multivitamins could mask B12

deficiency

Abbreviations as in Table 4

eficiencies in the fat-soluble vitamins A D E and K d

hich are important for driving many of the biologicalrocesses that help to regulate body size [29ndash31] As theate of noncompliance with prophylactic multivitamin sup-lementation increases the rate of postoperative deficiencyay increase almost twofold [32]In the past it has been thought that the specific nutri-

ional deficiencies commonly seen among malabsorptiverocedures would not be present in patients choosing aurely restrictive surgery such as the adjustable gastric bandAGB) However poor eating behavior low nutrient-denseood choices food intolerance and a restricted portion sizean contribute to potential nutrient deficiencies in theseatients as well Although the incidence of nutritional com-lications may be less frequent in this patient population itould be detrimental to assume that they do not existIt is important for the bariatric patient to take vitamin and

ineral supplements not only to prevent adverse healthonditions that can arise after surgery but because someutrients such as calcium can enhance weight loss and helprevent weight regain The nutrient deficiency might beroportional to the length of the absorptive area bypassed

RYGB BPDDS Comment

mdash

mdash

mdash

10000 IU of vitamin A

2000 IU of vitamin D

300 g of vitamin K

May begin 2ndash4weeks aftersurgery

1 servingd 1 servingd May begin on day 1after hospitaldischarge

ngd

uring surgical procedures and to a lesser extent to the

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tsar[iwisptmci

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oa

S81L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ercentage of weight lost Iron vitamin B12 and vitamin Deficiencies along with changes in calcium metabolism areommon after RYGB Protein fat-soluble vitamin andther micronutrient deficiencies as well as altered calciumetabolism are most notably found after BPDDS Folate

eficiency has been reported after AGB [33] Thiamin de-ciency is common among all surgical patients with fre-uent vomiting regardless of the type of procedure per-ormed Because many nutritional deficiencies progressith time patients should be monitored frequently and

egularly to prevent malnutrition [29] Reinforcement ofupplement compliance at each patient follow-up is alsomportant in the fight to enhance nutrition status and preventutritional complications

eight loss and nutrient deficits restrictionersus malabsorption

Malabsorptive procedures such as the BPDDS arehought to cause weight loss primarily through the malab-orption of macronutrients with as much as 25 of proteinnd 72 of fat malabsorbed Such primary malabsorptionesults in concomitant malabsorption of micronutrients3435] Vitamins and minerals relying on fat metabolismncluding vitamins D A E K and zinc may be affectedhen absorption is impaired [36] The decrease in gastro-

ntestinal transit time may also result in secondary malab-orption of a wide range of micronutrients related to by-assing the duodenum and jejunum or limited contact withhe brush border secondary to a short common limb Othericronutrient deficiency concerns reported for patients

hoosing a procedure with malabsorptive features includeron calcium vitamin B12 and folate

Nutrient deficiencies after RYGB can result from eitherrimary or secondary malabsorption or from inadequateietary intake A minimal amount of macronutrient malab-orption is thought to occur However specific micronutri-nts appear to be malabsorbed postoperatively and presents deficiencies without adequate vitamin and mineral sup-lementation Retrospective analyses of patients who havendergone gastric bypass have revealed predictable micro-utrient deficiencies including iron vitamin B12 and folate2627ndash39] Case reports have also shown that thiamin de-ciency can develop especially when persistent postopera-

ive vomiting occurs [40ndash43]Few studies that measure absorption after measured and

uantified intake have been published It can be hypothe-ized that the bypassed duodenum and proximal jejunumegatively affect nutrient assimilation Bradley et al [44]tudied patients who had undergone total gastrectomy therocedure from which the RYGB evolved The researchersound that most nutritional status changes in patients wereost likely due to changes in intake versus malabsorptionhese balance studies were conducted in a controlled re-

earch setting however they did not measure pre- and c

ostoperative changes nor include radioisotope labeling toeasure absorption of key nutrients and the subjects had

ndergone the procedure for reasons other than weight lossIt is unclear whether intestinal adaptation occurs after

ombination procedures and to what degree it affects long-erm weight maintenance and nutrition status Adaptation iscompensatory response that follows an abrupt decrease inucosal surface area and has been well studied in short-

owel patients who require bowel resection [45] The pro-ess includes both anatomic and functional changes thatncrease the gutrsquos digestive and absorptive capacity Al-hough these changes begin to take place in the early post-perative period total adaptation may take up to three yearso complete Adaptation in gastric bypass has not beenonsidered in absorption or metabolic studies This consid-ration could be important even when determining early andate macro- and micronutrient intake recommendations Theffect of pancreatic enzyme replacement therapy on vitaminnd mineral absorption in this population is also unknown

Purely restrictive procedures such as the AGB can resultn micronutrient deficiencies related to changes in dietaryntake It is commonly accepted that because no alteration isade in the absorptive pathway malabsorption does not

ccur as a result of AGB procedures However nutrienteficits would be likely to occur because of the low nutrientntake and avoidance of nutrient-rich foods in the earlyonths postoperatively and later possibly as a result of

xcessive band restriction Food with high nutritional valueuch as meat and fibrous fresh fruits and vegetables mighte poorly tolerated

Literature has been published that addresses the effect ofalabsorptive restrictive and combination surgical proce-

ures on acute and long-term nutritional status These stud-es have attempted for the most part to indirectly determinehe surgical impact on nutrition status by the evaluation ofetabolic and laboratory markers Although some studies

ave included certain aspects of absorption few have in-luded the necessary components to evaluate absorption ofprescribed andor monitored diet in a controlled metabolic

ettingThe following sections examine the pre- and postopera-

ive risks for nutritional deficiencies associated with RYGBPDDS and AGB It is important for all members of theedical team to increase their awareness of the nutritional

omplications and challenges that lie ahead for the patientontinued review of current research by the medical team

egarding advances in nutrition science beyond the bound-ries of the present report cannot be emphasized enough

hiamin (vitamin B1)

Beriberi is a thiamin deficiency that can affect variousrgan systems including the heart gastrointestinal tractnd peripheral and central nervous systems Although the

ondition is generally considered rare a number of reported

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S82 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nd possibly a much greater number of unreported or un-iagnosed cases of beriberi have occurred among individ-als who have undergone surgery for morbid obesity Earlyetection and prompt treatment of thiamin deficits in thesendividuals can help to prevent serious health consequencesf beriberi is misdiagnosed or goes undetected for even ahort period the bariatric patient can develop irreversibleeuromuscular disorders permanent defects in learning andhort-term memory coma and even death Because of theife-altering and potentially life-threatening nature of a thi-min deficiency it is important that healthcare professionalsn the field of bariatric surgery have knowledge of thetiology of the condition and its signs and symptomsreatment and prevention

tiology of potential deficiency Thiamin is a water-solubleitamin that is absorbed in the proximal jejunum by anctive (saturable high-affinity) transport system [4647] Inhe body thiamin is found in high concentrations in therain heart muscle liver and kidneys However withoutegular and sufficient intake these tissues become rapidlyevoid of thiamin [4647] The total amount of thiamin inhe body of an adult is approximately 30 mg with a half-lifef only 9ndash18 days Persistent vomiting a diet deficient inhe vitamin or the bodyrsquos excessive utilization of thiaminse can result in a severe state of thiamin depletion withinnly a short period producing symptoms of beriberi46ndash48]

Bariatric surgery increases the risk of beriberi through ex-cerbation of pre-existing thiamin deficits low nutrient intakealabsorption and episodes of nausea and vomiting [49ndash51]hronic or acute thiamin deficiencies in bariatric patients oftenresent with symptoms of peripheral neuropathy or Wer-ickersquos encephalopathy and Korsakoffrsquos psychoses [2148ndash4] Early diagnosis of the signs and symptoms of these con-itions is extremely important to prevent serious adverse healthonsequences Even if treatment is initiated recovery can bencomplete with cognitive andor neuromuscular impairmentsersisting long term or permanently

igns symptoms and treatment of deficiency (seeppendix Table A1)

reoperative risk The risk of the development of beriberifter bariatric surgery is far greater for individuals present-ng for surgery with low thiamin levels Investigators at theleveland Clinic of Florida reported that 15 of their pre-perative bariatric patients had deficiencies in thiamin be-ore surgery [52] A study by Flancbaum et al [21] similarlyound that 29 of their preoperative patients had low thia-in levels Data obtained by that study also showed a

ignificant difference between ethnicity and preoperativehiamin levels Although only 67 of whites presentedith thiamin deficiencies before surgery nearly one third

31) of African Americans and almost one half (47) of

ispanics had thiamin deficits The results of these studies S

uggested a need for preoperative thiamin testing as well ashiamin repletion by diet or supplementation to reduce theisk of ldquobariatricrdquo beriberi postoperatively

ostoperative risk Beriberi has been observed after gastricestrictive and malabsorptive procedures A number of casesf Wernicke-Korsakoff syndrome (WKS) as well as periph-ral neuropathy have been reported for patients havingndergone vertical banded gastroplasty [53ndash61] A fewncidences of WKS have also been reported after AGB436263] Additionally reports of thiamin deficiencies and

KS after RYGB [404164ndash73] and several cases of WKSnd neuropathy in patients who had undergone BPD [74]ave been published Many more cases of WKS are be-ieved to have occurred with bariatric procedures that haveither not been reported or have been misdiagnosed becausef limited knowledge regarding the signs and symptoms ofcute or severe thiamin deficits Because many foods areortified with thiamin beriberi has been nearly eradicatedhroughout the world except for patients with severe alco-olism severe vomiting during pregnancy (hyperemesisravidarium) or those malnourished and starved For thiseason few healthcare professionals until recently havead a patient present with beriberi

According to the published reports of thiamin deficitsfter bariatric procedures most patients develop such defi-iencies in the early postoperative months after an episodef intractable vomiting Nausea and vomiting are relativelyommon after all bariatric procedures early in the postop-rative period Thiamin stores in the body are small andaintenance of appropriate thiamin levels requires daily

eplenishment A deficiency of thiamin for only a couple ofeeks or less caused by persistent vomiting can deplete

hiamin stores Symptoms of WKS were reported in aYGB patient after only two weeks of persistent vomiting

67]Bariatric beriberi can also develop in postoperative patients

ho are given infusate containing dextrose without thiaminnd other vitamins which is often the case for patients inritical care units postoperative patients with complicationsnterfering with the ingestion of food or patients dehydratedrom persistent vomiting Malnutrition caused by a lack ofppetite and dietary intake postoperatively also contributes toariatric beriberi as does noncompliance in taking postopera-ive vitamin supplements

Although most cases of beriberi occur in the early post-perative periods cases of patients with severe thiamineficiency more than one year after surgery have beeneported One study reported WKS in association with al-ohol abuse 13 years after RYGB [75] Other conditionsontributing to late cases of bariatric beriberi include ahiamin-poor diet a diet high in carbohydrates anorexiand bulimia [46ndash48]

uggested supplementation Because of the greater likeli-

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S83L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ood of low dietary thiamin intake patients should be sup-lemented with thiamin This is usually accomplishedhrough daily intake of a multivitamin Most multivitaminsontain thiamin at 100 of the daily value Patients havingpisodes of nausea and vomiting and those who are anorec-ic might require sublingual intramuscular or intravenoushiamin to avoid depletion of thiamin stores and beriberiaution should be used when infusing bariatric patientsith solutions containing dextrose without additional vita-ins and thiamin because an increase in glucose utilizationithout additional thiamin can deplete thiamin stores [76]Thiamin deficiency in bariatric patients is treated with

hiamin together with other B-complex vitamins and mag-esium for maximal thiamin absorption and appropriateeurologic function [46 ndash 48] Early symptoms of neuropa-hy can often be resolved by providing the patient with oralhiamin doses of 20ndash30 mgd until symptoms disappear Forore advanced signs of neuropathy or for individuals with

rotracted vomiting 50ndash100 mgd of intravenous or intra-uscular thiamin may be necessary for resolution or im-

rovement of symptoms or for the prevention of suchatients with WKS generally require 100 mg thiamindministered intravenously for several days or longer fol-owed by intramuscular thiamin or high oral doses untilymptoms have resolved or significantly improved This canequire months to years Some patients might have to takehiamin for life to prevent the reoccurrence of neuropathy

itamin B12 and folate

Vitamin B12 (cobalamin) and folate (folic acid) are bothnvolved in the maturation of red blood cells and are com-only discussed in the literature together Over time a

eficiency in either vitamin B12 or folate can lead to mac-ocytic anemia a condition characterized by the productionf fewer but larger red blood cells and a decreased abilityo carry oxygen Most (95) cases of megaloblastic anemiacharacterized by large immature abnormal undifferenti-ted red blood cells in bone marrow) are attributed toitamin B12 or folate deficiency [77]

itamin B12

tiology of potential deficiency RYGB patients have bothncomplete digestion and release of vitamin B12 from pro-ein foods With a significant decrease in hydrochloric acidepsinogen is not converted into pepsin which is necessaryor the release of vitamin B12 from protein [78] BecauseGB patients have an artificial restriction yet complete usef the stomach and BPD patients do not have as great aestriction in stomach capacity and parietal cells as RYGBatients the reduction in hydrochloric acid and subsequentitamin B12 deficiency is not as prevalent with these tworocedures

Intrinsic factor (IF) is produced by the parietal cells of

he stomach and in certain conditions (eg atrophic gastri- a

is resected small bowel elderly patients) can be impairedausing an IF deficiency Subsequent vitamin B12 deficiencypernicious anemia) occurs without IF production or useecause IF is needed to absorb vitamin B12 in the terminalleum [77] Factors that increase the risk of vitamin B12

eficiency relevant to bariatric surgery include the follow-ng

An inability to release protein-bound vitamin B12

from food particularly in hypochlorhydria andatrophic gastritis

Malabsorption due to inadequate IF in perniciousanemia

Gastrectomy and gastric bypassResection or disease of terminal ileumLong-term vegan dietMedications such as neomycin metformin colch-

icines medications used in the management ofbowel inflammation and gastroesophageal refluxand ulcers (eg proton pump inhibitors) and anti-convulsant agents [79]

Cobalamin stores are known to exist for long periods3ndash5 yr) and are dependent on dietary repletion and dailyepletion However gastric bypass patients have both aecreased production of stomach acid and a decreased avail-bility of IF thus a vitamin B12 deficiency could developithout appropriate supplementation Because the typical

bsorption pathway cannot be relied on the surgical weightoss patient must rely on passive absorption of B12 whichccurs independent of IF

igns symptoms and treatment of deficiency (seeppendix Table A3)

reoperative risk Several medications common to preop-rative bariatric patients have been noted to affect preoper-tive vitamin B12 absorption and stores Of patients takingetformin 10ndash30 present with reduced vitamin B12 ab-

orption [80] Additionally patients with obesity have aigh incidence of gastroesophageal reflux disease for whichhey take proton pump inhibitors thus increasing the poten-ial to develop a vitamin B12 deficiency

Flancbaum et al [21] conducted a retrospective study of79 (320 women and 59 men) pre-operative patients Vita-in B12 deficiency was reported as negative in all patients

f various ethnic backgrounds [21] No clinical criteria orymptoms for vitamin B12 deficiency were noted In theeneral population 5ndash10 present with neurologic symp-oms with vitamin B12 levels of 200ndash400 pgmL Amongreoperative gastric bypass patients Madan et al [27] foundhat 13 (n 59) of patients were deficient in vitamin B12n a comparison of patients presenting for either RYGB orPD Skroubis et al [81] recently reported that preoperativeitamin B12 levels were low-normal in both groups Itould be prudent to screen for and treat IF deficiency

ndor vitamin B12 deficiency in all patients preoperatively

bd

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Eri

S84 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ut it is essential for RYGB patients so as not to hasten theevelopment of a potential postoperative deficiency

ostoperative risk Vitamin B12 deficiency has been fre-uently reported after RYGB Schilling et al [82] estimatedhe prevalence of vitamin B12 deficiency to be 12ndash33ther researchers have suggested a much greater prevalencef B12 deficiency in up to 75 of postoperative RYGBatients however most reports have cited approximately5 of postoperative RYGB patients as vitamin B12 defi-ient [82ndash87] Brolin et al [87] reported that low levels ofitamin B12 might be seen as soon as six months afterariatric surgery but most often occurring more than oneear postoperatively as liver stores become depleted Sk-oubis et al [88] predicted that the deficiency will mostikely occur 7 months after RYGB and 79 months afterPDDS although their research did not consider compro-ised preoperative status and its correlation to postopera-

ive deficiency After the first postoperative year the prev-lence of vitamin B12 deficiency appears to increase yearlyn RYGB patients [89]

Although the bodyrsquos storage of vitamin B12 is significant2000 g) compared with daily needs (24 gd) thisarticular deficiency has been found within 1ndash9 years ofastric bypass surgery [29] Brolin et al [84] reported thatne third of RYGB patients are deficient at four yearsostoperatively However non-surgical variables were notxplored and many patients might have had preoperativealues near the lower end of the normal range Ocon Bretont al [90] compared micronutrient deficiencies among two-ear postoperative BPDDS and RYGB patients and foundhat all nutritional deficiencies were more common amongPDDS patients except for vitamin B12 for which theeficiency was more common among the RYGB patientstudied A lack of B12 deficiency among BPDDS patientsight result from a better tolerance of animal proteins in a

arger pouch greater pepsingastric acid production to re-ease protein-bound B12 and increased availability and in-eraction of IF with the pouch contents

Experts have noted the significance of subclinical defi-iency in the low-normal cobalamin range in nongastricypass patients who do not exhibit clinical evidence ofeficiency The methylmalonic acid (MMA) assay is thereferred marker of B12 status because metabolic changesften precede low B12 levels in the progression to defi-iency Serum B12 assays may miss as much as 25ndash30 of

12 deficiencies making them less reliable than the MMAssay [91] It has been suggested that early signs of vitamin

12 deficiency can be detected if the serum levels of bothMA and homocysteine are measured [91] Vitamin B12

eficiency after RYGB has been associated with megalo-lastic anemia [92] Some vitamin B12-deficient patientsevelop significant symptoms such as polyneuropathy par-

sthesia and permanent neural impairment On occasion

ome patients may experience extreme delusions halluci-ations and even overt psychosis [93]

uggested supplementation Because of the frequent lack ofymptoms of vitamin B12 deficiency the suggested dili-ence in following up or treating these values among thosesymptomatic patients has been questioned The decisionot to supplement or routinely screen patients for B12 defi-iency should be examined very carefully given the risk ofrreversible neurologic damage if vitamin B12 goes un-reated for long periods At least one case report has beenublished of an exclusively breastfed infant with vitamin

12 deficiency who was born of an asymptomatic motherho had undergone gastric bypass surgery [94]Deficiency of vitamin B12 is typically defined at levels

200 pgmL However about 50 of patients with obviousigns and symptoms of deficiency have normal vitamin B12

evels [31] Kaplan et al [95] reported that vitamin B12

eficiency usually resolves after several weeks of treatmentith 700ndash2000 gwk Rhode et al [96] found that aosage of 350ndash600 gd of oral B12 prevented vitamin B12

eficiency in 95 of patients and an oral dose of 500 gdas sufficient to overcome an existing deficiency as re-orted by Brolin et al [87] in a similar study Thereforeupplementation of RYGB patients with 350ndash500 gd mayrevent most postoperative vitamin B12 deficiency

While most vitamin B12 in normal adults is absorbed inhe ileum in the presence of IF approximately 1 of sup-lemented B12 will be absorbed passively (by diffusion)long the entire length of the (non-bypassed) intestine byurgical weight loss patients given a high-dose oral supple-ent [97] Thus the consumption of 350ndash500 g yields a

5ndash50-g absorption which is greater than the daily re-uirement Although the use of monthly intramuscular in-ections or a weekly oral dose of vitamin B12 is commonmong practices it relies on patient compliance Practitio-ers should assess the patientrsquos preference and the potentialor compliance when considering a daily weekly oronthly regimen of B12 supplementation In addition to oral

upplements or intramuscular injections nasal sprays andublingual sources of vitamin B12 are also available Pa-ients should be monitored closely for their lifetime becauseevere anemia can develop with or without supplementation98]

olate

tiology of potential deficiency Factors that increase theisk of folic acid deficiency relevant to bariatric surgerynclude the following

Inadequate dietary intakeNoncompliance with multivitamin supplementationMalabsorptionMedications (anticonvulsants oral contraceptives

and cancer treating agents) [79]

pmo

SA

PAtArBatbhptl5

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cbct

pntiat

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Soiwt[2tpbvhsfowbmftm

I

dspbiwiu

S85L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Folic acid stores can be depleted within a few monthsostoperatively unless replenished by a multivitamin supple-ent and dietary sources (ie green leafy vegetables fruits

rgan meats liver dried yeast and fortified grain products)

igns symptoms and treatment of deficiency (seeppendix Table A4)

reoperative risk The goals of the 1998 Food and Drugdministration policy requiring all enriched grain products

o be fortified with folate included increasing the averagemerican diet by 100 g folate daily and decreasing the

ate of neural tube defects in childbearing women [99]entley et al [100] reported that the proportion of womenged 15ndash44 years old (in the general population) who meethe recommended dietary intake of 400 gd folate variesetween 23 and 33 With the increasing popularity ofigh proteinlow carbohydrate diets one cannot assume thatreoperative patients consume dietary sources of folatehrough fortified grain products fruits and vegetables Boy-an et al [26] found folate deficiencies preoperatively in6 of RYGB patients studied

ostoperative risk Although it has been observed that fo-ate deficiency after RYGB surgery is less common than B12

eficiency and is thought to occur because of decreasedietary or multivitamin supplement intake low serum folateevels have been cited from 6 to 65 among RYGBatients [2686101] Additionally folate deficiencies haveccurred postoperatively even with supplementation Boy-an et al [26] found that 47 (n 17) of RYGB patientsad low folate levels six months postoperatively and 41n 17) had low levels at one year This deficiency oc-urred despite patient adherence to taking a multivitaminupplement that contained at least the daily value for folate00 g [26] Postoperative bariatric patients with rapideight loss might have an increased risk of micronutrienteficiencies MacLean et al [86] reported that 65 ofostoperative patients had low folate levels These sameatients exhibited additional B vitamin deficiencies 24itamin B12 and 50 thiamin [86] An increased risk ofeficiency has also been noted among AGB patients pos-ibly because of decreased folate intake Gasteyger et al33] found a significant decrease in serum folate levels441) between the baseline and 24-month postoperativeeasurementsDixon and OrsquoBrien [101] reported elevated serum ho-

ocysteine levels in patients after bariatric surgery regard-ess of the type of procedure (restrictive or malabsorptive)levated homocysteine levels can indicate not only low

olate levels and a greater risk of neural tube defects but canlso be indicative of an independent risk factor for heartisease andor oxidative stress in the nonbariatric popula-ion [102] However unlike iron and vitamin B12 the folate

ontained in the multivitamin supplementation essentially e

orrects the deficiency in the vast majority of postoperativeariatric patients [103] Therefore persistent folate defi-iency might indicate a patientrsquos lack of compliance withhe prescribed vitamin protocol [32]

It is common knowledge that folic acid deficiency amongregnant women has been associated with a greater risk ofeural tube defects in newborns Consistent supplementa-ion and monitoring among women of child-bearing agencluding pre- and postoperative bariatric patients is vital inn effort to prevent the possibility of neural tube defects inhe developing fetus

Because folate does not affect the myelin of nerveseurologic damage is not as common with folate such as ishe case for vitamin B12 deficiency In contrast patientsith folate deficiency often present with forgetfulness irri-

ability hostility and even paranoid behaviors [29] Similaro that evidenced with vitamin B12 most postoperativeYGB patients who are folate deficient are asymptomatic orave subclinical symptoms therefore these deficient statesay not be easily identified

uggested supplementation Even though folate absorptionccurs preferentially in the proximal portion of the smallntestine it can occur along the entire length of the small bowelith postoperative adaptation Therefore it is generally agreed

hat folate deficiency is corrected with 1000 mgd folic acid32] and is preventable with supplementation that provides00 of the daily value (800 g) This level can also benefithe fetus in a female patient unaware of her postoperativeregnancy Folate supplementation 1000 mgd has noteen recommended because of the potential for maskingitamin B12 deficiency Carmel et al [104] suggested thatomocysteine is the most sensitive marker of folic acidtatus in conjunction with erythrocyte folate Althougholic acid deficiency could potentially occur among post-perative bariatric surgery patients it has not been seenidely in recent studies especially when patients haveeen compliant with postoperative multivitamin supple-entation Therefore it is imperative to closely follow

olic acid both pre- and postoperatively especially inhose patients suspected to be noncompliant with theirultivitamin supplementation

ron

Much of the iron and surgical weight loss research con-ucted to date has been generated from a limited number ofurgeons and scientists however the data have consistentlyointed toward the risk of iron deficiency and anemia afterariatric procedures Iron deficiency is defined as a decreasen the total iron body content Iron deficiency anemia occurshen erythropoiesis is impaired as a result of the lack of

ron stores In the absence of anemia iron deficiency issually asymptomatic Fatigue and a diminished capacity to

xercise however are common symptoms of anemia

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S86 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

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S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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S90 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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S91L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

gba

SA

Cphctrpw[nvfiisitCbg

Oafp[woofc(1hpritt

P

E

tgpoo

ccpcglcppmtttwaw

ailmsmtsbtciaspomtsa

bompo(almqmmbbEc

S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

(admcas

ihtpacbsT

ovBfted

fbsalumlcatspie

P

laTofmndef

pocimhphcsatpa

P

awrywaoirfiotnrsafRe

strwsviaratrlsgt

S93L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

[ntnriasiB(cdip

afedmvfllBrpem

D1mypei

iecalbcBmpmtta

ciru

iipafcfui

foaowppartptpthc

P

iwEvln6wdeapctnstat

S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

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apcptaasosdbc

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TI

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HILLMPTTV

TC

P

C

C

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H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

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Dmdcn4pm1[

C

twsottCaectnpupu

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itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

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[

[

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[

[

[

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[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

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[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

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[

[

[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

s

aildquo

T

T

DFF

F

E

A

D

T

T

P

DFF

S

D

T

S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

DFF

S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 6: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

Table 4Continued

Vitaminmineral Screening Normal range Additional laboratoryindexes

Critical range Preoperative deficiency Postoperativedeficiency

Comments

Vitamin D 25(OH)D 25ndash40 ngmL 2Serum phosphorus1Alkaline phosphatase1Serum PTH2Urinary calcium

Serum 25(OH)D 20ngmL suggestsdeficiency 20ndash30 ngmL suggestsinsufficiency

Common 60ndash70 Common with BPDDS after 1 yr mayoccur with RYGBprevalenceunknown

With deficiency serumcalcium may be low ornormal serumphosphorus maydecrease serum alkalinephosphatase increasesPTH elevated

Vitamin E Plasma alphatocopherol

5ndash20 gmL Plasma lipids 5 gmL Uncommon Uncommon Low plasma alphatocopherol to plasmalipids (08 mgg totallipid) should be usedwith hyperlipidemia

Vitamin K PT 10ndash13 seconds 1DCP 2Plasmaphylloquinone

Variable Uncommon Common with BPDDS after 1 yr

PT is not a sensitivemeasure of vitamin Kstatus

Zinc Plasma zinc 60ndash130 gdL 2RBC zinc Plasma zinc 70 gdL Uncommon but increasedrisk of low levelsassociated with obesity

Common with BPDDS after 1 yr mayoccur with RYGB

Monitor albumin levelsand interpret zincaccordingly albumin isprimary binding proteinfor zinc no reliablemethod of determiningzinc status is availableplasma zinc is methodgenerally used studiescited in this report didnot adequately describemethods of zinc analysis

Protein Serum albuminSerum totalprotein

4ndash6 gdL6ndash8 gdL

2Serum prealbumin(transthyretin)

Albumin 30 gdLPrealbumin 20 mgdL

Uncommon Rare but can occurwith RYGB AGBand BPDDS ifprotein intake islow in total intakeor indispensableamino acids

Half-life for prealbumin is2ndash4 d and reflectschanges in nutritionalstatus sooner thanalbumin a nonspecificprotein carrier with ahalf-life of 22 d

RYGB Roux-en-Y gastric bypass AGB adjustable gastric banding BPDDS biliopancreatic diversionduodenal switch PLP pyridoxal-5rsquo-phosphate RBC red blood cell MMA methylmalonic acid tHcy total homocysteine CRT creatinine PPIs protein pump inhibitors FIGLU formiminogluatmic acid CBC complete blood count TIBC total iron binding capacityHgb hemoglobin Hct hematocrit RPB retinol binding protein PTH parathyroid hormone 25(OH)D 25-hydroxyvitamin D PT prothrombin time DCP des-gamma-carboxypromthrom-bin

In general laboratory values should be reviewed annually or as indicated by clinical presentation Laboratory normal values vary among laboratory settings and are method dependent This chart providesa brief summary of monitoring tools See the Appendix for additional detail and diagnostic tools

copy Jeanne Blankenship MS RD Used with permission

S78L

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al

Surgeryfor

Obesity

andR

elatedD

iseases4

(2008)S73-S108

TS

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S79L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able 5uggested Postoperative Vitamin Supplementation

upplement AGB RYGB BPDDS Comment

ultivitamin-mineral supplementA high-potency vitamin containing 100 of daily value for

at least 23 of nutrients100 of daily

value

200 of dailyvalue

200 of daily value Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to whole tabletcapsule as toleratedAvoid time-released supplementsAvoid enteric coatingChoose a complete formula with at least 18 mg iron 400

g folic acid and containing selenium and zinc in eachserving

Avoid childrenrsquos formulas that are incompleteMay improve gastrointestinal tolerance when taken close to

food intakeMay separate dosageDo not mix multivitamin containing iron with calcium

supplement take at least 2 hr apartIndividual brands should be reviewed for absorption rate and

bioavailabilitySpecialized bariatric formulations are available

dditional cobalamin (B12)Available forms include sublingual tablets liquid drops

mouth spray or nasal gelsprayIntramuscular injection mdash 1000 gmo mdash Begin 0ndash3 mo after

surgeryOral tablet (crystalline form) mdash 350ndash500 gd mdashSupplementation after AGB and BPDDS may be required

dditional elemental calciumChoose a brand that contains calcium citrate and vitamin D3

Begin with chewable or liquidProgress to whole tabletcapsule as tolerated

1500 mgd 1500ndash 2000 mgd 1800ndash 2400 mgd May begin on day 1after hospitaldischarge orwithin 1 mo aftersurgery

Split into 500ndash600 mg doses be mindful of serving size onsupplement label

Space doses evenly throughout daySuggest a brand that contains magnesium especially for

BPDDSDo not combine calcium with iron containing supplements

To maximize absorptionTo minimize gastrointestinal intoleranceWait 2 h after taking multivitamin or iron supplement

Promote intake of dairy beverages andor foods that aresignificant sources of dietary calcium in addition torecommended supplements up to 3 servings daily

Combined dietary and supplemental calcium intake 1700mgd may be required to prevent bone loss during rapidweight loss

dditional elemental iron (above that provided by mvi)Recommended for menstruating women and those at risk of

anemia (total goal intake 50-100 mg elemental irond)

mdash Add a minimumof 18ndash27 mgdelemental

Add a minimum of18ndash27 mgdelemental

Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to tablet as toleratedDosage may need to be adjusted based on biochemical

markersNo enteric coatingDo not mix iron and calcium supplements take 2 h apartAvoid excessive intake of tea due to tannin interactionEncourage foods rich in heme iron

Vitamin C may enhance absorption of non-heme iron sources

wa

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tpp(fcppw

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S80 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hich in turn causes metabolic changes that favor fatccumulation [23ndash25]

Several of the B-complex vitamins important for appro-riate metabolism of carbohydrate and neural functions thategulate appetite have been found to be deficient in someatients with morbid obesity [212627] Iron deficiencieshich would significantly hinder energy use have been

eported in nearly 50 of morbidly obese preoperativeandidates [21] Zinc and selenium deficits have been re-orted as well as deficits in vitamins A E and C allmportant antioxidants helpful in regulating energy produc-ion and various other processes of body weight manage-ent [1926ndash28]The risk of micronutrient depletion continues to be quite

igh particularly after surgeries that affect the digestion andbsorption of nutrients such as Roux-en-Y gastric bypassRYGB) and biliopancreatic diversion with or without du-denal switch (BPDDS) RYGB increases the risk of vita-in B12 and other B vitamin deficits in addition to iron and

alcium BPDDS procedures may also cause an increasedisk of iron and calcium deficits along with significant

able 5ontinued

upplement AGB

at-soluble vitaminsWith all procedures higher maintenance doses may be

required for those with a history of deficiencyWater-soluble preparations of fat-soluble vitamins are

availableRetinol sources of vitamin A should be used to calculatedosageMost supplements contain a high percentage of beta

carotene which does not contribute to vitamin A toxicityIntake of 2000 IU Vitamin D3 may be achieved with careful

selection of multivitamin and calcium supplementsNo toxic effect known for vitamin K1 phytonadione

(phyloquinone)

mdash

mdash

mdash

Vitamin K requirement varies with dietary sources andcolonic production

Caution with vitamin K supplementation for patientsreceiving coagulation therapy

Vitamin E deficiency has been suggested but is notprevalent in published studies

ptional B complexB-50 dosageLiquid form is available

1 servi

Avoid time released tabletsNo known risk of toxicityMay provide additional prophylaxis against B-vitamin

deficiencies including thiamin especially for BPDDSprocedures as water-soluble vitamins are absorbed in theproximal jejunum

Note 1000 mg of supplemental folic acid provided incombination with multivitamins could mask B12

deficiency

Abbreviations as in Table 4

eficiencies in the fat-soluble vitamins A D E and K d

hich are important for driving many of the biologicalrocesses that help to regulate body size [29ndash31] As theate of noncompliance with prophylactic multivitamin sup-lementation increases the rate of postoperative deficiencyay increase almost twofold [32]In the past it has been thought that the specific nutri-

ional deficiencies commonly seen among malabsorptiverocedures would not be present in patients choosing aurely restrictive surgery such as the adjustable gastric bandAGB) However poor eating behavior low nutrient-denseood choices food intolerance and a restricted portion sizean contribute to potential nutrient deficiencies in theseatients as well Although the incidence of nutritional com-lications may be less frequent in this patient population itould be detrimental to assume that they do not existIt is important for the bariatric patient to take vitamin and

ineral supplements not only to prevent adverse healthonditions that can arise after surgery but because someutrients such as calcium can enhance weight loss and helprevent weight regain The nutrient deficiency might beroportional to the length of the absorptive area bypassed

RYGB BPDDS Comment

mdash

mdash

mdash

10000 IU of vitamin A

2000 IU of vitamin D

300 g of vitamin K

May begin 2ndash4weeks aftersurgery

1 servingd 1 servingd May begin on day 1after hospitaldischarge

ngd

uring surgical procedures and to a lesser extent to the

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S81L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ercentage of weight lost Iron vitamin B12 and vitamin Deficiencies along with changes in calcium metabolism areommon after RYGB Protein fat-soluble vitamin andther micronutrient deficiencies as well as altered calciumetabolism are most notably found after BPDDS Folate

eficiency has been reported after AGB [33] Thiamin de-ciency is common among all surgical patients with fre-uent vomiting regardless of the type of procedure per-ormed Because many nutritional deficiencies progressith time patients should be monitored frequently and

egularly to prevent malnutrition [29] Reinforcement ofupplement compliance at each patient follow-up is alsomportant in the fight to enhance nutrition status and preventutritional complications

eight loss and nutrient deficits restrictionersus malabsorption

Malabsorptive procedures such as the BPDDS arehought to cause weight loss primarily through the malab-orption of macronutrients with as much as 25 of proteinnd 72 of fat malabsorbed Such primary malabsorptionesults in concomitant malabsorption of micronutrients3435] Vitamins and minerals relying on fat metabolismncluding vitamins D A E K and zinc may be affectedhen absorption is impaired [36] The decrease in gastro-

ntestinal transit time may also result in secondary malab-orption of a wide range of micronutrients related to by-assing the duodenum and jejunum or limited contact withhe brush border secondary to a short common limb Othericronutrient deficiency concerns reported for patients

hoosing a procedure with malabsorptive features includeron calcium vitamin B12 and folate

Nutrient deficiencies after RYGB can result from eitherrimary or secondary malabsorption or from inadequateietary intake A minimal amount of macronutrient malab-orption is thought to occur However specific micronutri-nts appear to be malabsorbed postoperatively and presents deficiencies without adequate vitamin and mineral sup-lementation Retrospective analyses of patients who havendergone gastric bypass have revealed predictable micro-utrient deficiencies including iron vitamin B12 and folate2627ndash39] Case reports have also shown that thiamin de-ciency can develop especially when persistent postopera-

ive vomiting occurs [40ndash43]Few studies that measure absorption after measured and

uantified intake have been published It can be hypothe-ized that the bypassed duodenum and proximal jejunumegatively affect nutrient assimilation Bradley et al [44]tudied patients who had undergone total gastrectomy therocedure from which the RYGB evolved The researchersound that most nutritional status changes in patients wereost likely due to changes in intake versus malabsorptionhese balance studies were conducted in a controlled re-

earch setting however they did not measure pre- and c

ostoperative changes nor include radioisotope labeling toeasure absorption of key nutrients and the subjects had

ndergone the procedure for reasons other than weight lossIt is unclear whether intestinal adaptation occurs after

ombination procedures and to what degree it affects long-erm weight maintenance and nutrition status Adaptation iscompensatory response that follows an abrupt decrease inucosal surface area and has been well studied in short-

owel patients who require bowel resection [45] The pro-ess includes both anatomic and functional changes thatncrease the gutrsquos digestive and absorptive capacity Al-hough these changes begin to take place in the early post-perative period total adaptation may take up to three yearso complete Adaptation in gastric bypass has not beenonsidered in absorption or metabolic studies This consid-ration could be important even when determining early andate macro- and micronutrient intake recommendations Theffect of pancreatic enzyme replacement therapy on vitaminnd mineral absorption in this population is also unknown

Purely restrictive procedures such as the AGB can resultn micronutrient deficiencies related to changes in dietaryntake It is commonly accepted that because no alteration isade in the absorptive pathway malabsorption does not

ccur as a result of AGB procedures However nutrienteficits would be likely to occur because of the low nutrientntake and avoidance of nutrient-rich foods in the earlyonths postoperatively and later possibly as a result of

xcessive band restriction Food with high nutritional valueuch as meat and fibrous fresh fruits and vegetables mighte poorly tolerated

Literature has been published that addresses the effect ofalabsorptive restrictive and combination surgical proce-

ures on acute and long-term nutritional status These stud-es have attempted for the most part to indirectly determinehe surgical impact on nutrition status by the evaluation ofetabolic and laboratory markers Although some studies

ave included certain aspects of absorption few have in-luded the necessary components to evaluate absorption ofprescribed andor monitored diet in a controlled metabolic

ettingThe following sections examine the pre- and postopera-

ive risks for nutritional deficiencies associated with RYGBPDDS and AGB It is important for all members of theedical team to increase their awareness of the nutritional

omplications and challenges that lie ahead for the patientontinued review of current research by the medical team

egarding advances in nutrition science beyond the bound-ries of the present report cannot be emphasized enough

hiamin (vitamin B1)

Beriberi is a thiamin deficiency that can affect variousrgan systems including the heart gastrointestinal tractnd peripheral and central nervous systems Although the

ondition is generally considered rare a number of reported

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S82 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nd possibly a much greater number of unreported or un-iagnosed cases of beriberi have occurred among individ-als who have undergone surgery for morbid obesity Earlyetection and prompt treatment of thiamin deficits in thesendividuals can help to prevent serious health consequencesf beriberi is misdiagnosed or goes undetected for even ahort period the bariatric patient can develop irreversibleeuromuscular disorders permanent defects in learning andhort-term memory coma and even death Because of theife-altering and potentially life-threatening nature of a thi-min deficiency it is important that healthcare professionalsn the field of bariatric surgery have knowledge of thetiology of the condition and its signs and symptomsreatment and prevention

tiology of potential deficiency Thiamin is a water-solubleitamin that is absorbed in the proximal jejunum by anctive (saturable high-affinity) transport system [4647] Inhe body thiamin is found in high concentrations in therain heart muscle liver and kidneys However withoutegular and sufficient intake these tissues become rapidlyevoid of thiamin [4647] The total amount of thiamin inhe body of an adult is approximately 30 mg with a half-lifef only 9ndash18 days Persistent vomiting a diet deficient inhe vitamin or the bodyrsquos excessive utilization of thiaminse can result in a severe state of thiamin depletion withinnly a short period producing symptoms of beriberi46ndash48]

Bariatric surgery increases the risk of beriberi through ex-cerbation of pre-existing thiamin deficits low nutrient intakealabsorption and episodes of nausea and vomiting [49ndash51]hronic or acute thiamin deficiencies in bariatric patients oftenresent with symptoms of peripheral neuropathy or Wer-ickersquos encephalopathy and Korsakoffrsquos psychoses [2148ndash4] Early diagnosis of the signs and symptoms of these con-itions is extremely important to prevent serious adverse healthonsequences Even if treatment is initiated recovery can bencomplete with cognitive andor neuromuscular impairmentsersisting long term or permanently

igns symptoms and treatment of deficiency (seeppendix Table A1)

reoperative risk The risk of the development of beriberifter bariatric surgery is far greater for individuals present-ng for surgery with low thiamin levels Investigators at theleveland Clinic of Florida reported that 15 of their pre-perative bariatric patients had deficiencies in thiamin be-ore surgery [52] A study by Flancbaum et al [21] similarlyound that 29 of their preoperative patients had low thia-in levels Data obtained by that study also showed a

ignificant difference between ethnicity and preoperativehiamin levels Although only 67 of whites presentedith thiamin deficiencies before surgery nearly one third

31) of African Americans and almost one half (47) of

ispanics had thiamin deficits The results of these studies S

uggested a need for preoperative thiamin testing as well ashiamin repletion by diet or supplementation to reduce theisk of ldquobariatricrdquo beriberi postoperatively

ostoperative risk Beriberi has been observed after gastricestrictive and malabsorptive procedures A number of casesf Wernicke-Korsakoff syndrome (WKS) as well as periph-ral neuropathy have been reported for patients havingndergone vertical banded gastroplasty [53ndash61] A fewncidences of WKS have also been reported after AGB436263] Additionally reports of thiamin deficiencies and

KS after RYGB [404164ndash73] and several cases of WKSnd neuropathy in patients who had undergone BPD [74]ave been published Many more cases of WKS are be-ieved to have occurred with bariatric procedures that haveither not been reported or have been misdiagnosed becausef limited knowledge regarding the signs and symptoms ofcute or severe thiamin deficits Because many foods areortified with thiamin beriberi has been nearly eradicatedhroughout the world except for patients with severe alco-olism severe vomiting during pregnancy (hyperemesisravidarium) or those malnourished and starved For thiseason few healthcare professionals until recently havead a patient present with beriberi

According to the published reports of thiamin deficitsfter bariatric procedures most patients develop such defi-iencies in the early postoperative months after an episodef intractable vomiting Nausea and vomiting are relativelyommon after all bariatric procedures early in the postop-rative period Thiamin stores in the body are small andaintenance of appropriate thiamin levels requires daily

eplenishment A deficiency of thiamin for only a couple ofeeks or less caused by persistent vomiting can deplete

hiamin stores Symptoms of WKS were reported in aYGB patient after only two weeks of persistent vomiting

67]Bariatric beriberi can also develop in postoperative patients

ho are given infusate containing dextrose without thiaminnd other vitamins which is often the case for patients inritical care units postoperative patients with complicationsnterfering with the ingestion of food or patients dehydratedrom persistent vomiting Malnutrition caused by a lack ofppetite and dietary intake postoperatively also contributes toariatric beriberi as does noncompliance in taking postopera-ive vitamin supplements

Although most cases of beriberi occur in the early post-perative periods cases of patients with severe thiamineficiency more than one year after surgery have beeneported One study reported WKS in association with al-ohol abuse 13 years after RYGB [75] Other conditionsontributing to late cases of bariatric beriberi include ahiamin-poor diet a diet high in carbohydrates anorexiand bulimia [46ndash48]

uggested supplementation Because of the greater likeli-

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S83L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ood of low dietary thiamin intake patients should be sup-lemented with thiamin This is usually accomplishedhrough daily intake of a multivitamin Most multivitaminsontain thiamin at 100 of the daily value Patients havingpisodes of nausea and vomiting and those who are anorec-ic might require sublingual intramuscular or intravenoushiamin to avoid depletion of thiamin stores and beriberiaution should be used when infusing bariatric patientsith solutions containing dextrose without additional vita-ins and thiamin because an increase in glucose utilizationithout additional thiamin can deplete thiamin stores [76]Thiamin deficiency in bariatric patients is treated with

hiamin together with other B-complex vitamins and mag-esium for maximal thiamin absorption and appropriateeurologic function [46 ndash 48] Early symptoms of neuropa-hy can often be resolved by providing the patient with oralhiamin doses of 20ndash30 mgd until symptoms disappear Forore advanced signs of neuropathy or for individuals with

rotracted vomiting 50ndash100 mgd of intravenous or intra-uscular thiamin may be necessary for resolution or im-

rovement of symptoms or for the prevention of suchatients with WKS generally require 100 mg thiamindministered intravenously for several days or longer fol-owed by intramuscular thiamin or high oral doses untilymptoms have resolved or significantly improved This canequire months to years Some patients might have to takehiamin for life to prevent the reoccurrence of neuropathy

itamin B12 and folate

Vitamin B12 (cobalamin) and folate (folic acid) are bothnvolved in the maturation of red blood cells and are com-only discussed in the literature together Over time a

eficiency in either vitamin B12 or folate can lead to mac-ocytic anemia a condition characterized by the productionf fewer but larger red blood cells and a decreased abilityo carry oxygen Most (95) cases of megaloblastic anemiacharacterized by large immature abnormal undifferenti-ted red blood cells in bone marrow) are attributed toitamin B12 or folate deficiency [77]

itamin B12

tiology of potential deficiency RYGB patients have bothncomplete digestion and release of vitamin B12 from pro-ein foods With a significant decrease in hydrochloric acidepsinogen is not converted into pepsin which is necessaryor the release of vitamin B12 from protein [78] BecauseGB patients have an artificial restriction yet complete usef the stomach and BPD patients do not have as great aestriction in stomach capacity and parietal cells as RYGBatients the reduction in hydrochloric acid and subsequentitamin B12 deficiency is not as prevalent with these tworocedures

Intrinsic factor (IF) is produced by the parietal cells of

he stomach and in certain conditions (eg atrophic gastri- a

is resected small bowel elderly patients) can be impairedausing an IF deficiency Subsequent vitamin B12 deficiencypernicious anemia) occurs without IF production or useecause IF is needed to absorb vitamin B12 in the terminalleum [77] Factors that increase the risk of vitamin B12

eficiency relevant to bariatric surgery include the follow-ng

An inability to release protein-bound vitamin B12

from food particularly in hypochlorhydria andatrophic gastritis

Malabsorption due to inadequate IF in perniciousanemia

Gastrectomy and gastric bypassResection or disease of terminal ileumLong-term vegan dietMedications such as neomycin metformin colch-

icines medications used in the management ofbowel inflammation and gastroesophageal refluxand ulcers (eg proton pump inhibitors) and anti-convulsant agents [79]

Cobalamin stores are known to exist for long periods3ndash5 yr) and are dependent on dietary repletion and dailyepletion However gastric bypass patients have both aecreased production of stomach acid and a decreased avail-bility of IF thus a vitamin B12 deficiency could developithout appropriate supplementation Because the typical

bsorption pathway cannot be relied on the surgical weightoss patient must rely on passive absorption of B12 whichccurs independent of IF

igns symptoms and treatment of deficiency (seeppendix Table A3)

reoperative risk Several medications common to preop-rative bariatric patients have been noted to affect preoper-tive vitamin B12 absorption and stores Of patients takingetformin 10ndash30 present with reduced vitamin B12 ab-

orption [80] Additionally patients with obesity have aigh incidence of gastroesophageal reflux disease for whichhey take proton pump inhibitors thus increasing the poten-ial to develop a vitamin B12 deficiency

Flancbaum et al [21] conducted a retrospective study of79 (320 women and 59 men) pre-operative patients Vita-in B12 deficiency was reported as negative in all patients

f various ethnic backgrounds [21] No clinical criteria orymptoms for vitamin B12 deficiency were noted In theeneral population 5ndash10 present with neurologic symp-oms with vitamin B12 levels of 200ndash400 pgmL Amongreoperative gastric bypass patients Madan et al [27] foundhat 13 (n 59) of patients were deficient in vitamin B12n a comparison of patients presenting for either RYGB orPD Skroubis et al [81] recently reported that preoperativeitamin B12 levels were low-normal in both groups Itould be prudent to screen for and treat IF deficiency

ndor vitamin B12 deficiency in all patients preoperatively

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S84 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ut it is essential for RYGB patients so as not to hasten theevelopment of a potential postoperative deficiency

ostoperative risk Vitamin B12 deficiency has been fre-uently reported after RYGB Schilling et al [82] estimatedhe prevalence of vitamin B12 deficiency to be 12ndash33ther researchers have suggested a much greater prevalencef B12 deficiency in up to 75 of postoperative RYGBatients however most reports have cited approximately5 of postoperative RYGB patients as vitamin B12 defi-ient [82ndash87] Brolin et al [87] reported that low levels ofitamin B12 might be seen as soon as six months afterariatric surgery but most often occurring more than oneear postoperatively as liver stores become depleted Sk-oubis et al [88] predicted that the deficiency will mostikely occur 7 months after RYGB and 79 months afterPDDS although their research did not consider compro-ised preoperative status and its correlation to postopera-

ive deficiency After the first postoperative year the prev-lence of vitamin B12 deficiency appears to increase yearlyn RYGB patients [89]

Although the bodyrsquos storage of vitamin B12 is significant2000 g) compared with daily needs (24 gd) thisarticular deficiency has been found within 1ndash9 years ofastric bypass surgery [29] Brolin et al [84] reported thatne third of RYGB patients are deficient at four yearsostoperatively However non-surgical variables were notxplored and many patients might have had preoperativealues near the lower end of the normal range Ocon Bretont al [90] compared micronutrient deficiencies among two-ear postoperative BPDDS and RYGB patients and foundhat all nutritional deficiencies were more common amongPDDS patients except for vitamin B12 for which theeficiency was more common among the RYGB patientstudied A lack of B12 deficiency among BPDDS patientsight result from a better tolerance of animal proteins in a

arger pouch greater pepsingastric acid production to re-ease protein-bound B12 and increased availability and in-eraction of IF with the pouch contents

Experts have noted the significance of subclinical defi-iency in the low-normal cobalamin range in nongastricypass patients who do not exhibit clinical evidence ofeficiency The methylmalonic acid (MMA) assay is thereferred marker of B12 status because metabolic changesften precede low B12 levels in the progression to defi-iency Serum B12 assays may miss as much as 25ndash30 of

12 deficiencies making them less reliable than the MMAssay [91] It has been suggested that early signs of vitamin

12 deficiency can be detected if the serum levels of bothMA and homocysteine are measured [91] Vitamin B12

eficiency after RYGB has been associated with megalo-lastic anemia [92] Some vitamin B12-deficient patientsevelop significant symptoms such as polyneuropathy par-

sthesia and permanent neural impairment On occasion

ome patients may experience extreme delusions halluci-ations and even overt psychosis [93]

uggested supplementation Because of the frequent lack ofymptoms of vitamin B12 deficiency the suggested dili-ence in following up or treating these values among thosesymptomatic patients has been questioned The decisionot to supplement or routinely screen patients for B12 defi-iency should be examined very carefully given the risk ofrreversible neurologic damage if vitamin B12 goes un-reated for long periods At least one case report has beenublished of an exclusively breastfed infant with vitamin

12 deficiency who was born of an asymptomatic motherho had undergone gastric bypass surgery [94]Deficiency of vitamin B12 is typically defined at levels

200 pgmL However about 50 of patients with obviousigns and symptoms of deficiency have normal vitamin B12

evels [31] Kaplan et al [95] reported that vitamin B12

eficiency usually resolves after several weeks of treatmentith 700ndash2000 gwk Rhode et al [96] found that aosage of 350ndash600 gd of oral B12 prevented vitamin B12

eficiency in 95 of patients and an oral dose of 500 gdas sufficient to overcome an existing deficiency as re-orted by Brolin et al [87] in a similar study Thereforeupplementation of RYGB patients with 350ndash500 gd mayrevent most postoperative vitamin B12 deficiency

While most vitamin B12 in normal adults is absorbed inhe ileum in the presence of IF approximately 1 of sup-lemented B12 will be absorbed passively (by diffusion)long the entire length of the (non-bypassed) intestine byurgical weight loss patients given a high-dose oral supple-ent [97] Thus the consumption of 350ndash500 g yields a

5ndash50-g absorption which is greater than the daily re-uirement Although the use of monthly intramuscular in-ections or a weekly oral dose of vitamin B12 is commonmong practices it relies on patient compliance Practitio-ers should assess the patientrsquos preference and the potentialor compliance when considering a daily weekly oronthly regimen of B12 supplementation In addition to oral

upplements or intramuscular injections nasal sprays andublingual sources of vitamin B12 are also available Pa-ients should be monitored closely for their lifetime becauseevere anemia can develop with or without supplementation98]

olate

tiology of potential deficiency Factors that increase theisk of folic acid deficiency relevant to bariatric surgerynclude the following

Inadequate dietary intakeNoncompliance with multivitamin supplementationMalabsorptionMedications (anticonvulsants oral contraceptives

and cancer treating agents) [79]

pmo

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S85L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Folic acid stores can be depleted within a few monthsostoperatively unless replenished by a multivitamin supple-ent and dietary sources (ie green leafy vegetables fruits

rgan meats liver dried yeast and fortified grain products)

igns symptoms and treatment of deficiency (seeppendix Table A4)

reoperative risk The goals of the 1998 Food and Drugdministration policy requiring all enriched grain products

o be fortified with folate included increasing the averagemerican diet by 100 g folate daily and decreasing the

ate of neural tube defects in childbearing women [99]entley et al [100] reported that the proportion of womenged 15ndash44 years old (in the general population) who meethe recommended dietary intake of 400 gd folate variesetween 23 and 33 With the increasing popularity ofigh proteinlow carbohydrate diets one cannot assume thatreoperative patients consume dietary sources of folatehrough fortified grain products fruits and vegetables Boy-an et al [26] found folate deficiencies preoperatively in6 of RYGB patients studied

ostoperative risk Although it has been observed that fo-ate deficiency after RYGB surgery is less common than B12

eficiency and is thought to occur because of decreasedietary or multivitamin supplement intake low serum folateevels have been cited from 6 to 65 among RYGBatients [2686101] Additionally folate deficiencies haveccurred postoperatively even with supplementation Boy-an et al [26] found that 47 (n 17) of RYGB patientsad low folate levels six months postoperatively and 41n 17) had low levels at one year This deficiency oc-urred despite patient adherence to taking a multivitaminupplement that contained at least the daily value for folate00 g [26] Postoperative bariatric patients with rapideight loss might have an increased risk of micronutrienteficiencies MacLean et al [86] reported that 65 ofostoperative patients had low folate levels These sameatients exhibited additional B vitamin deficiencies 24itamin B12 and 50 thiamin [86] An increased risk ofeficiency has also been noted among AGB patients pos-ibly because of decreased folate intake Gasteyger et al33] found a significant decrease in serum folate levels441) between the baseline and 24-month postoperativeeasurementsDixon and OrsquoBrien [101] reported elevated serum ho-

ocysteine levels in patients after bariatric surgery regard-ess of the type of procedure (restrictive or malabsorptive)levated homocysteine levels can indicate not only low

olate levels and a greater risk of neural tube defects but canlso be indicative of an independent risk factor for heartisease andor oxidative stress in the nonbariatric popula-ion [102] However unlike iron and vitamin B12 the folate

ontained in the multivitamin supplementation essentially e

orrects the deficiency in the vast majority of postoperativeariatric patients [103] Therefore persistent folate defi-iency might indicate a patientrsquos lack of compliance withhe prescribed vitamin protocol [32]

It is common knowledge that folic acid deficiency amongregnant women has been associated with a greater risk ofeural tube defects in newborns Consistent supplementa-ion and monitoring among women of child-bearing agencluding pre- and postoperative bariatric patients is vital inn effort to prevent the possibility of neural tube defects inhe developing fetus

Because folate does not affect the myelin of nerveseurologic damage is not as common with folate such as ishe case for vitamin B12 deficiency In contrast patientsith folate deficiency often present with forgetfulness irri-

ability hostility and even paranoid behaviors [29] Similaro that evidenced with vitamin B12 most postoperativeYGB patients who are folate deficient are asymptomatic orave subclinical symptoms therefore these deficient statesay not be easily identified

uggested supplementation Even though folate absorptionccurs preferentially in the proximal portion of the smallntestine it can occur along the entire length of the small bowelith postoperative adaptation Therefore it is generally agreed

hat folate deficiency is corrected with 1000 mgd folic acid32] and is preventable with supplementation that provides00 of the daily value (800 g) This level can also benefithe fetus in a female patient unaware of her postoperativeregnancy Folate supplementation 1000 mgd has noteen recommended because of the potential for maskingitamin B12 deficiency Carmel et al [104] suggested thatomocysteine is the most sensitive marker of folic acidtatus in conjunction with erythrocyte folate Althougholic acid deficiency could potentially occur among post-perative bariatric surgery patients it has not been seenidely in recent studies especially when patients haveeen compliant with postoperative multivitamin supple-entation Therefore it is imperative to closely follow

olic acid both pre- and postoperatively especially inhose patients suspected to be noncompliant with theirultivitamin supplementation

ron

Much of the iron and surgical weight loss research con-ucted to date has been generated from a limited number ofurgeons and scientists however the data have consistentlyointed toward the risk of iron deficiency and anemia afterariatric procedures Iron deficiency is defined as a decreasen the total iron body content Iron deficiency anemia occurshen erythropoiesis is impaired as a result of the lack of

ron stores In the absence of anemia iron deficiency issually asymptomatic Fatigue and a diminished capacity to

xercise however are common symptoms of anemia

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S86 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

tsmp

lsnfwTlopaechc

Rtbwdsaar

fdaiwiiedasdt

Stbadtbpcwl

mccmacdrrT

C

EeamadmsDfd

dbdh7DtnDcwsh

SA

Pcptt[hmtlcgc

S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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S88 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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S89L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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S91L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

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hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

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S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

ratbrdd

aebaaa

apcptaasosdbc

afciitdmptpcrsPEv

TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

[

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[

[

[

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[

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[

[

[

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[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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T

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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c

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S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

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S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

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D

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T

T

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DFFS

D

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S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 7: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

TS

S

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A

A

A

S79L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able 5uggested Postoperative Vitamin Supplementation

upplement AGB RYGB BPDDS Comment

ultivitamin-mineral supplementA high-potency vitamin containing 100 of daily value for

at least 23 of nutrients100 of daily

value

200 of dailyvalue

200 of daily value Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to whole tabletcapsule as toleratedAvoid time-released supplementsAvoid enteric coatingChoose a complete formula with at least 18 mg iron 400

g folic acid and containing selenium and zinc in eachserving

Avoid childrenrsquos formulas that are incompleteMay improve gastrointestinal tolerance when taken close to

food intakeMay separate dosageDo not mix multivitamin containing iron with calcium

supplement take at least 2 hr apartIndividual brands should be reviewed for absorption rate and

bioavailabilitySpecialized bariatric formulations are available

dditional cobalamin (B12)Available forms include sublingual tablets liquid drops

mouth spray or nasal gelsprayIntramuscular injection mdash 1000 gmo mdash Begin 0ndash3 mo after

surgeryOral tablet (crystalline form) mdash 350ndash500 gd mdashSupplementation after AGB and BPDDS may be required

dditional elemental calciumChoose a brand that contains calcium citrate and vitamin D3

Begin with chewable or liquidProgress to whole tabletcapsule as tolerated

1500 mgd 1500ndash 2000 mgd 1800ndash 2400 mgd May begin on day 1after hospitaldischarge orwithin 1 mo aftersurgery

Split into 500ndash600 mg doses be mindful of serving size onsupplement label

Space doses evenly throughout daySuggest a brand that contains magnesium especially for

BPDDSDo not combine calcium with iron containing supplements

To maximize absorptionTo minimize gastrointestinal intoleranceWait 2 h after taking multivitamin or iron supplement

Promote intake of dairy beverages andor foods that aresignificant sources of dietary calcium in addition torecommended supplements up to 3 servings daily

Combined dietary and supplemental calcium intake 1700mgd may be required to prevent bone loss during rapidweight loss

dditional elemental iron (above that provided by mvi)Recommended for menstruating women and those at risk of

anemia (total goal intake 50-100 mg elemental irond)

mdash Add a minimumof 18ndash27 mgdelemental

Add a minimum of18ndash27 mgdelemental

Begin on day 1 afterhospital discharge

Begin with chewable or liquidProgress to tablet as toleratedDosage may need to be adjusted based on biochemical

markersNo enteric coatingDo not mix iron and calcium supplements take 2 h apartAvoid excessive intake of tea due to tannin interactionEncourage foods rich in heme iron

Vitamin C may enhance absorption of non-heme iron sources

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S80 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hich in turn causes metabolic changes that favor fatccumulation [23ndash25]

Several of the B-complex vitamins important for appro-riate metabolism of carbohydrate and neural functions thategulate appetite have been found to be deficient in someatients with morbid obesity [212627] Iron deficiencieshich would significantly hinder energy use have been

eported in nearly 50 of morbidly obese preoperativeandidates [21] Zinc and selenium deficits have been re-orted as well as deficits in vitamins A E and C allmportant antioxidants helpful in regulating energy produc-ion and various other processes of body weight manage-ent [1926ndash28]The risk of micronutrient depletion continues to be quite

igh particularly after surgeries that affect the digestion andbsorption of nutrients such as Roux-en-Y gastric bypassRYGB) and biliopancreatic diversion with or without du-denal switch (BPDDS) RYGB increases the risk of vita-in B12 and other B vitamin deficits in addition to iron and

alcium BPDDS procedures may also cause an increasedisk of iron and calcium deficits along with significant

able 5ontinued

upplement AGB

at-soluble vitaminsWith all procedures higher maintenance doses may be

required for those with a history of deficiencyWater-soluble preparations of fat-soluble vitamins are

availableRetinol sources of vitamin A should be used to calculatedosageMost supplements contain a high percentage of beta

carotene which does not contribute to vitamin A toxicityIntake of 2000 IU Vitamin D3 may be achieved with careful

selection of multivitamin and calcium supplementsNo toxic effect known for vitamin K1 phytonadione

(phyloquinone)

mdash

mdash

mdash

Vitamin K requirement varies with dietary sources andcolonic production

Caution with vitamin K supplementation for patientsreceiving coagulation therapy

Vitamin E deficiency has been suggested but is notprevalent in published studies

ptional B complexB-50 dosageLiquid form is available

1 servi

Avoid time released tabletsNo known risk of toxicityMay provide additional prophylaxis against B-vitamin

deficiencies including thiamin especially for BPDDSprocedures as water-soluble vitamins are absorbed in theproximal jejunum

Note 1000 mg of supplemental folic acid provided incombination with multivitamins could mask B12

deficiency

Abbreviations as in Table 4

eficiencies in the fat-soluble vitamins A D E and K d

hich are important for driving many of the biologicalrocesses that help to regulate body size [29ndash31] As theate of noncompliance with prophylactic multivitamin sup-lementation increases the rate of postoperative deficiencyay increase almost twofold [32]In the past it has been thought that the specific nutri-

ional deficiencies commonly seen among malabsorptiverocedures would not be present in patients choosing aurely restrictive surgery such as the adjustable gastric bandAGB) However poor eating behavior low nutrient-denseood choices food intolerance and a restricted portion sizean contribute to potential nutrient deficiencies in theseatients as well Although the incidence of nutritional com-lications may be less frequent in this patient population itould be detrimental to assume that they do not existIt is important for the bariatric patient to take vitamin and

ineral supplements not only to prevent adverse healthonditions that can arise after surgery but because someutrients such as calcium can enhance weight loss and helprevent weight regain The nutrient deficiency might beroportional to the length of the absorptive area bypassed

RYGB BPDDS Comment

mdash

mdash

mdash

10000 IU of vitamin A

2000 IU of vitamin D

300 g of vitamin K

May begin 2ndash4weeks aftersurgery

1 servingd 1 servingd May begin on day 1after hospitaldischarge

ngd

uring surgical procedures and to a lesser extent to the

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S81L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ercentage of weight lost Iron vitamin B12 and vitamin Deficiencies along with changes in calcium metabolism areommon after RYGB Protein fat-soluble vitamin andther micronutrient deficiencies as well as altered calciumetabolism are most notably found after BPDDS Folate

eficiency has been reported after AGB [33] Thiamin de-ciency is common among all surgical patients with fre-uent vomiting regardless of the type of procedure per-ormed Because many nutritional deficiencies progressith time patients should be monitored frequently and

egularly to prevent malnutrition [29] Reinforcement ofupplement compliance at each patient follow-up is alsomportant in the fight to enhance nutrition status and preventutritional complications

eight loss and nutrient deficits restrictionersus malabsorption

Malabsorptive procedures such as the BPDDS arehought to cause weight loss primarily through the malab-orption of macronutrients with as much as 25 of proteinnd 72 of fat malabsorbed Such primary malabsorptionesults in concomitant malabsorption of micronutrients3435] Vitamins and minerals relying on fat metabolismncluding vitamins D A E K and zinc may be affectedhen absorption is impaired [36] The decrease in gastro-

ntestinal transit time may also result in secondary malab-orption of a wide range of micronutrients related to by-assing the duodenum and jejunum or limited contact withhe brush border secondary to a short common limb Othericronutrient deficiency concerns reported for patients

hoosing a procedure with malabsorptive features includeron calcium vitamin B12 and folate

Nutrient deficiencies after RYGB can result from eitherrimary or secondary malabsorption or from inadequateietary intake A minimal amount of macronutrient malab-orption is thought to occur However specific micronutri-nts appear to be malabsorbed postoperatively and presents deficiencies without adequate vitamin and mineral sup-lementation Retrospective analyses of patients who havendergone gastric bypass have revealed predictable micro-utrient deficiencies including iron vitamin B12 and folate2627ndash39] Case reports have also shown that thiamin de-ciency can develop especially when persistent postopera-

ive vomiting occurs [40ndash43]Few studies that measure absorption after measured and

uantified intake have been published It can be hypothe-ized that the bypassed duodenum and proximal jejunumegatively affect nutrient assimilation Bradley et al [44]tudied patients who had undergone total gastrectomy therocedure from which the RYGB evolved The researchersound that most nutritional status changes in patients wereost likely due to changes in intake versus malabsorptionhese balance studies were conducted in a controlled re-

earch setting however they did not measure pre- and c

ostoperative changes nor include radioisotope labeling toeasure absorption of key nutrients and the subjects had

ndergone the procedure for reasons other than weight lossIt is unclear whether intestinal adaptation occurs after

ombination procedures and to what degree it affects long-erm weight maintenance and nutrition status Adaptation iscompensatory response that follows an abrupt decrease inucosal surface area and has been well studied in short-

owel patients who require bowel resection [45] The pro-ess includes both anatomic and functional changes thatncrease the gutrsquos digestive and absorptive capacity Al-hough these changes begin to take place in the early post-perative period total adaptation may take up to three yearso complete Adaptation in gastric bypass has not beenonsidered in absorption or metabolic studies This consid-ration could be important even when determining early andate macro- and micronutrient intake recommendations Theffect of pancreatic enzyme replacement therapy on vitaminnd mineral absorption in this population is also unknown

Purely restrictive procedures such as the AGB can resultn micronutrient deficiencies related to changes in dietaryntake It is commonly accepted that because no alteration isade in the absorptive pathway malabsorption does not

ccur as a result of AGB procedures However nutrienteficits would be likely to occur because of the low nutrientntake and avoidance of nutrient-rich foods in the earlyonths postoperatively and later possibly as a result of

xcessive band restriction Food with high nutritional valueuch as meat and fibrous fresh fruits and vegetables mighte poorly tolerated

Literature has been published that addresses the effect ofalabsorptive restrictive and combination surgical proce-

ures on acute and long-term nutritional status These stud-es have attempted for the most part to indirectly determinehe surgical impact on nutrition status by the evaluation ofetabolic and laboratory markers Although some studies

ave included certain aspects of absorption few have in-luded the necessary components to evaluate absorption ofprescribed andor monitored diet in a controlled metabolic

ettingThe following sections examine the pre- and postopera-

ive risks for nutritional deficiencies associated with RYGBPDDS and AGB It is important for all members of theedical team to increase their awareness of the nutritional

omplications and challenges that lie ahead for the patientontinued review of current research by the medical team

egarding advances in nutrition science beyond the bound-ries of the present report cannot be emphasized enough

hiamin (vitamin B1)

Beriberi is a thiamin deficiency that can affect variousrgan systems including the heart gastrointestinal tractnd peripheral and central nervous systems Although the

ondition is generally considered rare a number of reported

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S82 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nd possibly a much greater number of unreported or un-iagnosed cases of beriberi have occurred among individ-als who have undergone surgery for morbid obesity Earlyetection and prompt treatment of thiamin deficits in thesendividuals can help to prevent serious health consequencesf beriberi is misdiagnosed or goes undetected for even ahort period the bariatric patient can develop irreversibleeuromuscular disorders permanent defects in learning andhort-term memory coma and even death Because of theife-altering and potentially life-threatening nature of a thi-min deficiency it is important that healthcare professionalsn the field of bariatric surgery have knowledge of thetiology of the condition and its signs and symptomsreatment and prevention

tiology of potential deficiency Thiamin is a water-solubleitamin that is absorbed in the proximal jejunum by anctive (saturable high-affinity) transport system [4647] Inhe body thiamin is found in high concentrations in therain heart muscle liver and kidneys However withoutegular and sufficient intake these tissues become rapidlyevoid of thiamin [4647] The total amount of thiamin inhe body of an adult is approximately 30 mg with a half-lifef only 9ndash18 days Persistent vomiting a diet deficient inhe vitamin or the bodyrsquos excessive utilization of thiaminse can result in a severe state of thiamin depletion withinnly a short period producing symptoms of beriberi46ndash48]

Bariatric surgery increases the risk of beriberi through ex-cerbation of pre-existing thiamin deficits low nutrient intakealabsorption and episodes of nausea and vomiting [49ndash51]hronic or acute thiamin deficiencies in bariatric patients oftenresent with symptoms of peripheral neuropathy or Wer-ickersquos encephalopathy and Korsakoffrsquos psychoses [2148ndash4] Early diagnosis of the signs and symptoms of these con-itions is extremely important to prevent serious adverse healthonsequences Even if treatment is initiated recovery can bencomplete with cognitive andor neuromuscular impairmentsersisting long term or permanently

igns symptoms and treatment of deficiency (seeppendix Table A1)

reoperative risk The risk of the development of beriberifter bariatric surgery is far greater for individuals present-ng for surgery with low thiamin levels Investigators at theleveland Clinic of Florida reported that 15 of their pre-perative bariatric patients had deficiencies in thiamin be-ore surgery [52] A study by Flancbaum et al [21] similarlyound that 29 of their preoperative patients had low thia-in levels Data obtained by that study also showed a

ignificant difference between ethnicity and preoperativehiamin levels Although only 67 of whites presentedith thiamin deficiencies before surgery nearly one third

31) of African Americans and almost one half (47) of

ispanics had thiamin deficits The results of these studies S

uggested a need for preoperative thiamin testing as well ashiamin repletion by diet or supplementation to reduce theisk of ldquobariatricrdquo beriberi postoperatively

ostoperative risk Beriberi has been observed after gastricestrictive and malabsorptive procedures A number of casesf Wernicke-Korsakoff syndrome (WKS) as well as periph-ral neuropathy have been reported for patients havingndergone vertical banded gastroplasty [53ndash61] A fewncidences of WKS have also been reported after AGB436263] Additionally reports of thiamin deficiencies and

KS after RYGB [404164ndash73] and several cases of WKSnd neuropathy in patients who had undergone BPD [74]ave been published Many more cases of WKS are be-ieved to have occurred with bariatric procedures that haveither not been reported or have been misdiagnosed becausef limited knowledge regarding the signs and symptoms ofcute or severe thiamin deficits Because many foods areortified with thiamin beriberi has been nearly eradicatedhroughout the world except for patients with severe alco-olism severe vomiting during pregnancy (hyperemesisravidarium) or those malnourished and starved For thiseason few healthcare professionals until recently havead a patient present with beriberi

According to the published reports of thiamin deficitsfter bariatric procedures most patients develop such defi-iencies in the early postoperative months after an episodef intractable vomiting Nausea and vomiting are relativelyommon after all bariatric procedures early in the postop-rative period Thiamin stores in the body are small andaintenance of appropriate thiamin levels requires daily

eplenishment A deficiency of thiamin for only a couple ofeeks or less caused by persistent vomiting can deplete

hiamin stores Symptoms of WKS were reported in aYGB patient after only two weeks of persistent vomiting

67]Bariatric beriberi can also develop in postoperative patients

ho are given infusate containing dextrose without thiaminnd other vitamins which is often the case for patients inritical care units postoperative patients with complicationsnterfering with the ingestion of food or patients dehydratedrom persistent vomiting Malnutrition caused by a lack ofppetite and dietary intake postoperatively also contributes toariatric beriberi as does noncompliance in taking postopera-ive vitamin supplements

Although most cases of beriberi occur in the early post-perative periods cases of patients with severe thiamineficiency more than one year after surgery have beeneported One study reported WKS in association with al-ohol abuse 13 years after RYGB [75] Other conditionsontributing to late cases of bariatric beriberi include ahiamin-poor diet a diet high in carbohydrates anorexiand bulimia [46ndash48]

uggested supplementation Because of the greater likeli-

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S83L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ood of low dietary thiamin intake patients should be sup-lemented with thiamin This is usually accomplishedhrough daily intake of a multivitamin Most multivitaminsontain thiamin at 100 of the daily value Patients havingpisodes of nausea and vomiting and those who are anorec-ic might require sublingual intramuscular or intravenoushiamin to avoid depletion of thiamin stores and beriberiaution should be used when infusing bariatric patientsith solutions containing dextrose without additional vita-ins and thiamin because an increase in glucose utilizationithout additional thiamin can deplete thiamin stores [76]Thiamin deficiency in bariatric patients is treated with

hiamin together with other B-complex vitamins and mag-esium for maximal thiamin absorption and appropriateeurologic function [46 ndash 48] Early symptoms of neuropa-hy can often be resolved by providing the patient with oralhiamin doses of 20ndash30 mgd until symptoms disappear Forore advanced signs of neuropathy or for individuals with

rotracted vomiting 50ndash100 mgd of intravenous or intra-uscular thiamin may be necessary for resolution or im-

rovement of symptoms or for the prevention of suchatients with WKS generally require 100 mg thiamindministered intravenously for several days or longer fol-owed by intramuscular thiamin or high oral doses untilymptoms have resolved or significantly improved This canequire months to years Some patients might have to takehiamin for life to prevent the reoccurrence of neuropathy

itamin B12 and folate

Vitamin B12 (cobalamin) and folate (folic acid) are bothnvolved in the maturation of red blood cells and are com-only discussed in the literature together Over time a

eficiency in either vitamin B12 or folate can lead to mac-ocytic anemia a condition characterized by the productionf fewer but larger red blood cells and a decreased abilityo carry oxygen Most (95) cases of megaloblastic anemiacharacterized by large immature abnormal undifferenti-ted red blood cells in bone marrow) are attributed toitamin B12 or folate deficiency [77]

itamin B12

tiology of potential deficiency RYGB patients have bothncomplete digestion and release of vitamin B12 from pro-ein foods With a significant decrease in hydrochloric acidepsinogen is not converted into pepsin which is necessaryor the release of vitamin B12 from protein [78] BecauseGB patients have an artificial restriction yet complete usef the stomach and BPD patients do not have as great aestriction in stomach capacity and parietal cells as RYGBatients the reduction in hydrochloric acid and subsequentitamin B12 deficiency is not as prevalent with these tworocedures

Intrinsic factor (IF) is produced by the parietal cells of

he stomach and in certain conditions (eg atrophic gastri- a

is resected small bowel elderly patients) can be impairedausing an IF deficiency Subsequent vitamin B12 deficiencypernicious anemia) occurs without IF production or useecause IF is needed to absorb vitamin B12 in the terminalleum [77] Factors that increase the risk of vitamin B12

eficiency relevant to bariatric surgery include the follow-ng

An inability to release protein-bound vitamin B12

from food particularly in hypochlorhydria andatrophic gastritis

Malabsorption due to inadequate IF in perniciousanemia

Gastrectomy and gastric bypassResection or disease of terminal ileumLong-term vegan dietMedications such as neomycin metformin colch-

icines medications used in the management ofbowel inflammation and gastroesophageal refluxand ulcers (eg proton pump inhibitors) and anti-convulsant agents [79]

Cobalamin stores are known to exist for long periods3ndash5 yr) and are dependent on dietary repletion and dailyepletion However gastric bypass patients have both aecreased production of stomach acid and a decreased avail-bility of IF thus a vitamin B12 deficiency could developithout appropriate supplementation Because the typical

bsorption pathway cannot be relied on the surgical weightoss patient must rely on passive absorption of B12 whichccurs independent of IF

igns symptoms and treatment of deficiency (seeppendix Table A3)

reoperative risk Several medications common to preop-rative bariatric patients have been noted to affect preoper-tive vitamin B12 absorption and stores Of patients takingetformin 10ndash30 present with reduced vitamin B12 ab-

orption [80] Additionally patients with obesity have aigh incidence of gastroesophageal reflux disease for whichhey take proton pump inhibitors thus increasing the poten-ial to develop a vitamin B12 deficiency

Flancbaum et al [21] conducted a retrospective study of79 (320 women and 59 men) pre-operative patients Vita-in B12 deficiency was reported as negative in all patients

f various ethnic backgrounds [21] No clinical criteria orymptoms for vitamin B12 deficiency were noted In theeneral population 5ndash10 present with neurologic symp-oms with vitamin B12 levels of 200ndash400 pgmL Amongreoperative gastric bypass patients Madan et al [27] foundhat 13 (n 59) of patients were deficient in vitamin B12n a comparison of patients presenting for either RYGB orPD Skroubis et al [81] recently reported that preoperativeitamin B12 levels were low-normal in both groups Itould be prudent to screen for and treat IF deficiency

ndor vitamin B12 deficiency in all patients preoperatively

bd

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S84 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ut it is essential for RYGB patients so as not to hasten theevelopment of a potential postoperative deficiency

ostoperative risk Vitamin B12 deficiency has been fre-uently reported after RYGB Schilling et al [82] estimatedhe prevalence of vitamin B12 deficiency to be 12ndash33ther researchers have suggested a much greater prevalencef B12 deficiency in up to 75 of postoperative RYGBatients however most reports have cited approximately5 of postoperative RYGB patients as vitamin B12 defi-ient [82ndash87] Brolin et al [87] reported that low levels ofitamin B12 might be seen as soon as six months afterariatric surgery but most often occurring more than oneear postoperatively as liver stores become depleted Sk-oubis et al [88] predicted that the deficiency will mostikely occur 7 months after RYGB and 79 months afterPDDS although their research did not consider compro-ised preoperative status and its correlation to postopera-

ive deficiency After the first postoperative year the prev-lence of vitamin B12 deficiency appears to increase yearlyn RYGB patients [89]

Although the bodyrsquos storage of vitamin B12 is significant2000 g) compared with daily needs (24 gd) thisarticular deficiency has been found within 1ndash9 years ofastric bypass surgery [29] Brolin et al [84] reported thatne third of RYGB patients are deficient at four yearsostoperatively However non-surgical variables were notxplored and many patients might have had preoperativealues near the lower end of the normal range Ocon Bretont al [90] compared micronutrient deficiencies among two-ear postoperative BPDDS and RYGB patients and foundhat all nutritional deficiencies were more common amongPDDS patients except for vitamin B12 for which theeficiency was more common among the RYGB patientstudied A lack of B12 deficiency among BPDDS patientsight result from a better tolerance of animal proteins in a

arger pouch greater pepsingastric acid production to re-ease protein-bound B12 and increased availability and in-eraction of IF with the pouch contents

Experts have noted the significance of subclinical defi-iency in the low-normal cobalamin range in nongastricypass patients who do not exhibit clinical evidence ofeficiency The methylmalonic acid (MMA) assay is thereferred marker of B12 status because metabolic changesften precede low B12 levels in the progression to defi-iency Serum B12 assays may miss as much as 25ndash30 of

12 deficiencies making them less reliable than the MMAssay [91] It has been suggested that early signs of vitamin

12 deficiency can be detected if the serum levels of bothMA and homocysteine are measured [91] Vitamin B12

eficiency after RYGB has been associated with megalo-lastic anemia [92] Some vitamin B12-deficient patientsevelop significant symptoms such as polyneuropathy par-

sthesia and permanent neural impairment On occasion

ome patients may experience extreme delusions halluci-ations and even overt psychosis [93]

uggested supplementation Because of the frequent lack ofymptoms of vitamin B12 deficiency the suggested dili-ence in following up or treating these values among thosesymptomatic patients has been questioned The decisionot to supplement or routinely screen patients for B12 defi-iency should be examined very carefully given the risk ofrreversible neurologic damage if vitamin B12 goes un-reated for long periods At least one case report has beenublished of an exclusively breastfed infant with vitamin

12 deficiency who was born of an asymptomatic motherho had undergone gastric bypass surgery [94]Deficiency of vitamin B12 is typically defined at levels

200 pgmL However about 50 of patients with obviousigns and symptoms of deficiency have normal vitamin B12

evels [31] Kaplan et al [95] reported that vitamin B12

eficiency usually resolves after several weeks of treatmentith 700ndash2000 gwk Rhode et al [96] found that aosage of 350ndash600 gd of oral B12 prevented vitamin B12

eficiency in 95 of patients and an oral dose of 500 gdas sufficient to overcome an existing deficiency as re-orted by Brolin et al [87] in a similar study Thereforeupplementation of RYGB patients with 350ndash500 gd mayrevent most postoperative vitamin B12 deficiency

While most vitamin B12 in normal adults is absorbed inhe ileum in the presence of IF approximately 1 of sup-lemented B12 will be absorbed passively (by diffusion)long the entire length of the (non-bypassed) intestine byurgical weight loss patients given a high-dose oral supple-ent [97] Thus the consumption of 350ndash500 g yields a

5ndash50-g absorption which is greater than the daily re-uirement Although the use of monthly intramuscular in-ections or a weekly oral dose of vitamin B12 is commonmong practices it relies on patient compliance Practitio-ers should assess the patientrsquos preference and the potentialor compliance when considering a daily weekly oronthly regimen of B12 supplementation In addition to oral

upplements or intramuscular injections nasal sprays andublingual sources of vitamin B12 are also available Pa-ients should be monitored closely for their lifetime becauseevere anemia can develop with or without supplementation98]

olate

tiology of potential deficiency Factors that increase theisk of folic acid deficiency relevant to bariatric surgerynclude the following

Inadequate dietary intakeNoncompliance with multivitamin supplementationMalabsorptionMedications (anticonvulsants oral contraceptives

and cancer treating agents) [79]

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S85L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Folic acid stores can be depleted within a few monthsostoperatively unless replenished by a multivitamin supple-ent and dietary sources (ie green leafy vegetables fruits

rgan meats liver dried yeast and fortified grain products)

igns symptoms and treatment of deficiency (seeppendix Table A4)

reoperative risk The goals of the 1998 Food and Drugdministration policy requiring all enriched grain products

o be fortified with folate included increasing the averagemerican diet by 100 g folate daily and decreasing the

ate of neural tube defects in childbearing women [99]entley et al [100] reported that the proportion of womenged 15ndash44 years old (in the general population) who meethe recommended dietary intake of 400 gd folate variesetween 23 and 33 With the increasing popularity ofigh proteinlow carbohydrate diets one cannot assume thatreoperative patients consume dietary sources of folatehrough fortified grain products fruits and vegetables Boy-an et al [26] found folate deficiencies preoperatively in6 of RYGB patients studied

ostoperative risk Although it has been observed that fo-ate deficiency after RYGB surgery is less common than B12

eficiency and is thought to occur because of decreasedietary or multivitamin supplement intake low serum folateevels have been cited from 6 to 65 among RYGBatients [2686101] Additionally folate deficiencies haveccurred postoperatively even with supplementation Boy-an et al [26] found that 47 (n 17) of RYGB patientsad low folate levels six months postoperatively and 41n 17) had low levels at one year This deficiency oc-urred despite patient adherence to taking a multivitaminupplement that contained at least the daily value for folate00 g [26] Postoperative bariatric patients with rapideight loss might have an increased risk of micronutrienteficiencies MacLean et al [86] reported that 65 ofostoperative patients had low folate levels These sameatients exhibited additional B vitamin deficiencies 24itamin B12 and 50 thiamin [86] An increased risk ofeficiency has also been noted among AGB patients pos-ibly because of decreased folate intake Gasteyger et al33] found a significant decrease in serum folate levels441) between the baseline and 24-month postoperativeeasurementsDixon and OrsquoBrien [101] reported elevated serum ho-

ocysteine levels in patients after bariatric surgery regard-ess of the type of procedure (restrictive or malabsorptive)levated homocysteine levels can indicate not only low

olate levels and a greater risk of neural tube defects but canlso be indicative of an independent risk factor for heartisease andor oxidative stress in the nonbariatric popula-ion [102] However unlike iron and vitamin B12 the folate

ontained in the multivitamin supplementation essentially e

orrects the deficiency in the vast majority of postoperativeariatric patients [103] Therefore persistent folate defi-iency might indicate a patientrsquos lack of compliance withhe prescribed vitamin protocol [32]

It is common knowledge that folic acid deficiency amongregnant women has been associated with a greater risk ofeural tube defects in newborns Consistent supplementa-ion and monitoring among women of child-bearing agencluding pre- and postoperative bariatric patients is vital inn effort to prevent the possibility of neural tube defects inhe developing fetus

Because folate does not affect the myelin of nerveseurologic damage is not as common with folate such as ishe case for vitamin B12 deficiency In contrast patientsith folate deficiency often present with forgetfulness irri-

ability hostility and even paranoid behaviors [29] Similaro that evidenced with vitamin B12 most postoperativeYGB patients who are folate deficient are asymptomatic orave subclinical symptoms therefore these deficient statesay not be easily identified

uggested supplementation Even though folate absorptionccurs preferentially in the proximal portion of the smallntestine it can occur along the entire length of the small bowelith postoperative adaptation Therefore it is generally agreed

hat folate deficiency is corrected with 1000 mgd folic acid32] and is preventable with supplementation that provides00 of the daily value (800 g) This level can also benefithe fetus in a female patient unaware of her postoperativeregnancy Folate supplementation 1000 mgd has noteen recommended because of the potential for maskingitamin B12 deficiency Carmel et al [104] suggested thatomocysteine is the most sensitive marker of folic acidtatus in conjunction with erythrocyte folate Althougholic acid deficiency could potentially occur among post-perative bariatric surgery patients it has not been seenidely in recent studies especially when patients haveeen compliant with postoperative multivitamin supple-entation Therefore it is imperative to closely follow

olic acid both pre- and postoperatively especially inhose patients suspected to be noncompliant with theirultivitamin supplementation

ron

Much of the iron and surgical weight loss research con-ucted to date has been generated from a limited number ofurgeons and scientists however the data have consistentlyointed toward the risk of iron deficiency and anemia afterariatric procedures Iron deficiency is defined as a decreasen the total iron body content Iron deficiency anemia occurshen erythropoiesis is impaired as a result of the lack of

ron stores In the absence of anemia iron deficiency issually asymptomatic Fatigue and a diminished capacity to

xercise however are common symptoms of anemia

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S86 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

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S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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S88 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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S89L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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S90 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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msmpdr

Sab2omh

dumRameod

maailo

fmRr

CdcBstpcbtpo

O

VcslwAwvIvmtbrvsee

S91L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

gba

SA

Cphctrpw[nvfiisitCbg

Oafp[woofc(1hpritt

P

E

tgpoo

ccpcglcppmtttwaw

ailmsmtsbtciaspomtsa

bompo(almqmmbbEc

S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

(admcas

ihtpacbsT

ovBfted

fbsalumlcatspie

P

laTofmndef

pocimhphcsatpa

P

awrywaoirfiotnrsafRe

strwsviaratrlsgt

S93L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

[ntnriasiB(cdip

afedmvfllBrpem

D1mypei

iecalbcBmpmtta

ciru

iipafcfui

foaowppartptpthc

P

iwEvln6wdeapctnstat

S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

ratbrdd

aebaaa

apcptaasosdbc

afciitdmptpcrsPEv

TI

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HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

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[

[

[

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[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

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[

[

[

[

[

[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 8: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S80 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hich in turn causes metabolic changes that favor fatccumulation [23ndash25]

Several of the B-complex vitamins important for appro-riate metabolism of carbohydrate and neural functions thategulate appetite have been found to be deficient in someatients with morbid obesity [212627] Iron deficiencieshich would significantly hinder energy use have been

eported in nearly 50 of morbidly obese preoperativeandidates [21] Zinc and selenium deficits have been re-orted as well as deficits in vitamins A E and C allmportant antioxidants helpful in regulating energy produc-ion and various other processes of body weight manage-ent [1926ndash28]The risk of micronutrient depletion continues to be quite

igh particularly after surgeries that affect the digestion andbsorption of nutrients such as Roux-en-Y gastric bypassRYGB) and biliopancreatic diversion with or without du-denal switch (BPDDS) RYGB increases the risk of vita-in B12 and other B vitamin deficits in addition to iron and

alcium BPDDS procedures may also cause an increasedisk of iron and calcium deficits along with significant

able 5ontinued

upplement AGB

at-soluble vitaminsWith all procedures higher maintenance doses may be

required for those with a history of deficiencyWater-soluble preparations of fat-soluble vitamins are

availableRetinol sources of vitamin A should be used to calculatedosageMost supplements contain a high percentage of beta

carotene which does not contribute to vitamin A toxicityIntake of 2000 IU Vitamin D3 may be achieved with careful

selection of multivitamin and calcium supplementsNo toxic effect known for vitamin K1 phytonadione

(phyloquinone)

mdash

mdash

mdash

Vitamin K requirement varies with dietary sources andcolonic production

Caution with vitamin K supplementation for patientsreceiving coagulation therapy

Vitamin E deficiency has been suggested but is notprevalent in published studies

ptional B complexB-50 dosageLiquid form is available

1 servi

Avoid time released tabletsNo known risk of toxicityMay provide additional prophylaxis against B-vitamin

deficiencies including thiamin especially for BPDDSprocedures as water-soluble vitamins are absorbed in theproximal jejunum

Note 1000 mg of supplemental folic acid provided incombination with multivitamins could mask B12

deficiency

Abbreviations as in Table 4

eficiencies in the fat-soluble vitamins A D E and K d

hich are important for driving many of the biologicalrocesses that help to regulate body size [29ndash31] As theate of noncompliance with prophylactic multivitamin sup-lementation increases the rate of postoperative deficiencyay increase almost twofold [32]In the past it has been thought that the specific nutri-

ional deficiencies commonly seen among malabsorptiverocedures would not be present in patients choosing aurely restrictive surgery such as the adjustable gastric bandAGB) However poor eating behavior low nutrient-denseood choices food intolerance and a restricted portion sizean contribute to potential nutrient deficiencies in theseatients as well Although the incidence of nutritional com-lications may be less frequent in this patient population itould be detrimental to assume that they do not existIt is important for the bariatric patient to take vitamin and

ineral supplements not only to prevent adverse healthonditions that can arise after surgery but because someutrients such as calcium can enhance weight loss and helprevent weight regain The nutrient deficiency might beroportional to the length of the absorptive area bypassed

RYGB BPDDS Comment

mdash

mdash

mdash

10000 IU of vitamin A

2000 IU of vitamin D

300 g of vitamin K

May begin 2ndash4weeks aftersurgery

1 servingd 1 servingd May begin on day 1after hospitaldischarge

ngd

uring surgical procedures and to a lesser extent to the

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S81L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ercentage of weight lost Iron vitamin B12 and vitamin Deficiencies along with changes in calcium metabolism areommon after RYGB Protein fat-soluble vitamin andther micronutrient deficiencies as well as altered calciumetabolism are most notably found after BPDDS Folate

eficiency has been reported after AGB [33] Thiamin de-ciency is common among all surgical patients with fre-uent vomiting regardless of the type of procedure per-ormed Because many nutritional deficiencies progressith time patients should be monitored frequently and

egularly to prevent malnutrition [29] Reinforcement ofupplement compliance at each patient follow-up is alsomportant in the fight to enhance nutrition status and preventutritional complications

eight loss and nutrient deficits restrictionersus malabsorption

Malabsorptive procedures such as the BPDDS arehought to cause weight loss primarily through the malab-orption of macronutrients with as much as 25 of proteinnd 72 of fat malabsorbed Such primary malabsorptionesults in concomitant malabsorption of micronutrients3435] Vitamins and minerals relying on fat metabolismncluding vitamins D A E K and zinc may be affectedhen absorption is impaired [36] The decrease in gastro-

ntestinal transit time may also result in secondary malab-orption of a wide range of micronutrients related to by-assing the duodenum and jejunum or limited contact withhe brush border secondary to a short common limb Othericronutrient deficiency concerns reported for patients

hoosing a procedure with malabsorptive features includeron calcium vitamin B12 and folate

Nutrient deficiencies after RYGB can result from eitherrimary or secondary malabsorption or from inadequateietary intake A minimal amount of macronutrient malab-orption is thought to occur However specific micronutri-nts appear to be malabsorbed postoperatively and presents deficiencies without adequate vitamin and mineral sup-lementation Retrospective analyses of patients who havendergone gastric bypass have revealed predictable micro-utrient deficiencies including iron vitamin B12 and folate2627ndash39] Case reports have also shown that thiamin de-ciency can develop especially when persistent postopera-

ive vomiting occurs [40ndash43]Few studies that measure absorption after measured and

uantified intake have been published It can be hypothe-ized that the bypassed duodenum and proximal jejunumegatively affect nutrient assimilation Bradley et al [44]tudied patients who had undergone total gastrectomy therocedure from which the RYGB evolved The researchersound that most nutritional status changes in patients wereost likely due to changes in intake versus malabsorptionhese balance studies were conducted in a controlled re-

earch setting however they did not measure pre- and c

ostoperative changes nor include radioisotope labeling toeasure absorption of key nutrients and the subjects had

ndergone the procedure for reasons other than weight lossIt is unclear whether intestinal adaptation occurs after

ombination procedures and to what degree it affects long-erm weight maintenance and nutrition status Adaptation iscompensatory response that follows an abrupt decrease inucosal surface area and has been well studied in short-

owel patients who require bowel resection [45] The pro-ess includes both anatomic and functional changes thatncrease the gutrsquos digestive and absorptive capacity Al-hough these changes begin to take place in the early post-perative period total adaptation may take up to three yearso complete Adaptation in gastric bypass has not beenonsidered in absorption or metabolic studies This consid-ration could be important even when determining early andate macro- and micronutrient intake recommendations Theffect of pancreatic enzyme replacement therapy on vitaminnd mineral absorption in this population is also unknown

Purely restrictive procedures such as the AGB can resultn micronutrient deficiencies related to changes in dietaryntake It is commonly accepted that because no alteration isade in the absorptive pathway malabsorption does not

ccur as a result of AGB procedures However nutrienteficits would be likely to occur because of the low nutrientntake and avoidance of nutrient-rich foods in the earlyonths postoperatively and later possibly as a result of

xcessive band restriction Food with high nutritional valueuch as meat and fibrous fresh fruits and vegetables mighte poorly tolerated

Literature has been published that addresses the effect ofalabsorptive restrictive and combination surgical proce-

ures on acute and long-term nutritional status These stud-es have attempted for the most part to indirectly determinehe surgical impact on nutrition status by the evaluation ofetabolic and laboratory markers Although some studies

ave included certain aspects of absorption few have in-luded the necessary components to evaluate absorption ofprescribed andor monitored diet in a controlled metabolic

ettingThe following sections examine the pre- and postopera-

ive risks for nutritional deficiencies associated with RYGBPDDS and AGB It is important for all members of theedical team to increase their awareness of the nutritional

omplications and challenges that lie ahead for the patientontinued review of current research by the medical team

egarding advances in nutrition science beyond the bound-ries of the present report cannot be emphasized enough

hiamin (vitamin B1)

Beriberi is a thiamin deficiency that can affect variousrgan systems including the heart gastrointestinal tractnd peripheral and central nervous systems Although the

ondition is generally considered rare a number of reported

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S82 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nd possibly a much greater number of unreported or un-iagnosed cases of beriberi have occurred among individ-als who have undergone surgery for morbid obesity Earlyetection and prompt treatment of thiamin deficits in thesendividuals can help to prevent serious health consequencesf beriberi is misdiagnosed or goes undetected for even ahort period the bariatric patient can develop irreversibleeuromuscular disorders permanent defects in learning andhort-term memory coma and even death Because of theife-altering and potentially life-threatening nature of a thi-min deficiency it is important that healthcare professionalsn the field of bariatric surgery have knowledge of thetiology of the condition and its signs and symptomsreatment and prevention

tiology of potential deficiency Thiamin is a water-solubleitamin that is absorbed in the proximal jejunum by anctive (saturable high-affinity) transport system [4647] Inhe body thiamin is found in high concentrations in therain heart muscle liver and kidneys However withoutegular and sufficient intake these tissues become rapidlyevoid of thiamin [4647] The total amount of thiamin inhe body of an adult is approximately 30 mg with a half-lifef only 9ndash18 days Persistent vomiting a diet deficient inhe vitamin or the bodyrsquos excessive utilization of thiaminse can result in a severe state of thiamin depletion withinnly a short period producing symptoms of beriberi46ndash48]

Bariatric surgery increases the risk of beriberi through ex-cerbation of pre-existing thiamin deficits low nutrient intakealabsorption and episodes of nausea and vomiting [49ndash51]hronic or acute thiamin deficiencies in bariatric patients oftenresent with symptoms of peripheral neuropathy or Wer-ickersquos encephalopathy and Korsakoffrsquos psychoses [2148ndash4] Early diagnosis of the signs and symptoms of these con-itions is extremely important to prevent serious adverse healthonsequences Even if treatment is initiated recovery can bencomplete with cognitive andor neuromuscular impairmentsersisting long term or permanently

igns symptoms and treatment of deficiency (seeppendix Table A1)

reoperative risk The risk of the development of beriberifter bariatric surgery is far greater for individuals present-ng for surgery with low thiamin levels Investigators at theleveland Clinic of Florida reported that 15 of their pre-perative bariatric patients had deficiencies in thiamin be-ore surgery [52] A study by Flancbaum et al [21] similarlyound that 29 of their preoperative patients had low thia-in levels Data obtained by that study also showed a

ignificant difference between ethnicity and preoperativehiamin levels Although only 67 of whites presentedith thiamin deficiencies before surgery nearly one third

31) of African Americans and almost one half (47) of

ispanics had thiamin deficits The results of these studies S

uggested a need for preoperative thiamin testing as well ashiamin repletion by diet or supplementation to reduce theisk of ldquobariatricrdquo beriberi postoperatively

ostoperative risk Beriberi has been observed after gastricestrictive and malabsorptive procedures A number of casesf Wernicke-Korsakoff syndrome (WKS) as well as periph-ral neuropathy have been reported for patients havingndergone vertical banded gastroplasty [53ndash61] A fewncidences of WKS have also been reported after AGB436263] Additionally reports of thiamin deficiencies and

KS after RYGB [404164ndash73] and several cases of WKSnd neuropathy in patients who had undergone BPD [74]ave been published Many more cases of WKS are be-ieved to have occurred with bariatric procedures that haveither not been reported or have been misdiagnosed becausef limited knowledge regarding the signs and symptoms ofcute or severe thiamin deficits Because many foods areortified with thiamin beriberi has been nearly eradicatedhroughout the world except for patients with severe alco-olism severe vomiting during pregnancy (hyperemesisravidarium) or those malnourished and starved For thiseason few healthcare professionals until recently havead a patient present with beriberi

According to the published reports of thiamin deficitsfter bariatric procedures most patients develop such defi-iencies in the early postoperative months after an episodef intractable vomiting Nausea and vomiting are relativelyommon after all bariatric procedures early in the postop-rative period Thiamin stores in the body are small andaintenance of appropriate thiamin levels requires daily

eplenishment A deficiency of thiamin for only a couple ofeeks or less caused by persistent vomiting can deplete

hiamin stores Symptoms of WKS were reported in aYGB patient after only two weeks of persistent vomiting

67]Bariatric beriberi can also develop in postoperative patients

ho are given infusate containing dextrose without thiaminnd other vitamins which is often the case for patients inritical care units postoperative patients with complicationsnterfering with the ingestion of food or patients dehydratedrom persistent vomiting Malnutrition caused by a lack ofppetite and dietary intake postoperatively also contributes toariatric beriberi as does noncompliance in taking postopera-ive vitamin supplements

Although most cases of beriberi occur in the early post-perative periods cases of patients with severe thiamineficiency more than one year after surgery have beeneported One study reported WKS in association with al-ohol abuse 13 years after RYGB [75] Other conditionsontributing to late cases of bariatric beriberi include ahiamin-poor diet a diet high in carbohydrates anorexiand bulimia [46ndash48]

uggested supplementation Because of the greater likeli-

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imdrot(av

V

EitpfAorpvp

t

tc(bidi

(ddawalo

SA

Peamshtt

3mosgtptIBvw

S83L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ood of low dietary thiamin intake patients should be sup-lemented with thiamin This is usually accomplishedhrough daily intake of a multivitamin Most multivitaminsontain thiamin at 100 of the daily value Patients havingpisodes of nausea and vomiting and those who are anorec-ic might require sublingual intramuscular or intravenoushiamin to avoid depletion of thiamin stores and beriberiaution should be used when infusing bariatric patientsith solutions containing dextrose without additional vita-ins and thiamin because an increase in glucose utilizationithout additional thiamin can deplete thiamin stores [76]Thiamin deficiency in bariatric patients is treated with

hiamin together with other B-complex vitamins and mag-esium for maximal thiamin absorption and appropriateeurologic function [46 ndash 48] Early symptoms of neuropa-hy can often be resolved by providing the patient with oralhiamin doses of 20ndash30 mgd until symptoms disappear Forore advanced signs of neuropathy or for individuals with

rotracted vomiting 50ndash100 mgd of intravenous or intra-uscular thiamin may be necessary for resolution or im-

rovement of symptoms or for the prevention of suchatients with WKS generally require 100 mg thiamindministered intravenously for several days or longer fol-owed by intramuscular thiamin or high oral doses untilymptoms have resolved or significantly improved This canequire months to years Some patients might have to takehiamin for life to prevent the reoccurrence of neuropathy

itamin B12 and folate

Vitamin B12 (cobalamin) and folate (folic acid) are bothnvolved in the maturation of red blood cells and are com-only discussed in the literature together Over time a

eficiency in either vitamin B12 or folate can lead to mac-ocytic anemia a condition characterized by the productionf fewer but larger red blood cells and a decreased abilityo carry oxygen Most (95) cases of megaloblastic anemiacharacterized by large immature abnormal undifferenti-ted red blood cells in bone marrow) are attributed toitamin B12 or folate deficiency [77]

itamin B12

tiology of potential deficiency RYGB patients have bothncomplete digestion and release of vitamin B12 from pro-ein foods With a significant decrease in hydrochloric acidepsinogen is not converted into pepsin which is necessaryor the release of vitamin B12 from protein [78] BecauseGB patients have an artificial restriction yet complete usef the stomach and BPD patients do not have as great aestriction in stomach capacity and parietal cells as RYGBatients the reduction in hydrochloric acid and subsequentitamin B12 deficiency is not as prevalent with these tworocedures

Intrinsic factor (IF) is produced by the parietal cells of

he stomach and in certain conditions (eg atrophic gastri- a

is resected small bowel elderly patients) can be impairedausing an IF deficiency Subsequent vitamin B12 deficiencypernicious anemia) occurs without IF production or useecause IF is needed to absorb vitamin B12 in the terminalleum [77] Factors that increase the risk of vitamin B12

eficiency relevant to bariatric surgery include the follow-ng

An inability to release protein-bound vitamin B12

from food particularly in hypochlorhydria andatrophic gastritis

Malabsorption due to inadequate IF in perniciousanemia

Gastrectomy and gastric bypassResection or disease of terminal ileumLong-term vegan dietMedications such as neomycin metformin colch-

icines medications used in the management ofbowel inflammation and gastroesophageal refluxand ulcers (eg proton pump inhibitors) and anti-convulsant agents [79]

Cobalamin stores are known to exist for long periods3ndash5 yr) and are dependent on dietary repletion and dailyepletion However gastric bypass patients have both aecreased production of stomach acid and a decreased avail-bility of IF thus a vitamin B12 deficiency could developithout appropriate supplementation Because the typical

bsorption pathway cannot be relied on the surgical weightoss patient must rely on passive absorption of B12 whichccurs independent of IF

igns symptoms and treatment of deficiency (seeppendix Table A3)

reoperative risk Several medications common to preop-rative bariatric patients have been noted to affect preoper-tive vitamin B12 absorption and stores Of patients takingetformin 10ndash30 present with reduced vitamin B12 ab-

orption [80] Additionally patients with obesity have aigh incidence of gastroesophageal reflux disease for whichhey take proton pump inhibitors thus increasing the poten-ial to develop a vitamin B12 deficiency

Flancbaum et al [21] conducted a retrospective study of79 (320 women and 59 men) pre-operative patients Vita-in B12 deficiency was reported as negative in all patients

f various ethnic backgrounds [21] No clinical criteria orymptoms for vitamin B12 deficiency were noted In theeneral population 5ndash10 present with neurologic symp-oms with vitamin B12 levels of 200ndash400 pgmL Amongreoperative gastric bypass patients Madan et al [27] foundhat 13 (n 59) of patients were deficient in vitamin B12n a comparison of patients presenting for either RYGB orPD Skroubis et al [81] recently reported that preoperativeitamin B12 levels were low-normal in both groups Itould be prudent to screen for and treat IF deficiency

ndor vitamin B12 deficiency in all patients preoperatively

bd

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Eri

S84 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ut it is essential for RYGB patients so as not to hasten theevelopment of a potential postoperative deficiency

ostoperative risk Vitamin B12 deficiency has been fre-uently reported after RYGB Schilling et al [82] estimatedhe prevalence of vitamin B12 deficiency to be 12ndash33ther researchers have suggested a much greater prevalencef B12 deficiency in up to 75 of postoperative RYGBatients however most reports have cited approximately5 of postoperative RYGB patients as vitamin B12 defi-ient [82ndash87] Brolin et al [87] reported that low levels ofitamin B12 might be seen as soon as six months afterariatric surgery but most often occurring more than oneear postoperatively as liver stores become depleted Sk-oubis et al [88] predicted that the deficiency will mostikely occur 7 months after RYGB and 79 months afterPDDS although their research did not consider compro-ised preoperative status and its correlation to postopera-

ive deficiency After the first postoperative year the prev-lence of vitamin B12 deficiency appears to increase yearlyn RYGB patients [89]

Although the bodyrsquos storage of vitamin B12 is significant2000 g) compared with daily needs (24 gd) thisarticular deficiency has been found within 1ndash9 years ofastric bypass surgery [29] Brolin et al [84] reported thatne third of RYGB patients are deficient at four yearsostoperatively However non-surgical variables were notxplored and many patients might have had preoperativealues near the lower end of the normal range Ocon Bretont al [90] compared micronutrient deficiencies among two-ear postoperative BPDDS and RYGB patients and foundhat all nutritional deficiencies were more common amongPDDS patients except for vitamin B12 for which theeficiency was more common among the RYGB patientstudied A lack of B12 deficiency among BPDDS patientsight result from a better tolerance of animal proteins in a

arger pouch greater pepsingastric acid production to re-ease protein-bound B12 and increased availability and in-eraction of IF with the pouch contents

Experts have noted the significance of subclinical defi-iency in the low-normal cobalamin range in nongastricypass patients who do not exhibit clinical evidence ofeficiency The methylmalonic acid (MMA) assay is thereferred marker of B12 status because metabolic changesften precede low B12 levels in the progression to defi-iency Serum B12 assays may miss as much as 25ndash30 of

12 deficiencies making them less reliable than the MMAssay [91] It has been suggested that early signs of vitamin

12 deficiency can be detected if the serum levels of bothMA and homocysteine are measured [91] Vitamin B12

eficiency after RYGB has been associated with megalo-lastic anemia [92] Some vitamin B12-deficient patientsevelop significant symptoms such as polyneuropathy par-

sthesia and permanent neural impairment On occasion

ome patients may experience extreme delusions halluci-ations and even overt psychosis [93]

uggested supplementation Because of the frequent lack ofymptoms of vitamin B12 deficiency the suggested dili-ence in following up or treating these values among thosesymptomatic patients has been questioned The decisionot to supplement or routinely screen patients for B12 defi-iency should be examined very carefully given the risk ofrreversible neurologic damage if vitamin B12 goes un-reated for long periods At least one case report has beenublished of an exclusively breastfed infant with vitamin

12 deficiency who was born of an asymptomatic motherho had undergone gastric bypass surgery [94]Deficiency of vitamin B12 is typically defined at levels

200 pgmL However about 50 of patients with obviousigns and symptoms of deficiency have normal vitamin B12

evels [31] Kaplan et al [95] reported that vitamin B12

eficiency usually resolves after several weeks of treatmentith 700ndash2000 gwk Rhode et al [96] found that aosage of 350ndash600 gd of oral B12 prevented vitamin B12

eficiency in 95 of patients and an oral dose of 500 gdas sufficient to overcome an existing deficiency as re-orted by Brolin et al [87] in a similar study Thereforeupplementation of RYGB patients with 350ndash500 gd mayrevent most postoperative vitamin B12 deficiency

While most vitamin B12 in normal adults is absorbed inhe ileum in the presence of IF approximately 1 of sup-lemented B12 will be absorbed passively (by diffusion)long the entire length of the (non-bypassed) intestine byurgical weight loss patients given a high-dose oral supple-ent [97] Thus the consumption of 350ndash500 g yields a

5ndash50-g absorption which is greater than the daily re-uirement Although the use of monthly intramuscular in-ections or a weekly oral dose of vitamin B12 is commonmong practices it relies on patient compliance Practitio-ers should assess the patientrsquos preference and the potentialor compliance when considering a daily weekly oronthly regimen of B12 supplementation In addition to oral

upplements or intramuscular injections nasal sprays andublingual sources of vitamin B12 are also available Pa-ients should be monitored closely for their lifetime becauseevere anemia can develop with or without supplementation98]

olate

tiology of potential deficiency Factors that increase theisk of folic acid deficiency relevant to bariatric surgerynclude the following

Inadequate dietary intakeNoncompliance with multivitamin supplementationMalabsorptionMedications (anticonvulsants oral contraceptives

and cancer treating agents) [79]

pmo

SA

PAtArBatbhptl5

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pntiat

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Soiwt[2tpbvhsfowbmftm

I

dspbiwiu

S85L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Folic acid stores can be depleted within a few monthsostoperatively unless replenished by a multivitamin supple-ent and dietary sources (ie green leafy vegetables fruits

rgan meats liver dried yeast and fortified grain products)

igns symptoms and treatment of deficiency (seeppendix Table A4)

reoperative risk The goals of the 1998 Food and Drugdministration policy requiring all enriched grain products

o be fortified with folate included increasing the averagemerican diet by 100 g folate daily and decreasing the

ate of neural tube defects in childbearing women [99]entley et al [100] reported that the proportion of womenged 15ndash44 years old (in the general population) who meethe recommended dietary intake of 400 gd folate variesetween 23 and 33 With the increasing popularity ofigh proteinlow carbohydrate diets one cannot assume thatreoperative patients consume dietary sources of folatehrough fortified grain products fruits and vegetables Boy-an et al [26] found folate deficiencies preoperatively in6 of RYGB patients studied

ostoperative risk Although it has been observed that fo-ate deficiency after RYGB surgery is less common than B12

eficiency and is thought to occur because of decreasedietary or multivitamin supplement intake low serum folateevels have been cited from 6 to 65 among RYGBatients [2686101] Additionally folate deficiencies haveccurred postoperatively even with supplementation Boy-an et al [26] found that 47 (n 17) of RYGB patientsad low folate levels six months postoperatively and 41n 17) had low levels at one year This deficiency oc-urred despite patient adherence to taking a multivitaminupplement that contained at least the daily value for folate00 g [26] Postoperative bariatric patients with rapideight loss might have an increased risk of micronutrienteficiencies MacLean et al [86] reported that 65 ofostoperative patients had low folate levels These sameatients exhibited additional B vitamin deficiencies 24itamin B12 and 50 thiamin [86] An increased risk ofeficiency has also been noted among AGB patients pos-ibly because of decreased folate intake Gasteyger et al33] found a significant decrease in serum folate levels441) between the baseline and 24-month postoperativeeasurementsDixon and OrsquoBrien [101] reported elevated serum ho-

ocysteine levels in patients after bariatric surgery regard-ess of the type of procedure (restrictive or malabsorptive)levated homocysteine levels can indicate not only low

olate levels and a greater risk of neural tube defects but canlso be indicative of an independent risk factor for heartisease andor oxidative stress in the nonbariatric popula-ion [102] However unlike iron and vitamin B12 the folate

ontained in the multivitamin supplementation essentially e

orrects the deficiency in the vast majority of postoperativeariatric patients [103] Therefore persistent folate defi-iency might indicate a patientrsquos lack of compliance withhe prescribed vitamin protocol [32]

It is common knowledge that folic acid deficiency amongregnant women has been associated with a greater risk ofeural tube defects in newborns Consistent supplementa-ion and monitoring among women of child-bearing agencluding pre- and postoperative bariatric patients is vital inn effort to prevent the possibility of neural tube defects inhe developing fetus

Because folate does not affect the myelin of nerveseurologic damage is not as common with folate such as ishe case for vitamin B12 deficiency In contrast patientsith folate deficiency often present with forgetfulness irri-

ability hostility and even paranoid behaviors [29] Similaro that evidenced with vitamin B12 most postoperativeYGB patients who are folate deficient are asymptomatic orave subclinical symptoms therefore these deficient statesay not be easily identified

uggested supplementation Even though folate absorptionccurs preferentially in the proximal portion of the smallntestine it can occur along the entire length of the small bowelith postoperative adaptation Therefore it is generally agreed

hat folate deficiency is corrected with 1000 mgd folic acid32] and is preventable with supplementation that provides00 of the daily value (800 g) This level can also benefithe fetus in a female patient unaware of her postoperativeregnancy Folate supplementation 1000 mgd has noteen recommended because of the potential for maskingitamin B12 deficiency Carmel et al [104] suggested thatomocysteine is the most sensitive marker of folic acidtatus in conjunction with erythrocyte folate Althougholic acid deficiency could potentially occur among post-perative bariatric surgery patients it has not been seenidely in recent studies especially when patients haveeen compliant with postoperative multivitamin supple-entation Therefore it is imperative to closely follow

olic acid both pre- and postoperatively especially inhose patients suspected to be noncompliant with theirultivitamin supplementation

ron

Much of the iron and surgical weight loss research con-ucted to date has been generated from a limited number ofurgeons and scientists however the data have consistentlyointed toward the risk of iron deficiency and anemia afterariatric procedures Iron deficiency is defined as a decreasen the total iron body content Iron deficiency anemia occurshen erythropoiesis is impaired as a result of the lack of

ron stores In the absence of anemia iron deficiency issually asymptomatic Fatigue and a diminished capacity to

xercise however are common symptoms of anemia

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ifftBibfagowtimiB

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S86 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

tsmp

lsnfwTlopaechc

Rtbwdsaar

fdaiwiiedasdt

Stbadtbpcwl

mccmacdrrT

C

EeamadmsDfd

dbdh7DtnDcwsh

SA

Pcptt[hmtlcgc

S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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S88 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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S89L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

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hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

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S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

ratbrdd

aebaaa

apcptaasosdbc

afciitdmptpcrsPEv

TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

[

[

[

[

[

[

[

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[

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[

[

[

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[

[

[

[

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[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

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S

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T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

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S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

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S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

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S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 9: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S81L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ercentage of weight lost Iron vitamin B12 and vitamin Deficiencies along with changes in calcium metabolism areommon after RYGB Protein fat-soluble vitamin andther micronutrient deficiencies as well as altered calciumetabolism are most notably found after BPDDS Folate

eficiency has been reported after AGB [33] Thiamin de-ciency is common among all surgical patients with fre-uent vomiting regardless of the type of procedure per-ormed Because many nutritional deficiencies progressith time patients should be monitored frequently and

egularly to prevent malnutrition [29] Reinforcement ofupplement compliance at each patient follow-up is alsomportant in the fight to enhance nutrition status and preventutritional complications

eight loss and nutrient deficits restrictionersus malabsorption

Malabsorptive procedures such as the BPDDS arehought to cause weight loss primarily through the malab-orption of macronutrients with as much as 25 of proteinnd 72 of fat malabsorbed Such primary malabsorptionesults in concomitant malabsorption of micronutrients3435] Vitamins and minerals relying on fat metabolismncluding vitamins D A E K and zinc may be affectedhen absorption is impaired [36] The decrease in gastro-

ntestinal transit time may also result in secondary malab-orption of a wide range of micronutrients related to by-assing the duodenum and jejunum or limited contact withhe brush border secondary to a short common limb Othericronutrient deficiency concerns reported for patients

hoosing a procedure with malabsorptive features includeron calcium vitamin B12 and folate

Nutrient deficiencies after RYGB can result from eitherrimary or secondary malabsorption or from inadequateietary intake A minimal amount of macronutrient malab-orption is thought to occur However specific micronutri-nts appear to be malabsorbed postoperatively and presents deficiencies without adequate vitamin and mineral sup-lementation Retrospective analyses of patients who havendergone gastric bypass have revealed predictable micro-utrient deficiencies including iron vitamin B12 and folate2627ndash39] Case reports have also shown that thiamin de-ciency can develop especially when persistent postopera-

ive vomiting occurs [40ndash43]Few studies that measure absorption after measured and

uantified intake have been published It can be hypothe-ized that the bypassed duodenum and proximal jejunumegatively affect nutrient assimilation Bradley et al [44]tudied patients who had undergone total gastrectomy therocedure from which the RYGB evolved The researchersound that most nutritional status changes in patients wereost likely due to changes in intake versus malabsorptionhese balance studies were conducted in a controlled re-

earch setting however they did not measure pre- and c

ostoperative changes nor include radioisotope labeling toeasure absorption of key nutrients and the subjects had

ndergone the procedure for reasons other than weight lossIt is unclear whether intestinal adaptation occurs after

ombination procedures and to what degree it affects long-erm weight maintenance and nutrition status Adaptation iscompensatory response that follows an abrupt decrease inucosal surface area and has been well studied in short-

owel patients who require bowel resection [45] The pro-ess includes both anatomic and functional changes thatncrease the gutrsquos digestive and absorptive capacity Al-hough these changes begin to take place in the early post-perative period total adaptation may take up to three yearso complete Adaptation in gastric bypass has not beenonsidered in absorption or metabolic studies This consid-ration could be important even when determining early andate macro- and micronutrient intake recommendations Theffect of pancreatic enzyme replacement therapy on vitaminnd mineral absorption in this population is also unknown

Purely restrictive procedures such as the AGB can resultn micronutrient deficiencies related to changes in dietaryntake It is commonly accepted that because no alteration isade in the absorptive pathway malabsorption does not

ccur as a result of AGB procedures However nutrienteficits would be likely to occur because of the low nutrientntake and avoidance of nutrient-rich foods in the earlyonths postoperatively and later possibly as a result of

xcessive band restriction Food with high nutritional valueuch as meat and fibrous fresh fruits and vegetables mighte poorly tolerated

Literature has been published that addresses the effect ofalabsorptive restrictive and combination surgical proce-

ures on acute and long-term nutritional status These stud-es have attempted for the most part to indirectly determinehe surgical impact on nutrition status by the evaluation ofetabolic and laboratory markers Although some studies

ave included certain aspects of absorption few have in-luded the necessary components to evaluate absorption ofprescribed andor monitored diet in a controlled metabolic

ettingThe following sections examine the pre- and postopera-

ive risks for nutritional deficiencies associated with RYGBPDDS and AGB It is important for all members of theedical team to increase their awareness of the nutritional

omplications and challenges that lie ahead for the patientontinued review of current research by the medical team

egarding advances in nutrition science beyond the bound-ries of the present report cannot be emphasized enough

hiamin (vitamin B1)

Beriberi is a thiamin deficiency that can affect variousrgan systems including the heart gastrointestinal tractnd peripheral and central nervous systems Although the

ondition is generally considered rare a number of reported

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S82 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nd possibly a much greater number of unreported or un-iagnosed cases of beriberi have occurred among individ-als who have undergone surgery for morbid obesity Earlyetection and prompt treatment of thiamin deficits in thesendividuals can help to prevent serious health consequencesf beriberi is misdiagnosed or goes undetected for even ahort period the bariatric patient can develop irreversibleeuromuscular disorders permanent defects in learning andhort-term memory coma and even death Because of theife-altering and potentially life-threatening nature of a thi-min deficiency it is important that healthcare professionalsn the field of bariatric surgery have knowledge of thetiology of the condition and its signs and symptomsreatment and prevention

tiology of potential deficiency Thiamin is a water-solubleitamin that is absorbed in the proximal jejunum by anctive (saturable high-affinity) transport system [4647] Inhe body thiamin is found in high concentrations in therain heart muscle liver and kidneys However withoutegular and sufficient intake these tissues become rapidlyevoid of thiamin [4647] The total amount of thiamin inhe body of an adult is approximately 30 mg with a half-lifef only 9ndash18 days Persistent vomiting a diet deficient inhe vitamin or the bodyrsquos excessive utilization of thiaminse can result in a severe state of thiamin depletion withinnly a short period producing symptoms of beriberi46ndash48]

Bariatric surgery increases the risk of beriberi through ex-cerbation of pre-existing thiamin deficits low nutrient intakealabsorption and episodes of nausea and vomiting [49ndash51]hronic or acute thiamin deficiencies in bariatric patients oftenresent with symptoms of peripheral neuropathy or Wer-ickersquos encephalopathy and Korsakoffrsquos psychoses [2148ndash4] Early diagnosis of the signs and symptoms of these con-itions is extremely important to prevent serious adverse healthonsequences Even if treatment is initiated recovery can bencomplete with cognitive andor neuromuscular impairmentsersisting long term or permanently

igns symptoms and treatment of deficiency (seeppendix Table A1)

reoperative risk The risk of the development of beriberifter bariatric surgery is far greater for individuals present-ng for surgery with low thiamin levels Investigators at theleveland Clinic of Florida reported that 15 of their pre-perative bariatric patients had deficiencies in thiamin be-ore surgery [52] A study by Flancbaum et al [21] similarlyound that 29 of their preoperative patients had low thia-in levels Data obtained by that study also showed a

ignificant difference between ethnicity and preoperativehiamin levels Although only 67 of whites presentedith thiamin deficiencies before surgery nearly one third

31) of African Americans and almost one half (47) of

ispanics had thiamin deficits The results of these studies S

uggested a need for preoperative thiamin testing as well ashiamin repletion by diet or supplementation to reduce theisk of ldquobariatricrdquo beriberi postoperatively

ostoperative risk Beriberi has been observed after gastricestrictive and malabsorptive procedures A number of casesf Wernicke-Korsakoff syndrome (WKS) as well as periph-ral neuropathy have been reported for patients havingndergone vertical banded gastroplasty [53ndash61] A fewncidences of WKS have also been reported after AGB436263] Additionally reports of thiamin deficiencies and

KS after RYGB [404164ndash73] and several cases of WKSnd neuropathy in patients who had undergone BPD [74]ave been published Many more cases of WKS are be-ieved to have occurred with bariatric procedures that haveither not been reported or have been misdiagnosed becausef limited knowledge regarding the signs and symptoms ofcute or severe thiamin deficits Because many foods areortified with thiamin beriberi has been nearly eradicatedhroughout the world except for patients with severe alco-olism severe vomiting during pregnancy (hyperemesisravidarium) or those malnourished and starved For thiseason few healthcare professionals until recently havead a patient present with beriberi

According to the published reports of thiamin deficitsfter bariatric procedures most patients develop such defi-iencies in the early postoperative months after an episodef intractable vomiting Nausea and vomiting are relativelyommon after all bariatric procedures early in the postop-rative period Thiamin stores in the body are small andaintenance of appropriate thiamin levels requires daily

eplenishment A deficiency of thiamin for only a couple ofeeks or less caused by persistent vomiting can deplete

hiamin stores Symptoms of WKS were reported in aYGB patient after only two weeks of persistent vomiting

67]Bariatric beriberi can also develop in postoperative patients

ho are given infusate containing dextrose without thiaminnd other vitamins which is often the case for patients inritical care units postoperative patients with complicationsnterfering with the ingestion of food or patients dehydratedrom persistent vomiting Malnutrition caused by a lack ofppetite and dietary intake postoperatively also contributes toariatric beriberi as does noncompliance in taking postopera-ive vitamin supplements

Although most cases of beriberi occur in the early post-perative periods cases of patients with severe thiamineficiency more than one year after surgery have beeneported One study reported WKS in association with al-ohol abuse 13 years after RYGB [75] Other conditionsontributing to late cases of bariatric beriberi include ahiamin-poor diet a diet high in carbohydrates anorexiand bulimia [46ndash48]

uggested supplementation Because of the greater likeli-

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S83L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ood of low dietary thiamin intake patients should be sup-lemented with thiamin This is usually accomplishedhrough daily intake of a multivitamin Most multivitaminsontain thiamin at 100 of the daily value Patients havingpisodes of nausea and vomiting and those who are anorec-ic might require sublingual intramuscular or intravenoushiamin to avoid depletion of thiamin stores and beriberiaution should be used when infusing bariatric patientsith solutions containing dextrose without additional vita-ins and thiamin because an increase in glucose utilizationithout additional thiamin can deplete thiamin stores [76]Thiamin deficiency in bariatric patients is treated with

hiamin together with other B-complex vitamins and mag-esium for maximal thiamin absorption and appropriateeurologic function [46 ndash 48] Early symptoms of neuropa-hy can often be resolved by providing the patient with oralhiamin doses of 20ndash30 mgd until symptoms disappear Forore advanced signs of neuropathy or for individuals with

rotracted vomiting 50ndash100 mgd of intravenous or intra-uscular thiamin may be necessary for resolution or im-

rovement of symptoms or for the prevention of suchatients with WKS generally require 100 mg thiamindministered intravenously for several days or longer fol-owed by intramuscular thiamin or high oral doses untilymptoms have resolved or significantly improved This canequire months to years Some patients might have to takehiamin for life to prevent the reoccurrence of neuropathy

itamin B12 and folate

Vitamin B12 (cobalamin) and folate (folic acid) are bothnvolved in the maturation of red blood cells and are com-only discussed in the literature together Over time a

eficiency in either vitamin B12 or folate can lead to mac-ocytic anemia a condition characterized by the productionf fewer but larger red blood cells and a decreased abilityo carry oxygen Most (95) cases of megaloblastic anemiacharacterized by large immature abnormal undifferenti-ted red blood cells in bone marrow) are attributed toitamin B12 or folate deficiency [77]

itamin B12

tiology of potential deficiency RYGB patients have bothncomplete digestion and release of vitamin B12 from pro-ein foods With a significant decrease in hydrochloric acidepsinogen is not converted into pepsin which is necessaryor the release of vitamin B12 from protein [78] BecauseGB patients have an artificial restriction yet complete usef the stomach and BPD patients do not have as great aestriction in stomach capacity and parietal cells as RYGBatients the reduction in hydrochloric acid and subsequentitamin B12 deficiency is not as prevalent with these tworocedures

Intrinsic factor (IF) is produced by the parietal cells of

he stomach and in certain conditions (eg atrophic gastri- a

is resected small bowel elderly patients) can be impairedausing an IF deficiency Subsequent vitamin B12 deficiencypernicious anemia) occurs without IF production or useecause IF is needed to absorb vitamin B12 in the terminalleum [77] Factors that increase the risk of vitamin B12

eficiency relevant to bariatric surgery include the follow-ng

An inability to release protein-bound vitamin B12

from food particularly in hypochlorhydria andatrophic gastritis

Malabsorption due to inadequate IF in perniciousanemia

Gastrectomy and gastric bypassResection or disease of terminal ileumLong-term vegan dietMedications such as neomycin metformin colch-

icines medications used in the management ofbowel inflammation and gastroesophageal refluxand ulcers (eg proton pump inhibitors) and anti-convulsant agents [79]

Cobalamin stores are known to exist for long periods3ndash5 yr) and are dependent on dietary repletion and dailyepletion However gastric bypass patients have both aecreased production of stomach acid and a decreased avail-bility of IF thus a vitamin B12 deficiency could developithout appropriate supplementation Because the typical

bsorption pathway cannot be relied on the surgical weightoss patient must rely on passive absorption of B12 whichccurs independent of IF

igns symptoms and treatment of deficiency (seeppendix Table A3)

reoperative risk Several medications common to preop-rative bariatric patients have been noted to affect preoper-tive vitamin B12 absorption and stores Of patients takingetformin 10ndash30 present with reduced vitamin B12 ab-

orption [80] Additionally patients with obesity have aigh incidence of gastroesophageal reflux disease for whichhey take proton pump inhibitors thus increasing the poten-ial to develop a vitamin B12 deficiency

Flancbaum et al [21] conducted a retrospective study of79 (320 women and 59 men) pre-operative patients Vita-in B12 deficiency was reported as negative in all patients

f various ethnic backgrounds [21] No clinical criteria orymptoms for vitamin B12 deficiency were noted In theeneral population 5ndash10 present with neurologic symp-oms with vitamin B12 levels of 200ndash400 pgmL Amongreoperative gastric bypass patients Madan et al [27] foundhat 13 (n 59) of patients were deficient in vitamin B12n a comparison of patients presenting for either RYGB orPD Skroubis et al [81] recently reported that preoperativeitamin B12 levels were low-normal in both groups Itould be prudent to screen for and treat IF deficiency

ndor vitamin B12 deficiency in all patients preoperatively

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S84 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ut it is essential for RYGB patients so as not to hasten theevelopment of a potential postoperative deficiency

ostoperative risk Vitamin B12 deficiency has been fre-uently reported after RYGB Schilling et al [82] estimatedhe prevalence of vitamin B12 deficiency to be 12ndash33ther researchers have suggested a much greater prevalencef B12 deficiency in up to 75 of postoperative RYGBatients however most reports have cited approximately5 of postoperative RYGB patients as vitamin B12 defi-ient [82ndash87] Brolin et al [87] reported that low levels ofitamin B12 might be seen as soon as six months afterariatric surgery but most often occurring more than oneear postoperatively as liver stores become depleted Sk-oubis et al [88] predicted that the deficiency will mostikely occur 7 months after RYGB and 79 months afterPDDS although their research did not consider compro-ised preoperative status and its correlation to postopera-

ive deficiency After the first postoperative year the prev-lence of vitamin B12 deficiency appears to increase yearlyn RYGB patients [89]

Although the bodyrsquos storage of vitamin B12 is significant2000 g) compared with daily needs (24 gd) thisarticular deficiency has been found within 1ndash9 years ofastric bypass surgery [29] Brolin et al [84] reported thatne third of RYGB patients are deficient at four yearsostoperatively However non-surgical variables were notxplored and many patients might have had preoperativealues near the lower end of the normal range Ocon Bretont al [90] compared micronutrient deficiencies among two-ear postoperative BPDDS and RYGB patients and foundhat all nutritional deficiencies were more common amongPDDS patients except for vitamin B12 for which theeficiency was more common among the RYGB patientstudied A lack of B12 deficiency among BPDDS patientsight result from a better tolerance of animal proteins in a

arger pouch greater pepsingastric acid production to re-ease protein-bound B12 and increased availability and in-eraction of IF with the pouch contents

Experts have noted the significance of subclinical defi-iency in the low-normal cobalamin range in nongastricypass patients who do not exhibit clinical evidence ofeficiency The methylmalonic acid (MMA) assay is thereferred marker of B12 status because metabolic changesften precede low B12 levels in the progression to defi-iency Serum B12 assays may miss as much as 25ndash30 of

12 deficiencies making them less reliable than the MMAssay [91] It has been suggested that early signs of vitamin

12 deficiency can be detected if the serum levels of bothMA and homocysteine are measured [91] Vitamin B12

eficiency after RYGB has been associated with megalo-lastic anemia [92] Some vitamin B12-deficient patientsevelop significant symptoms such as polyneuropathy par-

sthesia and permanent neural impairment On occasion

ome patients may experience extreme delusions halluci-ations and even overt psychosis [93]

uggested supplementation Because of the frequent lack ofymptoms of vitamin B12 deficiency the suggested dili-ence in following up or treating these values among thosesymptomatic patients has been questioned The decisionot to supplement or routinely screen patients for B12 defi-iency should be examined very carefully given the risk ofrreversible neurologic damage if vitamin B12 goes un-reated for long periods At least one case report has beenublished of an exclusively breastfed infant with vitamin

12 deficiency who was born of an asymptomatic motherho had undergone gastric bypass surgery [94]Deficiency of vitamin B12 is typically defined at levels

200 pgmL However about 50 of patients with obviousigns and symptoms of deficiency have normal vitamin B12

evels [31] Kaplan et al [95] reported that vitamin B12

eficiency usually resolves after several weeks of treatmentith 700ndash2000 gwk Rhode et al [96] found that aosage of 350ndash600 gd of oral B12 prevented vitamin B12

eficiency in 95 of patients and an oral dose of 500 gdas sufficient to overcome an existing deficiency as re-orted by Brolin et al [87] in a similar study Thereforeupplementation of RYGB patients with 350ndash500 gd mayrevent most postoperative vitamin B12 deficiency

While most vitamin B12 in normal adults is absorbed inhe ileum in the presence of IF approximately 1 of sup-lemented B12 will be absorbed passively (by diffusion)long the entire length of the (non-bypassed) intestine byurgical weight loss patients given a high-dose oral supple-ent [97] Thus the consumption of 350ndash500 g yields a

5ndash50-g absorption which is greater than the daily re-uirement Although the use of monthly intramuscular in-ections or a weekly oral dose of vitamin B12 is commonmong practices it relies on patient compliance Practitio-ers should assess the patientrsquos preference and the potentialor compliance when considering a daily weekly oronthly regimen of B12 supplementation In addition to oral

upplements or intramuscular injections nasal sprays andublingual sources of vitamin B12 are also available Pa-ients should be monitored closely for their lifetime becauseevere anemia can develop with or without supplementation98]

olate

tiology of potential deficiency Factors that increase theisk of folic acid deficiency relevant to bariatric surgerynclude the following

Inadequate dietary intakeNoncompliance with multivitamin supplementationMalabsorptionMedications (anticonvulsants oral contraceptives

and cancer treating agents) [79]

pmo

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S85L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Folic acid stores can be depleted within a few monthsostoperatively unless replenished by a multivitamin supple-ent and dietary sources (ie green leafy vegetables fruits

rgan meats liver dried yeast and fortified grain products)

igns symptoms and treatment of deficiency (seeppendix Table A4)

reoperative risk The goals of the 1998 Food and Drugdministration policy requiring all enriched grain products

o be fortified with folate included increasing the averagemerican diet by 100 g folate daily and decreasing the

ate of neural tube defects in childbearing women [99]entley et al [100] reported that the proportion of womenged 15ndash44 years old (in the general population) who meethe recommended dietary intake of 400 gd folate variesetween 23 and 33 With the increasing popularity ofigh proteinlow carbohydrate diets one cannot assume thatreoperative patients consume dietary sources of folatehrough fortified grain products fruits and vegetables Boy-an et al [26] found folate deficiencies preoperatively in6 of RYGB patients studied

ostoperative risk Although it has been observed that fo-ate deficiency after RYGB surgery is less common than B12

eficiency and is thought to occur because of decreasedietary or multivitamin supplement intake low serum folateevels have been cited from 6 to 65 among RYGBatients [2686101] Additionally folate deficiencies haveccurred postoperatively even with supplementation Boy-an et al [26] found that 47 (n 17) of RYGB patientsad low folate levels six months postoperatively and 41n 17) had low levels at one year This deficiency oc-urred despite patient adherence to taking a multivitaminupplement that contained at least the daily value for folate00 g [26] Postoperative bariatric patients with rapideight loss might have an increased risk of micronutrienteficiencies MacLean et al [86] reported that 65 ofostoperative patients had low folate levels These sameatients exhibited additional B vitamin deficiencies 24itamin B12 and 50 thiamin [86] An increased risk ofeficiency has also been noted among AGB patients pos-ibly because of decreased folate intake Gasteyger et al33] found a significant decrease in serum folate levels441) between the baseline and 24-month postoperativeeasurementsDixon and OrsquoBrien [101] reported elevated serum ho-

ocysteine levels in patients after bariatric surgery regard-ess of the type of procedure (restrictive or malabsorptive)levated homocysteine levels can indicate not only low

olate levels and a greater risk of neural tube defects but canlso be indicative of an independent risk factor for heartisease andor oxidative stress in the nonbariatric popula-ion [102] However unlike iron and vitamin B12 the folate

ontained in the multivitamin supplementation essentially e

orrects the deficiency in the vast majority of postoperativeariatric patients [103] Therefore persistent folate defi-iency might indicate a patientrsquos lack of compliance withhe prescribed vitamin protocol [32]

It is common knowledge that folic acid deficiency amongregnant women has been associated with a greater risk ofeural tube defects in newborns Consistent supplementa-ion and monitoring among women of child-bearing agencluding pre- and postoperative bariatric patients is vital inn effort to prevent the possibility of neural tube defects inhe developing fetus

Because folate does not affect the myelin of nerveseurologic damage is not as common with folate such as ishe case for vitamin B12 deficiency In contrast patientsith folate deficiency often present with forgetfulness irri-

ability hostility and even paranoid behaviors [29] Similaro that evidenced with vitamin B12 most postoperativeYGB patients who are folate deficient are asymptomatic orave subclinical symptoms therefore these deficient statesay not be easily identified

uggested supplementation Even though folate absorptionccurs preferentially in the proximal portion of the smallntestine it can occur along the entire length of the small bowelith postoperative adaptation Therefore it is generally agreed

hat folate deficiency is corrected with 1000 mgd folic acid32] and is preventable with supplementation that provides00 of the daily value (800 g) This level can also benefithe fetus in a female patient unaware of her postoperativeregnancy Folate supplementation 1000 mgd has noteen recommended because of the potential for maskingitamin B12 deficiency Carmel et al [104] suggested thatomocysteine is the most sensitive marker of folic acidtatus in conjunction with erythrocyte folate Althougholic acid deficiency could potentially occur among post-perative bariatric surgery patients it has not been seenidely in recent studies especially when patients haveeen compliant with postoperative multivitamin supple-entation Therefore it is imperative to closely follow

olic acid both pre- and postoperatively especially inhose patients suspected to be noncompliant with theirultivitamin supplementation

ron

Much of the iron and surgical weight loss research con-ucted to date has been generated from a limited number ofurgeons and scientists however the data have consistentlyointed toward the risk of iron deficiency and anemia afterariatric procedures Iron deficiency is defined as a decreasen the total iron body content Iron deficiency anemia occurshen erythropoiesis is impaired as a result of the lack of

ron stores In the absence of anemia iron deficiency issually asymptomatic Fatigue and a diminished capacity to

xercise however are common symptoms of anemia

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S86 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

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S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

(admcas

ihtpacbsT

ovBfted

fbsalumlcatspie

P

laTofmndef

pocimhphcsatpa

P

awrywaoirfiotnrsafRe

strwsviaratrlsgt

S93L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

[ntnriasiB(cdip

afedmvfllBrpem

D1mypei

iecalbcBmpmtta

ciru

iipafcfui

foaowppartptpthc

P

iwEvln6wdeapctnstat

S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

ratbrdd

aebaaa

apcptaasosdbc

afciitdmptpcrsPEv

TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

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S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

s

aildquo

T

T

DFF

F

E

A

D

T

T

P

DFF

S

D

T

S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

DFF

S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 10: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S82 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

nd possibly a much greater number of unreported or un-iagnosed cases of beriberi have occurred among individ-als who have undergone surgery for morbid obesity Earlyetection and prompt treatment of thiamin deficits in thesendividuals can help to prevent serious health consequencesf beriberi is misdiagnosed or goes undetected for even ahort period the bariatric patient can develop irreversibleeuromuscular disorders permanent defects in learning andhort-term memory coma and even death Because of theife-altering and potentially life-threatening nature of a thi-min deficiency it is important that healthcare professionalsn the field of bariatric surgery have knowledge of thetiology of the condition and its signs and symptomsreatment and prevention

tiology of potential deficiency Thiamin is a water-solubleitamin that is absorbed in the proximal jejunum by anctive (saturable high-affinity) transport system [4647] Inhe body thiamin is found in high concentrations in therain heart muscle liver and kidneys However withoutegular and sufficient intake these tissues become rapidlyevoid of thiamin [4647] The total amount of thiamin inhe body of an adult is approximately 30 mg with a half-lifef only 9ndash18 days Persistent vomiting a diet deficient inhe vitamin or the bodyrsquos excessive utilization of thiaminse can result in a severe state of thiamin depletion withinnly a short period producing symptoms of beriberi46ndash48]

Bariatric surgery increases the risk of beriberi through ex-cerbation of pre-existing thiamin deficits low nutrient intakealabsorption and episodes of nausea and vomiting [49ndash51]hronic or acute thiamin deficiencies in bariatric patients oftenresent with symptoms of peripheral neuropathy or Wer-ickersquos encephalopathy and Korsakoffrsquos psychoses [2148ndash4] Early diagnosis of the signs and symptoms of these con-itions is extremely important to prevent serious adverse healthonsequences Even if treatment is initiated recovery can bencomplete with cognitive andor neuromuscular impairmentsersisting long term or permanently

igns symptoms and treatment of deficiency (seeppendix Table A1)

reoperative risk The risk of the development of beriberifter bariatric surgery is far greater for individuals present-ng for surgery with low thiamin levels Investigators at theleveland Clinic of Florida reported that 15 of their pre-perative bariatric patients had deficiencies in thiamin be-ore surgery [52] A study by Flancbaum et al [21] similarlyound that 29 of their preoperative patients had low thia-in levels Data obtained by that study also showed a

ignificant difference between ethnicity and preoperativehiamin levels Although only 67 of whites presentedith thiamin deficiencies before surgery nearly one third

31) of African Americans and almost one half (47) of

ispanics had thiamin deficits The results of these studies S

uggested a need for preoperative thiamin testing as well ashiamin repletion by diet or supplementation to reduce theisk of ldquobariatricrdquo beriberi postoperatively

ostoperative risk Beriberi has been observed after gastricestrictive and malabsorptive procedures A number of casesf Wernicke-Korsakoff syndrome (WKS) as well as periph-ral neuropathy have been reported for patients havingndergone vertical banded gastroplasty [53ndash61] A fewncidences of WKS have also been reported after AGB436263] Additionally reports of thiamin deficiencies and

KS after RYGB [404164ndash73] and several cases of WKSnd neuropathy in patients who had undergone BPD [74]ave been published Many more cases of WKS are be-ieved to have occurred with bariatric procedures that haveither not been reported or have been misdiagnosed becausef limited knowledge regarding the signs and symptoms ofcute or severe thiamin deficits Because many foods areortified with thiamin beriberi has been nearly eradicatedhroughout the world except for patients with severe alco-olism severe vomiting during pregnancy (hyperemesisravidarium) or those malnourished and starved For thiseason few healthcare professionals until recently havead a patient present with beriberi

According to the published reports of thiamin deficitsfter bariatric procedures most patients develop such defi-iencies in the early postoperative months after an episodef intractable vomiting Nausea and vomiting are relativelyommon after all bariatric procedures early in the postop-rative period Thiamin stores in the body are small andaintenance of appropriate thiamin levels requires daily

eplenishment A deficiency of thiamin for only a couple ofeeks or less caused by persistent vomiting can deplete

hiamin stores Symptoms of WKS were reported in aYGB patient after only two weeks of persistent vomiting

67]Bariatric beriberi can also develop in postoperative patients

ho are given infusate containing dextrose without thiaminnd other vitamins which is often the case for patients inritical care units postoperative patients with complicationsnterfering with the ingestion of food or patients dehydratedrom persistent vomiting Malnutrition caused by a lack ofppetite and dietary intake postoperatively also contributes toariatric beriberi as does noncompliance in taking postopera-ive vitamin supplements

Although most cases of beriberi occur in the early post-perative periods cases of patients with severe thiamineficiency more than one year after surgery have beeneported One study reported WKS in association with al-ohol abuse 13 years after RYGB [75] Other conditionsontributing to late cases of bariatric beriberi include ahiamin-poor diet a diet high in carbohydrates anorexiand bulimia [46ndash48]

uggested supplementation Because of the greater likeli-

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S83L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ood of low dietary thiamin intake patients should be sup-lemented with thiamin This is usually accomplishedhrough daily intake of a multivitamin Most multivitaminsontain thiamin at 100 of the daily value Patients havingpisodes of nausea and vomiting and those who are anorec-ic might require sublingual intramuscular or intravenoushiamin to avoid depletion of thiamin stores and beriberiaution should be used when infusing bariatric patientsith solutions containing dextrose without additional vita-ins and thiamin because an increase in glucose utilizationithout additional thiamin can deplete thiamin stores [76]Thiamin deficiency in bariatric patients is treated with

hiamin together with other B-complex vitamins and mag-esium for maximal thiamin absorption and appropriateeurologic function [46 ndash 48] Early symptoms of neuropa-hy can often be resolved by providing the patient with oralhiamin doses of 20ndash30 mgd until symptoms disappear Forore advanced signs of neuropathy or for individuals with

rotracted vomiting 50ndash100 mgd of intravenous or intra-uscular thiamin may be necessary for resolution or im-

rovement of symptoms or for the prevention of suchatients with WKS generally require 100 mg thiamindministered intravenously for several days or longer fol-owed by intramuscular thiamin or high oral doses untilymptoms have resolved or significantly improved This canequire months to years Some patients might have to takehiamin for life to prevent the reoccurrence of neuropathy

itamin B12 and folate

Vitamin B12 (cobalamin) and folate (folic acid) are bothnvolved in the maturation of red blood cells and are com-only discussed in the literature together Over time a

eficiency in either vitamin B12 or folate can lead to mac-ocytic anemia a condition characterized by the productionf fewer but larger red blood cells and a decreased abilityo carry oxygen Most (95) cases of megaloblastic anemiacharacterized by large immature abnormal undifferenti-ted red blood cells in bone marrow) are attributed toitamin B12 or folate deficiency [77]

itamin B12

tiology of potential deficiency RYGB patients have bothncomplete digestion and release of vitamin B12 from pro-ein foods With a significant decrease in hydrochloric acidepsinogen is not converted into pepsin which is necessaryor the release of vitamin B12 from protein [78] BecauseGB patients have an artificial restriction yet complete usef the stomach and BPD patients do not have as great aestriction in stomach capacity and parietal cells as RYGBatients the reduction in hydrochloric acid and subsequentitamin B12 deficiency is not as prevalent with these tworocedures

Intrinsic factor (IF) is produced by the parietal cells of

he stomach and in certain conditions (eg atrophic gastri- a

is resected small bowel elderly patients) can be impairedausing an IF deficiency Subsequent vitamin B12 deficiencypernicious anemia) occurs without IF production or useecause IF is needed to absorb vitamin B12 in the terminalleum [77] Factors that increase the risk of vitamin B12

eficiency relevant to bariatric surgery include the follow-ng

An inability to release protein-bound vitamin B12

from food particularly in hypochlorhydria andatrophic gastritis

Malabsorption due to inadequate IF in perniciousanemia

Gastrectomy and gastric bypassResection or disease of terminal ileumLong-term vegan dietMedications such as neomycin metformin colch-

icines medications used in the management ofbowel inflammation and gastroesophageal refluxand ulcers (eg proton pump inhibitors) and anti-convulsant agents [79]

Cobalamin stores are known to exist for long periods3ndash5 yr) and are dependent on dietary repletion and dailyepletion However gastric bypass patients have both aecreased production of stomach acid and a decreased avail-bility of IF thus a vitamin B12 deficiency could developithout appropriate supplementation Because the typical

bsorption pathway cannot be relied on the surgical weightoss patient must rely on passive absorption of B12 whichccurs independent of IF

igns symptoms and treatment of deficiency (seeppendix Table A3)

reoperative risk Several medications common to preop-rative bariatric patients have been noted to affect preoper-tive vitamin B12 absorption and stores Of patients takingetformin 10ndash30 present with reduced vitamin B12 ab-

orption [80] Additionally patients with obesity have aigh incidence of gastroesophageal reflux disease for whichhey take proton pump inhibitors thus increasing the poten-ial to develop a vitamin B12 deficiency

Flancbaum et al [21] conducted a retrospective study of79 (320 women and 59 men) pre-operative patients Vita-in B12 deficiency was reported as negative in all patients

f various ethnic backgrounds [21] No clinical criteria orymptoms for vitamin B12 deficiency were noted In theeneral population 5ndash10 present with neurologic symp-oms with vitamin B12 levels of 200ndash400 pgmL Amongreoperative gastric bypass patients Madan et al [27] foundhat 13 (n 59) of patients were deficient in vitamin B12n a comparison of patients presenting for either RYGB orPD Skroubis et al [81] recently reported that preoperativeitamin B12 levels were low-normal in both groups Itould be prudent to screen for and treat IF deficiency

ndor vitamin B12 deficiency in all patients preoperatively

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S84 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ut it is essential for RYGB patients so as not to hasten theevelopment of a potential postoperative deficiency

ostoperative risk Vitamin B12 deficiency has been fre-uently reported after RYGB Schilling et al [82] estimatedhe prevalence of vitamin B12 deficiency to be 12ndash33ther researchers have suggested a much greater prevalencef B12 deficiency in up to 75 of postoperative RYGBatients however most reports have cited approximately5 of postoperative RYGB patients as vitamin B12 defi-ient [82ndash87] Brolin et al [87] reported that low levels ofitamin B12 might be seen as soon as six months afterariatric surgery but most often occurring more than oneear postoperatively as liver stores become depleted Sk-oubis et al [88] predicted that the deficiency will mostikely occur 7 months after RYGB and 79 months afterPDDS although their research did not consider compro-ised preoperative status and its correlation to postopera-

ive deficiency After the first postoperative year the prev-lence of vitamin B12 deficiency appears to increase yearlyn RYGB patients [89]

Although the bodyrsquos storage of vitamin B12 is significant2000 g) compared with daily needs (24 gd) thisarticular deficiency has been found within 1ndash9 years ofastric bypass surgery [29] Brolin et al [84] reported thatne third of RYGB patients are deficient at four yearsostoperatively However non-surgical variables were notxplored and many patients might have had preoperativealues near the lower end of the normal range Ocon Bretont al [90] compared micronutrient deficiencies among two-ear postoperative BPDDS and RYGB patients and foundhat all nutritional deficiencies were more common amongPDDS patients except for vitamin B12 for which theeficiency was more common among the RYGB patientstudied A lack of B12 deficiency among BPDDS patientsight result from a better tolerance of animal proteins in a

arger pouch greater pepsingastric acid production to re-ease protein-bound B12 and increased availability and in-eraction of IF with the pouch contents

Experts have noted the significance of subclinical defi-iency in the low-normal cobalamin range in nongastricypass patients who do not exhibit clinical evidence ofeficiency The methylmalonic acid (MMA) assay is thereferred marker of B12 status because metabolic changesften precede low B12 levels in the progression to defi-iency Serum B12 assays may miss as much as 25ndash30 of

12 deficiencies making them less reliable than the MMAssay [91] It has been suggested that early signs of vitamin

12 deficiency can be detected if the serum levels of bothMA and homocysteine are measured [91] Vitamin B12

eficiency after RYGB has been associated with megalo-lastic anemia [92] Some vitamin B12-deficient patientsevelop significant symptoms such as polyneuropathy par-

sthesia and permanent neural impairment On occasion

ome patients may experience extreme delusions halluci-ations and even overt psychosis [93]

uggested supplementation Because of the frequent lack ofymptoms of vitamin B12 deficiency the suggested dili-ence in following up or treating these values among thosesymptomatic patients has been questioned The decisionot to supplement or routinely screen patients for B12 defi-iency should be examined very carefully given the risk ofrreversible neurologic damage if vitamin B12 goes un-reated for long periods At least one case report has beenublished of an exclusively breastfed infant with vitamin

12 deficiency who was born of an asymptomatic motherho had undergone gastric bypass surgery [94]Deficiency of vitamin B12 is typically defined at levels

200 pgmL However about 50 of patients with obviousigns and symptoms of deficiency have normal vitamin B12

evels [31] Kaplan et al [95] reported that vitamin B12

eficiency usually resolves after several weeks of treatmentith 700ndash2000 gwk Rhode et al [96] found that aosage of 350ndash600 gd of oral B12 prevented vitamin B12

eficiency in 95 of patients and an oral dose of 500 gdas sufficient to overcome an existing deficiency as re-orted by Brolin et al [87] in a similar study Thereforeupplementation of RYGB patients with 350ndash500 gd mayrevent most postoperative vitamin B12 deficiency

While most vitamin B12 in normal adults is absorbed inhe ileum in the presence of IF approximately 1 of sup-lemented B12 will be absorbed passively (by diffusion)long the entire length of the (non-bypassed) intestine byurgical weight loss patients given a high-dose oral supple-ent [97] Thus the consumption of 350ndash500 g yields a

5ndash50-g absorption which is greater than the daily re-uirement Although the use of monthly intramuscular in-ections or a weekly oral dose of vitamin B12 is commonmong practices it relies on patient compliance Practitio-ers should assess the patientrsquos preference and the potentialor compliance when considering a daily weekly oronthly regimen of B12 supplementation In addition to oral

upplements or intramuscular injections nasal sprays andublingual sources of vitamin B12 are also available Pa-ients should be monitored closely for their lifetime becauseevere anemia can develop with or without supplementation98]

olate

tiology of potential deficiency Factors that increase theisk of folic acid deficiency relevant to bariatric surgerynclude the following

Inadequate dietary intakeNoncompliance with multivitamin supplementationMalabsorptionMedications (anticonvulsants oral contraceptives

and cancer treating agents) [79]

pmo

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dspbiwiu

S85L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Folic acid stores can be depleted within a few monthsostoperatively unless replenished by a multivitamin supple-ent and dietary sources (ie green leafy vegetables fruits

rgan meats liver dried yeast and fortified grain products)

igns symptoms and treatment of deficiency (seeppendix Table A4)

reoperative risk The goals of the 1998 Food and Drugdministration policy requiring all enriched grain products

o be fortified with folate included increasing the averagemerican diet by 100 g folate daily and decreasing the

ate of neural tube defects in childbearing women [99]entley et al [100] reported that the proportion of womenged 15ndash44 years old (in the general population) who meethe recommended dietary intake of 400 gd folate variesetween 23 and 33 With the increasing popularity ofigh proteinlow carbohydrate diets one cannot assume thatreoperative patients consume dietary sources of folatehrough fortified grain products fruits and vegetables Boy-an et al [26] found folate deficiencies preoperatively in6 of RYGB patients studied

ostoperative risk Although it has been observed that fo-ate deficiency after RYGB surgery is less common than B12

eficiency and is thought to occur because of decreasedietary or multivitamin supplement intake low serum folateevels have been cited from 6 to 65 among RYGBatients [2686101] Additionally folate deficiencies haveccurred postoperatively even with supplementation Boy-an et al [26] found that 47 (n 17) of RYGB patientsad low folate levels six months postoperatively and 41n 17) had low levels at one year This deficiency oc-urred despite patient adherence to taking a multivitaminupplement that contained at least the daily value for folate00 g [26] Postoperative bariatric patients with rapideight loss might have an increased risk of micronutrienteficiencies MacLean et al [86] reported that 65 ofostoperative patients had low folate levels These sameatients exhibited additional B vitamin deficiencies 24itamin B12 and 50 thiamin [86] An increased risk ofeficiency has also been noted among AGB patients pos-ibly because of decreased folate intake Gasteyger et al33] found a significant decrease in serum folate levels441) between the baseline and 24-month postoperativeeasurementsDixon and OrsquoBrien [101] reported elevated serum ho-

ocysteine levels in patients after bariatric surgery regard-ess of the type of procedure (restrictive or malabsorptive)levated homocysteine levels can indicate not only low

olate levels and a greater risk of neural tube defects but canlso be indicative of an independent risk factor for heartisease andor oxidative stress in the nonbariatric popula-ion [102] However unlike iron and vitamin B12 the folate

ontained in the multivitamin supplementation essentially e

orrects the deficiency in the vast majority of postoperativeariatric patients [103] Therefore persistent folate defi-iency might indicate a patientrsquos lack of compliance withhe prescribed vitamin protocol [32]

It is common knowledge that folic acid deficiency amongregnant women has been associated with a greater risk ofeural tube defects in newborns Consistent supplementa-ion and monitoring among women of child-bearing agencluding pre- and postoperative bariatric patients is vital inn effort to prevent the possibility of neural tube defects inhe developing fetus

Because folate does not affect the myelin of nerveseurologic damage is not as common with folate such as ishe case for vitamin B12 deficiency In contrast patientsith folate deficiency often present with forgetfulness irri-

ability hostility and even paranoid behaviors [29] Similaro that evidenced with vitamin B12 most postoperativeYGB patients who are folate deficient are asymptomatic orave subclinical symptoms therefore these deficient statesay not be easily identified

uggested supplementation Even though folate absorptionccurs preferentially in the proximal portion of the smallntestine it can occur along the entire length of the small bowelith postoperative adaptation Therefore it is generally agreed

hat folate deficiency is corrected with 1000 mgd folic acid32] and is preventable with supplementation that provides00 of the daily value (800 g) This level can also benefithe fetus in a female patient unaware of her postoperativeregnancy Folate supplementation 1000 mgd has noteen recommended because of the potential for maskingitamin B12 deficiency Carmel et al [104] suggested thatomocysteine is the most sensitive marker of folic acidtatus in conjunction with erythrocyte folate Althougholic acid deficiency could potentially occur among post-perative bariatric surgery patients it has not been seenidely in recent studies especially when patients haveeen compliant with postoperative multivitamin supple-entation Therefore it is imperative to closely follow

olic acid both pre- and postoperatively especially inhose patients suspected to be noncompliant with theirultivitamin supplementation

ron

Much of the iron and surgical weight loss research con-ucted to date has been generated from a limited number ofurgeons and scientists however the data have consistentlyointed toward the risk of iron deficiency and anemia afterariatric procedures Iron deficiency is defined as a decreasen the total iron body content Iron deficiency anemia occurshen erythropoiesis is impaired as a result of the lack of

ron stores In the absence of anemia iron deficiency issually asymptomatic Fatigue and a diminished capacity to

xercise however are common symptoms of anemia

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S86 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

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S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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S90 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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S91L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

gba

SA

Cphctrpw[nvfiisitCbg

Oafp[woofc(1hpritt

P

E

tgpoo

ccpcglcppmtttwaw

ailmsmtsbtciaspomtsa

bompo(almqmmbbEc

S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

(admcas

ihtpacbsT

ovBfted

fbsalumlcatspie

P

laTofmndef

pocimhphcsatpa

P

awrywaoirfiotnrsafRe

strwsviaratrlsgt

S93L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

[ntnriasiB(cdip

afedmvfllBrpem

D1mypei

iecalbcBmpmtta

ciru

iipafcfui

foaowppartptpthc

P

iwEvln6wdeapctnstat

S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

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apcptaasosdbc

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TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

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[

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[

[

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[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

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[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

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[

[

[

[

[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

s

aildquo

T

T

DFF

F

E

A

D

T

T

P

DFF

S

D

T

S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

DFF

S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 11: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S83L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ood of low dietary thiamin intake patients should be sup-lemented with thiamin This is usually accomplishedhrough daily intake of a multivitamin Most multivitaminsontain thiamin at 100 of the daily value Patients havingpisodes of nausea and vomiting and those who are anorec-ic might require sublingual intramuscular or intravenoushiamin to avoid depletion of thiamin stores and beriberiaution should be used when infusing bariatric patientsith solutions containing dextrose without additional vita-ins and thiamin because an increase in glucose utilizationithout additional thiamin can deplete thiamin stores [76]Thiamin deficiency in bariatric patients is treated with

hiamin together with other B-complex vitamins and mag-esium for maximal thiamin absorption and appropriateeurologic function [46 ndash 48] Early symptoms of neuropa-hy can often be resolved by providing the patient with oralhiamin doses of 20ndash30 mgd until symptoms disappear Forore advanced signs of neuropathy or for individuals with

rotracted vomiting 50ndash100 mgd of intravenous or intra-uscular thiamin may be necessary for resolution or im-

rovement of symptoms or for the prevention of suchatients with WKS generally require 100 mg thiamindministered intravenously for several days or longer fol-owed by intramuscular thiamin or high oral doses untilymptoms have resolved or significantly improved This canequire months to years Some patients might have to takehiamin for life to prevent the reoccurrence of neuropathy

itamin B12 and folate

Vitamin B12 (cobalamin) and folate (folic acid) are bothnvolved in the maturation of red blood cells and are com-only discussed in the literature together Over time a

eficiency in either vitamin B12 or folate can lead to mac-ocytic anemia a condition characterized by the productionf fewer but larger red blood cells and a decreased abilityo carry oxygen Most (95) cases of megaloblastic anemiacharacterized by large immature abnormal undifferenti-ted red blood cells in bone marrow) are attributed toitamin B12 or folate deficiency [77]

itamin B12

tiology of potential deficiency RYGB patients have bothncomplete digestion and release of vitamin B12 from pro-ein foods With a significant decrease in hydrochloric acidepsinogen is not converted into pepsin which is necessaryor the release of vitamin B12 from protein [78] BecauseGB patients have an artificial restriction yet complete usef the stomach and BPD patients do not have as great aestriction in stomach capacity and parietal cells as RYGBatients the reduction in hydrochloric acid and subsequentitamin B12 deficiency is not as prevalent with these tworocedures

Intrinsic factor (IF) is produced by the parietal cells of

he stomach and in certain conditions (eg atrophic gastri- a

is resected small bowel elderly patients) can be impairedausing an IF deficiency Subsequent vitamin B12 deficiencypernicious anemia) occurs without IF production or useecause IF is needed to absorb vitamin B12 in the terminalleum [77] Factors that increase the risk of vitamin B12

eficiency relevant to bariatric surgery include the follow-ng

An inability to release protein-bound vitamin B12

from food particularly in hypochlorhydria andatrophic gastritis

Malabsorption due to inadequate IF in perniciousanemia

Gastrectomy and gastric bypassResection or disease of terminal ileumLong-term vegan dietMedications such as neomycin metformin colch-

icines medications used in the management ofbowel inflammation and gastroesophageal refluxand ulcers (eg proton pump inhibitors) and anti-convulsant agents [79]

Cobalamin stores are known to exist for long periods3ndash5 yr) and are dependent on dietary repletion and dailyepletion However gastric bypass patients have both aecreased production of stomach acid and a decreased avail-bility of IF thus a vitamin B12 deficiency could developithout appropriate supplementation Because the typical

bsorption pathway cannot be relied on the surgical weightoss patient must rely on passive absorption of B12 whichccurs independent of IF

igns symptoms and treatment of deficiency (seeppendix Table A3)

reoperative risk Several medications common to preop-rative bariatric patients have been noted to affect preoper-tive vitamin B12 absorption and stores Of patients takingetformin 10ndash30 present with reduced vitamin B12 ab-

orption [80] Additionally patients with obesity have aigh incidence of gastroesophageal reflux disease for whichhey take proton pump inhibitors thus increasing the poten-ial to develop a vitamin B12 deficiency

Flancbaum et al [21] conducted a retrospective study of79 (320 women and 59 men) pre-operative patients Vita-in B12 deficiency was reported as negative in all patients

f various ethnic backgrounds [21] No clinical criteria orymptoms for vitamin B12 deficiency were noted In theeneral population 5ndash10 present with neurologic symp-oms with vitamin B12 levels of 200ndash400 pgmL Amongreoperative gastric bypass patients Madan et al [27] foundhat 13 (n 59) of patients were deficient in vitamin B12n a comparison of patients presenting for either RYGB orPD Skroubis et al [81] recently reported that preoperativeitamin B12 levels were low-normal in both groups Itould be prudent to screen for and treat IF deficiency

ndor vitamin B12 deficiency in all patients preoperatively

bd

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Eri

S84 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ut it is essential for RYGB patients so as not to hasten theevelopment of a potential postoperative deficiency

ostoperative risk Vitamin B12 deficiency has been fre-uently reported after RYGB Schilling et al [82] estimatedhe prevalence of vitamin B12 deficiency to be 12ndash33ther researchers have suggested a much greater prevalencef B12 deficiency in up to 75 of postoperative RYGBatients however most reports have cited approximately5 of postoperative RYGB patients as vitamin B12 defi-ient [82ndash87] Brolin et al [87] reported that low levels ofitamin B12 might be seen as soon as six months afterariatric surgery but most often occurring more than oneear postoperatively as liver stores become depleted Sk-oubis et al [88] predicted that the deficiency will mostikely occur 7 months after RYGB and 79 months afterPDDS although their research did not consider compro-ised preoperative status and its correlation to postopera-

ive deficiency After the first postoperative year the prev-lence of vitamin B12 deficiency appears to increase yearlyn RYGB patients [89]

Although the bodyrsquos storage of vitamin B12 is significant2000 g) compared with daily needs (24 gd) thisarticular deficiency has been found within 1ndash9 years ofastric bypass surgery [29] Brolin et al [84] reported thatne third of RYGB patients are deficient at four yearsostoperatively However non-surgical variables were notxplored and many patients might have had preoperativealues near the lower end of the normal range Ocon Bretont al [90] compared micronutrient deficiencies among two-ear postoperative BPDDS and RYGB patients and foundhat all nutritional deficiencies were more common amongPDDS patients except for vitamin B12 for which theeficiency was more common among the RYGB patientstudied A lack of B12 deficiency among BPDDS patientsight result from a better tolerance of animal proteins in a

arger pouch greater pepsingastric acid production to re-ease protein-bound B12 and increased availability and in-eraction of IF with the pouch contents

Experts have noted the significance of subclinical defi-iency in the low-normal cobalamin range in nongastricypass patients who do not exhibit clinical evidence ofeficiency The methylmalonic acid (MMA) assay is thereferred marker of B12 status because metabolic changesften precede low B12 levels in the progression to defi-iency Serum B12 assays may miss as much as 25ndash30 of

12 deficiencies making them less reliable than the MMAssay [91] It has been suggested that early signs of vitamin

12 deficiency can be detected if the serum levels of bothMA and homocysteine are measured [91] Vitamin B12

eficiency after RYGB has been associated with megalo-lastic anemia [92] Some vitamin B12-deficient patientsevelop significant symptoms such as polyneuropathy par-

sthesia and permanent neural impairment On occasion

ome patients may experience extreme delusions halluci-ations and even overt psychosis [93]

uggested supplementation Because of the frequent lack ofymptoms of vitamin B12 deficiency the suggested dili-ence in following up or treating these values among thosesymptomatic patients has been questioned The decisionot to supplement or routinely screen patients for B12 defi-iency should be examined very carefully given the risk ofrreversible neurologic damage if vitamin B12 goes un-reated for long periods At least one case report has beenublished of an exclusively breastfed infant with vitamin

12 deficiency who was born of an asymptomatic motherho had undergone gastric bypass surgery [94]Deficiency of vitamin B12 is typically defined at levels

200 pgmL However about 50 of patients with obviousigns and symptoms of deficiency have normal vitamin B12

evels [31] Kaplan et al [95] reported that vitamin B12

eficiency usually resolves after several weeks of treatmentith 700ndash2000 gwk Rhode et al [96] found that aosage of 350ndash600 gd of oral B12 prevented vitamin B12

eficiency in 95 of patients and an oral dose of 500 gdas sufficient to overcome an existing deficiency as re-orted by Brolin et al [87] in a similar study Thereforeupplementation of RYGB patients with 350ndash500 gd mayrevent most postoperative vitamin B12 deficiency

While most vitamin B12 in normal adults is absorbed inhe ileum in the presence of IF approximately 1 of sup-lemented B12 will be absorbed passively (by diffusion)long the entire length of the (non-bypassed) intestine byurgical weight loss patients given a high-dose oral supple-ent [97] Thus the consumption of 350ndash500 g yields a

5ndash50-g absorption which is greater than the daily re-uirement Although the use of monthly intramuscular in-ections or a weekly oral dose of vitamin B12 is commonmong practices it relies on patient compliance Practitio-ers should assess the patientrsquos preference and the potentialor compliance when considering a daily weekly oronthly regimen of B12 supplementation In addition to oral

upplements or intramuscular injections nasal sprays andublingual sources of vitamin B12 are also available Pa-ients should be monitored closely for their lifetime becauseevere anemia can develop with or without supplementation98]

olate

tiology of potential deficiency Factors that increase theisk of folic acid deficiency relevant to bariatric surgerynclude the following

Inadequate dietary intakeNoncompliance with multivitamin supplementationMalabsorptionMedications (anticonvulsants oral contraceptives

and cancer treating agents) [79]

pmo

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S85L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Folic acid stores can be depleted within a few monthsostoperatively unless replenished by a multivitamin supple-ent and dietary sources (ie green leafy vegetables fruits

rgan meats liver dried yeast and fortified grain products)

igns symptoms and treatment of deficiency (seeppendix Table A4)

reoperative risk The goals of the 1998 Food and Drugdministration policy requiring all enriched grain products

o be fortified with folate included increasing the averagemerican diet by 100 g folate daily and decreasing the

ate of neural tube defects in childbearing women [99]entley et al [100] reported that the proportion of womenged 15ndash44 years old (in the general population) who meethe recommended dietary intake of 400 gd folate variesetween 23 and 33 With the increasing popularity ofigh proteinlow carbohydrate diets one cannot assume thatreoperative patients consume dietary sources of folatehrough fortified grain products fruits and vegetables Boy-an et al [26] found folate deficiencies preoperatively in6 of RYGB patients studied

ostoperative risk Although it has been observed that fo-ate deficiency after RYGB surgery is less common than B12

eficiency and is thought to occur because of decreasedietary or multivitamin supplement intake low serum folateevels have been cited from 6 to 65 among RYGBatients [2686101] Additionally folate deficiencies haveccurred postoperatively even with supplementation Boy-an et al [26] found that 47 (n 17) of RYGB patientsad low folate levels six months postoperatively and 41n 17) had low levels at one year This deficiency oc-urred despite patient adherence to taking a multivitaminupplement that contained at least the daily value for folate00 g [26] Postoperative bariatric patients with rapideight loss might have an increased risk of micronutrienteficiencies MacLean et al [86] reported that 65 ofostoperative patients had low folate levels These sameatients exhibited additional B vitamin deficiencies 24itamin B12 and 50 thiamin [86] An increased risk ofeficiency has also been noted among AGB patients pos-ibly because of decreased folate intake Gasteyger et al33] found a significant decrease in serum folate levels441) between the baseline and 24-month postoperativeeasurementsDixon and OrsquoBrien [101] reported elevated serum ho-

ocysteine levels in patients after bariatric surgery regard-ess of the type of procedure (restrictive or malabsorptive)levated homocysteine levels can indicate not only low

olate levels and a greater risk of neural tube defects but canlso be indicative of an independent risk factor for heartisease andor oxidative stress in the nonbariatric popula-ion [102] However unlike iron and vitamin B12 the folate

ontained in the multivitamin supplementation essentially e

orrects the deficiency in the vast majority of postoperativeariatric patients [103] Therefore persistent folate defi-iency might indicate a patientrsquos lack of compliance withhe prescribed vitamin protocol [32]

It is common knowledge that folic acid deficiency amongregnant women has been associated with a greater risk ofeural tube defects in newborns Consistent supplementa-ion and monitoring among women of child-bearing agencluding pre- and postoperative bariatric patients is vital inn effort to prevent the possibility of neural tube defects inhe developing fetus

Because folate does not affect the myelin of nerveseurologic damage is not as common with folate such as ishe case for vitamin B12 deficiency In contrast patientsith folate deficiency often present with forgetfulness irri-

ability hostility and even paranoid behaviors [29] Similaro that evidenced with vitamin B12 most postoperativeYGB patients who are folate deficient are asymptomatic orave subclinical symptoms therefore these deficient statesay not be easily identified

uggested supplementation Even though folate absorptionccurs preferentially in the proximal portion of the smallntestine it can occur along the entire length of the small bowelith postoperative adaptation Therefore it is generally agreed

hat folate deficiency is corrected with 1000 mgd folic acid32] and is preventable with supplementation that provides00 of the daily value (800 g) This level can also benefithe fetus in a female patient unaware of her postoperativeregnancy Folate supplementation 1000 mgd has noteen recommended because of the potential for maskingitamin B12 deficiency Carmel et al [104] suggested thatomocysteine is the most sensitive marker of folic acidtatus in conjunction with erythrocyte folate Althougholic acid deficiency could potentially occur among post-perative bariatric surgery patients it has not been seenidely in recent studies especially when patients haveeen compliant with postoperative multivitamin supple-entation Therefore it is imperative to closely follow

olic acid both pre- and postoperatively especially inhose patients suspected to be noncompliant with theirultivitamin supplementation

ron

Much of the iron and surgical weight loss research con-ucted to date has been generated from a limited number ofurgeons and scientists however the data have consistentlyointed toward the risk of iron deficiency and anemia afterariatric procedures Iron deficiency is defined as a decreasen the total iron body content Iron deficiency anemia occurshen erythropoiesis is impaired as a result of the lack of

ron stores In the absence of anemia iron deficiency issually asymptomatic Fatigue and a diminished capacity to

xercise however are common symptoms of anemia

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S86 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

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S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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S90 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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S91L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

gba

SA

Cphctrpw[nvfiisitCbg

Oafp[woofc(1hpritt

P

E

tgpoo

ccpcglcppmtttwaw

ailmsmtsbtciaspomtsa

bompo(almqmmbbEc

S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

(admcas

ihtpacbsT

ovBfted

fbsalumlcatspie

P

laTofmndef

pocimhphcsatpa

P

awrywaoirfiotnrsafRe

strwsviaratrlsgt

S93L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

[ntnriasiB(cdip

afedmvfllBrpem

D1mypei

iecalbcBmpmtta

ciru

iipafcfui

foaowppartptpthc

P

iwEvln6wdeapctnstat

S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

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apcptaasosdbc

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TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

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[

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[

[

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[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

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[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

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[

[

[

[

[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

s

aildquo

T

T

DFF

F

E

A

D

T

T

P

DFF

S

D

T

S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

DFF

S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 12: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S84 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ut it is essential for RYGB patients so as not to hasten theevelopment of a potential postoperative deficiency

ostoperative risk Vitamin B12 deficiency has been fre-uently reported after RYGB Schilling et al [82] estimatedhe prevalence of vitamin B12 deficiency to be 12ndash33ther researchers have suggested a much greater prevalencef B12 deficiency in up to 75 of postoperative RYGBatients however most reports have cited approximately5 of postoperative RYGB patients as vitamin B12 defi-ient [82ndash87] Brolin et al [87] reported that low levels ofitamin B12 might be seen as soon as six months afterariatric surgery but most often occurring more than oneear postoperatively as liver stores become depleted Sk-oubis et al [88] predicted that the deficiency will mostikely occur 7 months after RYGB and 79 months afterPDDS although their research did not consider compro-ised preoperative status and its correlation to postopera-

ive deficiency After the first postoperative year the prev-lence of vitamin B12 deficiency appears to increase yearlyn RYGB patients [89]

Although the bodyrsquos storage of vitamin B12 is significant2000 g) compared with daily needs (24 gd) thisarticular deficiency has been found within 1ndash9 years ofastric bypass surgery [29] Brolin et al [84] reported thatne third of RYGB patients are deficient at four yearsostoperatively However non-surgical variables were notxplored and many patients might have had preoperativealues near the lower end of the normal range Ocon Bretont al [90] compared micronutrient deficiencies among two-ear postoperative BPDDS and RYGB patients and foundhat all nutritional deficiencies were more common amongPDDS patients except for vitamin B12 for which theeficiency was more common among the RYGB patientstudied A lack of B12 deficiency among BPDDS patientsight result from a better tolerance of animal proteins in a

arger pouch greater pepsingastric acid production to re-ease protein-bound B12 and increased availability and in-eraction of IF with the pouch contents

Experts have noted the significance of subclinical defi-iency in the low-normal cobalamin range in nongastricypass patients who do not exhibit clinical evidence ofeficiency The methylmalonic acid (MMA) assay is thereferred marker of B12 status because metabolic changesften precede low B12 levels in the progression to defi-iency Serum B12 assays may miss as much as 25ndash30 of

12 deficiencies making them less reliable than the MMAssay [91] It has been suggested that early signs of vitamin

12 deficiency can be detected if the serum levels of bothMA and homocysteine are measured [91] Vitamin B12

eficiency after RYGB has been associated with megalo-lastic anemia [92] Some vitamin B12-deficient patientsevelop significant symptoms such as polyneuropathy par-

sthesia and permanent neural impairment On occasion

ome patients may experience extreme delusions halluci-ations and even overt psychosis [93]

uggested supplementation Because of the frequent lack ofymptoms of vitamin B12 deficiency the suggested dili-ence in following up or treating these values among thosesymptomatic patients has been questioned The decisionot to supplement or routinely screen patients for B12 defi-iency should be examined very carefully given the risk ofrreversible neurologic damage if vitamin B12 goes un-reated for long periods At least one case report has beenublished of an exclusively breastfed infant with vitamin

12 deficiency who was born of an asymptomatic motherho had undergone gastric bypass surgery [94]Deficiency of vitamin B12 is typically defined at levels

200 pgmL However about 50 of patients with obviousigns and symptoms of deficiency have normal vitamin B12

evels [31] Kaplan et al [95] reported that vitamin B12

eficiency usually resolves after several weeks of treatmentith 700ndash2000 gwk Rhode et al [96] found that aosage of 350ndash600 gd of oral B12 prevented vitamin B12

eficiency in 95 of patients and an oral dose of 500 gdas sufficient to overcome an existing deficiency as re-orted by Brolin et al [87] in a similar study Thereforeupplementation of RYGB patients with 350ndash500 gd mayrevent most postoperative vitamin B12 deficiency

While most vitamin B12 in normal adults is absorbed inhe ileum in the presence of IF approximately 1 of sup-lemented B12 will be absorbed passively (by diffusion)long the entire length of the (non-bypassed) intestine byurgical weight loss patients given a high-dose oral supple-ent [97] Thus the consumption of 350ndash500 g yields a

5ndash50-g absorption which is greater than the daily re-uirement Although the use of monthly intramuscular in-ections or a weekly oral dose of vitamin B12 is commonmong practices it relies on patient compliance Practitio-ers should assess the patientrsquos preference and the potentialor compliance when considering a daily weekly oronthly regimen of B12 supplementation In addition to oral

upplements or intramuscular injections nasal sprays andublingual sources of vitamin B12 are also available Pa-ients should be monitored closely for their lifetime becauseevere anemia can develop with or without supplementation98]

olate

tiology of potential deficiency Factors that increase theisk of folic acid deficiency relevant to bariatric surgerynclude the following

Inadequate dietary intakeNoncompliance with multivitamin supplementationMalabsorptionMedications (anticonvulsants oral contraceptives

and cancer treating agents) [79]

pmo

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PAtArBatbhptl5

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I

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S85L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Folic acid stores can be depleted within a few monthsostoperatively unless replenished by a multivitamin supple-ent and dietary sources (ie green leafy vegetables fruits

rgan meats liver dried yeast and fortified grain products)

igns symptoms and treatment of deficiency (seeppendix Table A4)

reoperative risk The goals of the 1998 Food and Drugdministration policy requiring all enriched grain products

o be fortified with folate included increasing the averagemerican diet by 100 g folate daily and decreasing the

ate of neural tube defects in childbearing women [99]entley et al [100] reported that the proportion of womenged 15ndash44 years old (in the general population) who meethe recommended dietary intake of 400 gd folate variesetween 23 and 33 With the increasing popularity ofigh proteinlow carbohydrate diets one cannot assume thatreoperative patients consume dietary sources of folatehrough fortified grain products fruits and vegetables Boy-an et al [26] found folate deficiencies preoperatively in6 of RYGB patients studied

ostoperative risk Although it has been observed that fo-ate deficiency after RYGB surgery is less common than B12

eficiency and is thought to occur because of decreasedietary or multivitamin supplement intake low serum folateevels have been cited from 6 to 65 among RYGBatients [2686101] Additionally folate deficiencies haveccurred postoperatively even with supplementation Boy-an et al [26] found that 47 (n 17) of RYGB patientsad low folate levels six months postoperatively and 41n 17) had low levels at one year This deficiency oc-urred despite patient adherence to taking a multivitaminupplement that contained at least the daily value for folate00 g [26] Postoperative bariatric patients with rapideight loss might have an increased risk of micronutrienteficiencies MacLean et al [86] reported that 65 ofostoperative patients had low folate levels These sameatients exhibited additional B vitamin deficiencies 24itamin B12 and 50 thiamin [86] An increased risk ofeficiency has also been noted among AGB patients pos-ibly because of decreased folate intake Gasteyger et al33] found a significant decrease in serum folate levels441) between the baseline and 24-month postoperativeeasurementsDixon and OrsquoBrien [101] reported elevated serum ho-

ocysteine levels in patients after bariatric surgery regard-ess of the type of procedure (restrictive or malabsorptive)levated homocysteine levels can indicate not only low

olate levels and a greater risk of neural tube defects but canlso be indicative of an independent risk factor for heartisease andor oxidative stress in the nonbariatric popula-ion [102] However unlike iron and vitamin B12 the folate

ontained in the multivitamin supplementation essentially e

orrects the deficiency in the vast majority of postoperativeariatric patients [103] Therefore persistent folate defi-iency might indicate a patientrsquos lack of compliance withhe prescribed vitamin protocol [32]

It is common knowledge that folic acid deficiency amongregnant women has been associated with a greater risk ofeural tube defects in newborns Consistent supplementa-ion and monitoring among women of child-bearing agencluding pre- and postoperative bariatric patients is vital inn effort to prevent the possibility of neural tube defects inhe developing fetus

Because folate does not affect the myelin of nerveseurologic damage is not as common with folate such as ishe case for vitamin B12 deficiency In contrast patientsith folate deficiency often present with forgetfulness irri-

ability hostility and even paranoid behaviors [29] Similaro that evidenced with vitamin B12 most postoperativeYGB patients who are folate deficient are asymptomatic orave subclinical symptoms therefore these deficient statesay not be easily identified

uggested supplementation Even though folate absorptionccurs preferentially in the proximal portion of the smallntestine it can occur along the entire length of the small bowelith postoperative adaptation Therefore it is generally agreed

hat folate deficiency is corrected with 1000 mgd folic acid32] and is preventable with supplementation that provides00 of the daily value (800 g) This level can also benefithe fetus in a female patient unaware of her postoperativeregnancy Folate supplementation 1000 mgd has noteen recommended because of the potential for maskingitamin B12 deficiency Carmel et al [104] suggested thatomocysteine is the most sensitive marker of folic acidtatus in conjunction with erythrocyte folate Althougholic acid deficiency could potentially occur among post-perative bariatric surgery patients it has not been seenidely in recent studies especially when patients haveeen compliant with postoperative multivitamin supple-entation Therefore it is imperative to closely follow

olic acid both pre- and postoperatively especially inhose patients suspected to be noncompliant with theirultivitamin supplementation

ron

Much of the iron and surgical weight loss research con-ucted to date has been generated from a limited number ofurgeons and scientists however the data have consistentlyointed toward the risk of iron deficiency and anemia afterariatric procedures Iron deficiency is defined as a decreasen the total iron body content Iron deficiency anemia occurshen erythropoiesis is impaired as a result of the lack of

ron stores In the absence of anemia iron deficiency issually asymptomatic Fatigue and a diminished capacity to

xercise however are common symptoms of anemia

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S86 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

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S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

(admcas

ihtpacbsT

ovBfted

fbsalumlcatspie

P

laTofmndef

pocimhphcsatpa

P

awrywaoirfiotnrsafRe

strwsviaratrlsgt

S93L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

[ntnriasiB(cdip

afedmvfllBrpem

D1mypei

iecalbcBmpmtta

ciru

iipafcfui

foaowppartptpthc

P

iwEvln6wdeapctnstat

S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

ratbrdd

aebaaa

apcptaasosdbc

afciitdmptpcrsPEv

TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

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S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

s

aildquo

T

T

DFF

F

E

A

D

T

T

P

DFF

S

D

T

S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

DFF

S

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D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

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T

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S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 13: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S85L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

Folic acid stores can be depleted within a few monthsostoperatively unless replenished by a multivitamin supple-ent and dietary sources (ie green leafy vegetables fruits

rgan meats liver dried yeast and fortified grain products)

igns symptoms and treatment of deficiency (seeppendix Table A4)

reoperative risk The goals of the 1998 Food and Drugdministration policy requiring all enriched grain products

o be fortified with folate included increasing the averagemerican diet by 100 g folate daily and decreasing the

ate of neural tube defects in childbearing women [99]entley et al [100] reported that the proportion of womenged 15ndash44 years old (in the general population) who meethe recommended dietary intake of 400 gd folate variesetween 23 and 33 With the increasing popularity ofigh proteinlow carbohydrate diets one cannot assume thatreoperative patients consume dietary sources of folatehrough fortified grain products fruits and vegetables Boy-an et al [26] found folate deficiencies preoperatively in6 of RYGB patients studied

ostoperative risk Although it has been observed that fo-ate deficiency after RYGB surgery is less common than B12

eficiency and is thought to occur because of decreasedietary or multivitamin supplement intake low serum folateevels have been cited from 6 to 65 among RYGBatients [2686101] Additionally folate deficiencies haveccurred postoperatively even with supplementation Boy-an et al [26] found that 47 (n 17) of RYGB patientsad low folate levels six months postoperatively and 41n 17) had low levels at one year This deficiency oc-urred despite patient adherence to taking a multivitaminupplement that contained at least the daily value for folate00 g [26] Postoperative bariatric patients with rapideight loss might have an increased risk of micronutrienteficiencies MacLean et al [86] reported that 65 ofostoperative patients had low folate levels These sameatients exhibited additional B vitamin deficiencies 24itamin B12 and 50 thiamin [86] An increased risk ofeficiency has also been noted among AGB patients pos-ibly because of decreased folate intake Gasteyger et al33] found a significant decrease in serum folate levels441) between the baseline and 24-month postoperativeeasurementsDixon and OrsquoBrien [101] reported elevated serum ho-

ocysteine levels in patients after bariatric surgery regard-ess of the type of procedure (restrictive or malabsorptive)levated homocysteine levels can indicate not only low

olate levels and a greater risk of neural tube defects but canlso be indicative of an independent risk factor for heartisease andor oxidative stress in the nonbariatric popula-ion [102] However unlike iron and vitamin B12 the folate

ontained in the multivitamin supplementation essentially e

orrects the deficiency in the vast majority of postoperativeariatric patients [103] Therefore persistent folate defi-iency might indicate a patientrsquos lack of compliance withhe prescribed vitamin protocol [32]

It is common knowledge that folic acid deficiency amongregnant women has been associated with a greater risk ofeural tube defects in newborns Consistent supplementa-ion and monitoring among women of child-bearing agencluding pre- and postoperative bariatric patients is vital inn effort to prevent the possibility of neural tube defects inhe developing fetus

Because folate does not affect the myelin of nerveseurologic damage is not as common with folate such as ishe case for vitamin B12 deficiency In contrast patientsith folate deficiency often present with forgetfulness irri-

ability hostility and even paranoid behaviors [29] Similaro that evidenced with vitamin B12 most postoperativeYGB patients who are folate deficient are asymptomatic orave subclinical symptoms therefore these deficient statesay not be easily identified

uggested supplementation Even though folate absorptionccurs preferentially in the proximal portion of the smallntestine it can occur along the entire length of the small bowelith postoperative adaptation Therefore it is generally agreed

hat folate deficiency is corrected with 1000 mgd folic acid32] and is preventable with supplementation that provides00 of the daily value (800 g) This level can also benefithe fetus in a female patient unaware of her postoperativeregnancy Folate supplementation 1000 mgd has noteen recommended because of the potential for maskingitamin B12 deficiency Carmel et al [104] suggested thatomocysteine is the most sensitive marker of folic acidtatus in conjunction with erythrocyte folate Althougholic acid deficiency could potentially occur among post-perative bariatric surgery patients it has not been seenidely in recent studies especially when patients haveeen compliant with postoperative multivitamin supple-entation Therefore it is imperative to closely follow

olic acid both pre- and postoperatively especially inhose patients suspected to be noncompliant with theirultivitamin supplementation

ron

Much of the iron and surgical weight loss research con-ucted to date has been generated from a limited number ofurgeons and scientists however the data have consistentlyointed toward the risk of iron deficiency and anemia afterariatric procedures Iron deficiency is defined as a decreasen the total iron body content Iron deficiency anemia occurshen erythropoiesis is impaired as a result of the lack of

ron stores In the absence of anemia iron deficiency issually asymptomatic Fatigue and a diminished capacity to

xercise however are common symptoms of anemia

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S86 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

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S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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S88 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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S89L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

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hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

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S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

ratbrdd

aebaaa

apcptaasosdbc

afciitdmptpcrsPEv

TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

[

[

[

[

[

[

[

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[

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[

[

[

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[

[

[

[

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[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

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S

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T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

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S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

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S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

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S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 14: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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tiology of potential deficiency As with other vitamins andinerals the possible reasons for iron deficiency related to

urgical weight loss are multifactorial and not fully ex-lained in the literature Iron deficiency can be associatedith malabsorptive procedures combination procedures

nd AGB although the etiology of the deficiency is likely toe unique with each procedure Although the absorption ofron can occur throughout the small intestine it is mostfficient in the duodenum and proximal jejunum which isypassed after RYGB leading to decreased overall absorp-ion Important receptors in the apical membrane of thenterocyte including duodenal cytochrome b are involvedn the reduction of ferric iron and subsequent transporting ofron into the cell [105] The effect of bariatric surgery onhese transporters has not been defined but it is likely thatt least initially fewer receptors are available to transportron With malabsorptive procedures there is likely a de-rease in transit time during which dietary iron has lessontact with the lumen in addition to the bypass of theuodenum resulting in decreased absorption In RYGBrocedures decreased absorption is coupled with reducedietary intake of iron-rich foods such as meats enrichedrains and vegetables Those patients who are able to tol-rate meat have been shown to have a lower risk of ironeficiency [38] however patient tolerance varies consider-bly and red meat in particular is often cited as a poorlyolerated food source Iron-fortified grain products are oftenimited because of the emphasis on protein-rich foods andestricted carbohydrate intake Finally decreased hydro-hloric acid production in the stomach after RYGB [106]an affect the reduction of iron from the ferric (Fe3) to thebsorbable ferrous state (Fe2) Notably vitamin C foundn both dietary and supplemental sources can enhance ironbsorption of non-heme iron making it a worthy recom-endation for inclusion in the postoperative diet [39]

igns symptoms and treatment of deficiency (seeppendix Table A5)

reoperative risk The prevalence of iron deficiency in thenited States is well documented Premenopausal women

re at increased risk of deficiency because of menstrualosses especially when oral contraceptives are not usedhe use of oral contraceptives alone decreases blood loss

rom menstruation by as much as 60 and decreases theecommended daily allowance to 11 mgd (instead of 15gd) [105] Women of child-bearing age comprise a large

ercentage (80) of the bariatric surgery cases performedach year The propensity of this population to be at risk ofron deficiency and related anemia is relatively independentf bariatric surgery and thus should be evaluated before therocedure to establish baseline measures of iron status ando treat a deficiency if indicated

Women however are not the only group at risk of iron

eficiency obese men and younger (25 yr) surgical can- h

idates have also been found to be iron deficient preopera-ively In one retrospective study of consecutive cases (n 79) 44 of bariatric surgery candidates were iron defi-ient [21] In this report men were more likely than womeno be anemic (407 versus 191) as determined by ab-ormal hemoglobin values Women however were moreikely to have abnormal ferritin levels Anemia and ironeficiency were more common in patients 25 years of ageompared with those 60 years of age Of these 79 ofounger patients versus 42 of older patients presentedith preoperative iron deficiency as determined by low

erum iron values Another study found iron levels to bebnormal in 16 of patients despite a low proportion ofatients for whom data were available (64) These studiesre in contrast to earlier reports of limited preoperative ironeficiency [32107]

ostoperative risk Iron deficiency is common after gastricypass surgery with reports of deficiency ranging from 20 to9 [3298107108] Up to 51 of female patients in oneeries were iron deficient confirming the high-risk nature ofhis population [87] Among patients with super obesity un-ergoing RYGB with varying limb length iron deficiency haseen identified in 49ndash52 and anemia in 35ndash74 of subjectsp to 3 years postoperatively [84]

In one study the prevalence of iron deficiency was sim-lar among RYGB and BPD subjects Skroubis et al [88]ollowed both RYGB and BPD subjects for five years Theerritin levels at two years were significantly different be-ween the two groups with 38 of RYGB versus 15 ofPD subjects having low levels The percentage of patients

ncluded in the follow-up data decreased considerably inoth groups and must be taken into account Although dataor 70 RYGB subjects and 60 BPD subjects were recordedt one year only eight and one subject remained in theroups respectively at five years It is difficult to commentn the iron status and other clinical parameters given theeight of the data For example the investigators reported

hat 100 of BPD subjects were deficient in hemoglobinron and ferritin However only one subject remainedaking the later results nongeneralizable Additional stud-

es investigating iron absorption and status are warranted forPDDS procedures

Menstruating women and adolescents who undergo bariat-ic surgery might require additional iron One randomizedtudy of premenopausal RYGB women (n 56) demonstratedhat 320 mg of supplemental oral iron (ferrous sulfate) givenwice daily prevented the development of iron deficiency butid not protect against the development of anemia [107] No-ably those patients who developed anemia were not regularlyaking their iron supplements (5 timeswk) during the periodreceding diagnosis In that study a significant correlation wasound between the resolution of iron deficiency and adhering tohe prescribed oral iron supplement regimen Ferritin levels

ad decreased at two years in the untreated group but those in

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he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

gba

SA

Cphctrpw[nvfiisitCbg

Oafp[woofc(1hpritt

P

E

tgpoo

ccpcglcppmtttwaw

ailmsmtsbtciaspomtsa

bompo(almqmmbbEc

S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

(admcas

ihtpacbsT

ovBfted

fbsalumlcatspie

P

laTofmndef

pocimhphcsatpa

P

awrywaoirfiotnrsafRe

strwsviaratrlsgt

S93L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

[ntnriasiB(cdip

afedmvfllBrpem

D1mypei

iecalbcBmpmtta

ciru

iipafcfui

foaowppartptpthc

P

iwEvln6wdeapctnstat

S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

ratbrdd

aebaaa

apcptaasosdbc

afciitdmptpcrsPEv

TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

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[

[

[

[

[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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D

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T

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S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

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D

T

T

T

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D

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S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

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TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 15: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S87L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he supplemented group remained within the normal rangeuggesting dietary intake and one multivitamin (containing 18g iron) might be inadequate to maintain iron stores in RYGB

atientsA significant decline in the iron status of surgical weight

oss patients can occur over time In one series 63 ofubjects followed for two years after RYGB developedutritional deficiencies including iron vitamin B12 andolate [32] In this study those subjects who were compliantith a daily multivitamin could not prevent iron deficiencywo thirds (67) of those who did develop iron deficiency

ater became anemic Their findings suggest that the amountf iron in a standard multivitamin alone is not adequate torevent deficiency Similarly Avinoah et al [38] found thatt 67 years postoperatively weight loss (56 22xcess body weight) had been relatively stable for the pre-eding five years (n 200) however the iron saturationemoglobin and mean corpuscular volume values had de-lined progressively and significantly

Recently case reports of a re-emergence of pica afterYGB might also be linked to iron deficiency [109] Pica is

he ingestion of nonfood substances and historically haseen common in some parts of the world during pregnancyith gastrointestinal blood loss and in those with sickle cellisease Although perhaps less detrimental than consumingtarch or clay the consumption of ice (pagophagia) is alsoform of pica that might not be routinely identified In the

forementioned case series iron treatment was noted toesolve pica within eight weeks in five women after RYGB

Screening for iron status can include the use of serumerritin levels Such levels however should not be used toiagnose a deficiency Ferritin is an acute-phase reactantnd can fluctuate with age inflammation and infectionmdashncluding the common cold Measuring serum iron alongith the total iron binding capacity is preferred to determine

ron status Hemoglobin and hematocrit changes reflect lateron-deficient anemia and are less valuable in identifyingarly anemia but are frequently used in the bariatric data toefine anemia because of their widespread clinical avail-bility Serum iron along with total iron binding capacityhould be measured at 6 months postoperatively because aeficiency can occur rapidly and then annually in additiono analyzing the complete blood count

uggested supplementation In addition to the iron found inwo multivitamins menstruating women and adolescents ofoth sexes may require additional supplementation tochieve a total oral intake of 50ndash100 mg of elemental ironaily although the long-term efficacy of such prophylacticreatment is unknown [87107] This amount of oral iron cane achieved by the addition of ferrous sulfate or otherreparations such as ferrous fumarate gluconate polysac-haride or iron protein succinylate forms Those womenho use oral contraceptives have significantly less blood

oss and therefore may have lower requirements for supple- y

ental iron This is an important consideration during thelinical interview The use of two complete multivitaminsollectively providing 36 mg of iron (typically ferrous fu-arate) is customary for low-risk patients including men

nd postmenopausal women A history of anemia or ahange in laboratory values may indicate the need for ad-itional supplementation in conjunction with age sex andeproductive considerations Treatment of iron deficiencyequires additional supplementation as noted in Appendixable A5

alcium and vitamin D

tiology of potential deficiency Calcium is absorbed pref-rentially in the duodenum and proximal jejunum and itsbsorption is facilitated by vitamin D in an acid environ-ent Vitamin D is absorbed preferentially in the jejunum

nd ileum As the malabsorptive effects of surgical proce-ures increase so does the likelihood of fat-soluble vitaminalabsorption related to the bypassing of the stomach ab-

orption sites of the intestine and poor mixing of bile saltsecreased dietary intake of calcium and vitamin D-rich

oods related to intolerance can also increase the risk ofeficiency after all surgical procedures

Low vitamin D levels are associated with a decrease inietary calcium absorption but are not always accompaniedy a reduction in serum calcium As blood calcium ionsecrease parathyroid hormone levels increase Secondaryyperparathyroidism allows the kidney and liver to convert-dehydroxycholecalciferol into the active form of vitamin 125 dihydroxycholecalciferol and stimulates the intes-

ine to increase absorption of calcium If dietary calcium isot available or intestinal absorption is impaired by vitamin

deficiency calcium homeostasis is maintained by in-reases in bone resorption and in conservation of calcium byay of the kidneys Therefore calcium deficiency (low

erum calcium) would not be expected until osteoporosisas severely depleted the skeleton of calcium stores

igns symptoms and treatment of deficiency (seeppendix Tables A6 and A7)

reoperative risk Although vitamin D deficiency and in-reased bone remodeling can be expected after malabsorptiverocedures it is very important to consider the prevalence ofhese conditions preoperatively Buffington et al [19] foundhat 62 of women (n 60) had 25-hydroxyvitamin D25(OH)D] levels at less than normal values confirming theypothesis that vitamin D deficiency might be associated withorbid obesity A negative correlation between BMI and vi-

amin D levels was noted suggesting that individuals with aarger BMI might be more prone to develop vitamin D defi-iency [19] In addition a positive correlation exists between areater BMI and increased parathyroid hormone [110] Re-ently Flancbaum et al [21] completed a retrospective anal-

sis of 379 preoperative gastric bypass patients and found

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S88 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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S89L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

ww

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S90 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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S91L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

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S93L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

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S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

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S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

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[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

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FF

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D

T

T

V

D

FF

EA

D

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T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

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T

T

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DFFS

D

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S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

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TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 16: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S88 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

81 were deficient in 25(OH)D Vitamin D deficiency wasess common among Hispanics (564) than among whites788) and African Americans (704) [21] Ybarra et al20] also found 80 of a screened population of patientsresented with similar patterns of low vitamin D levels andecondary hyperparathyroidism

Several mechanisms have been suggested to explain theause of the increased risk of vitamin D deficiency amongreoperative obese individuals They include the decreasedioavailability of vitamin D because of enhanced uptakend clearance by adipose tissue 125-dihydroxyvitamin Dnhancement and negative feedback control on the hepaticynthesis of 25(OH)D underexposure to solar ultravioletadiation and malabsorption [111ndash114] with the majorause being decreased availability of vitamin D secondaryo the preoperative fat mass

Considering the evidence from both observational stud-es and clinical trials that calcium malnutrition and hypovi-aminosis D are predisposing conditions for various com-on chronic diseases the need for the early identification ofdeficiency is paramount to protect the preoperative patientith obesity from serious complications and adverse ef-

ects In addition to skeletal disorders calcium and vitamindeficits increase the risk of malignancies (in particular of

he colon breast and prostate gland) of chronic inflamma-ory and autoimmune disease (eg diabetes mellitus type 1nflammatory bowel disease multiple sclerosis rheumatoidrthritis) of metabolic disorders (metabolic syndrome andypertension) as well as peripheral vascular disease115116]

ostoperative risk An increased long-term risk of meta-olic bone disease has been well documented after BPDDSnd RYGB Slater et al [36] followed BPDDS patients fourears postoperatively and found vitamin D deficiency in3 hypocalcemia in 48 and a corresponding increase inarathyroid hormone (PTH) in 69 of patients Anothereries found at a median follow-up of 32 months that59 of patients were hypokalemic 50 had low vitamin and 631 had elevated PTH despite taking multivita-ins [117] The bypass of the duodenum and a shorter

ommon channel in BPDDS patients increases the risk ofeveloping hyperparathyroidism This could be related toeduced calcium and 25(OH)D absorption [118] Similarlyhe increased incidence of vitamin D deficiency and sec-ndary hyperparathyroidism has also been found in RYGBatients related to the bypass of the duodenum [119]

Goode et al [120] using urinary markers consistent withone degradation found that postmenopausal womenhowed evidence of secondary hyperparathyroidism ele-ated bone resorption and patterns of bone loss afterYGB Dietary supplementation with vitamin D and 1200g calcium per day did not affect these measures indicating

he need for greater supplementation [120] Secondary ele-

ated PTH and urinary bone marker levels consistent with (

ncreased bone turnover postoperatively were also found inne small short-term series (n 15) followed by Coates etl [121] The subjects were found to have significanthanges in total hip trochanter and total body bone mineralensity as a result of increased bone resorption beginning asarly as three months postoperatively These changes oc-urred despite increased dietary intake of calcium and vita-in D The significance of elevated PTH is clearly an

mportant area of investigation in postoperative patientsecause high PTH levels could be an early sign of boneisease in some patients A decrease in serum estradiolevels has also been found to alter calcium metabolism afterYGB-induced weight loss [122]

Fewer studies have reported vitamin Dcalcium deficitsnd elevated PTH in AGB patient Pugnale et al [123] andiusti et al [124] followed premenopausal women under-oing gastric banding one and two years postoperativelynd found no significant decrease in vitamin D serumalcium or PTH levels however serum telopeptide-C in-reased by 100 indicative of an increase in bone turnoverurthermore the bone mass density and bone mineral con-entration decreased especially in the femoral neck aseight loss occurred Despite the absence of secondaryyperparathyroidism after gastric banding biochemicalone markers have continued to show a negative remodel-ng balance characterized by an increase in bone resorption123124] Bone loss has also been reported in a series ofen and women undergoing vertical banded gastroplasty oredical weight loss therapy The investigators attributed the

educed estradiol levels in female patients studied to explainhe increased bone turnover [125] Reidt et al [126] sug-ested that an increase in bone turnover with weight lossould occur from a decrease in estradiol secondary to a lossf adipose tissue or to other conditions associated witheight loss such as an increase in PTH an increase in

ortisol or to a decrease in weight-bearing bone stresshese investigators found that increasing the dosage ofalcium citrate from 1000 mg to 1700 mgd (including 400U vitamin D) was able to reduce bone loss with weightoss but not stop it [126] If left undiagnosed and untreatedt would only be a matter of time before the vitamin Dcal-ium deficits and hormonal mechanisms such as secondaryyperparathyroidism would result in osteopenia osteoporo-is and ultimately osteomalacia [127]

alcium citrate versus calcium carbonate Supplementationith calcium and vitamin D during all weight loss modal-

ties is critical to preventing bone resorption [121] Thereferred form of calcium supplementation is an area ofebate in current clinical practice In a low acid environ-ent such as occurs with the negligible secretion of acid by

he pouch created with gastric bypass absorption of calciumarbonate is poor [128] Studies have found in nongastricypass postmenopausal female subjects that calcium citrate

not calcium carbonate) decreased markers of bone resorp-

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S89L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

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hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

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S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

ratbrdd

aebaaa

apcptaasosdbc

afciitdmptpcrsPEv

TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

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[

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[

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[

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[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

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S

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T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

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S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

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D

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S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

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S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 17: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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ion and did not increase PTH or calcium excretion [129] Aeta-analysis of calcium bioavailability suggested that cal-

ium citrate is more effectively absorbed than calcium car-onate by 22ndash27 regardless of whether it was taken on anmpty stomach or with meals [130] These findings suggesthat it is appropriate to advise calcium citrate supplementa-ion despite the limited evidence because of the potentialenefit without additional risk

Patients who have a history of requiring antiseizure orlucocorticoid medications as well as long-term use ofhyroid hormone methotrexate heparin or cholestyramineould also have an increased risk of metabolic bone diseaseherefore close monitoring of these individuals is also ap-ropriate [131]

uggested supplementation In view of the increased risksf poor bone health in the patient with morbid obesity allurgical candidates should be screened for vitamin D defi-iency and bone density abnormalities preoperatively Ifitamin D deficiency is present a suggested dose for cor-ection is 50000 IU ergocalciferol taken orally onceeekly for 8 weeks [21] It is no longer acceptable to

ssume that postoperative prophylaxis calcium and vitaminsupplementation will prevent an increase in bone turn-

ver Therefore life-long screening and aggressive treat-ent to improve bone health needs to become integrated

nto postoperative patient care protocolsIt appears that 1200 mg of daily calcium supplementa-

ion and the 400ndash800 IU of vitamin D contained in standardultivitamins might not provide adequate protection for

ostoperative patients against an increase in PTH and boneesorption [120121132] Riedt et al [122] estimated that

50 of RYGB postoperative postmenopausal womenould have a negative calcium balance even with 1200 mgf calcium intake daily Another study reported that increas-ng the dosage of vitamin D to 1600ndash2000 IUd producedo appreciable change in PTH 25(OH)D corrected cal-ium or alkaline phosphatase levels for BPDDS patients118] Increasing calcium citrate to 1700 mgd (with 400 IUitamin D) during caloric restriction was able to ameliorateone loss in nonoperative postmenopausal women but didot prevent it [125] Some investigators have suggested thatlthough increased calcium intake can positively influenceone turnover after RYGB it is unlikely that additionalalcium supplementation beyond current recommendationsapproximately 1500 mgd for postoperative postmeno-ausal patients) would attenuate the elevated levels of boneesorption [122] It remains to be seen with additional re-earch whether more aggressive therapy including greateroses of calcium and vitamin D can correct secondaryyperparathyroidism or whether perhaps a threshold of sup-lementation exists

Patient supplementation compliance is often a commononcern among healthcare practitioners Weight loss can

elp to eliminate many co-morbid conditions associated g

ith obesity however without calcium and vitamin D sup-lementation it can be at the cost of bone health Theenefits of vitaminmineral compliance and lifestylehanges offering protection need to be frequently rein-orced The promotion of physical activity such as weight-earing exercise increasing the dietary intake of calciumnd vitamin D-rich foods moderate sun exposure smokingessation and reducing onersquos intake of alcohol caffeinend phosphoric acid are additional measures the patient canake in the pursuit of strong and healthy bones [133]

itamins A E K and zinc

tiology of potential deficiency The risk of fat-soluble vi-amin deficiencies among bariatric surgery patients such asitamins A E and K has been elucidated particularlymong patients who have undergone BPD surgery [34ndash6134] BPDDS surgery results in decreased intestinalietary fat absorption caused by the delay in the mixing ofastric and pancreatic enzymes with bile until the final0ndash100 cm of the ileum also known as the common chan-el [36] BPD surgery has been shown to decrease fatbsorption by 72 [34] It would therefore seem plausiblehat particularly among postoperative BPD patients fat-oluble vitamin absorption would be at risk Researchersave also discovered fat-soluble vitamin deficiencies amongYGB and AGB patients [263084135] which might notave been previously suspected

Normal absorption of fat-soluble vitamins occurs pas-ively in the upper small intestine The digestion of dietaryat and subsequent micellation of triacylglycerides (triglyc-rides) is associated with fat-soluble vitamin absorptiondditionally the transport of fat-soluble vitamins to tissues

s reliant on lipid components such as chylomicrons andipoproteins The changes in fat digestion produced by sur-ical weight loss procedures consequently alters the diges-ion absorption and transport of fat-soluble vitamins

igns symptoms and treatment of deficiency (seeppendix Tables A8 A9 A10 A11)

itamin A

Slater et al [36] evaluated the prevalence of serum fat-oluble vitamin deficiencies after malabsorptive surgery Ofhe 170 subjects in their study who returned for follow uphe incidence of vitamin A deficiency was 52 at one yearfter BPD (n 46) and increased annually to 69 (n 27)y postoperative year four

In a study comparing the nutritional consequences ofonventional therapy for obesity AGB and RYGB Ledouxt al [135] found that the serum concentrations of vitaminmarkedly decreased in the RYGB group (n 40) comparedith the conventional treatment group (n 110) and the AGBroup (n 51) The prevalence of vitamin A deficiency was25 in the RYGB group compared with 255 in the AGB

roup (P 001) The follow-up period for the RYGB group

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as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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S91L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

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hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

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S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

ratbrdd

aebaaa

apcptaasosdbc

afciitdmptpcrsPEv

TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

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[

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[

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[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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T

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F

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A

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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c

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S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

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T

T

V

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EA

D

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S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

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S

D

T

T

T

V

DFFS

D

T

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S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

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S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 18: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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as approximately 16 9 months and for the AGB groupas 30 12 months a significant difference (P 0001)Madan et al [27] investigated vitamin and trace minerals

efore and after RYGB in 100 subjects and found severaleficiencies before surgery and up to one year postopera-ively including vitamin B12 vitamin D iron seleniumitamin A zinc and folic acid Vitamin A was low among of preoperative patients (n 55) and 17 (n 30) atne year postoperatively However at the three- and six-onth postoperative points the subjects (n 55) had

eached a peak deficiency of 28 at six months but only7 were deficient at one year The number of subjectsollowed up at one year is considerably less than the previ-us time points and the data must be viewed in this context

Brolin et al [84] reported in a series comparing shortnd distal RYGB that shorter limb gastric bypass patientsith super obesity typically were not monitored for fat-

oluble vitamin deficiency and deficiencies were not notedn this group However in the distal RYGB group (n 39)0 of subjects had vitamin A deficiency and 50 wereitamin D deficient These findings suggest that longeroux limb lengths result in increased nutritional risks com-ared with shorter limb lengths As such dietitians andthers completing nutrition assessments should be familiarith the limb lengths of patients during their nutrition as-

essments to fully appreciate the risk of deficiency Suger-an et al [136] reported in their series comparing distalYGB and shorter limb lengths that supplementation with0000 U of vitamin A in addition to other vitamins andinerals appeared to be adequate to prevent vitamin A

eficiency The laboratory values in this series were abnor-al for other vitamins and minerals including iron B12

itamin D and vitamin E [136]Although the clinical manifestations of vitamin A defi-

iency are believed to be rare case studies have demon-trated the occurrence of ophthalmologic consequencesuch as night blindness [137ndash139] Chae and Foroozan140] reported on vitamin A deficiency in patients with aemote history of intestinal surgery including bariatric sur-ery using a retrospective review of all patients with vita-in A deficiency seen during one year in a neuro-ophthal-ic practice A total of four patients with vitamin A

eficiency were discovered three of whom had undergonentestinal surgery 18 years before the development ofisual symptoms It was concluded that vitamin A defi-iency should be suspected among patients with an unex-lained decreased vision and a history of intestinal surgeryegardless of the length of time since the surgery had beenerformed

Significant unexpected consequences can occur as a re-ult of vitamin A deficiency Lee et al [141] for instanceeported a case study of a 39-year-old woman three yearsfter RYGB who presented with xerophthalmia nyctalopianight blindness) and visual deterioration to legal blindness

n association with vitamin noncompliance during an 18- p

onth period postoperatively [141] Because vitamin Aupplementation beyond that found in a multivitamin is notoutine for the RYGB patient it is likely that this individualad insufficient intake of dietary vitamin A although thisas not considered by the investigators They concluded

hat the increasing prevalence of patients who have under-one gastric bypass surgery warrants patient and physicianducation regarding the importance of adherence to therescribed vitamin supplementation regimen to prevent aossible epidemic of iatrogenic xerophthalmia and blind-ess Purvin [142] also reported a case of nycalopia in a3-year-old postoperative bariatric patient that was reversedith vitamin A supplementation

itamin K

In the series by Slater et al [36] the vitamin K levelsere suboptimal in 51 (n 35) of the patients one year

fter BPD By the fourth year the deficiency had increasedo 68 (n 19) with 42 of patientsrsquo serum vitamin Kevels at less than the measurable range of 01 nmolLompared with 14 at the end of the first year of the studyitamin K deficiency was also considered by Ledoux et al

135] using the prothrombin time as an indicator of defi-iency The mean prothrombin time percentage was lowern the RYGB group versus both the AGB and conventionalreatment groups which suggests vitamin K deficiency135]

Among the unusual and rare complications after bariatricurgery Cone et al [143] cited a case report in which anlder woman with significant weight loss and diarrhea thatad been caused by the bacterium Clostridium difficileeveloped Streptococcal pneumonia sepsis after gastric by-ass surgery The researchers hypothesized that malabsorp-ion of vitamin K-dependent proteins C S and antithrom-in resulting from the gastric bypass predisposed theatient to purpura fulminans and disseminated intravascularoagulation

itamin E

A review of the literature revealed that most studies havexamined the postoperative and do not consider the preop-rative fat-soluble vitamin deficiencies Boylan et al [26]ound that 23 of RYGB patients studied (n 22) had lowitamin E levels preoperatively Even though the food in-ake of all subjects was sharply decreased after surgeryost patients who were taking a multivitamin supplement

hat provided 100 of the daily value of vitamin E wereound to maintain normal vitamin E levels In a study ofPDDS patients the vitamin E levels were normal in all

he patients less than one year postoperatively (n 44) andemained normal among 96 (n 24) of patients up to fourears after surgery [36] In a study comparing various sur-ical procedures Ledoux et al [135] found a significant

revalence of vitamin E deficiency among the RYGB com-

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ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

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hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

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In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

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A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

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[

[

[

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[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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T

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A

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

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FF

S

D

T

m

T

F

D

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T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

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V

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S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

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D

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S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

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S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 19: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

p1r

Z

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Sab2omh

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fmRr

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O

VcslwAwvIvmtbrvsee

S91L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ared with the AGB group (P 005) with 225 and18 of subjects presenting with a vitamin E deficiencyespectively

inc

Although zinc deficiency has not been fully explorednd its metabolic sequelae have not been clearly delineatedt is a nutrient that depends on fat absorption [36] thereforehe likelihood of deficiency of this mineral among surgicalatients appears plausible Slater et al [36] found that seruminc levels were abnormally low in 51 of BPDDS sub-ects (n 43) at one year postoperatively and remaineduboptimal among 50 of patients (n 26) at four yearsostoperatively In RYGB patients Madan et al [27] de-ermined that zinc levels were suboptimal among 28 ofreoperative patients (n 69) and 36 of one-year post-perative patients (n 33) In addition Cominetti et al144] researched the zinc status of pre- and postoperativeYGB patients and found that the greatest changes were

een among erythrocyte and urinary zinc concentrationsersus plasma zinc levels They postulated that RYGB pa-ients might have a lower dietary zinc intake in the postop-rative period that could put them at a risk of deficiency Aower dietary zinc intake could be related to food intoler-nces especially that of red meat

Burge [145] studied whether RYGB patients hadhanges in taste acuity postoperatively and whether zinconcentrations were affected Taste acuity and serum zincevels were measured in 14 subjects preoperatively and at 6nd 12 weeks postoperatively Although the researchers didot find changes in zinc concentrations during the study atix weeks postoperatively all patients reported that foodsasted sweeter and they had modified food selections ac-ordingly Finally Scruggs et al [146] found that afterYGB surgery a significant upregulation in taste acuity foritter and sour was observed as well as a trend toward aecrease in salt and sweet detection and recognition thresh-lds The researchers concluded that among other thingsaste effectors such as zinc when in the normal range doot alter thresholds of the four basic tastes

Although zinc has been preliminarily investigated theethods of analysis have not be rigorously evaluated Many

tudies reporting suboptimal zinc levels did not report theethod used to determine the status or how the analysis was

erformed The method and accurate assessment of theietary intake of zinc is critical to the evaluation of theeported data

uggested supplementation Ledoux et al [135] did not findsignificant difference in fat-soluble vitamin deficiencies

etween those subjects who consumed a multivitamin (n 4) and those who did not (n 16) The small sample sizef the study and that the subjects were not randomized forultivitamin supplementation versus no supplementation

ave made the data less meaningful In addition the level of e

ietary intake of these nutrients was not considered It isnknown whether the two groups (with and without supple-ents) consumed similar diets They proposed that allYGB patients should be supplemented with multivitaminss complete as possible including fat-soluble vitamins andinerals A recommendation of 50000 IU of vitamin A

very two weeks and 500 mg of vitamin E daily amongther supplements was suggested to correct most cases ofeficiency [135]

Slater et al [36] suggested life-long annual measure-ents of fat-soluble nutrients after BPDDS procedures

long with continued nutrition counseling and education Inddition to multivitaminmineral recommendations whichncluded zinc vitamin D and calcium they recommendedife-long daily supplementation of a minimum of 10000 IUf vitamin A and 300 g of vitamin K [36]

Finally Madan et al [27] also concluded that water andat-soluble vitamin and trace mineral deficiencies are com-on both pre- and postoperatively among RYGB patientsoutine evaluation of serum vitamin and mineral levels was

ecommended for this patient population

onclusion The reports cited in this section illustrate thateficiencies of vitamins A E K and zinc have been dis-overed among bariatric surgery patients AlthoughPDDS patients have been known to be at risk of fat-

oluble vitamin deficiencies the reports cited have illus-rated that bariatric patients in general including RYGBatients may also be at risk In addition rare and unusualomplications such as visual and taste disturbances mighte attributable to these deficiencies Routine supplementa-ion including multivitaminsminerals along with closere- and postoperative monitoring could attenuate the riskf these deficiencies

ther micronutrients

itamin B6 Little information is available pertaining tohanges in vitamin B6 (pyridoxal phosphate) with bariatricurgery because vitamin B6 is not routinely measured Boy-an et al [26] found that vitamin B6 levels before surgeryere adequate in only 36 of their surgical candidatesfter gastric bypass a normal status for vitamin B6 levelsas achieved in patients using supplements containing theitamin at amounts close to the US Dietary Referencentake Turkki et al [147] also found normal levels ofitamin B6 after gastroplasty for patients receiving supple-entation However these investigators subsequently found

hat the serum levels might not be reflective of vitamin B6

iologic status [148] When co-enzyme activation of eryth-ocyte aminotransferase activities was used as a marker ofitamin B6 status rather than the serum vitamin levelsupplementation of vitamin B6 at the US Dietary Refer-nce Intake recommended amounts (16 mg ) proved inad-quate for co-enzyme activation of these enzymes in the

arly postoperative period These findings suggest that

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S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

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S93L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

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S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

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S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

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D

paswaimpp

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pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

[

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[

[

[

[

[

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[

[

[

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S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 20: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S92 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

reater than the recommended amounts of vitamin B6 mighte required for normalization of vitamin B6 status in bari-tric patients

igns symptoms and treatment of deficiency (seeppendix Table A2)

opper Although copper is absorbed by the stomach androximal gut copper is rarely measured in patients whoave undergone RYGB or BPDDS Deficiencies in copperan not only cause anemia but also myelopathy similar tohat found with deficiencies in vitamin B12 [149150] Cur-ently only two cases of copper deficiency have been re-orted in gastric bypass patients both of whom presentedith symptoms of myelopathy (ie ataxia paresthesia)

149150] Other cases of copper deficiency and demyeli-ating neuropathy however have been reported for indi-iduals who have undergone gastrectomies [150] Thesendings suggest that the copper status needs to be examined

n RYGB and BPDDS patients presenting with signs andymptoms of neuropathy and normal B12 levels The find-ngs would also suggest multivitamin supplementation con-aining adequate amounts of copper (2 mg daily value)aution should be used when prescribing zinc supplementsecause copper depletion occurs when 50 mg zinc isiven for a long period of time

ther mineral deficiencies Various other trace elementsnd minerals could be deficient postoperatively Seleniumor instance has been found to be deficient in surgicalatients both pre- and postoperatively [27] Dolan et al134] found that 145 of patients undergoing BPDDSere selenium deficient These investigators as well asthers [151152] have also reported inadequate magnesiumr potassium status with bariatric surgery Dolan et al [134]ound that 5 of patients undergoing BPDDS were defi-ient in magnesium Schauer et al [151] found that 107) of gastric bypass patients were magnesium deficientndash31 months postoperatively These same investigatorsowever reported hypokalemia in 5 of their gastric by-ass population Crowley et al [152] in a much earliereport also found low potassium levels after gastric bypassn 24 of patients The findings of these studies emphasizehe need for recommendations of multivitamin supplementshat are complete in minerals

rotein

tiology of potential deficiency

Thorough mastication of food is an important first step inhe overall digestion process to compensate for the reducedrinding capacity of the pouch Breaking food into smallerarticles and moistening it with saliva will facilitate a bolusf animal protein to pass from the esophagus into the pouch

r through the band In normal digestion hydrochloric acid a

onverts the inactive proteolytic enzyme pepsinogen (se-reted in the middle of the stomach) into its active formepsin This allows the digestion of collagen to begin as theontents of the stomach continues to grind and mix withastric secretions Cholecystokinin and enterokinase are re-eased as the chyme comes in contact with intestinal mu-osa allowing the secretion and activation of pancreaticroteolytic enzymes trypsin chymotrypsin and carboxy-olypeptidase which facilitate the breakdown of proteinolecules into smaller polypeptides and amino acids Pro-

eolytic peptidases located in the brush border of the intes-ine allow additional breakdown into tripeptides and dipep-ides These small peptides cross the brush border intacthere peptide hydrolases complete digestion into amino

cids so they can be absorbed and transported to the liver byay of the portal veinQuite often it is thought that if a bolus of protein is not

ble to mix with the hydrochloric acid and pepsin producedn the antrum of the stomach that maldigestion will resulteading to significant protein deficiencies in patients withalabsorptive or combination procedures However the

tomachrsquos role in the digestion of protein is very small withost digestion and absorption occurring in the small intes-

ine Strong evidence cannot be found in the literature toupport the theory that the malabsorptive components ofariatric surgery alone cause deficiency Protein malnutri-ion (PM) is usually associated with other contemporaneousircumstances that lead to decreased dietary intake includ-ng anorexia prolonged vomiting diarrhea food intoler-nce depression fear of weight regain alcoholdrug abuseocioeconomic status or other reasons that might cause aatient to avoid protein and limit caloric intake All post-perative patients are therefore at risk of developing pri-ary PM andor protein-energy malnutrition (PEM) related

o decreased oral intake BPDDS patients are at risk ofecondary PMPEM because of the greater degree of mal-bsorption produced by this procedure

When nutrition is withheld for whatever reason theody is able to metabolically adapt for survival As a resultf decreased caloric intake hypoinsulinemia allows fat anduscle breakdown to supply the amino acids needed to

reserve the visceral pool Gluconeogenesis and fatty acidxidation help maintain a supply of energy to vital organsthe brain heart and kidney) Protein sparing is eventuallychieved as the body enters into ketosis Initially weightoss occurs as a result of water loss resulting from theetabolism of liver and muscle glycogen stores Subse-

uent weight loss occurs with the breakdown of muscleass and a reduction of adipose tissue as the body strives toaintain homeostasis A low protein intake can be tolerated

y the body because it will adjust to the negative nitrogenalance over several days but only to a certain extentventually without adequate intake a deficiency will oc-ur characterized by decreased hepatic proteins including

lbumin muscle wasting asthenia (weakness) and alopecia

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S93L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

[ntnriasiB(cdip

afedmvfllBrpem

D1mypei

iecalbcBmpmtta

ciru

iipafcfui

foaowppartptpthc

P

iwEvln6wdeapctnstat

S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

ratbrdd

aebaaa

apcptaasosdbc

afciitdmptpcrsPEv

TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

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S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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T

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F

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A

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

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S

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D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 21: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

(admcas

ihtpacbsT

ovBfted

fbsalumlcatspie

P

laTofmndef

pocimhphcsatpa

P

awrywaoirfiotnrsafRe

strwsviaratrlsgt

S93L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

hair loss) Protein-energy malnutrition is typically associ-ted with anemia related to iron B12 folate andor coppereficiency Deficiencies in zinc thiamin and B6 are com-only found with a deficient protein status In addition

atabolism of lean body mass and diuresis cause electrolytend mineral disturbances with sodium potassium magne-ium and phosphorus

If the protein deficit occurs in conjunction with excessiventake of carbohydrate calories hyperinsulinemia will in-ibit fat and muscle breakdown When the body is not ableo hormonally adapt to spare protein a decrease in visceralrotein synthesis will result along with hypoalbuminemianemia and impaired immunity If left undiagnosed thisan result in an illness in which fat stores are preserved leanody mass is decreased and appropriate weight loss is noteen because of the accumulation of extracellular waterhis edema is associated with PM [34153154]

Unfortunately loss of muscle mass is an inevitable partf the weight loss process after obesity surgery or anyery-low-calorie diet Patients especially those undergoingPDDS should be encouraged to focus on protein-rich

oods of high biologic value in meal planning while por-ion size is significantly decreased during the early postop-rative period This might help compensate for the naturalaily endogenous loss of protein in the gut

It is important for the medical team members to beamiliar with the process of extreme weight loss and theodyrsquos ability to metabolically adapt for survival in theemistarvation state that is commonly produced after bari-tric surgery Perhaps explaining the mechanism of weightoss and the desired outcome in terms the patient cannderstand would help to promote compliance and provideotivation to choose quality foods consisting of high bio-

ogic value protein balanced with nutrient dense complexarbohydrates and healthy food sources of essential fattycids In addition to consistent biochemical screening arained professional (typically a Registered Dietitian)hould regularly complete a thorough assessment of theatientrsquos nutritional status to ensure adequate protein intaken the midst of a calorie restriction This might help preventxcessive wasting of lean body mass and deficiency

reoperative risk

Preoperative protein deficiency is rarely reported in pub-ished studies Flancbaum et al [21] found ldquoabnormalrdquolbumin levels in 4 of 357 preoperative RYGB patientshis was reported as being insignificant They did not notether measures of protein deficiency Rabkin et al [155]ollowed 589 consecutive DS patients and found no abnor-al protein metabolism preoperatively Although it does

ot appear that preoperative patients are at risk of proteineficiency it would be unwise to assume that it does notxist among the morbidly obese with todayrsquos popularity of

ood faddism and the well-documented disordered eating s

atterns among the morbidly obese The idea that the pre-perative patient is overnourished from the stand point ofalories does not reflect the nutritional quality of the dietaryntake Routine preoperative screening including laboratoryeasures of albumin transferrin and lymphocyte count are

elpful in the diagnosis of PM [76] and assessing visceralrotein status Other hepatic protein measures with shorteralf-lives such as retinol binding protein and prealbuminould be useful in diagnosing acute changes in proteintatus Clinical signs of deficiency might be masked by thedipose tissue edema and general malaise experienced byhe bariatric patient It is not appropriate to assume that theatient that appears to look well has good nutritional statusnd appropriate dietary intake

ostoperative risk

Protein deficiency (albumin 35 gdL) is not commonfter RYGB Brolin et al [84] reported that 13 of patientsho had undergone distal RYGB as part of a prospective

andomized study were found to have hypoalbuminemia twoears after surgery Those with short Roux limbs (150 cm)ere not found to have decreased albumin levels [84] In

nother prospective randomized study of long-limb superbese gastric bypass patients protein deficiency was not foundn patients at a mean of 43 months postoperatively [156] Twoetrospective studies determined that hypoalbuminemia (de-ned as albumin 40 gdL in one and 30 gdL in thether) was negligible in both RYGB and BPD patients oneo two years postoperatively [88157] The investigatorsoted the few cases of hypoalbuminemia that did occuresulted from patient ldquononcompliancerdquo with nutrition in-truction and were treated with protein supplementation Inddition no evidence of protein or energy malnutrition wasound by Avinnoah et al [158] six to eight years afterYGB despite a high prevalence of long-term meat intol-rance among the subjects

Protein deficiency is more likely to be noted in publishedtudies in association with BPD procedures usually duringhe first or second year postoperatively Sporadic cases ofecurrent late PM have been reported requiring two to threeeeks of parenteral feeding for correction The pathogene-

is of this PM after BPD is multifactorial Operation-relatedariables include stomach volume intestinal limb lengthndividual capacity of intestinal absorption and adaptations well as the amount of endogenous nitrogen loss Patient-elated variables include customary eating habits ability todapt to the nutrition requirements and socioeconomic sta-us Early occurrences of PM are typically due to patient-elated factors and recurrent late episodes of PM are moreikely to be caused by excessive malabsorption as a result ofurgery Correction in these cases typically requires elon-ation of the common limb [34] By varying the length ofhe intestinal limbs and common channel protein malab-

orption can be increased or decreased [35]

[ntnriasiB(cdip

afedmvfllBrpem

D1mypei

iecalbcBmpmtta

ciru

iipafcfui

foaowppartptpthc

P

iwEvln6wdeapctnstat

S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

uat1m3mtfc

M

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aebaaa

apcptaasosdbc

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TI

Ia

HILLMPTTV

TC

P

C

C

A

H

S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

paswaimpp

C

pncaallbscb

F

cuucadmtrp

P

btscdedisft

M

mctgai

D

u

S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

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[

[

[

[

[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

s

aildquo

T

T

DFF

F

E

A

D

T

T

P

DFF

S

D

T

S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

DFF

S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 22: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S94 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

In a controlled environment (n 15) Scopinaro et al159] found intestinal albumin absorption to be 73 anditrogen absorption 57 after BPD This indicates greaterhan normal loss of endogenous nitrogen The investigatorsoted that the percentage of nitrogen absorption tended toemain constant when intake varied Therefore an increasen alimentary protein intake would result in an increasedbsolute amount absorbed They postulated that the ob-erved 30 protein malabsorption that had been identifiedn previous studies did not explain the PM that occurs afterPD It was concluded that loss of endogenous nitrogen

approximately fivefold the normal value) plays a signifi-ant role in the development of PM after BPD especiallyuring the early postoperative period when restricted foodntake might cause a negative balance in both calories androtein [159]

The incidence of PM after BPD has been reported to bepproximately 7ndash21 [35] However Totte et al [160]ollowed 180 BPD patients (using the method of Scopinarot al [35] with a 50-cm common channel) and found proteineficiency developed in only two patients at 16 and 24onths postoperatively requiring parenteral nutrition con-

ersion of the alimentary tract and psychiatric counselingor correction Both cases were attributed to causes unre-ated to the operation that had disrupted the patientsrsquo normalife It was concluded that metabolic complications afterPD were the result of patient noncompliance with dietary

ecommendations (70ndash80 gd protein) that had been ex-lained during preoperative counseling by a Registered Di-titian [160] Marinari et al [161] reported mild hypoalbu-inemia in 11 and severe in 24 of BPD patientsRabkin et al [155] followed a cohort of 589 sequential

S patients (with a gastric sleeve and common channel of00 cm) and found annual laboratory measures of serumarkers for protein metabolism to slightly decrease at one

ear postoperatively but then stabilize at two and three yearsostoperatively well within normal limits Similarly in anarlier study Marceau et al [162] also reported no signif-cant decrease in albumin levels among BPDDS patients

Body composition has also been studied postoperativelyn malabsorptive and restrictive surgical patients Tacchinot al [163] studied changes in total and segmental bodyomposition in 101 women preoperatively and at 2 6 12nd 24 months after BPD A significant reduction in fat andean body mass was observed postoperatively that stabilizedetween 12ndash24 months at levels similar to those of theontrols The investigators concluded that weight loss afterPD was achieved with an appropriate decline of lean bodyass In addition the visceralmuscle ratio in pre-BPD

atients was preserved in the post-BPD patients at 24onths [163] Benedetti et al [164] studied body composi-

ion and energy expenditure after BPD (n 30) and foundhat after one year of weight stabilization the subjects had

greater fat free mass and basal metabolic rate then did the [

ontrols The postoperative patients had an increased caloricntake and physical activity expenditure This aided in theetention of the fat free mass after weight loss and contrib-ted to the greater basal metabolic rate [164]

Because AGB patients have weight loss due to a signif-cant reduction in caloric intake and can experience foodntolerances leading to aversion of protein foods it is im-ortant to consider the loss of body protein in these patientss well A small series (n 17) of AGB patients wereollowed for two years postoperatively Total weight lossonsisted of 301 fat mass and a 123 reduction in fatree mass No significant change was found in the potassi-mnitrogen ratio after surgery and the loss of fat mass wasn proportion to that usually seen in weight loss [165]

When a deficiency occurs and no mechanical explanationor vomiting or food intolerance is present patients canften be successfully treated with a high-protein liquid dietnd slow progression to a regular diet [76] Reinforcementf proper eating style (small bites of tender food chewedell eaten slowly) is always important to address duringatient consultation in an effort to improve intake As therotein deficiency is corrected and edema is decreasedround the anastomosis food tolerance and vomiting mayesolve Although rare severe PM can occur regardless ofhe type of surgery performed This typically requires hos-italization parenteral treatment to sufficiently return theotal body protein to normal levels and might warrantsychological evaluation andor counseling It is importanto rule out all the possible underlying mechanical and be-avioral causes before considering lengthening the commonhannel or surgery reversal

rotein intake

Current clinical practice recommendations for proteinntake after surgery without complications are consistentith those for medically supervised modified protein fastsxperts recommend up to 70 gd during weight loss onery-low-calorie diets [167] The recommended dietary al-owance (RDA) for protein is approximately 50 gd forormal adults [166] Many programs recommend a range of0ndash80 gd total protein intake or 10ndash15 gkg ideal bodyeight (IBW) although the exact needs have yet to beefined The use of 15 g of proteinkg IBWday after thearly postoperative phase is probably greater than the met-bolic requirements for noncomplicated patients and mightrevent the consumption of other macronutrients in theontext of volume restriction An analysis of RYGB pa-ientrsquos typical nutrient intake at one year post surgery foundo significant changes in albumin with daily protein con-umption at 11 gkg IBW [168] After BPDDS procedureshe amount of protein should be increased by 30 toccommodate for malabsorption making the average pro-ein requirement for these patients approximately 90 gd

36]

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S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

Ye

No

No

Va

Tpmtsw

cmostHwisnahprcqct

parWwcaiibmcmTa

D

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S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 23: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S95L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

During the early postoperative period incorporating liq-id supplements into the patientrsquos daily oral intake providesn important source of calories and protein that help preventhe loss of lean body mass Experts have noted that adding00 gd of carbohydrate decreases nitrogen loss by 40 inodified protein fasts [34] One popular myth is that only

0 ghr of protein can be absorbed Although this is com-only found in both lay and some professional literature

here is no scientific basis for this claim It is possible thatrom a volume standpoint patients might only realisticallyonsume 30 gmeal of protein during the first year

odular protein supplements

It is commonly known that adequate dietary intake isequired to supply the 9 indispensable (essential) aminocids (IAAs) and adequate substrate for the production ofhe 11 dispensable (nonessential) amino acids that composeody protein This is referred to as the nonspecific nitrogenequirement In the presence of physiologic stress or certainisease states the body cannot produce enough of certainispensable amino acids to satisfy onersquos need To this end

able 6ndispensable and Dispensable Amino Acids [169]

ndispensablemino acids

EAR(mgg pro)

Dispensable aminoacids

Conditionallyindispensableamino acids

istidinesoleucineeucineysineethionine

henylalaninehreonineryptophanaline

172352472341246

29

AlanineAspartic acidAsparagineArginineCysteine (23)Glutamic acidGlutamineGlycineProlineSerineTyrosine

ArginineCysteineGlutamineGlycineProlineTyrosine (41)

EAR estimated average requirement

able 7ategories of Modular Protein Supplements

rotein category Derived from

omplete proteinconcentrates

Egg white soy or milk (caseinwhey fractions)

ollagen-basedconcentrates

Hydrolyzed collagen some are combined withcasein or other complete proteins

mino acid dose Large doses of 1 DAAs (ie arginineglutamine) or amino acid precursors

ybrids of proteinplus an aminoacid dose

Complete protein concentrate or collagen baseplus 1 DAAs

IAAs indispensable amino acids DAAs dispensable amino acids

Adapted from Castellanos et al [170] with permission

third category of conditionally indispensable amino acidsxists potentially increasing the bodyrsquos protein requirementeyond the RDA The Institutes of Medicine has establishedn estimated average requirement (EAR) for the essentialmino acids that may be used as a reference value whenssessing protein supplements (Table 6)

Commercially produced modular protein supplementsre widely available that can be used to complement aatientrsquos dietary intake after surgery Clinicians are oftenhallenged when choosing the best product to meet theatientrsquos nutritional needs Although convenience tasteexture ease in mixing and price are important consider-tions that may improve intake compliance the productrsquosmino acid profile should be the first priority A proteinupplement that provides all the indispensable amino acidsr a combination of products must be used when proteinupplements are the sole source of dietary protein intakeuring rapid weight loss Reputable manufacturers shoulde able to provide accurate information substantiatinglaims made about the amino acid profile of their products

In a comprehensive review completed by Castellanos etl [170] modular protein supplements were classified intoour categories (Table 7) They noted that the amino acidontent of various protein supplements differs dramaticallyn that a given quantity of a supplement from one categorys not nutritionally equivalent to the same quantity of pro-ein from a different category Although peer-reviewed datao not exist to determine the quality of the various com-ercial products through traditional methods such as net

rotein use biologic value and protein efficiency ratiohese assessments have been conducted on the commonrotein sources used in commercial products (ie wheyasein egg soy) In 1991 the ldquoprotein digestibility cor-ected amino acidrdquo (PDCAA) score was established as auperior method for the evaluation of protein qualityDCAAs compare the IAA content of a protein to theAR for each IAA mgg of protein (The EAR referencealues used to calculate PDCAAs are noted in Table 6)

mplete Intended use

s contains all 9 IAAs relative tohuman requirement

Provides IAAs in dietary protein

contains low levels of 8 of 9IAAmdashlacks tryptophan

Provides DAAs in dietaryprotein contains highproportion of nitrogen insmall volume

Provides conditionally IAAspromotes wound healing

ries Meets protein needs andincreases intake ofconditionally IAAs

Co

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S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

[

[

[

[

[

[

[

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[

[

[

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S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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D

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c

T

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DFF

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T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

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D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 24: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S96 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

he PDCAA score indicates the overall quality of arotein because it represents the relative adequacy of itsost limiting amino acid The PDCAA score indicates

he bodyrsquos ability to use that product for protein synthe-is The PDCAA score is equal to 100 for milk caseinhey egg white and soy [170]Caution should be used when recommending any type of

ollagen-based protein supplement Although some com-ercial collagen products can be combined with casein or

ther complete proteins the resulting combination mighttill provide insufficient amounts of several IAAs Theseypes of products are typically not considered ldquocompleterdquoowever because collagen contains a high level of nitrogenithin a small volume it might be useful for the patient who

s able to consume enough good-quality dietary protein toupply the needed IAAs yet not be consuming enough totalitrogen to meet the nonspecific nitrogen requirement andchieve balance [171] In this case the patient would alsoave to be consuming enough calories to spare the IAAs forrotein synthesis It is very important for the practitioner toeview the amino acid composition of the patientrsquos selectedommercial protein products to ensure they include ade-uate amounts of all the IAAs The loss of lean body massan occur despite meeting a daily oral intake protein goal inhe presence of IAA deficiency

The highest quality protein products are made of wheyrotein which provides high levels of branched-chainmino acids (important to prevent lean tissue breakdown)emain soluble in the stomach and are rapidly digested

hey concentrates can contain varying amounts of lactosehile whey protein isolates are lactose free This can be a

onsideration for those individuals with a severe intoler-nce Meal replacement supplements and protein bars typ-cally contain a blend of whey casein and soy proteins (tomprove texture and palatability) varying amounts of car-ohydrate and fiber as well as greater levels of vitamins andinerals than simple protein supplements Many commer-

ial protein drinks and bars are designed to supplement aixed diet including animal and plant sources of proteinhey are not intended to provide the sole source of proteinnd calories for long periods of time

iet and texture progression

The purpose of nutrition care after surgical weight lossrocedures is twofold First adequate energy and nutrientsre required to support tissue healing after surgery and toupport the preservation of lean body mass during extremeeight loss Second the foods and beverages consumed

fter surgery must minimize reflux early satiety and dump-ng syndrome while maximizing weight loss and ulti-ately weight maintenance Many surgical weight loss

rograms encourage the use of a multiphase diet to accom-

lish these goals d

lear liquid diet

A clear liquid diet is often used as the first step inostoperative nutrition despite some evidence that it mightot be warranted [172] Sugar-free or low sugar bariatriclear liquid diets supply fluid electrolytes and a limitedmount of energy and encourage the restoration of gutctivity after surgery The foods that are included in cleariquid diets are typically liquid at body temperature andeave a minimal amount of gastrointestinal residue Gastricypass clear liquid diets are nutritionally inadequate andhould not be continued without the inclusion of commer-ial low-residue or clear liquid oral nutrition supplementseyond 24ndash48 hours

ull liquid diet

Sugar-free or low-sugar full liquid diets often follow thelear liquid phase Full liquid diets include milk milk prod-cts milk alternatives and other liquids that contain sol-tes Full liquid diets have slightly more texture and in-reased gastric residue compared with clear liquid diets Inddition the calories and nutrients provided by full liquidiets that include protein supplements can closely approxi-ate the needs of surgical weight loss patients The liquid

exture is thought to further allow healing and the caloricestriction provides energy and protein equivalent to thatrovided by very-low-calorie diets

ureed diet

The bariatric pureed diet consists of foods that have beenlended or liquefied with adequate fluid resulting in foodshat range from milkshake to pudding to mash potato con-istency In addition foods such as scrambled eggs andanned fish (tuna or salmon) can be incorporated into theiet Fruits and vegetables may be included although themphasis of this phase is usually on protein-rich foods Thisiet fosters additional tolerance of a gradually progressivencrease in gastric residue and gut tolerance of increasedolute and fiber The protein supplements used during theull liquid phase are often continued during the puree phaseo complement dietary protein intake

echanically altered soft diet

The bariatric soft diet provides foods that are texture-odified require minimal chewing and that will theoreti-

ally pass easily from the gastric pouch through the gas-rojejunostomy into the jejunum or through the adjustableastric band This diet is considered a transition diet that ischieved by chopping grinding mashing flaking or puree-ng foods [173]

iet and texture progression survey

Given the limited availability of research to support these of multiphase diets after surgical weight loss proce-

ures dietitians who were members of the American Soci-

eicmsS

DnMarc

PplrT(piBc2np

Dupgfsfdfa

ftcsas

popa

1picc

gcsac

ddcsdoAwas

awdmarb

pppw

TCN

D

CFPMR

TR

F

S

CFHSTNC

S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

pTtvs

FattsroihtIamwcrc

Dmdcn4pm1[

C

twsottCaectnpupu

A

itteNampStccap

D

BAci

R

S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

DFF

S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 25: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S97L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ty for Metabolic and Bariatric Surgery were surveyed us-ng an on-line survey in May 2007 to determine currentlinical practice with regard to texture and diet advance-ent Overall 68 dietitians responded to the survey repre-

enting 50 of the dietitian membership within Americanociety for Metabolic and Bariatric Surgery

emographics Most of the respondents were from commu-ity hospitals (50) and academic medical centers (24)ost of the programs surveyed performed 101ndash300 RYGBs

nd 50 AGBs annually Most of the programs (62)eported that their institution did not perform BPDDS pro-edures or performed 50yr (31)

ouch size and limb lengths The most commonly reportedouch size for RYGB was 30ndash39 cm3 (54) with a Rouximb length of 70 to 100 cm (44) Nearly 38 ofespondents reported that the limb length was 125ndash150 cmhe most common pouch size for AGB was 30ndash39 cm3

37) however almost 19 of respondents could not re-ort the pouch size most commonly created by the surgeonsn their respective programs For those programs offeringPDDS the most common pouch size was 120 to 180m3 (55) The common channel was reported to be 101ndash00 cm (34) by most respondents however 28 couldot identify the length of the common channel used by theirrogram

iet phases The dietitians reported that multiple phases aresed for postoperative recommendations Most programs re-orted clear liquid (95) full liquid (94) puree (77)round or soft (67) and ultimately regular diets with sugarat andor fiber restrictions (87) For the purposes of theurvey it was assumed that each progressive phase allowedoods from earlier phases Thus items allowed on a clear liquidiet were assumed to be included in a full liquid diet and soorth For example protein supplements were commonly listeds being included in all phases of diet progression

Clear liquid diets were reported by most programs to lastor 1ndash2 days for both RYGB (60) and AGB (40) pa-ients The foods commonly reported to be included in thelear liquid diet were diet gelatin broth sugar-free pop-icles decafherbal teas artificially sweetened beveragesnd protein supplements Although regular juices contain

able 8urrent Texture Advancement in Clinical Practice foroncomplicated Patients

iet phase Duration(d)

lear liquid 1ndash2ull liquid 10ndash14uree 10ndash14echanically altered soft 14egular mdash

ignificant amounts of fruit sugar 40 of respondents re-A

orted that diluted fruit juice was offered during this phasef the diet Caution should be used when encouraging sim-le carbohydrate intake because this could facilitate gutdaptation

Full liquid diets were most commonly advised for0 ndash14 days for both RYGB (38) and AGB (28)atients Common foods included in the full liquid dietncluded milk and alternatives vegetable juice artifi-ially sweetened yogurt strained cream soups creamereals and sugar-free puddings

Pureed diets were most commonly reported as beingiven for 10 days for RYGB and AGB The foods mostommonly included in the puree phase were reported to becrambled eggs and egg substitute pureed meat flaked fishnd meat alternatives pureed fruits and vegetables softheeses and hot cereal

Most respondents reported that a traditional ldquogroundietrdquo was not included in the diet progression Instead a softiet that included mechanically altered meats was mostommonly recommended Traditionally a ldquosoft dietrdquo con-ists of low-residue foods however for surgical weight lossiets the term ldquosoftrdquo most commonly relates to the texturef the food rather than residue Both RYGB (55) andGB (42) diet progressions most commonly included14 days of a soft diet Foods included in the soft diet phaseere ground and chopped tender cuts of meats and meat

lternatives canned fruit soft fresh fruit canned vegetablesoft cooked vegetables and grains as tolerated

Most of the programs reported that diet advancement tosurgical weight loss regular diet occurred after eight

eeks for RYGB and after six to eight weeks for AGB Theiets for RYGB and AGB were strikingly similar as sum-arized in Table 8 This was perhaps a result of program

dministration and resource constraints or could have beenelated to the limited number of AGB procedures performedy the institutions responding to the survey

Similar to AGB and RYGB programs offering DSBPDrocedures reported that the clear liquid diet phase is em-loyed for one to two days after surgery The full liquidhase was most commonly noted to last 10 to 14 dayshile the pureed phase was reported to be 14 days Most

able 9ecommended Foods to Avoid or Delay Reintroduction

ood type Recommendation

ugar sugar-containing foodsconcentrated sweets

Avoid

arbonated beverages Avoiddelayruit juice Avoidigh-saturated fat fried foods Avoidoft ldquodoughyrdquo bread pasta rice Avoiddelayough dry red meat Avoiddelayuts popcorn other fibrous foods Delayaffeine Avoiddelay in moderation

lcohol Avoiddelay in moderation

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S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

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[

[

[

[

[

[

[

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[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

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[

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[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

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[

[

[

[

[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

s

aildquo

T

T

DFF

F

E

A

D

T

T

P

DFF

S

D

T

S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

DFF

S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 26: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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FattsroihtIamwcrc

Dmdcn4pm1[

C

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D

BAci

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S98 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

rograms report that a ground texture phase is not utilizedhe soft diet phase was reported to last 14 days Finally

hose programs offering DSBPD most often reported ad-ancing patients to a regular diet five to eight weeks afterurgery

oods commonly restricted The American Society for Met-bolic and Bariatric Surgery members reported in the surveyhat patients were instructed to avoid or delay the introduc-ion of several foods as noted in Table 9 Research toupport these clinical practices is limited especially withegard to caffeine and carbonation Practitioners might the-rize that certain foods and beverages will cause gastricrritation outlet obstruction intolerance delayed woundealing or alter the weight loss course however much ofhe information is anecdotal and lacks empirical evidencen addition although practitioners recommend that patientsvoid or delay the introduction of these foods little infor-ation is known as to whether patients actually complyith these recommendations and whether those who do not

omply have altered outcomes or clinical histories Oneetrospective survey suggested that many patients are non-ompliant with diet and exercise recommendations [174]

iet advancement and nutrition intervention Diet advance-ent was most commonly advised at the discretion of the

ietitians (74) however other members of the team in-luding the surgeon nurse or midlevel provider were alsooted to make recommendations for advancement Almost0 of respondents reported that patients followed a writtenrotocol for diet advancement Nutrition interventions wereost commonly conducted as individual appointments at

ndash2 weeks 1 2 3 6 and 9 months and then annually175]

onclusion

It was the intent of this paper to serve as an educa-ional tool for not only dietitians but all those providersorking with patients with severe obesity Current re-

earch and expert opinion were reviewed to provide anverview of the elements that are important to the nutri-ional care of the bariatric patient While the extent ofhis paper has been broad the Allied Health Executiveouncil of the American Society for Metabolic and Bari-tric Surgery realizes there are many areas for futurexpansion that may change the paradigm for nutritionalare The Ad Hoc Nutrition Committee sincerely hopeshat this document will serve to elucidate the generalutrition knowledge necessary for the care of the pre- andostoperative patient with consideration for the individ-al patientrsquos unique medical needs as well as the variablerotocol established among surgical centers and individ-

al practices

cknowledgments

We would like to thank Dr Harvey Sugerman for allow-ng the use of the following manuscript cited in the bookitled ldquoManaging Morbid Obesityrdquo as the starting point forhis paper Blankenship J Wolfe BM Nutrition and Roux-n-Y Gastric Bypass Surgery In Sugerman HJ NguyenT eds Management of morbid obesity New York Taylor

Francis 2006 We thank our senior advisors Scotthikora MD FACS and Bill Gourash NP-C for

heir advice and support We also thank the American So-iety for Metabolic and Bariatric Surgery Executive Coun-il the Allied Health Executive Council the Foundationnd the Corporate Council for their commitment to theublication of this white paper

isclosures

J Blankenship is on the Medical Advisory Board forariMD and the Advisory Board for Celebrate Vitamins Lills C Buffington M Furtado and J Parrott claim noommercial associations that might be a conflict of interestn relation to this article

eferences

[1] Cottam DR Atkinson JA Anderson A Grace B Fisher B Acase-controlled matched-pair cohort study of laparoscopic Roux-en-Y gastric bypass and Lap-Bandreg patients in a single US centerwith three-year follow-up Obes Surg 200616534ndash40

[2] Cummings DE Shannon MH Ghrelin and gastric bypass is there ahormonal contribution to surgical weight loss J Clin EndocrinolMetab 2003882999ndash3002

[3] Position of the American Dietetic Association Weight Manage-ment J Am Diet Assoc 20021021145ndash55

[4] Dietal M Recommendations for reporting weight loss Obes Surg200313159ndash60

[5] Buchwald H Avidor Y Braunwald E et al Bariatric surgery asystematic review and meta-analysis JAMA 20042921724ndash37

[6] MacLean LD Rhode BM Samplais J et al Results of the surgicaltreatment of obesity Am J Surg 1993165155ndash9

[7] Kuczmarski RJ Carrol MD Flegal KM et al Varying body massindex cutoff points to describe overweight prevalence among USadults NHANES III (1988 to 1944) Obes Res 19975542ndash8

[8] Neidman DC Trone GA Austin MD A new handheld device formeasuring resting metabolic rate and oxygen consumption J AmDiet Assoc 2003103588

[9] Hsu LK Sullivan SP Benotti PN Eating disturbances and outcomeof gastric bypass surgery a pilot study Int J Disord 199721385ndash90

[10] Saunders R Grazing A High risk behavior Obes Surg 20041498ndash102

[11] Malone M Alger-Mayer S Binge status and quality of life aftergastric bypass surgery a one-year study Obes Res 200412473ndash81

[12] Marcus E Bariatric surgery the role of the RD in patient assessmentand management SCANrsquos Pulse a newsletter of the Sports Car-diovascular and Wellness Nutrition Practice Group of the AmericanDietetic Association 200524(2)18ndash20

[13] National Institutes of HealthNational Heart Lung and Blood Insti-tute North American Association for the Study of Obesity in Adults

Bethesda National Institutes of Health 2000

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

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[

[

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[

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[

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[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

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T

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F

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A

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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c

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S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

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S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

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T

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D

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S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 27: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

S99L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[14] Ray EC Nickels NW Sayeed S et al Predicting success aftergastric bypass the role of psychological and behavioral factorsSurgery 2003134555ndash63

[15] Rosal MC Ebbeling CB Lofgren I et al Facilitating dietarychange the patient centered counseling model J Am Diet Assoc2001101332ndash41

[16] Wing RR Hill JD Successful weight loss maintenance Annu RevNutr 200121323

[17] Harrisonrsquos on line Disorders of vitamin and mineral metabolismidentifying vitamin deficiencies Available from httpwwwMerckMedicuscom Accessed November 17 2006

[18] AGA AGA technical review of short bowel syndrome and intestinaltransplantation Gastroenterology 20031241111ndash34

[19] Buffington CK Walker B Cowan GS et al Vitamin D deficiency inthe morbidly obese Obes Surg 19933421ndash4

[20] Ybarra J Sanchez-Hernandez J Vich I et al Unchanged hypovita-minosis D and secondary hyperparathyroidism in morbid obesityalter bariatric surgery Obes Surg 200515330ndash5

[21] Flancbaum L Belsley S Drake V et al Preoperative nutritionalstatus of patients undergoing Roux-en-Y gastric bypass for morbidobesity J Gastrointest Surg 2006101033ndash7

[22] Carlin AM Rao DS Meslemani AM et al Prevalence of vitamin-osis D depletion among morbidly obese patients seeking bypasssurgery Surg Obes Related Dis 2006298ndash103

[23] El-Kadre LJ Roca PR de Almeida Tinoco AC et al Calciummetabolism in pre and postmenopausal morbidly obese women atbaseline and after laparoscopic Roux-en-Y gastric bypass ObesSurg 2004141062ndash6

[24] Schrager S Dietary calcium intake and obesity J Am Board FamPract 200518205ndash10

[25] Zemel MB Richards J Mathis S Milstead A Gebhardt Silva EDairy augmentation of total and central fat loss in obese subjects IntJ Obes 200529391ndash7

[26] Boylan LM Sugerman HJ Driskell JA Vitamin E vitamin B-6vitamin B-12 and folate status of gastric bypass surgery patientsJ Am Diet Assoc 198888579ndash85

[27] Madan AK Orth WS Tichansky DS Ternovits CA Vitamin andtrace mineral levels after laparoscopic gastric bypass Obes Surg200616603ndash6

[28] Reitman A Friedrich I Ben-Amotz A Levy Y Low plasma anti-oxidants and normal plasma B vitamins and homocysteine in pa-tients with severe obesity Isr Med Assoc J 20024590ndash3

[29] Alvarez-Leite JI Nutrient deficiencies secondary to bariatric sur-gery Curr Opin Clin Nutr Metab Care 20047569ndash75

[30] Bloomberg RD Fleishman A Nalle JE et al Nutritional deficien-cies following bariatric surgery what have we learned Obes Surg200515145ndash54

[31] Malinowski SS Nutritional and metabolic complications of bariatricsurgery Am J Med Sci 2006331219ndash25

[32] Brolin RE Gorman RC Milgrim LM Kenler HA Multivitaminprophylaxis in prevention of post-gastric bypass vitamin and mineraldeficiencies Int J Obes 199115661ndash7

[33] Gasteyger C Suter M Calmes JM Gaillard RC Giusti V Changesin body composition metabolic profile and nutritional status 24months after gastric banding Obes Surg 200616243ndash50

[34] Scopinaro N Adami GF Marinari GM et al Biliopancreatic diver-sion World J Surg 199822936ndash46

[35] Scopinaro N Gianetta E Adami GF et al Biliopancreatic diversionfor obesity at eighteen years Surgery 1996119261ndash8

[36] Slater GH Ren CJ Seigel N et al Serum fat-soluble vitamindeficiency and abnormal calcium metabolism after malabsorptivebariatric surgery J Gastrointest Surg 2004848ndash55

[37] Halverson JD Micronutrient deficiencies after gastric bypass for

morbid obesity Am Surg 198652594ndash8

[38] Avinoah E Ovant A Charuzi I Nutrition status seven years afterRoux-en-Y gastric bypass surgery Surgery 1992111137ndash42

[39] Rhode BM Shustik C Christou NV et al Iron absorption andtherapy after gastric bypass Obes Surg 1999917ndash21

[40] Salas-Salvado J Garcia-Lourda P Cuatrecasas G et al Wernickersquossyndrome after bariatric surgery Clin Nutr 200012371ndash3

[41] Loh Y Watson WD Verma A et al Acute Wernickersquos encepha-lopathy following bariatric surgery clinical course and MRI corre-lation Obes Surg 200414129ndash32

[42] Chaves L Faintuch J Kahwage S et al A cluster of polyneuropathyand Wernicke-Korsakoff syndrome in a bariatric unit Obes Surg200212328ndash34

[43] Sola E Morillas C Garzon S et al Rapid onset of Wernickersquosencephalopathy following gastric restrictive surgery Obes Surg200313661ndash2

[44] Bradley EL Issacs J Hersh T et al Nutritional consequences oftotal gastrectomy Ann Surg 1975182415ndash29

[45] OrsquoBrien DP Nelson LA Huang FS et al Intestinal adaptationstructure function and regulation Semin Pediatr Surg 20011056ndash64

[46] Higdon H Thiamin The Linus Pauling Institute Micronutrient Infor-mation Center Available from httplpioregonstateeduinfocentervitaminsthiaminindexhtml Accessed September 20 2006

[47] National Institutes of Health Beriberi Available from httpwwwnlmnihgovmedlineplusencyarticle000339htm Accessed Sep-tember 20 2006

[48] National Institutes of Health Wernick-Korsakoff syndrome Avail-able from httpwwwnlmnihgovmedlineplusencyarticle000771htm Accessed September 20 2006

[49] Koffman BM Greenfield LJ Ali II Pirzada NA Neurologic com-plications after surgery for obesity Muscle Nerve 200633166ndash76

[50] Gollobin C Marcus W Bariatric beriberi Obes Surg 200212309ndash11

[51] Nautiyal A Singh S Alaimo D Wernicke encephalopathymdashanemerging trend after bariatric surgery Am J Med 2004117804ndash5

[52] Carrodeguas L Kaidar-Person O Szomstein S Antozzi P Preop-erative thiamin deficiency in obese population undergoing laparo-scopic bariatric surgery Surg Obes Relat Dis 20051517ndash22

[53] Seehra H MacDermott N Lascelles RG Taylor TV Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity BMJ 1996312434

[54] Munoz-Farjas E Jerico I Pascual-Millan LF Mauri JA Morales-Asin F Neuropathic beriberi as a complication of surgery of morbidobesity Rev Neurol 199624456ndash8

[55] Christodoulakis M Maris T Plaitakis A et al Wernickersquos enceph-alopathy after vertical banded gastroplasty for morbid obesity EurJ Surg 1997163473ndash4

[56] Toth C Voll C Wernickersquos encephalopathy following gastroplastyfor morbid obesity Can J Neurol Sci 20012889ndash92

[57] Fawcett S Young GB Holliday RL Wernickersquos encephalopathyafter gastric partitioning for morbid obesity Can J Surg 198427169ndash70

[58] Oczkowski WJ Kertesz A Wernickersquos encephalopathy after gas-troplasty for morbid obesity Neurology 19853599ndash101

[59] Abarbanel J Berginer V Osimani A et al Neurologic complica-tions after gastric restriction surgery for morbid obesity Neurology198737196ndash200

[60] Houdent C Verger N Courtois H Ahtoy P Teniere P Wernickersquosencephalopathy after vertical banded gastroplasty for morbid obe-sity Rev Med Interne 200324476ndash7

[61] Cirignotta F Manconi M Mondini S Buzzi G Ambrosetto PWernicke-Korsakoff encephalopathy and polyneuropathy after gas-troplasty for morbid obesity report of a case Arch Neurol 2000

571356ndash9

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

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S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

s

aildquo

T

T

DFF

F

E

A

D

T

T

P

DFF

S

D

T

S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

DFF

S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 28: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

[

[

[

[

[

[

[

[

[

S100 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

[62] Bozboa A Coskun H Ozarmagan S et al A rare complication ofadjustable gastric banding Wernickersquos encephalopathy Obes Surg200019274ndash5

[63] Wadstrom C Backman L Polyneuropathy following gastric band-ing for obesity Case report Acta Chir Scand 198955131ndash4

[64] Angstadt JD Bodziner RA Peripheral polyneuropathy from thiamindeficiency following laparoscopic Roux-en-Y gastric bypass ObesSurg 200515890ndash92

[65] Nakamura D Roberson E Reilly L et al Polyneuropathy followinggastric bypass surgery Am J Med 2003115679ndash80

[66] Escalona A Perez G Leon F et al Wernickersquos encephalopathy afterRoux-en-Y gastric bypass Obes Surg 2004141135ndash7

[67] Al-Fahad T Ismael A Soliman MO et al Very early onset ofWernickersquos encephalopathy after gastric bypass Obes Surg 200616671ndash2

[68] Maryniak O Severe peripheral neuropathy following gastric bypasssurgery for morbid obesity Can Med Assoc J 1984131119ndash20

[69] Alves LF Goncalves RMN Cordeiro GV Lauria MW Ramos AVBeriberi after bariatric surgery not an unusual complication ArqBras Endocrinol Metabol 200650564ndash8

[70] Worden RW Allen HM Wernickersquos encephalopathy after gastricbypass that masqueraded as acute psychosis Curr Surg 200663114ndash6

[71] Towbin A Inge TH Garcia VF et al Beriberi after gastric bypassin adolescence J Pediatr 2005146263ndash7

[72] Fandino JN Benchimol AK Fandino LN et al Eating avoidancedisorder and Wernicke-Korsakoff syndrome following gastric by-pass an under-diagnosed association Obes Surg 2005151207ndash12

[73] Kulkani S Lee AG Holstein SA Warner JE You are what you eatSurv Ophthalmol 200550389ndash93

[74] Primavera A Brusa G Novello P et al Wernicke-Korsakoff en-cephalopathy following biliopancreatic diversion Obes Surg 19983175ndash77

[75] Grace DM Alfieri MA Leung FY Alcohol and poor compliance asfactors in Wernickersquos encephalopathy diagnosed 13 years after gas-tric bypass Can J Surg 199841389ndash92

[76] Mason EE Starvation injury after gastric reduction for obesityWorld J Surg 1998221002ndash7

[77] Mahan LK Escott-Stump S eds Medical nutrition therapy foranemia Krausersquos food nutrition and diet therapy 10th edPhila-delphiaWB Saunders2000 p 781ndash99

[78] Ponsky TA Brody F Pucci E Alterations in gastrointestinal phys-iology after Roux-en-Y gastric bypass J Am Coll Surg 2005201125ndash31

[79] Charney P Malone A eds ADA pocket guide to nutrition assess-ment ChicagoAmerican Dietetic Association 2004

[80] Bauman WA Shaw S Jayatilleke K Spungen AM Herbert VIncreased intake of calcium reverses the B-12 malabsorption in-duced by metformin Diab Care 2000231227ndash31

[81] Skroubis G Anesidis S Kehagias L et al Roux-en-Y gastric bypassversus a variant of BPD in a non-superobese population prospectivecomparison of the efficacy and the incidence of metabolic deficien-cies Obes Surg 200616488ndash95

[82] Schilling RD Gohdes PN Hardie GH Vitamin B-12 deficiencyafter gastric bypass for obesity Ann Intern Med 1984101501ndash2

[83] Kushner R Managing the obese patient after bariatric surgery acase report of severe malnutrition and review of the literature JPENJ Parenter Enteral Nutr 200024126ndash32

[84] Brolin RE LaMarca LB Henler HA Cody RP Malabsorptivegastric bypass in patients with super-obesity J Gastrointest Surg20026195ndash203

[85] Rhode BM Arseneau P Cooper BA et al Vitamin B-12 deficiencyafter gastric surgery for obesity Am J Clin Nutr 199663103ndash9

[86] MacLean LD Rhode BM Shizgal HM Nutrition following gastric

operations for morbid obesity Ann Surg 1983198347ndash55

[87] Brolin RE Gorman JH Gorman RC et al Are vitamin B-12 andfolate deficiency clinically important after Roux-en-Y gastric by-pass J Gastrointest Surg 19982436ndash42

[88] Skroubis G Sakellarapoulos G Pouggouras K Comparison of nu-tritional deficiencies after Roux-en-Y gastric bypass and biliopan-creatic diversion with Roux-en-Y gastric bypass Obes Surg 200212551ndash8

[89] Fujioka K Follow-up of nutritional and metabolic problems afterbariatric surgery Diab Care 200528481ndash4

[90] Ocon Breton J Perez Naranjo S Gimeno Laborda S Benito RuescaP Garcia Hernandez R Effectiveness and complications of bariatricsurgery in the treatment of morbid obesity Nutr Hosp 200520409ndash14

[91] Sumner AE Elevated methylmalonic acid and total homocysteinelevels show high prevalence of vitamin B-12 deficiency after gastricsurgery Ann Intern Med 1996124469ndash76

[92] Crowley LV Olson RW Megaloblastic anemia after gastric bypassfor obesity Am J Gastroenterol 19833181720ndash8

[93] Smith CD Herkes SB Behrns KE et al Gastric acid secretion andvitamin B-12 absorption after vertical Roux-en-Y gastric bypass formorbid obesity Ann Surg 199321891ndash6

[94] Grange DK Finlay JL Nutritional vitamin B-12 deficiency in abreastfed infant following maternal gastric bypass Pediatr HematolOncol 199411311ndash8

[95] Kaplan LM Pharmacological therapies for obesity GastroenterolClin North Am 20053491ndash104

[96] Rhode BM Tamim H Gilfix MB Treatment of vitamin B-12deficiency after gastric bypass surgery for severe obesity Obes Surg19955154ndash8

[97] Herbert V Das KC Folic acid and vitamin B-12 In Shill MEOlson J Shike M eds Modern nutrition in health and disease 8thed Philadelphia Lea amp Febriger 1994 p 402ndash25

[98] Amaral JF Thompson WR Caldwell MD Martin HF Randall HTProspective hematologic evaluation of gastric exclusion surgery formorbid obesity Ann Surg 1985201186ndash93

[99] US Food and Drug Administration Food standards amendmentsof standards of identity for enriched grain products to require addi-tion of folic acid Fed Regist 1996618781ndash97

100] Bentley TGK Willett W Weinstein MC Kuntz KM Population-level changes in folate intake by age gender raceethnicity afterfolic acid fortification Am J Pub Health 2006962040ndash7

101] Dixon ME OrsquoBrien PE Elevated homocysteine levels with weightloss after Lap-Band surgery higher folate and vitamin B-12 levelsrequired to maintain homocysteine level Int J Obes Relat MetabDisord 200125219ndash27

102] Hirsch S Serum folate and homocysteine levels in obese femaleswith non-alcoholic fatty liver Nutrition 200521137ndash41

103] Mallory GN Macgregor AM Folate status following gastric bypasssurgery (the great folate mystery) Obes Surg 1991169ndash72

104] Carmel R Green R Rosenblatt DS Watkins D Update on cobal-amin folate and homocysteine Hematology 200362ndash81

105] Wood RJ Ronnenberg AG Iron In Shils ME Shike M Ross ACCaballero B Cousins RJ eds Modern nutrition in health and dis-ease 10th ed Philadelphia Lippincott Williams amp Wilkins 2006

106] Behrns KE Smith CD Sarr MG Prospective evaluation of gastricacid secretion and cobalamin absorption following gastric bypass forclinically severe obesity Digest Dis Sci 199439315ndash20

107] Brolin RE Gorman JH Gorman RC et al Prophylactic iron sup-plementation after Roux-en-Y gastric bypass a prospective double-blind randomized study Arch Surg 1998133740ndash4

108] Halverson JD Zuckerman GR Koehler RE et al Gastric bypass formorbid obesity a medical-surgical assessment Ann Surg 1981194

152ndash60

[

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[

[

[

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[

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[

[

[

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[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

s

aildquo

T

T

DFF

F

E

A

D

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T

P

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S

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T

S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

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D

T

T

c

T

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DFF

S

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T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

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FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

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D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 29: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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S101L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

109] Kushner RF Shanta Retelny V Emergence of pica (ingestion ofnon-food substances) accompanying iron deficiency anemia aftergastric bypass surgery Obes Surg 2005151491ndash5

110] Hamoui N Anthone G Crookes P Calcium metabolism in themorbidly obese Obes Surg 2004149ndash12

111] Bell NH Epstein S Shary J Greene V Oexmann MJ Shaw SEvidence for alteration of the vitamin Dndashendocrine system in obesesubjects J Clin Invest 198576370ndash3

112] Compston JE Vedi S Ledger JE Webb A Gazet JC Pilkington TRVitamin D status and bone histomorphometry in gross obesity Am JNutr 1981342359ndash63

113] Wortsman J Matsuoka LY Chen TC Lu Z Holick MF Decreasedbioavailability of vitamin D in obesity Am J Nutr 200072690ndash3

114] Hey H Stokholm KH Lund B Lund B Sorensen OH Vitamin Ddeficiency in obese patients and changes in circulating vitamin Dmetabolism following jejunoileal bypass Int J Obes 19826473ndash9

115] Peterlik M Cross HS Vitamin D and calcium deficits predispose formultiple chronic diseases Eur J Clin Invest 200535290ndash304

116] Holik MF The vitamin D epidemic and its health consequences JNutr 20051352739Sndash48S

117] Newbury L Dolan K Hatzifotis M Fielding G Calcium and vita-min D depletion and elevated parathyroid hormone following bilio-pancreatic diversion Obes Surg 200313893ndash5

118] Hamoui N Kim K Anthone G Crookes PF The significance ofelevated levels of parathyroid hormone in patients with morbidobesity and after bariatric surgery Arch Surg 2003138891ndash7

119] Johnson JM Maher JW DeMaria EJ Downs RW Wolfe LGKellum JM The long term effects of gastric bypass on vitamin Dmetabolism Ann Surg 2006243701ndash4

120] Goode LR Brolin RE Chowdry HA Shapes SA Bone and gastricbypass surgery effects of dietary calcium and vitamin D Obes Res20041240ndash7

121] Coates PS Fernstrom JD Fernstrom MH Schauer PR GreenspanSL Gastric bypass surgery for morbid obesity leads to an increasein bone turnover and a decrease in bone mass J Clin EndocrinolMetab 2004891061ndash5

122] Reidt CS Brolin RE Sherrell RM Field PM Shapses SA Truefractional calcium absorption is decreased after Roux-en-Y gastricbypass surgery Obesity 2006141940ndash8

123] Pugnale N Giusti V Suter M et al Bone metabolism and risk ofsecondary hyperparathyroidism 12 months alter gastric banding inobese pre-menopausal women Int J Obes Relat Metab Disord 200327110ndash6

124] Giusti V Gasteyger C Suter M Heraief E Galliard RC BurckhardtP Gastric banding induces negative bone remodeling in the absenceof secondary hyperparathyroidism potential of serum telopeptidesfor follow-up Int J Obes 2005291429ndash35

125] Guney E Kisakol G Ozgen G Yilmaz C Yilmaz R Kabalak TEffect of weight loss on bone metabolism comparison of verticalbanded gastroplasty and medical intervention Obes Surg 200313383ndash8

126] Riedt CS Cifuentes M Stahl T Chowdhury HA Schlussel YShapses SA Overweight postmenopausal women lose bone withmoderate weight reduction and 1 gday calcium intake J BoneMineral Res 200520455ndash63

127] Golder WS OrsquoDorsio TM Dillon JS Mason EE Severe metabolicbone disease as a long-term complication of obesity surgery ObesSurg 200212685ndash92

128] Recker RR Calcium absorption and achlorhydria N Engl J Med198531370ndash3

129] Kenny AM Prestwood KM Biskup B et al Comparison of theeffects of calcium loading with calcium citrate or calcium carbonateon bone turnover in postmenopausal women Osteoporos Int 2004

4290ndash4

130] Sakhaee K Bhuket T Adams-Huet B Rao DS Meta-analysis ofcalcium bioavailability a comparison of calcium citrate with cal-cium carbonate Am J Ther 19996313ndash21

131] National Osteoporosis Foundation Risk factors for osteoporosisAvailable from httpnoforgpreventionriskhtml Accessed Octo-ber 16 2006

132] Collazo-Clavell ML Jimenez A Hodgson SF Sarr MG Osteoma-lacia alter Roux-en-Y gastric bypass Endocr Pract 200410195ndash198

133] National Institutes of Health Osteoporosis and related bone dis-easemdashNational Resource Center Available from httpwwwosteoorg Accessed October 16 2006

134] Dolan K Hatzifotis M Newbury L et al A clinical and nutritionalcomparison of biliopancreatic diversion with and without duodenalswitch Ann Surg 200424051ndash6

135] Ledoux S Msika S Moussa F et al Comparison of nutritionalconsequences of conventional therapy of obesity adjustable gastricbanding and gastric bypass Obes Surg 2006161041ndash9

136] Sugerman JH Kellum JM DeMaria EJ Conversion of proximal todistal gastric bypass for failed gastric bypass for superobesity JGastrointes Surg 19976517ndash25

137] Hatizifotis M Dolan K Newbury L et al Symptomatic vitamin Adeficiency following biliopancreatic diversion Obes Surg 200313655ndash7

138] Huerta S Rogers LM Li Z et al Vitamin A deficiency in a newbornresulting from maternal hypovitaminosis A after biliopancreaticdiversion for the treatment of morbid obesity Am J Clin Nutr200276426ndash9

139] Quaranta L Nascimbeni G Semeraro F et al Severe corneocon-junctival xerosis after biliopancreatic bypass for obesity (Scopin-arorsquos operation) Am J Ophthalmol 1994118817ndash8

140] Chae T Foroozan R Vitamin A deficiency in patients with a remotehistory of intestinal surgery Br J Ophthalmol 200690955ndash6

141] Lee WB Hamilton SM Harris JP Schwab IR Ocular complicationsof hypovitaminosis after bariatric surgery Ophthalmology 20051121031ndash4

142] Purvin V Through a shade darkly Surv Ophthalmol 199943335ndash40

143] Cone LA B Waterbor R Sofonia MV Purpura fulminans due toStreptococcus pneumoniae sepsis following gastric bypass ObesSurg 200414690ndash4

144] Cominetti C Garrido AB Jr Cozzolino SM Zinc nutritional statusof morbidly obese patients before and after Roux-en-Y gastric by-pass a preliminary report Obes Surg 200616448ndash53

145] Burge J Changes in patientsrsquo taste acuity after Roux-en-Y gastricbypass for clinically severe obesity J Am Diet Assoc 199595666ndash70

146] Scruggs DM Buffington C Cowan GS Taste acuity of the morbidlyobese before and after gastric bypass surgery Obes Surg 1994424ndash8

147] Turkki PR Ingerman L Schroeder LA Chung RS Chen M Dear-love J Plasma pyridoxal phosphate as indicator of vitamin B6 statusin morbidly obese women after gastric restriction surgery Nutrition19895229ndash35

148] Turkki PR Ingerman L Schroeder LA et al Thiamin and vitaminB6 intakes and erythrocyte transketolase and aminotransferase ac-tivities in morbidly obese females before and after gastroplastyJ Am Coll Nutr 199211272ndash82

149] Kumar N McEvoy KM Ahiskog JE Myelopathy due to copperdeficiency following gastrointestinal surgery Arch Neurol 2003601782ndash5

150] Kumar N Ahiskog JE Gross JB Jr Acquired hypocuremia after

gastric surgery Clin Gastroent Hepatol 200421074ndash9

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

s

aildquo

T

T

DFF

F

E

A

D

T

T

P

DFF

S

D

T

S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

DFF

S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 30: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

[

[

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[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

S102 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

151] Schauer PR Ikramuddin S Gourash W Ramanthan R Luketich JOutcomes after laparoscopic Roux-en-Y gastric bypass for morbidobesity Ann Surg 2000232515ndash29

152] Crowley LV Seay J Mullin G Late effects of gastric bypass forobesity Am J Gastroenterol 198479850ndash60

153] Mahan LK Escott-Stump S Krausersquos food nutrition and diettherapy 9th ed Philadelphia WB Saunders 1996

154] Shils ME Olson J Shike M Modern nutrition in health and disease8th ed Philadelphia Lea amp Febriger 1994

155] Rabkin RA Rabkin JM Metcalf B Lazo M Rossi M Lehman-Becker LB Nutritional markers following duodenal switch for mor-bid obesity Obes Surg 20041484ndash90

156] Brolin RE Kenler HA Gorman JH et al Long-limb gastric bypassin the superobese a prospective randomized study Ann Surg 1992215387ndash95

157] Skroubis G Stathis A Kehagias I et al Roux-en-Y gastricbypass versus a variant of biliopancreatic diversion in a non-superobese population prospective comparison of the efficacyand the incidence of metabolic deficiencies Obes Surg 200616488 ndash95

158] Avinnoah E Ovnat A Charuzi I Nutritional status seven years afterRoux-en-Y gastric bypass surgery Surgery 1990111137ndash42

159] Scopinaro N Marinari GM Camerini G et al Energy and nitrogenabsorption after biliopancreatic diversion Obes Surg 200010436ndash41

160] Totte E Hendrickx L van Hee R Biliopancreatic diversion fortreatment of morbid obesity experience in 180 consecutive casesObes Surg 19999161ndash5

161] Marinari GM Murelli F Camerini G et al A 15 year evaluation ofbiliopancreatic diversion according to the bariatric analysis report-ing outcome system (BAROS) Obes Surg 200414325ndash8

162] Marceau P Hould FS Simard S et al Biliopancreatic diversionwith duodenal switch World J Surg 199822947ndash54

163] Tacchino RM Mancini A Perrelli M et al Body compositionand energy expenditure relationship and changes in obese sub-jects before and after biliopancreatic diversion Metabolism

200352552ndash 8

164] Benedetti G Mingrone G Marcoccia S et al Body composition andenergy expenditure after weight loss following bariatric surgeryJ Am Coll Nutr 200019270ndash4

165] Strauss B Marks S Growcott J et al Body composition changesfollowing laparoscopic gastric banding for morbid obesity ActaDiabetol 200340S266ndash9

166] National Academy of Science Institute of Medicine Food andNutrition Board Dietary Reference Intake 2004 Available fromwwwnalusdagovfnic Accessed September 23 2007

167] Mahan LK Escott-Stump S Medical nutrition therapy for anemiaKrausersquos food nutrition and diet therapy 10th ed PhiladelphiaWB Saunders 2000 p 469

168] Moize V Geliebter A Gluck ME et al Obese patients have inad-equate protein intake related to protein intolerance up to 1 yearfollowing Roux-en-Y gastric bypass Obes Surg 20031323ndash8

169] Institute of Medicine of the National Academies Protein and aminoacids In Dietary reference intakes for energy carbohydrate fiberfat fatty acids cholesterol protein and amino acids Food andNutrition Board National Academy of Sciences Washington DCNational Academy Press 2005

170] Castellanos V Litchford M Campbell W Modular protein supplementsand their application to long-term care Nutr Clin Pract 200621485ndash504

171] Reeds P Dispensable and indispensable amino acids for humans JNutr 20001301835ndash40S

172] Jeffery KM Harkins B Cresci GA Martindale RG The clear liquiddiet is no longer a necessity in the routine postoperative manage-ment of surgical patients Am J Surg 199662167ndash70

173] American Dietetic Association Manual of clinical dietetics 6th edChicago American Dietetic Association 2000

174] Elkins G Whitfield P Marcus J Symmonds R Rodriguez J CookT Noncompliance with behavioral recommendations followingbariatric surgery Obes Surg 200515546ndash51

175] American Society for Metabolic and Bariatric Surgery Dietitiansurvey ASMBS members Unpublished data May 2007

176] Vitamins Food and Nutrition Board Dietary reference intakesrecommended intakes for individuals Bethesda Institutes of Med-

icine National Academy of Science 2004

AD

s

aildquo

T

T

DFF

F

E

A

D

T

T

P

DFF

S

D

T

S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

DFF

S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 31: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

AD

s

aildquo

T

T

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F

E

A

D

T

T

P

DFF

S

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S103L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

ppendix Identifying and Treating MicronutrienteficienciesTables A1 through A11 list by micronutrient the

ources functions interactions symptoms of deficiency f

RBC red blood cell

reatment Vitamin B6 50 mgd 100ndash200 mg if deficiency relate

nd recommended treatments for micronutrients discussedn this report [17154176] DRI and UL are defined asdietary reference intakerdquo and ldquoupper limitrdquo respectively

or all tables in Appendix A

able A1

hiamin (B1)

RI and UL DRI 11ndash12 mgd (females vs males) UL not determinableood sources Meat especially pork sunflower seeds grains vegetablesunctions Co-enzyme in carbohydrate metabolism protein metabolism central and peripheral nerve cell function

myocardial functionBody storage limited to 30 mg half life is 9ndash18 d

oodnutrient interactions Drinking teacoffee or decaffeinated teacoffee depletes thiamin in humansAscorbic acid improves thiamin statusThiamin is poorly absorbed when folate or protein deficiency present

arly symptoms of deficiency AnorexiaGait ataxiaParesthesiaMuscle crampsIrritability

dvanced symptoms of deficiency Wet beriberi high output heart failure with dyspnea due to peripheral vasodilation tachycardiacardiomegaly pulmonary and peripheral edema warm extremities mimicking cellulites

Dry beriberi symmetric motor and sensory neuropathy with pain paresthesia loss of reflexes andWernicke-Korsakoff syndromeWernickersquos encephalopathy classic triad includes encephalopathy ataxic gait and oculomotor

dysfunctionKorsakoff syndrome includes amnesia or changes in memory confabulation and impaired learning

iagnosis Decreased urinary thiamin excretionDecreased RBC transketolaseDecreased serum thiaminIncreased lactic acidIncreased pyruvate

reatment With hyperemesis parenteral doses of 100 mgd for first 7 d followed by daily oral doses of 50 mgduntil complete recovery simultaneous therapeutic doses of other water-soluble vitaminsmagnesium deficiency must be treated simultaneously administration with food reduces rate ofabsorption

able A2

yridoxine (B6)

RI and UL DRI 13 mg UL 100 mgdood sources Legumes nuts wheat bran and meat more bioavailable in animal sourcesunction Co-factor for 100 enzymes involved in amino acid metabolism

Involved in heme and neurotransmitter synthesis and in metabolism of glycogen lipids steroids sphingoid bases and severalvitamins such as conversion of tryptophan to niacin

ymptoms of deficiency Epithelial changes atrophic glossitisNeuropathy with severe deficiencyAbnormal electroencephalogram findingsDepression confusionMicrocytic hypochromic anemia (B6 required for hemoglobin production)Platelet dysfunctionHyperhomocystinemia

iagnosis Decreased plasma pyridoxal phosphateComplete blood count (anemia)Increased homocysteine

d to medication use

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

DFF

S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 32: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

T

C

D

FF

S

D

T

m

T

F

D

FF

S

D

T

T

S104 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A3

obalamin (B12)

RI and UL DRI 24 gd UL not determinableBody stores 4 mg one half stored in liver

ood sources Meat dairy eggs found with animal productsunction Maturation of RBC

Neural functionDNA synthesis related to folate co-enzymesCo-factor for methionine synthase and methylmalonylndashco-enzyme AB12 deficiency will cause folate deficiency

ymptoms of deficiency Pernicious anemia (due to absence of intrinsic factor)megaloblastic anemiaPale with slightly icteric skin and eyesFatigue light-headedness or vertigoShortness of breathTinnitus (ringing in ear)Palpitations rapid pulse angina and symptoms of congestive failureNumbness and paresthesia (tingling or prickly feeling) in extremitiesDemyelination and axonal degeneration especially of peripheral nerves spinal cord and cerebrumChanges in mental status ranging from mild irritability and forgetfulness to severe dementia or frank psychosisSore tongue smooth and beefy red appearanceAtaxia (poor muscle coordination) change in reflexesAnorexiaDiarrhea

iagnosis CBC elevated MCV high RDW Howell-Jolly bodies reticulocytopeniaLow serum B12

Increased MMA and increased homocysteineDecreased transcobalamin II-B12

Neurologic disease can occur with normal hematocritreatment 1000 gwk IM for 8 wk then 1000 gmo IM for life or 350ndash500 gd oral crystalline B12

Neurologic defects might not reverse with supplementation

CBC complete blood count MCV mean corpuscular volume RBC red blood cell RDW red blood cell distribution width MMA

ethylmalonic acid IM intramuscularly

able A4

olate

RI and UL DRI 400 gd UL 1000 gdBody stores 5ndash20 mg one half stored in liver deficiency can occur within months

ood sources Vegetables especially green leafy fruit enriched grains including bread pasta and riceunctions Maturation of RBCs

Synthesis of purines pyrimidines and methioninePrevention of fetal neural tube defects

ymptoms of deficiency Megaloblastic anemiaDiarrheaCheilosis and glossitisNeurologic abnormalities do not occur

iagnosis CBC elevated MCV high RDWDecreased RBC folate (not subject to acute fluctuations in oral folate intake as seen with serum folate)Normal MMA with increased homocysteine

reatment 1000 gd orally up to 5 mgd might be needed with severe malabsorptionCorrection can occur within 1ndash2 mo encourage consumption of folate-rich foods and abstinence from alcohol alcohol

interferes with folate absorption and metabolismoxicity 1000 gd can mask hematologic effects of B12 deficiency

RBC red blood cell CBC complete blood count MCV mean corpuscular volume RDW red blood cell distribution width

T

I

DFF

S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 33: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

T

I

DFF

S

S

D

T

T

c

T

C

DFF

S

D

T

S105L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A5

ron

RI and UL DRI 8 mgd for men 18 mgd for women 19ndash50 yr UL 45 mgdood sources Meats fish poultry eggs enriched grains dried fruit some vegetables and legumesunction obin and myoglobin formation

Cytochrome enzymesIron-sulfur proteins

ymptoms of deficiency AnemiaDysphagiaKoilonychiaEnteropathyFatigueRapid heart ratepalpitationsDecreased work performanceImpaired learning ability

tages of deficiency Stage 1 Serum ferritin decreases 20 ngmLStage 2 Serum iron decreases 50 gdL transferrin saturation 16Stage 3 Anemia with normal-appearing RBCs and indexes occursStage 4 Microcytosis and then hypochromia presentStage 5 Fe deficiency affects tissues resulting in symptoms and signs

iagnosis CBC low HgbHct low MCVDecreased serum ironDecreased percentage of saturationIncreased TIBCIncreased transferrinDecreased serum ferritin (affected by inflammation or infection)

reatment Typically for iron replacement therapy up to 300 mgd elemental iron given usually as 3 or 4 iron tablets (eachcontaining 50ndash65 mg elemental iron) given during course of the day ideally oral iron preparations should be takenon empty stomach because food can inhibit iron absorption When oral treatment has failed or with severe anemia IViron infusion should be considered

oxicity Nausea vomiting diarrhea constipation iron overload with organ damage acute systemic toxicity

RBCs red blood cells CBC complete blood count HgbHct hemoglobinhematocrit MCV mean corpuscular volume TIBC total iron binding

apacity IV intravenous

able A6

alcium

RI and UL DRI 1000ndash1200 mgd UL 2500 mgdood sources Diary products leafy green vegetables legumes fortified foods including breads and juicesunction Bone and tooth formation

Blood coagulationMuscle contractionMyocardial conduction

ymptoms of deficiency Leg crampingHypocalcemia and tetanyNeuromuscular hyperexcitabilityOsteoporosis

iagnosis Increased parathyroid hormoneDecreased 25-hydroxyvitamin DDecreased ionized calciumDecreased serum calcium (poor indicator of bone stores)Urinary cross-links and type 1 collagen telopeptidesDEXA scan findings

oxicity Renal insufficiency nephrolithiasis impaired iron absorption

DEXA dual-energy x-ray absorptiometry

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 34: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

T

V

D

FF

S

D

T

T

V

D

FF

EA

D

T

T

S106 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A7

itamin D

RI and UL DRI 5 gd for adults 10 gd for ages 50ndash70 yr 15 gd for ages 70 yr UL 50 gd1 g 40 IU

ood sources Fortified dairy products fatty fish eggs fortified cerealsunction Calcium and phosphorus absorption

Resorption mineralization and maturation of boneTubular resorption of calcium

ymptoms of deficiency OsteomalaciaDisorders of calcium deficiency rachitic tetany

iagnosis Decreased 25-hydroxycholecalciferolDecreased serum phosphorusIncreased serum alkaline phosphataseIncreased parathyroid hormoneDecreased urinary calciumDecreased or normal serum calcium

reatment 50000 IUwk ergocalciferol (D2) orally or intramuscularly for 8 wk

able A8

itamin A

RI and UL DRI 700 gd females 900 gd males UL 3000 mgd1 RAE 1 g retinol 12 g B-carotene for supplements 1 RE 1 RAE

ood sources Liver dairy products fish darkly colored fruits and leafy vegetablesunctions Photoreceptor mechanism of the retina format

Integrity of epitheliaLysosome stabilityGlycoprotein synthesisGene expressionReproduction and embryonic functionImmune function

arly symptoms of deficiency Nyctalopia xerosis Bitotrsquos spots poor wound healingdvanced symptoms of deficiency Corneal damage keratomalacia perforation endophthalmitis and blindness

Xerosis and hyperkeratinization of the skin loss of tasteiagnosis Decreased serum vitamin A

Decreased plasma retinolDecreased retinal binding protein

reatment Without corneal changes 10000ndash25000 IUd vitamin A orally until clinical improvement (usually 1ndash2 weeks)With corneal changes 50000ndash100000 IU vitamin A IM for 3 days followed by 50000 IUd IM for 2 weeksEvaluate for concurrent iron andor copper deficiency which can impair resolution of vitamin A deficiencyPotential antioxidant effects of carotene can be achieved with supplements of 25000-50000 IU of carotene

oxicity Hypercarotenosis results in staining of skin yellow-orange color but is otherwise benign skin changes mostmarked on palms and soles sclera remains white

Hypervitaminosis A occurs after ingestion of daily doses of 50000 IUd for 3 mo early manifestationsinclude dry scaly skin hair loss mouth sores painful hyperostosis anorexia and vomiting

Most serious findings include hypercalcemia increased intracranial pressure with papilledema headaches anddecreased cognition and hepatomegaly occasionally progressing to cirrhosis

Excessive vitamin A has also been related to increased risk of hip fractureDiagnosis elevated serum vitamin A levelsTreatment withdrawal of vitamin A from diet most symptoms improve rapidly

RAE retinol activity equivalent RE retinol equivalent IM intramuscularly

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

T

Z

DFF

S

D

TT

S108 L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 35: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

T

V

DFF

S

D

T

T

T

V

DFFS

D

T

T

S107L Aills et al Surgery for Obesity and Related Diseases 4 (2008) S73-S108

able A9

itamin E

RI and UL DRI 15 mgd UL 1000 mgdood sources Vegetable oils unprocessed cereal grains nuts fruits vegetables meatsunction Intracellular antioxidant

Scavenger or free radicals in biologic membranesymptoms of deficiency Hyporeflexia disturbances of gait decreased proprioception and vibration ophthalmoplegia

RBC hemolysisNeurologic damageCeroid deposition in muscleNyctalopiaMuscle weaknessNystagmus

iagnosis Decreased plasma alpha-tocopherolSerum level of vitamin E should be interpreted in relation to circulating lipidsIncreased urinary creatinineIncreased plasma creatine phosphokinase

reatment Optimal therapeutic dose of vitamin E has not been clearly defined potential antioxidant benefits of vitamin E canbe achieved with supplements of 100ndash400 IUd

oxicity Large doses have been taken for extended periods without harm although nausea flatulence and diarrhea have beenreported large doses of vitamin E can increase vitamin K requirement and can result in bleeding in patientstaking oral anticoagulants

RBC red blood count

able A10

itamin K

RI and UL DRI 90 gd females 120 gd males UL not determinableood sources Green vegetables Brussels sprouts cabbage plant oils and margarineunction Formation of prothrombin other coagulation factors and bone proteinsymptoms of deficiency Hemorrhage from deficiency of prothrombin and other factors

Easy bruisingBleeding gumsHeavy menstrual and nose bleedingDelayed blood clottingOsteoporosis

iagnosis Increased prothrombin timeReduced clotting factorIncreased partial prothrombin timeDecreased plasma phylloquinoneFibrinogen level thrombin time platelet count and bleeding time are in normal rangeIncreased des-gamma-carboxyprothrombinAlso known as protein-induced in vitamin K absenceMeasured with antibodies

reatment Parenteral dose of 10 mgFor chronic malabsorption 1ndash2 mgd orally or 1ndash2 mgwk parenterallyNote if elevated prothrombin time does not improve it is not due to vitamin K deficiencyNote Warfarin-type drugs inhibit conversion of vitamin K to its active form hydroquinone

oxicity High doses can impair actions of oral anticoagulants

No known toxicity from dietary sources of vitamin K

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able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies
Page 36: ASMBS Guidelines ASMBS Allied Health Nutritional ... · ness for change, realistic goal setting, general nutrition knowledge, as well as behavioral, cultural, psychosocial, and economic

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able A11

inc

RI and UL DRI 8 mgd females 11 mgd males UL 40 mgdood sources Meat liver eggs oysters peanuts whole grainsunction Components of enzymes

Synthesis of proteins DNA RNAGene expressionSkin and cell integrityWound healingReproduction and growth

ymptoms of deficiency Hypogeusia (decreased taste sensation)Alterations in sense of smellPoor appetitePoor wound healingIrritabilityImpaired immune functionDiarrheaHair lossMuscle wastingDermatitis

iagnosis Decreased plasma zincDecreased serum zincDecreased RBC or WBC zincDecreased alkaline phosphataseDecreased plasma testosterone

reatment 60 mg elemental zinc orally twice dailyoxicity Acute toxicity causes nausea vomiting and fever

Chronic large doses of zinc can depress immune function and cause hypochromic anemia as a result of copperdeficiency

RBC red blood cell WBC white blood cell

  • ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss Patient
    • Nutrition care
      • Biochemical monitoring for nutrition status
      • Vitamin supplementation
        • Rationale for recommendations
          • Importance of multivitamin and mineral supplementation
          • Weight loss and nutrient deficits restriction versus malabsorption
          • Thiamin (vitamin B1)
            • Etiology of potential deficiency
              • Signs symptoms and treatment of deficiency
                • Preoperative risk
                • Postoperative risk
                • Suggested supplementation
                  • Vitamin B12 and folate
                  • Vitamin B12
                    • Etiology of potential deficiency
                      • Signs symptoms and treatment of deficiency (see13Appendix Table A3)
                        • Preoperative risk
                        • Postoperative risk
                        • Suggested supplementation
                          • Folate
                            • Etiology of potential deficiency
                              • Signs symptoms and treatment of deficiency (see13Appendix Table A4)
                                • Preoperative risk
                                • Postoperative risk
                                • Suggested supplementation
                                  • Iron
                                    • Etiology of potential deficiency
                                      • Signs symptoms and treatment of deficiency (see13Appendix Table A5)
                                        • Preoperative risk
                                        • Postoperative risk
                                        • Suggested supplementation
                                          • Calcium and vitamin D
                                            • Etiology of potential deficiency
                                              • Signs symptoms and treatment of deficiency (see Appendix Tables A6 and A7)
                                                • Preoperative risk
                                                • Postoperative risk
                                                • Calcium citrate versus calcium carbonate
                                                • Suggested supplementation
                                                  • Vitamins A E K and zinc
                                                    • Etiology of potential deficiency
                                                      • Signs symptoms and treatment of deficiency (see Appendix Tables A8 A9 A10 A11)
                                                      • Vitamin A
                                                      • Vitamin K
                                                      • Vitamin E
                                                      • Zinc
                                                        • Suggested supplementation
                                                        • Conclusion
                                                          • Other micronutrients
                                                            • Vitamin B6
                                                              • Signs symptoms and treatment of deficiency
                                                                • Copper
                                                                • Other mineral deficiencies
                                                                    • Protein
                                                                      • Etiology of potential deficiency
                                                                      • Preoperative risk
                                                                      • Postoperative risk
                                                                      • Protein intake
                                                                      • Modular protein supplements
                                                                        • Diet and texture progression
                                                                          • Clear liquid diet
                                                                          • Full liquid diet
                                                                          • Pureed diet
                                                                          • Mechanically altered soft diet
                                                                          • Diet and texture progression survey
                                                                            • Demographics
                                                                            • Pouch size and limb lengths
                                                                            • Diet phases
                                                                            • Foods commonly restricted
                                                                            • Diet advancement and nutrition intervention
                                                                                • Conclusion
                                                                                • Disclosures
                                                                                • Acknowledgments
                                                                                • References
                                                                                • Appendix Identifying and Treating Micronutrient Deficiencies