The Gluten Truth and Other Things Pediatric GI

Kenneth Fine, M.D.

What is Gluten?

• A protein found in wheat, barley, rye, oats

– Poorly digested by humans

– Causes immune reactions in genetically susceptible individuals

– Can become autoimmune

In the Beginning… GrainsFertile Crescent - 8500 B.C.E.

•Wheat, barley, rye, oats among the first foods to be domesticated

•Genetically modified its ancestors

Diploid Tetraploid Hexaploid

WildAncestors

Modern

Wheat and SpeltEarly Cultivated Wheat and Spelt

Factors Favoring Grain to Remain Human Food

• Easily and quickly grown with large yields

– Short growing season (few months)

• Seeds could be stored, ground and cooked into good tasting food with high carb/cal availability

• Yeast +/- sugar added - baked, fermented, distilled, brewed tasty, pleasurable, addicting food/drink

“The Coeliac Affection” Described by 100 C.E.

Aretaeus the Cappadocian

“Patients have flatulence and heavy pains of the stomach”

“They are emaciated and atrophied, pale, feeble, incapable of performing any of their accustomed work”

“The stomach labors in digestion when diarrhea, consisting of undigested food in a fluid state, seizes the patient”

Celiac Disease: The Classic Gluten-Related

Disease• Present in 0.5-1% of Europeans

and Americans

• Gluten-induced immune damage of the small intestine with specific lesion

• Most often diagnosed by intestinal biopsy and blood tests

– Most people today do not have the classic syndrome or biopsy

Normal

Celiac disease

Spectrum of SB Histopathology in Celiac Sprue

Partial Villous Atrophy

Subtotal VA

Total VA

Normal

HLA Genes in Celiac Sprue

• Tightly associated with class II alleles

HLA-DQ2 90%

HLA-DQ8 most of those without DQ2

Celiac Endoscopic Abnormalities

Evidence that Celiac Sprue isan Autoimmune Disease

• Shares predisposing HLA alleles and is epidem-iologically associated with other autoimmune dz

• Antigen Substrate for AEA is a human enzyme

– Tissue transglutaminase - responsible for protein crosslinking in response to tissue injury

– Can bind gliadin as a substrate (Dieterich et al Nature Med 1996)

Duration of Gluten Consumption and Risk of Autoimmune Disease

0%

5%

10%

15%

20%

25%

30%

35%

<2 yrs 2-4 yrs 4-12 yrs 12-20 yrs >20 yrs

Age at Diagnosis of Celiac Sprue

Ventura et al Gastroenterology 1999;117:297

Main Autoimmune Diseases Associated with Celiac Sprue

• Diabetes mellitus, type 1

• Dermatitis herpetiformis

• Thyroiditis - hypothyroid

• Sjogren’s syndrome

• Psoriasis

• Rheumatoid arthritis

• Alopecia

• Autoimmune hepatitis

• Primary biliary cirrhosis

• Sclerosing cholangitis

Other Disorders Associated with Gluten Sensitivity

• Crohn’s disease, Ulcerative colitis

• Chronic diarrhea

• Gastroesophageal reflux disease

• Hepatitis C, many other liver diseases

• Female infertility, mother’s of spina bifida

• Psychiatric disease, Alcoholism, Depression

• Iron deficiency anemia

• GI cancers/Lymphoma

Microscopic Colitis Syndrome

• Chronic, watery, non-bloody diarrhea

• Etiology unknown

• Normal or near-normal colonoscopic appearance

• Histopathology: LP inflammation, intraepithelial lymphocytosis, surface epithelial flattening,

+/- thick subepithelial collagen band

Microscopic ColitisNormal colon “Collagenous colitis”

MC

Stained Collagen

MC Possesses Celiac-Like Clinicopathologic Characteristics

• Colon biopsy of MC identical to biopsy of CS

• 5% of treated CS patients get MC

• 75% of MC have celiac genes (DQ2, DQ8)

• 70% have mild SB damage but rarely CS

• Not much more antigliadin antibody in serum than general population; positive titers < CS

Fine et al Gastroenterology 1996

Fine et al Human Pathology 1998

Fine et al Am J Gastro 2000

Small Bowel Enteropathy in Microscopic Colitis With all these similarities to CS

suggesting that microscopic colitis patients are gluten-sensitive, why

are antibodies to gliadin not detected more often in serum?

If an immunologic reaction to gliadin was detectable, it would prove their immunologic gluten sensitivity, and rationalize treatment with a gluten-free diet

Follow-up* of 50 Patients with MC Treated with Bismuth Subsalicylate

• Well, no further treatment 31 (62%)

• Well, required retreatment x 1 7 (13%)

• Relapsed, required adjuvant Rx 10 (20%)

• Continued diarrhea 2 (5%)

* 15 - 55 monthsFine et al Gastroenterology 1998

Stratification of HLA, SB Bx, AGA Results in MC by Response to BSS

ResponsePattern n

DQ2 or1,3

AbnormalSmall Bowel

SerumAGA IgA

FecalAGA IgA

Response,no relapse

17 11 (65%) 3 (18%) 2 (12%) 3 (18%)

Response,relapse

22 22 (100%) 20 (91%) 5 (23%) 12 (55%)

Noresponse

6 6 (100%) 6 (100%) 1 (17%) 6 (100%)

Effect of a GFD in the First 25 MC Patients with Relapsing Diarrhea following Bismuth Subsalicylate

Resolution of diarrhea 19

Improved; less/sporadic diarrhea 4

No improvement 2

“Secondary” Gluten-Sensitivity in Microscopic Colitis

• In patients with microscopic colitis, low titers of antigliadin antibodies and mild small intestinal histopathology occur secondarily to the colonic inflammatory response, rather than the converse

• Dietary gluten in such patients likely fuels the immune fire of the primary colitic disorder

Poor Sensitivity of Celiac Blood Tests with Less Villous Atrophy• Partial villous atrophy - 31%

• Subtotal villous atrophy - 70%

• Total villous atrophy - 100%

Rostami et al Am J Gastro 1999;94:888 Dickey W Scand J Gastro 2000;35:181 Tursi A, Am J Gastroenterol. 2001;96:1507-10 Tursi A, J Clin Gastroenterol 2003;36:219-21Abrams JA, Dig Dis Sci. 2004;49:546-50 Sanders DS, BMJ. 2005;330:775-6

Problem with Biopsies: Not All Gluten-Sensitive People Have

Villous Atrophy • “Gluten-Sensitive Diarrhea” (Gastroenterology 1980;79:801)

• “Gluten-Sensitivity with Mild Enteropathy” (Gastro 1996;111:608)

• “Celiac-like Abnormalities in IBS patients” (Gastro 2001;121:1329)

• “Celiac Disease without Villous Atrophy” (Dig Dis Sci 2001;46:879)

– Pts. with diarrhea/steatorrhea, anemia, osteoporosis, mouth ulcers

– Small bowel biopsies with γ-δ IEL’s and react to gluten in vitro

– All patients became well on a GFD; Sx’s recurred with gluten

Antigliadin Ab Is Inside the Intestine but not Blood with Mild

Intestinal Damage• Researchers assessed blood and aspirated small

bowel fluid for antigliadin IgA antibody in:

– Celiacs: blood and SB aspirate was positive

– Normals: blood and SB aspirate was negative

– Celiacs after 1 yr on GFD: blood neg., intestine positive

• Used intestinal lavage and analysis of rectal effluent to test for the presence of intestinal antigliadin Ab – Called “a relatively non-invasive screening method for early celiac sprue”

O’Mahoney et al, Gut 1990

8yr Prospective Study of Fecal Testing for Gluten Sensitivity

• 10,246 pts. collected one stool

• Measured fecal antigliadin IgA, ATTA, fecal fat

• Buccal swab analyzed for HLA-DQB1

• Questionnaire for clinical data: symptoms, indications

• Follow-up symptoms, stool tests

Detection Frequency of AGASerum vs. Stool

Patient Group+ Serum AGA

IgG or IgA+ Fecal

AGA IgAAsymptomatic volunteers (n=56) 11% 29%

IBS-like Abd. Symptoms (n=1280) 12% 62%

FH Celiac Disease (n=2151) 14% 64%

Autoimmune Disease (n=6181) 13% 68%

Microscopic colitis (n=380) 9% 72%

Chronic Fatigue (n=141) 10% 63%

Untreated celiac sprue (n=57) 75% 99%

AGA = antigliadin antibody

Follow-Up: Gluten-Free Diet Rx for Non-Celiac Gluten Sensitivity

What improved on a GFD?

– In 6-12 months:

• All symptoms, subjective assessment of health

– In 2-3 years

• Fecal antibody levels (indicator of ongoing sensitivity)

• Fecal fat malabsorption (indicator of intestinal dysfunction)

– Diet had to be 100% strict for malabsorption to resolve

# of Symptoms* - Study Onset vs. 15 Mo. Follow-Up in IBS and MC

Treatment n Sx before Sx after P value†

100% Strict GFD 247 4.9 1.0 <0.0001

<100% Strict GFD 173 4.7 1.4 <0.0001

None 77 4.6 4.3 0.30

* Weight loss, fatigue, aphthae, abdominal pain, bloating, dyspepsia, vomiting, diarrhea, or constipation as assessed by questionnaire† Before vs. after in each group; two-tailed paired student’s t-test

Subjective Change in Health -15 Mo. Follow-Up vs. Study Onset

1%93%6%77None

2%11%87%173<100% Strict GFD

1%5%94% 247100% Strict GFD

WorseSameBetternTreatment

0

1 0

2 0

3 0

4 0

5 0

6 0

7 0

8 0

B a se l ine F o l l ow-U p

P=0.002

Mean40

0

1 0

2 0

3 0

4 0

5 0

6 0

7 0

8 0

Ba se l ine F o l l ow-U p

0

1 0

2 0

3 0

4 0

5 0

6 0

7 0

8 0

Ba sel ine F o l l o w-U p

100% GFD <100% GFD No GFD

Improvement of Fecal Anti-Gliadin IgA on GFD - Baseline and 42-Mo. 

Units

Normal Range

Mean11

Mean15

Mean30

Mean24

Mean36

P=0.10 P=0.71 0

1 0 0

2 0 03 0 0

4 0 05 0 0

6 0 07 0 0

8 0 0

9 0 0

Ba sel ine F o l l ow-U p

0

1 0 0

2 0 03 0 0

4 0 05 0 0

6 0 07 0 0

8 0 0

9 0 0

Ba sel ine F o l l ow-U p

0

1 0 0

2 0 03 0 0

4 0 05 0 0

6 0 07 0 0

8 0 0

9 0 0

Ba sel ine F o l l ow-U p

NormalRange

Improvement of Dietary Fat Malabsorption on 100% GFD 42mo

100% GFD <100% GFD No GFD

Units

Mean393

Mean151

Mean 300

Mean322

Mean323

Mean426

P=0.33P=022P=0.04

Reproducibility Studies AGA• Repeated Fecal Antigliadin IgA: Different Stools,

Same People over days to weeks

0

20

40

60

80

100

120

Fec

al A

nti

glia

din

IgA

(Un

its)

Negative Control GroupsGroup n % negative

Babies <10 mos 18 100%*

Cow manure 24 100%*

Dog Manure 10 100%*

Fecal IgG 168 100%†

* Fecal Antigliadin IgA † Fecal Antigliadin IgG

Non-Celiac Gluten Sensitivity• Chronic immune “sensitivity” to wheat, barley, rye, oats

without celiac-like damage of the small intestine

• Makes people ill in many ways:Neuropsychiatric disordersAbdominal symptoms/syndromesAutoimmune/asthma disordersGlandular dysfunctionSkin rashes and syndromes

• Before 2000, no simple yet sensitive method of diagnosis – Now diagnosable by fecal testing• blood tests for gluten antibodies insensitive

Inflammation, no villous atrophy

Non-Celiac Gluten Sensitivity The Majority of the Epidemic

Celiac Disease (0.5-1% )17 million in US, Europe, Mid East

Symptomatic Non-CeliacGluten Sensitivity (22%)

375 million Asymptomatic Non-CeliacGluten Sensitivity (25% )

425 million

At Genetic Risk for Non-Celiac Gluten Sensitivity (47%)

800 million%’s are of a population with a wheat-based diet

Whole iceberg increasing, celiac tip smaller

GS47%

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

Fecal AGA Normal Fecal AGA Elevated

No HLA-DQ2 or DQ8

HLA-DQ2 and/or DQ8

P=0.04

P=0.04

% w

ith o

r w

ithou

t a

Cel

iac

HLA

-DQ

Gen

eCeliac vs. Non-Celiac HLA-DQ

Alleles Segregated by Fecal AGA How Did Gluten-Sensitive Genes Become So Common?

• Esp. common in peoples initially cultivating gluten– Celiac genes (HLA-DQ 2 or 8) present in 42%

– Gluten sensitive genes (HLA-DQ 1, 7, 9) present in 57%• More common than Eastern Asians, Africans, Native Americans

• Did genes lend survival advantage (like CF, Sickle cell)?– Immune stimulation, may have protected against infection

– May be linked to lactose tolerance or another trait

– Linked to being alcoholic - makes you really mean

Research Supporting Non-Celiac Gluten-Sensitive HLA-DQ Genes

• DQ1,7 found more commonly in MC and RA, and the latter are linked to CS

• DQ1 found more commonly in gluten ataxia

• DQ9 facilitates T-cell recognition of gliadin

• DQ1,7,9 (w/o DQ2,8) present in non-celiac, rectally gluten-reactive siblings of celiacs; & in 1% of celiacs

• Only DQ4 = no increase risk of GS (rare in US 0.4%)Fine et al. Am J Gastro 2000;95:1974 Hadjivassiliou et al. Brain 2003;126:685Moustakas et al. Int Immunol 2000;12:1157 Troncone R, et al. Gastroenterology. 1996;111:318-24 Garrote JA, et al. Immunogenetics. 2000;51:1045-6 Karell K, et al. Hum Immunol. 2003;64:469-77

Approach to Gluten Sensitivity

Screening• Stool for Antibody and Malabsorption Testing

– Fecal anti-gliadin, anti-oat protein, and anti-TTG IgA

– Quantitative fecal fat microscopy

• Swab of inside of mouth for Gene Testing

– HLA-DQB1 typing for gluten sensitive/celiac genes

• Other stool tests: ASCA, other foods; lactoferrin for acute -chronic colitis, parasite test, pancreatic elastase

Quantitative Fecal Fat Microscopy *

• New method of fecal fat microscopy allowing quantitation of fecal fat output from a single stool

• Easily diagnoses intestinal nutrient malabsorption and establishes a numeric pretreatment baseline

• Correlates with quantitative fecal fat excretion measured in 72-hour stool collections

• More sensitive than qualitative fecal fat & 72-hour collections (30-50% do not collect all stools)

* Developed and offered exclusively by EnteroLab.com

y = 0.032x + 2.64R = 0.90

P < 0.001

0

20

40

60

80

100

120

140

160

180

0 500 1000 1500 2000 2500 3000 3500 4000

Fecal Fat Droplet Total Size-Number Product

Fec

al F

at O

utp

ut

(g/d

ay)

Nor

mal

ran

ge -

feca

l fat

mic

rosc

opy

Normal range - fecal fat output

Who Should Be Screened?

• Microscopic colitis, Crohn’s, UC, any IBD

• Relatives of gluten-sensitive individuals

• Chronic diarrhea of unknown origin

• Irritable bowel syndrome

• Gastroesophageal reflux disease

• Hepatitis C, Autoimmune/other liver disease

• Short stature in children, Down's syndrome

Who Should Be Screened?• Female infertility, mother of spina bifida

• Peripheral neuropathy,Seizure disorders

• Psychiatric Dz, Alcoholism, Depression, Autism

• Diabetes mellitus, type 1, type 2 (?)

• Rheumatoid arthritis, Sjogren's syndrome, Lupus, Autoimmune thyroid disease, Any autoimmune Dz

• Asthma, AIDS, Osteoporosis, Iron deficiency

• Everyone!

Gluten Sensitive Disorders Unique to Children

• Short stature/developmental delay

• Refractory seizures (brain calcification)• Abnormal behavior, mood, thought, sensory processing

– Oppositional defiant disorder (ODD), obsessive-compulsive disorder (OCD), attention-deficit disorder (ADD), hyperactivity (ADHD), autism, learning disorders

Short Stature in Children

• 7 y/o girl with short stature since age 2; abdominal bloating and pain when eating gluten

• Had severe cow’s milk protein sensitivity with malabsorption and GI bleeding as an infant

• Negative blood tests for celiac sprue (HLA-DQ2 +)

• Positive fecal AGA, ATTA, fat Age (years)

Hei

ght

(in) 50th %

5th %

PtPartialGFD

Gluten Sensitivity and Impaired School Performance

Learning Disorders Associated with Gluten Sensitivity

• Dyslexia

• Attention Deficit Disorder (+/- hyperactivity)

• Impaired short-term auditory memory

• Slow visual processing speed

• Dysnomia (trouble expressing the proper word)

• Dysgraphia (poor writing; trouble writing what you are thinking about)

• Autism/Asperger’s syndrome

Gluten Sensitivity and Writing

Wheat5 y/o

During ExposureBefore Exposure After Exposure

Rye6 y/o

Mechanism By Which Gluten Causes Learning Disabilities

• Gluten digests mimic morphine in the brain causing:

– CNS depression

– Slowed neurotransmission (altered information processing)

– Drowsiness, apathy, and mental confusion

– Vasodilation, altering normal blood flow distribution

• Malnutrition from gut damage, altering brain neurotransmitter and nutrient concentrations

• Immune reaction against vital brain centers

Food Sensitivity and Behavior Food Sensitivity and Behavior

• Proven reactions during food sensitivity testing:

– Hyperactivity, loudness, aggression, vulgarity

– Fatigue, depression, falling asleep, yawning

– Inability to sit still, concentrate, think, follow directions

– Easy distractibility, impulsiveness

– Crawling under furniture, into dark corners

– Refusal to be touched

Gluten Sensitivity and Behavior

From: “The Impossible Child”D. Rapp, M.D.D. Bamberg, R.N., Ed.D.

Behavior

Writing Name

Drawing

Milk Sensitivity and Behavior

Have You Ever Seen This? Learning/Emotional/PsychiatricDisorders Improve on a GFD

• Dyslexia*

• Dysgraphia*

• Autism*

• Depression, Schizophrenia*

• ADD/ADHD †

• Oppositional Defiant Disorder †

• Obsessive-Compulsive Disorder †

* Scientifically Proven† Much anecdotal experience

Why is Gluten Sensitivity More Common Now Than Ever?

• Greater immune stress from environment, toxins

• Flora less protective from antibiotics, Cl- water

• Gastric-acid suppression increasing food sensitivity

• GS genes very common, especially in Caucasians

• More wheat being eaten than ever

• Wheat hybridized - more gluten• Grown with a corporate mentality

Similarities of the Gluten Sensitivity Paradigm with

that of H. pylori• Both started with revolutionary discounted paradigms

• Both affect large percentages of the population with at least as many or more asymptomatic as symptomatic

– Those symptomatic may have severe, sometimes life-threatening illness/events requiring treatment

• Both have malignant potential by a similar antigenic-immune mechanism (GI lymphomas, carcinomas)

• Both paradigms took more than a decade to be accepted

• One is now fully accepted, the other is on its way

What Happened to the Bread of Life?

Medical School Dictum: “Don’t give the patient more

than one disease”

Could the inflammatory Dz, gluten sensitivity, and obesity epidemics (and cancer epidemic?) all have a common underlying cause?

My Diagnosis: IMRMATTC

(Pronounced I am Rheumatic)

Insidious Moderno-Rapido-Mucho-Anxieto-Toxico-Technico-Commercialitis

Rising Prevalence of Inflammatory Disorders

• Chemical Sensitivity 25%

• Autoimmune Disease 15%

• Irritable bowel syndrome 15%

• Chronic fatigue 11%

• Asthma 10%

• Fibromyalgia 4%

• Inflammatory Bowel Disease 1%– Heart disease and aging now linked to inflammation

Our Inflammatory Outer World

• Antigenic diet

• Environmental Toxins

• Hormones in prescriptions, food, toxins

• Stressful, fast-paced, modern lifestyle

• Urban noise, plane and road traffic

• Negativity on news, TV, media

Our Inflammatory Inner WorldAntigenic Food and Flora

• Food and flora expose us to millions of antigens

What type of gluten-free foods should be chosen?

• Is gluten-free enough for optimal health?

– Known since 1960’s that celiac patients have high prevalence of other food sensitivities

• If you stay in the same grain-based dietary paradigm, you will get the same results of the standard American diet, probably with less immune reactivity (but not none)

• Gluten

(wheat, barley, rye, oats)

• Cow’s milk/dairy foods

• Dietary Yeast

• Corn/Other grains

• Citrus

• Beef

• Pork

• Soy

• Eggs

• Peanuts/Other legumes

• Nightshades

(Potatoes, tomatoes, eggplant, peppers)

• Tree nuts

• High protein diet/foods/bars

Common Immune-Stimulating Foods

So Many Diets, So Little Time!

• Gluten-free diet

• Gluten-free/Casein-free diet

• “Against the Grain” diet

• Low oxalate diet

• Paleolithic diet• Alkaline vegetarian diet

• Hypoglycemia diet

• Raw/Live food diet

Anti-Inflammatory

Diet

Anti-Inflammatory Diet

Optional

Are Oats Tolerated and Safe?

• In studies, 20- 50% of patients are excluded because they cannot tolerate oats - Selects most tolerant subjects

• Up to 13% of patients getting oats withdrew from the study

• Because oats are the least toxic gluten grain, damage may take longer than study periods allow, or may never cause villous atrophy but still cause immune dysfunction

• More recent studies proving they can be a problem

• Most oats and other grains in US are cross-contaminated

What is the Collective Consciousness of Food in the U.S.?

• More is better, cheap is best

• Looking at food only as calories or nutrients

• Corporate is the only way

– Why should we expect raising plants or farm animals would be any different than raising our children with respect to how we treat them affects their growth and success (or failure)

• What are the consequences of all this?

What is the Consequent Problem?A High Prevalence of:

• Obesity/Overweight

• Autoimmune diseases - asthma, colitis, diabetes, etc.

• Attention Deficit Disorder/Hyperactivity

• Depression

• Learning disorders

• Substance abuse

• Violence; waning hope and negativity about future

Food-Borne Illness in 2013 -An Entirely New Meaning

• Immune/Autoimmune reactions

• Obesity

• Diabetes

• New and more virulent infectious organisms

• “Eating Disorders”

• Addiction

Food Addiction

• Gluten and dairy after digestion generate morphine-like substances that mimic its actions

– Gluteomorphine and caseomorphine

• Fulfills addiction definition

– Increasing dose for same effect

– Upon removal - psychological craving, physical symptoms/syndrome

The Link Between GlutenSensitivity and Alcoholism

• Gluten is wheat, barley, rye, and oats

• Most alcohol consumed in this country is derived from gluten-containing grains

– Gluten in food and alcohol can be associated with a similar withdrawal syndrome including strong cravings

– GFD may help treatment of alcoholism

• Ireland touts highest incidence of CS and Alcoholism

The Inseparable Relationship

Eat Right

Think Right

Feel RightAct Right

The Inseparable Relationship

Eat Wrong

Think Wrong

Feel WrongAct Wrong

Definitions of Overweight/Obese Adults

• Body Mass Index (BMI) - Weight (kg)/height 2 (m)

– Same ranges for men and women

– Normal 18.5 - 24.9 (e.g., 5’ 9”, 125-168 lbs.)

• Overweight - Weight > Ideal Body Weight (from tables)

– BMI 25 - 29.9 (e.g. 5’ 9”, 169-202 lbs.)

• Obesity - Weight > 20% over Ideal Body Weight

– BMI > 30 (e.g. 5’ 9”, >202 lbs.)

Definition of Overweight

Children

• Healthy weight 5th - 85th % for age

• At risk for overweight 85th - 95th % for age

• Overweight > 95th % for age

Overweight/Obesity: Main Causes

Overweight/obesity result from too many calories, not enough physical activity* Body weight is the result of genes, metabolism, culture,

behavior, environment, socioeconomic status, familial

• Hormonal imbalances - estrogen, leptin, thyroid, largely due to immune reaction to foods

– Gluten & dairy mainly

* U.S. Surgeon General’s Call to Action toPrevent and Decrease Overweight and Obesity, 2001

The Trend of OverweightKids in America 1978 vs. 2004

Source:CDC/NHANESNational Health and Nutrition Examination SurveyOverweight > 95% for age

Age 1978 2004

Overweight 2-5 y/o 5% 14% Overweight 6-11 y/o 6% 19%

Overweight 12-19 y/o 5% 17%

No Data <10% 10%–14% 15%–19%

Prevalence of Obesity in U.S. Adults1991

Source:CDC/BRFSSBehavioral Risk Factor Surveillance System

No Data <10% 10%–14% 15%–19%

Prevalence of Obesity in U.S. Adults 1996

Source:CDC/BRFSS

No Data <10% 10%–14% 15%–19% 20%–24% ≥25%

Prevalence of Obesity in U.S. Adults 2001

Source:CDC/BRFSS

No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%

Prevalence of Obesity in U.S. Adults 2006

Source:CDC/BRFSS

Children Do Not Feed Themselves

• The problem in children stems from the problem in adults

• Education must involve and mostly be directed at parents - must teach didactically and by example– As teachers and as parents, grandparents, etc.

• We must restore good health, physical fitness, and lean body mass as a family/societal value– Society needs to relearn how to eat and nutrition

To Be Part of the Solution:“Get on a Mission Of Nutrition”

• 5 main points of instruction– Importance of good nutrition and dietary habits

– Importance of exercise for health and happiness

– Anatomy and physiology of digestion and absorption

– Anti-tobacco, drug, and alcohol lesson; abstinence

– Importance of good values, choices, positive attitude

• Up to 5 Classroom settings of instruction– Homeroom, Science, P.E., Health, Music/Drama

Audio CD

“A Trip Down Intestinal Lane”“A Trip Down Intestinal Lane”

Summary – Conclusions

• 1. Grains have been consumed as food a relatively short period of time (10,000 years) and gluten sensitivity has been present for at least the last 2000.

• 2. Non Celiac Gluten sensitivity has been mentioned in the medical literature for 35 years and accounts for 99% of the problems relating to gluten; celiac disease is only 1% of the problem.

Summary – Conclusions

• 3. Blood tests fall short of being a good screening or diagnostic method of diagnosis; stool for antigliadin antibodies is 5-7X more sensitive than blood tests.

• 4. Gluten (wheat, barley, and rye) is not the only food antigen of concern. Dairy, soy, egg, yeast, oats, others are now also a problem for at least half gluten-sensitive people.

Summary – Conclusions• 5. The Gluten sensitivity epidemic is due to common

GS genes; more wheat eaten; over-hybridization of wheat; more immune stimulation from stress, sanitation, and hormone and toxin influences; widespread use of acid-blocking drugs.

• 6. Food-borne illness is more far reaching than ever, with obesity, eating disorders, and food addiction epidemics in their own right needing public health attention and coordinated professional solutions

Specialized clinical diagnostic laboratoryfor intestinal health testing

501(c)(3) non-profit medical research and

public health educational institute

www.IntestinalHealth.org

.com

www.SixSOS.orgLinks to all my Websites

Anti-Inflammatory Diet• Always eliminate gluten; also dairy, added yeast

– Soy, corn, eggs, specific nuts if suspected problem

– Grains, legumes, nightshades for optimal benefit

• Diet centered around non-acid fruits, vegetables, soaked nuts/seed, healthy vegetable fats– Healthy lean meats are optional

• Foods eaten in natural state as much as possible

Anti-Inflammatory Diet• Limit/Avoid

– Saturated/trans fat, animal protein (meat, dairy, eggs)

– Starchy carbohydrates (grains, potatoes)

– Sodium (salt, canned/pickled foods, processed meats)

– Chemical preservatives, pesticides

– Simple sugar (soda, cane sugar; most fruit ok)

– High calorie foods, desserts, fast food, “junk food”

– Foods to which you are immune sensitive

How To Find Your Best Anti-Inflammatory Diet

• Become conscious of how you feel within minutes, 2-4 hours, and 6-24 hours after eating a food

• Learn the language of your body’s food reactions

– Headaches, stiffness, arthritis, fibromyalgia, abdominal symptoms, sinus mucus, mood changes, mental effects

• Food elimination and reintroduction experiments

• Tests for food sensitivities can be a guide

Dietary Schemes to Optimize Mental Acuity and Energy

• Eat the minimum amount of food for hunger to be satiated (appetizer-dose concept), and eat frequently

– Small morning meal, mid-morning snack, modest midday meal, small afternoon snack, moderate dinner, after-dinner snack (every 2-3 hours)

• Mix healthy carbs/fiber (fruit/veggies), protein (nuts, seeds, healthy meat), and fat (avocados, nuts, oils)

• Avoid sugar, starchy carbs, gluten &/or dairy (if sensitive)

Published Studies of Others Fecal Gliadin Testing

• 1968 - Yale: Anti-gluten agglutination in 3 CS pts.– JAMA. 1968;203:887-8.

• 1994, a letter from France (Clin Chem. 1993;39:696-7)

– 10 patients with CS had detectable AGA in stool

– 2 did not have it in serum

• 2002, Italian study showing AGA, ATTA and AEA in 21 CS patients, 10 treated CS after challenge; higher concentrations in CS vs. normal

– (Am J Gastro 2002;97:95)

Other Studies of Fecal Gliadin Testing (cont.)

• 2004 German Study found higher fecal AGA in 26 CS than 167 healthy controls (Clin Lab 2004;50:551)

– One CS patient with neg. serum, positive stool

• 2006 German Study of 20 celiac kids (BMJ 2006;332:213)

– Did not alter serum method or calculation of positive

– 10% sensitive, 98% specific

• If used a lower cut off, was 82% sensitive, 58% specific

– Only applied to CS, not gluten sensitivity

Common Pitfalls When Adapting a Serum ELISA Method for Stool

• Stool sample is over-diluted prior to analysis

• Inadequate washing of ELISA plates (stool takes more)

• Not customizing mathematical conversion of OD to a Unit, or interpretation of calculated Unit

• Centrifuge speed for stool too high, or too low

• Inadequate volume, improper preservation

• For AGA, restriction to celiac paradigm