nutrition in complementary care · include impotence, amenorrhea, irrita-bility, depression, and...

NCC Newsletter 2000 • Volume 3, Issue 1 A Dietetic Practice Group of the ADA ❂ 1

continued on page 4 continued on page 8

Therapies . . .A Dietetic Practice Group of the American Dietetic Association Fall 2000 • Volume 3, Issue 1

Supplements . . .Translating Nutritionand GeneticInformation IntoClinical PracticeVyoone T. Lewis PhD, MPH, RD

The Human Genome Project providesus with the information necessary tounderstand how hereditary differencesmake each of us unique. The projecthighlights new approaches in molecularmedicine to the diagnosis, treatment, andmanagement of disease. Genes, which areshort segments of DNA, are instructionsthat tell cells how to behave. Asinformation continues to unravel on therole of genes and how they affect nutrientrequirements and/or individual responsesto dietary interventions, nutrition prac-titioners will need to incorporate thisinformation into their nutrition counselingpractices.

The interaction of genes, nutrients, andthe environment determines phenotype andthe development of an individual.1

Although many chronic diseases have agenetic component, changes in environ-mental factors, like diet and lifestyle,contribute to the development of thesediseases.2 Genetic variation impacts humannutrition and can account for individualnutrient requirements for therapeuticbenefit.

Genetic diseases are usually char-acterized as single gene defects,chromosomal disorders, congenitalmalformations, disorders of mitochondrialDNA (cytoplasmic inheritance), disordersdue to somatic cell mutations, andmultifactorial inheritance, which is thebasis for many common diseases.2

Some diseases are inherited in Men-delian fashion, which include autosomalrecessive, autosomal dominant, X-linkedrecessive, and X-linked dominant. Adominant gene is one that manifests its

HemochromatosisSusan Moore, MS, RDDescription and Prevalence

Hereditary hemochromatosis (HH) isa type of primary iron overloadcharacterized by a genetic mutation thatcauses increased intestinal absorption ofiron. The excess iron is deposited in theparenchymal cells of the liver, pancreas,heart, and joints and causes inflammationand subsequent fibrosis and destruction. Ifundetected and untreated, HH can resultin cirrhosis, hepatoma, diabetes, cardio-myopathy, arthritis, hypogonadism, anddeath.1,2 Previously considered to be rare,recent estimates place the prevalence of thehomozygous genotype at 1 in 250persons—roughly 1 million people—and about 1 in 9 people are carriers (peoplewith one defective and one normal gene),3

making HH more common than cysticfibrosis, sickle-cell anemia, orphenylketonuria.

DiagnosisHH is frequently under-diagnosed,

primarily because its sequelae are notspecific to iron overload. Consequently, theunderlying cause is not recognized ortreated and organ damage progresses. Theclinical manifestations of HH usually donot appear until a person reaches 40 to 60years of age, when sufficient iron hasaccumulated to cause organ damage. Byage 40 about 50% of men and 13-20% ofwomen with untreated HH will haveclinical manifestations of iron overloadsuch as gray or bronze skin pigmentation,diabetes, and chronic abdominal pain.4

However, early signs and symptoms of HHinclude impotence, amenorrhea, irrita-bility, depression, and fatigue.2 Abnormallaboratory values suggestive of progressiveiron overload are an asymptomaticelevation of the liver enzymes alanineaminotransferase and aspartate amino-transferase. Liver disease—particularlycirrhosis—is present in 30-94% of patients

NUTRITION IN COMPLEMENTARY CARENUTRITION IN COMPLEMENTARY CARENUTRITION IN COMPLEMENTARY CARENUTRITION IN COMPLEMENTARY CAREIn This Issue...TherapiesTranslating Nutrition and Genetic

Information Into Clinical Practice ...... 1SupplementsHemochromatosis ........................ 1Homocysteinemia ........................ 9

HerbsCarotenoids, Cancer, and theConnexin Gene ............................. 3

Functional FoodsFood Biotechnology ..................... 5

Point/CounterpointUse of Genetically EngineeredFoods ............................................. 6

ReaDer ReportsPreparing for the GeneticsRevolution................................... 16The Human Genome Project:Implications for DieteticsPractitioners ................................ 14

ResourcesBook Reviews ............................. 13

CPE ArticleGenetics and Nutrition:The Future is Now.......................17

Of InterestMembers in the News ............. ..10Annual Meeting...........................22Editorial Staff ..............................22Executive Committee ................ 24Chair’s Corner .................... 2

Editor’s Notes .................... 2

2 ❂ Nutrition in Complementary Care NCC Newsletter 2000 • Volume 3, Issue 1

Chair’s Corner . . .Changing Times…Cheryl Galligos, MA, RD

Today I picked up this week’s editionof Time magazine. And yes, “Times–theyare achangin’”. This issue of Time entitled“The Future of Technology” contains anarticle written by the infamous Bill Gatescalled “Will Frankenfood Feed theWorld?” Fittingly, this issue of the NCCnewsletter focuses on genetics andbiotechnology and the changes ahead forus as dietetics professionals. The world ofdietetics as we know it will never again bethe same. As the profession changes, somust we change.

The leadership of NCC and theeditorial board of the newsletter areconstantly working to keep pace with thesechanging times and provide cutting edgeinformation for our members. You willagree that NCC’s editorial staff is extra-ordinaire when producing a greatnewsletter covering the latest happeningsof nutritional complementary care. Otherchanges are coming to NCC. Rick Hall,NCC’s Webmaster, and Ruth DeBusk, ourPublications Chair, are planning excitingnew features for NCC Web site in the nearfuture. Be sure to bookmark www.complementarynutrition.com and visit usoften. Make it a priority also to be on linewith NCC’s electronic mail list bycontacting Gretchen Forsell at [email protected] to enroll. On line you willdiscover colleagues willing to answerquestions and share a wealth ofinformation.

The American Dietetic Association ischanging as can be seen in the new face ofthe 2000 annual meeting in Denver-TheFood and Nutrition Conference andExhibition (FNCE). Efforts are beingmade to keep the ADA in the forefront byproviding an annual meeting andexhibition that has something for everyone.Be sure to read about NCC activities beingplanned for the FCNE in Denver in thisissue. We hope to see you in DenverOctober 16-19, 2000.

Finally, I would like to recognize thechange in leadership of NCC. Newofficers in several positions are eager tohelp NCC keep pace with the times.Welcome to Rebecca, Felicia, Diane,

Sarah Harding Laidlaw, MS,RD, MPA

As Cheryl so aptly stated, “The times,they are (definitely) achanging! With thisissue you will observe the first majorchanging of the guard for NCC. This is ourthird year as a DPG, and what a memorableone it will be. Welcome to an exciting DPGand changing profession!

This past summer most of us could notturn on the news or open a newspaperwithout hearing about the mapping of thehuman genome. NCC was ahead of thegame, planning this issue on geneticsmonths before the “big” announcement. Iam sure that after you have read this issueyou will know that we, as a DPG, are inthe forefront. We understand that therelationship of clients’ genetics and howwe counsel them will determine whethertheir nutrition prescriptions will work ornot.

For a novice in the rapidly changingarea of genetics, I have already applied,with success, concepts that I have readabout in preparation for this issue. One sizediet prescription does not fit all. As theprofession changes, yes, we too mustchange with an open mind. I am sure thatmany of you will experience what I haveas you approach change with an open mind.

A heartfelt “thanks” goes to RuthDeBusk, RD, PhD the Publications Chair

The views expressed in this newsletter are those ofthe authors and do not necessarily reflect the policiesand/or official positions of the American DieteticAssociation.

We invite you to submit articles, news andcomments. Contact us for author guidelines.

Send change-of-address notification to theAmerican Dietetic Association, 216 W. Jackson Blvd,Ste. 800, Chicago, IL 60606-6995.

Copyright © 2000 Nutrition in ComplementaryCare, a Dietetic Practice Group of the AmericanDietetic Association. All material appearing in thisnewsletter is covered by copyright law and may bephotocopied or otherwise reproduced for noncommer-cial scientific or educational purposes only, providedthe source is acknowledged. For all other purposes, thewritten consent of the editor is required.

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For international orders, add $5 shipping andhandling per annual subscription and for eachback issue order of 1-4 issues. For 5 or moreissues, the cost is $5 for 4 issues plus $1.50 foreach additional issue.

Send checks payable to NCC-DPG#18 to theNewsletter Editor. See back cover for address.

ISSN 1524-5209

Geeta, Margaret, Sarah, and Esther (seecontact information on the back page).And a very special thank you to those whoare saying adieu..Pam, Leslie, Mari andTheresa. Lisa, of course, is still providingNCC with valued assistance in her positionas Past Chair.

As a new year begins for NCC, I saywelcome if you are new and thanks forjoining again if you are returning. Pleasecontact us to let us know how we can helpyou “keep up with the changing times”.Here’s to a great third year for NCC.

Editor’s Notes . . .

and first Editor of the NCC newsletter. Shehas been supportive and helpful during thistransition, and I look forward to continuingmy work with her in the future. Thanksalso to those who assisted in preparationof this issue, Ruth, as a major contributor,and all of the Section Editors. And also toEsther Trepal, RD who will be assumingthe role of Associate Editor; her help hasbeen invaluable in the past year!

I look forward to working with all 2100plus members of NCC, individuallywhenever possible. I encourage each ofyou to provide suggestions for how we cankeep the newsletter and Web site workingfor you. Your support of the DPG andnewsletter is what has made us, in a shortthree years, what we are today. I am certainthat I can speak for all of the ExecutiveCommittee when I say that we want thistrend to continue.

I hope to see you in Denver. Look forNCC Executive Committee members andmake yourself known! Your input isappreciated and wanted.


Herbs . . .Carotenoids, Cancer,and the ConnexinGeneJohn S. Bertram, PhD

In Western societies, it is now gener-ally accepted that lifestyle, rather than ge-netics, is the major contributory factor tocancer risk. In a landmark review, Doll andPeto estimated this risk to be approxi-mately 70%, with 30% attributable to useof tobacco products and the remainder todiet and lifestyle. 1 A consistent finding hasbeen that populations with low cancer riskconsume significantly higher amounts offruits and vegetables than populations withhigh cancer risk. Analysis of the types offruits and vegetables and of their constitu-ents has reliably implicated the carotenoidsas being associated with decreased cancerrisk. These findings have been confirmedin studies measuring plasma carotenoidlevels (reviewed in reference 2). Currently,26 carotenoids and their metabolites havebeen identified in serum, and risk reduc-tion has been linked to several. 2

Carotenoids are plant pigments in-volved in photosynthesis; they act to in-crease the efficiency of this process and toprotect plant cells from oxidative damage.Carotenoids may serve a similar protec-tive function in the human eye. High con-centrations are found in the macula, the so-called “yellow spot”, where highest expo-sure to photons occurs. The major caro-tenoids found in the human diet and inmany herbal supplements are alpha- andbeta-carotene, found in deep yellow andorange fruits and vegetables; lutein, foundextensively in green leaves, yellow fruitsand vegetables, and in eggs; and lycopene,a red-colored carotenoid found extensivelyin tomatoes and other red fruits. Becausecarotenoids contain many unsaturatedbonds, they act as efficient lipid-phase an-tioxidants. A few, those containing intactbeta ionone rings, can be converted bymammals into vitamin A.

Oxidative damage is known to be car-cinogenic and, because vitamin A itself isin some situations a cancer preventiveagent, these two properties of carotenoidswere thought to be responsible for the can-cer risk reduction. However, when we firststarted investigating the activity of caro-

tenoids under defined cell culture condi-tions, we found that neither activity corre-lated with their ability to inhibit experi-mentally induced cancer. Instead, all ac-tive carotenoids were found to causeupregulated (increased) expression of agene, connexin 43, which codes for a trans-membrane protein that is critical in theformation of gap junctions. 3

Gap junctions are necessary for cell-to-cell communication. Adjacent cells ina tissue communicate with each otherthrough gap junctions in their cell mem-branes, water-filled pores through whichsmall molecules in the cytoplasm of onecell can pass into the cytoplasm of the ad-jacent cell, forming a communication net-work among the cells in a tissue. Each poreis ringed with connexin proteins, six mol-ecules per pore. The connexins on one celldock with those on an adjacent cell to forma tunnel linking the two cells. Moleculesand ions pass through this tunnel. This pro-cess is called “junctional communication.”Connexin 43 is the most widely expressedconnexin protein and its genetic expres-sion is regulated by carotenoids.

This type of communication occurs invirtually all cell types and is the most di-rect and most rapid form of intercellularcommunication known. 4 These findingswere exciting since in other studies we hadfound that growth-inhibited normal cellscould inhibit proliferation of tumor cellswhen cells were in communication throughgap junctions. 5

Interestingly virtually all human tu-mors lack junctional communication. Evenin pre-cancerous dysplastic regions of theuterine cervix, connexin 43 is poorly ex-pressed in comparison with normal tissue. 6

Lack of communication in dysplastic cellswould lead to enhanced proliferation dueto isolation from surrounding normal cells;by enhancing gene expression, dietarycarotenoids could restore communication,decrease proliferation and decrease pro-gression to malignancy. How carotenoidsstimulate the expression of this gene is notknown.

To determine the significance of in-creased communication, we directly testedeffects in human cervical cancer cells. Wegenetically engineered these cells so thatthey would express connexin 43 only whentreated with tetracycline, which at the con-

continued on page 10

centrations used is not toxic to human cells.Any changes thus result from changes inexpression of the engineered gene. We se-lected carcinoma cells that did not expressthis gene and transferred the connexin geneto these carcinoma cells, which then be-gan to express large quantities of functionalgap junctions. When these cells were in-jected into immunodeficient athymic mice,tumor growth was strongly inhibited inthe mice in which connexin gene expres-sion was induced by tetracycline as com-pared with mice in which the connexingene was not expressed.6 A search is nowon to identify and characterize the natureof the junctionally transmitted signals in-volved in tumor growth inhibition.

Proliferation is central to the produc-tion of cancer. 7 Dietary carotenoids, ob-tained from foods or herbal supplements,counter the loss of junctional communica-tion that occurs in preneoplastic cells. Byencouraging cell/cell communication,carotenoids can help suppress abnormalproliferation and, thereby, act as cancerpreventive agents. Because all cells are ex-posed to DNA damage, all individualsprobably contain many cells that have amutation in a gene that, when the cell pro-liferates, the sequence of events that leadsto cancer is initiated. By preventing, or atleast decreasing, abnormal proliferation,carotenoids can decrease the rate at whichthese "initiated cells" are able to progressto malignancy. At present, carotenoids ap-pear to act preventively rather than thera-peutically. As in other diseases, however,it is better to aim for prevention than cure. 8

References1. Doll R, Peto R. The Cause of Cancer. Oxford:Oxford University Press; 1981.2. Mayne ST. Beta-carotene, carotenoids, anddisease prevention in humans. FASEB J.1996;10:690-701.3. Zhang L-X, Cooney RV, Bertram JS. Caro-tenoids up-regulate connexin 43 gene expressionindependent of their pro-vitamin A or antioxidantproperties. Cancer Res. 1992;52:5707-5712.4. Nicholson SM, Bruzzone R. Gap junctions:getting the message through. Curr Biol.1997;7:R340-344.5. Mehta PP, Bertram JS, Loewenstein WR.Growth inhibition of transformed cells correlateswith their junctional communication with normalcells. Cell 1986;44:187-196.6. King TJ, Fukushima LH, Hieber AD, et al.Reduced levels of connexin 43 in cervicaldysplasia: inducible expression in cervicalcarcinoma cell lines decreases neoplastic potentialwith implications for tumor progression. Carcino-genesis. 2000; in press.7. Ames BN, Gold LS. Mitogenesis, mutagenesis,and animal cancer tests. Chemically Induced CellProliferation: Implications for Risk Assessment.New York, NY: Wiley-Liss, Inc., 1991:1-20.


Therapies . . .(cont.)continued from page 1

phenotypic (recognizable) effect inheterozygotes (having one copy of amutant gene). A recessive gene causes aphenotypic effect only when present in thehomozygous state (having two copies of amutant gene). X-linked disorders can resultfrom any of several genes that controlmany aspects of development and functionand are transmitted on the X chromosome.

Inborn errors of metabolism are usuallysingle gene defects. For example,phenylketonuria (PKU) is an inborn errorof metabolism characterized by decreasedor deficient activity of the hepatic enzymephenylalanine hydroxylase (PAH), whichconverts phenylalanine to tyrosine. In theabsence of PAH, individuals have anaccumulation of phenylalanine and itsmetabolites. In addition, tyrosinedeficiency develops due to a block in itsproduction. Treatment involves correctingthe primary imbalance by restrictingdietary sources of phenylalanine andprescribing supplemental tyrosine.3

In diseases involving multifactorialinheritance, the phenotype is determinedby the interaction of several genes atdifferent loci, with an additive effect of anenvironmental component. There arecertain common alleles (variants at a singlelocus or polymorphism) that can predictindividual responses to environmentalchanges.

In humans, 30% of all loci (alleles)have polymorphic variants (two or morealleles with a frequency of at least 1% ormore). An average person is heterozygousat about 10% of the loci. Some alleles havea positive, sometimes proactive, advantagein the heterozygous state, and some arelinked to common diseases and are affectedby environmental factors. Nutritionecogenetics is an extension ofpharmacogenetics, the study of howgenetic variation impacts drug responsesand tolerances.

Like pharmacogenetics, the field ofnutrition ecogenetics is evolving as welearn more about genes and how theyinteract with nutrients and predictsusceptibility to certain diseases.Polymorphic variants as described belowcan impact responses to dietary recommen-dations.

The Apolipoprotein VariantsGenetic variants in apolipo-

protein E (Apo E2, 3 or 4) can predictresponse to a low cholesterol diet. Oneperson in 50 has the Apo E2 variant that isassociated with hypertriglyceridemiasecondary to increases in energy, trans fattyacid, or carbohydrate intake. This variantis expressed in the presence of obesity,diabetes, and hypothyroidism. The Apo E4variant is found in 15% of Caucasians,35% of African (30% of Nigerian) andAsian populations, 22.7% of Finns, 20.3%of Swedes and 9.4% of Italians.

Women with Apo 3/2 genotypes havea reduction in the more protective high-density lipoprotein (HDL) cholesterol andwould benefit from a high polyunsaturateddiet. However, a general recommendationof a low fat diet would not benefit thisgenotype. Men with the Apo 4/3 genotypeshow an improvement in LDL/HDL ratioon a low fat diet. In individuals with the 3/3 genotype, a decrease in serum cholesterolwhen consuming oat bran at four weeks isnoted compared to no changes in the E4/4or 4/3 genotypes.4

In the variant Apo A-IV-1/2, found in1 in 7 persons in the United States, adecrease in the response of plasmacholesterol concentration with dietarycholesterol restriction is reported.However, no changes in triglycerides orHDL cholesterol are demonstrated. Thus,not every individual with these variantswill respond to a general recommendationof a low fat, low cholesterol diet.

The Variant Associated With SodiumThe angiotensinogen gene that has

been suggested to influence salt sensitivityhas been described.5 Individuals with theAA and AG genotypes respond to a sodiumrestricted diet with decreases in bloodpressure. GG genotypes are less saltsensitive and will have decreases in bloodpressure in response to a low sodium dietbut not so significantly as the AA and AGgenotypes.

A polymorphic variant (Gly 460 Trp)is associated with changes in bloodpressure and can be used to identify whichpatients will respond to sodium restriction.Patients with this variant allele have agreater decrease in blood pressure withsodium restriction.5

Vitamin D Receptor VariantIn postmenopausal women with the BB

vitamin D receptor genotype, it has beenshown that they absorb less dietary calciumthan the bb genotype. Thus the BBgenotype women prescribed the currentDietary Reference Intake (DRI) forcalcium, 1000-1200 mg/day, may notabsorb adequate amounts of calcium andwould typically require more than theDRI.6

Translating to Clinical PracticeNutritional recommendations that are

universal do not take into account geneticvariations that determine an individual’sresponse to nutrition intervention. Thefollowing are tips for integrating thisinformation into counseling practices:

• Prior to counseling patients on generalrecommendations for disease managementor RDAs/DRIs for prevention of commonnutrition deficiencies, evaluate their familyhistories.• Make family history a part of yournutrition assessment tool. Obtain impor-tant demographic and ethnic informationto identify individuals at risk for geneticvariants.• Determine if individuals have undergonegenetic/biochemical testing to identify riskcategories for chronic disease develop-ment. Ascertaining this information canhelp to target dietary recommendations andnutrient requirements for that person.• Keep up to date on advances in theHuman Genome Project at www.nhgi.nih.gov or www.balancehealthsolutions.com.

References1. Velazquez A, Bourges H. Implications of theHuman Genome Project for understanding gene-environment interactions. Nutr Rev. 1999;II:S39-S42.2. Weatherall DJ. The New Genetics and ClinicalPractice. New York, NY: Oxford Press; 1991.3. The Ross Metabolic Formula System. NutritionSupport Protocols. 3rd ed., 1997.4. Simopoulos AP. Genetic variation and nutrition.NutrRev. 1999;II:S10-S19.5. Mongeau JG. Heredity and blood pressure. SeminNephrol. 1989;9:208-216.6. Morrison NA, Qi JC, Tokita A, et al. Prediction ofbone density from vitamin D receptor alleles.Nature. 1994;367:284-287.

Vyoone T. Lewis, PhD, MPH, RD is a board-eligible biochemical geneticist. CurrentlyExecutive Director of Balance Health Solutions,a subsidiary of Professional NetworkConsultants, LLC, Vyoone has authorednumerous publications, including Low CostAlternative Health Care Therapies. ContactVyoone at www.balancehealthsolutions.com.


Functional Foods…Food BiotechnologyLori Holladay, MPH, RD andFelicia Busch, MPH, RD,FADA

Do you eat cheese? If so, you’re a con-sumer of the benefits of biotechnology.Over half the rennet used in cheese mak-ing worldwide is produced through abiotech fermentation process that elimi-nates the “old-fashioned” method. (LauraIngalls Wilder describes the method in herLittle House on the Prairie books: sacri-ficing a baby calf for the rennet found inits stomach lining in order to make cheese).Rapid-rise yeast products that speed upbread-making were developed in Englandby rearranging and duplicating certainyeast genes. On the horizon are foods thatcontain higher amounts of health-promot-ing phytochemicals or possess disease- ordrought-resistance.

What Is Biotechnology?For centuries, farmers have bred crops

and animals to develop foods with greateryields, better drought resistance, or fasterripening. The objective of biotechnologyis to apply biologic methods to improvevarious characteristics of plants and/or ani-mals. Biotechnology allows for the trans-fer of genetic information in a more pre-cise manner. Traditional breeding involvesthe transfer of large blocks of genes,whereas biotechnology entails the trans-fer of only a limited number of genes.

Genetics – A Quick ReviewA brief review of genetics can be use-

ful in evaluating the role of biotechnologyin our food supply. In 1953 James Watsonand Francis Crick discovered the structureof DNA. This double helix molecule hastwo strands of DNA composed of pairs ofchemicals: adenine (A) with thymine (T);and guanine (G) with cytosine (C). Theseare the base pairs. A segment of DNA thatencodes enough information to make oneprotein is called a gene. It’s the specificorder of DNA’s base pairs that determineswhich specific genes code for specific pro-teins, which determine individual traits.

By 1973, scientists were able to iso-late individual genes, and by the 1980scould transfer genes from one organism toanother. With biotechnology, a single gene

may be added to the DNA strand in a pre-cise manner without having to transferlarge blocks of genes that are unrelated tothe traits sought (see Genetics and Nutri-tion: The Future is Now on p. 15 for anoverview).

Biotechnology vs. TraditionalAgriculture Methods

Farmers have routinely used theirknowledge of genetics to improve foodproduction. Corn, for example, looks noth-ing like it did one hundred years ago be-cause of plant breeding, which has helpedU.S. farmers produce almost 600% morecorn in 1985 than in 1930. Biotechnologyis the latest development in the evolutionof farming practices. Ideally, present daycorn is used as the base and then is furtherenhanced by adding to it another desirablecharacteristic, such as an improved aminoacid composition. Biotechnology allowsfor this precise insertion of genetic mate-rial. Traditional breeding using conven-tional technology, in contrast, will losecharacteristics of the original corn as partof the genetic reshuffling that occurs dur-ing the attempt to add the new trait. Thedifference between these two techniquesis dramatic.

Food, Nutrition and Health:Implications for Functional Foods

Many experts predict that the nextwave of biotechnology will be in the areaof efforts to develop functional foods. Asadditional healthful food components areidentified, biotechnology will provideways to incorporate these components intoplants and animals.

Nutrient profiles of certain foods arealready improved by biotechnology. A soy-bean that produces oil with a “hearthealthy” fatty acid profile targeted to im-prove cardiovascular health is on the mar-ket. Rice and oils have been produced toexpress high carotene levels, with the po-tential to reduce the incidence of vitaminA-related blindness found in many partsof the developing world.

Safety IssuesThe Food and Drug Administration

(FDA) provides primary oversight for thesafety of all foods. Foods are judged bywhether they are safe, not by the processby which they have been developed. Foodsdeveloped through biotechnology are

evaluated to assess their equivalence tothose foods developed through traditionalmethods. Equivalent in this context meansthere is no meaningful change or differ-ence in the nutrient composition or allergypotential of a food.

The FDA, the United States Depart-ment of Agriculture (USDA), and the En-vironmental Protection Agency (EPA),along with individual state governments,have been working together to ensure thatcrops produced through biotechnology aresafe to eat. In 1992 FDA resolved thatcrops produced using biotechnology mustmeet the same rigorous standards as thosecreated by traditional means. While thereis no such thing as zero risk for any food,consumers can be confident that foods pro-duced using biotechnology meet the strin-gent food safety standards enforced by thegovernment. In fact, biotechnology hasbeen studied and researched significantlymore than common food manufacturingtechniques such as freezing, canning, anddehydration.

Concern has been expressed about thetransfer of genes from animals to plants.Such transfer between species is possiblebecause plants and animals carry out simi-lar metabolic reactions and the genes forthese proteins are similar. Technically, anindividual gene is neither a plant nor ananimal gene. To date, no cross-speciesfoodstuffs have been developed – despitemedia headlines to the contrary.

Who Benefits From Biotechnology?Consumers and producers benefit from

food biotechnology. Direct benefits toconsumers include enhanced flavor andfreshness and improvements in taste, qual-ity, and nutritional value. A number of in-direct benefits to consumers include re-duced used of pesticides; more sustainabletillage practices, which address costly en-vironmental problems like water pollution;less potential exposure to chemical resi-dues by farmers and groundwater; and in-creased food yields (for developing coun-tries this could help to address food short-ages and hunger).

FDA Food Labeling PolicyFoods produced through biotechnology

will need to have a special label if a knownfood allergen has been introduced,

continued on page 11


Use of GeneticallyEngineered FoodsEdited by Rebecca Ephraim, RD

COUNTERPOINTLori B. Taylor, MEd, MS, RD

Genetic engineering is one of the mostintriguing and powerful tools developed byscience to manipulate the natural world.This technology has allowed majoradvances in the treatment of humandisease. Scientists have been able tosynthesize drug treatments that moreclosely approximate human proteins, suchas erythropoietin, human insulin,t-PA and rituxan. The side effects of thesedrugs are minimal compared to those oftheir predecessors and offer real hope forthe treatment of chronic disease.

Biotechnology has also been usedextensively in the plant kingdom.Genetically engineered (GE), also calledgenetically modified, foods such assoybeans and corn have been designed tohave herbicide tolerance, pest resistance,and altered nutritional profiles. Initially,these new foods offered great promise:they would be safer for the environment,have greater yields and be more nutritious.However, scientific evidence does notsupport these promises.

Assumed—not proven—safe.The regulatory process for assessing

the safety of GE foods assumes thatrecombinant DNA (rDNA) movement ofgenetic material between organisms isequivalent in risk to hybridization ornaturally occurring movement of geneticmaterial. The National Academy ofSciences (NAS) upheld this principle in anApril 2000 report stating that “there is noevidence that unique hazards exist eitherin the use of rDNA techniques or in themovement of genes between unrelatedorganisms.”1 This does not mean that GEfoods are safe; it means nothing harmfulhas been discovered or reported yet.

Many scientists predict direconsequences when it comes to GE foods.John Fagan, PhD, noted molecularbiologist and NCI cancer researcher, states“splicing foreign DNA into an organism’sgenome can cause unpredictabledisruptions in the behavior of one or more

or bacteria, which cause them to functionindependently of the host organism’sintricate regulatory system. Moreover, thepresence of these powerful promoters canalter the expression levels of the nativegenes. Due to such factors, the resultingfood could be rendered toxic, allergenic,or otherwise harmful.”2

Dr. Fagan is not alone in his concernabout the safety of GE foods. Some Foodand Drug Administration’s scientiststhemselves believe that there are differentrisks posed by GE foods that need to beassessed and that a more stringentregulatory process should be put intoplace.3

GE foods may pose health risk.Recent studies have shown the

potential for increased allergenicity andtoxicity in GE foods. When genesencoding a brazil nut protein sequencewere engineered into soybeans to increaseamino acid content, the allergenicproperties of the brazil nut were transferredas well.4 Rats fed GE potatoes developedboth immune and organ damage, as wellas a viral infection of the GI tract.5

GE foods can be of inferior nutrition.Genetically engineered foods have

altered protein content and thus have adifferent nutritive value than con-ventionally grown crops. Recent researchdiscovered that GE soybeans haddecreased levels of beneficial phyto-estrogens when compared to conventionalsoybeans.6 In what may be an attempt tocontrol research outcomes, the researchershave been refused further seed to repeattheir experiments.7

No environmental gains offered.In laboratory studies, scientists have

discovered that GE crops producing theBacillus thuringiensis (Bt) toxin causelethality of non-target, beneficial insects(Monarch butterflies8 and corn-borereating lacewings9). Bt toxin present in cropfoliage has also been found to have apersistent, negative effect on soilmicroecology.10 Since Bt crops producetoxin systemically, one wonders howcontinuous consumption of Bt toxin willaffect humans?

herbicides and inadvertent gene transferthat could produce new plant viruses andsuper weeds resistant to herbicides, thereport recommended only that the effectsbe monitored, not that rigorous, pre-markettesting be required to prevent theseeffects. 1

Increases in crop yield are inconsistent.In a study by the USDA, yields of GEsoybeans were not sub-stantially greaterthan conventional soybeans.11, 12

GE foods: who benefits?Given the health and environmental

risks and lack of sustained, measurablebenefit of GE foods to farmers, whoseinterests are GE foods serving? Is it largechemical and agricultural businesses thatintegrate their seed and chemical packagesand forbid farmers from keeping or sellingseed11 to ensure further economic benefitto the corporation?

Until rigorous pre-market safety testingand labeling happens, we are theexperimental group for human safety.Unfortunately, there is no control group.Without labeling, even retrospectiveresearch will be impossible to conduct, asfood origin will not be traceable.

Alternatives to GE foodsIn all the rhetoric, few look beyond the

two major options of farmingconventionally with pesticides or using GEfoods and herbicides. Long-termsustainable practices employing smallerfarms and “agroecological” technologiesare being used throughout the world withmuch success.11 Perhaps it’s time to lookat restructuring our agriculturalinfrastructure to support smaller, moresustainable forms of farming that improvethe physical and economic health offarmers and consumers.

References1. National Research Council. Genetically modifiedpest protected plants: science and regulation.Available at http://www.nap.edu/html/gmpp/.Accessed 5/4/00.2. Fagan J. Declaration of John Fagan, Ph.D. UnitedStates District Court for the District of Columbia,Civil Action No. 98-1300 (CKK). Available at http://www.bio-integrity.org/fagandeclaration.html.Accessed 5/12/00.3. Key FDA documents revealing (1) hazards ofgenetically engineered foods and (2) flaws with howthe agency made its policy. Available at http://www.bio-integrity.org/list.html. Accessed 5/12/00.

Point/Counterpoint . . .Although the NAS report admits to

the potential for crop resistance to GEactive genes. The foreign genes…areroutinely fused to promoters from viruses


4. Nordlee JA, Taylor SL, Townsend JA, et al.Identification of a Brazil-nut allergen in transgenicsoybeans. N Engl J Med. 1996;334:688-692.5. Ewen SW, Pusztai A. Effect of diets containinggenetically modified potatoes expressing Galanthusnivalis lectin on rat small intestine. Lancet.1999;354:1353-1354.6. Lappé MA, Bailey B, Childress C, Setchell KDR.Alterations in clinically important phytoestrogens ingenetically modified, herbicide-tolerant soybeans. JMed Food. 1999;1:241-245.7. Lappé MA, Bailey B. Letter to the Editor. StLouis Post-Dispatch, June 25, 1999. Available athttp://www.cetos.org/toxalts/ASAResponse.html.Accessed 5/12/00.8. Losey JE, Rayor LS, Carter ME. Transgenic pollenharms monarch larvae. Nature. 1999; 399:214. Letter.Abstract available at: http://www.ent.iastate.edu/entsoc/ncb99/prog/abs/D81.html. Accessed 5/12/00.9. Hilbeck A, Baumgartner M., Fried, PM, Bigler F.Effects of transgenic Bacillus thuringiensis corn-fedprey on mortality and development time of immatureChrysoperla carnea (Neuroptera: Chrysopiae).Environmental Entomology. 1998;27:480-487.10. Altieri MA and Rosset P. Ten reasons whybiotechnology will not ensure food security, protectthe environment and reduce poverty in the developingworld. Ag Bio Forum. 1999;2:155-162. Available athttp://www.agbioforum.org. Accessed 5/4/00.11. United States Department of Agriculture.Genetically engineered crops for pest management.Washington DC: USDA Economic Research Service;1999.12. Altieri MA and Rosset P (1999). Strengtheningthe case for why biotechnology will not help thedeveloping world: a response to McGlouglin.AgBioForum. 1999;2:226-236. Available at: http://www.agbioforum.org. Accessed 5/4/00.

Lori B. Taylor, M Ed, MS is in privatepractice in Oak Harbor, Washington andteaches nutrition through the distance-learning program at the University ofWashington. Contact Lori [email protected].

POINTChannapatna S. Prakash, PhD

I suspect that the average American,hearing or reading something aboutbiotechnology, is at a loss to understandall that is involved. For many, thediscussion of genes and proteins boilsdown to: Whom am I going to believe,those who oppose biotechnology or thosewho support it?

Without question, the scientificcommunity is overwhelmingly supportiveof the technology as evidenced by a seriesof recent reports:

• On April 5, 2000 the National Academyof Sciences (NAS) issued a statement thatthere is no evidence suggesting foodsproduced through biotechnology are anyless safe than conventional crops. 1 In fact,the scientific panel concluded thatgrowing such crops could haveenvironmental advantages over othercrops. NAS recommended a fewregulatory changes, mostly to improvepublic acceptance.

• Another report, issued on April 13, 2000by the Basic Research Subcommittee ofthe House Committee on Sciencesummarizes the testimony of leadingscientific experts who had appeared beforethe subcommittee. It makes a very strongcase for the safety of biotechnology andwarns against needless over-regulation,which could delay development of atechnology with great potential for good.www.house.gov/science

• On April 14, 2000 the National Centerfor Food and Agricultural Policy releaseda report about the benefits of transgenicsoybeans, which have been improved towithstand a certain herbicide. The report,funded by the Rockefeller Foundation,concludes that farmers, who had beenusing three to four herbicides to controlweeds in soybeans, were able to use justone herbicide, eliminating 16 million acretreatments of herbicide per year. Theannual savings to farmers was estimatedto be $220 million. www.ncfap.org

• Around the world, more than 2,000scientists, including two Nobel Prizewinners, have signed a petition in supportof genetically modified crops.Overwhelmingly, scientific organizations,professional societies, and internationalbodies such as the World HealthOrganization agree that oversight ofbiotech crops should focus on thecharacteristics of the plant, its intendeduse and the environment into which it willbe introduced, not on the method used toproduce it. In other words, the scientificcommunity is strongly united in the viewthat there is nothing inherently risky aboutbiotech crops than crops developedthrough conventional breeding methods.

Three agencies of the federalgovernment – the EnvironmentalProtection Agency, the Food and DrugAdministration, and the DepartmentofAgriculture – are responsible fortheregulation of biotechnology.2 Hundredsoffield studies and specifically designedtoxicology studies have demonstrated thatbiotech crops pose no greater risk than anyother crop.

Opponents of biotechnology ignorethese data and continually cite the samehandful of studies that have been done inartificial laboratory settings and have notbeen duplicated in actual field situations.The most notable example is a study

with Monarch butterflies, which showedthat larvae of the popular insect could beharmed if they ate enough pollen from cornimproved to resist harmful insects. Theauthor of the study cautioned that it wasonly a laboratory finding,3 but activistsseized upon it to stir emotions. Thefollowing summer, 20 scientists fromseveral major universities conducted manyfield studies, which showed that Monarchlarvae are rarely exposed to the corn pollenand, therefore, are not threatened.4

Scientific reviewers have soundlycriticized other studies cited by biotechopponents. The American SoybeanAssociation (ASA) criticized one study,which purports to show that biotechsoybeans differ in nutritional content fromconventional soybeans. ASA said there ismore variability among variousconventional soybean varieties than wasseen when biotech and conventionalsoybeans were compared.5 Another study,which alleged that genetically modifiedpotatoes harmed rats, was criticized by theRoyal Society, Britain’s independentscience academy, as seriously flawed.6

Furthermore, rather than testing acommercial product, the researcher usedpotatoes that had been altered to contain agene from a known toxin, which neverwould make it through existing regulatoryprocesses.

An April 2000 report from a U.S.House subcommittee, chaired by Rep.Nick Smith of Michigan, is an outstandingopportunity to read and understand in clearterms how biotechnology works and howit can help solve agricultural problems. Itdiscusses the risks and benefits, reviewsthe regulatory system, and shows whymany of the emotional issues raised byopponents have little scientific support.The discussion of the alleged threat toMonarch butterflies, described as“overblown and probably insignificant”,isan excellent example. Testimony from 17scientists, including some critics ofbiotechnology, was the basis for the report,which can be viewed at www.house.gov/science.

The report makes several findings,including: biotechnology is reducingchemical pesticide use and will continueto do so; there is no greater risk ofintroducing allergens into biotech cropsthan with traditionally bred crops; the risk


with HH.5 Therefore, HH should beconsidered in the evaluation of any liverabnormality. HH should be considered apossibility based on laboratory valuesindicating abnormal iron metabolism. TheCollege of American Pathologists (CAP)developed an algorithm that recommendsre-testing of trans-ferrin saturation (in thefasting state) in the event of an elevatedinitial value, > 60% in men and > 50% inwomen; if results remain high, measureserum ferritin. If serum ferritinconcentration is > 400 mg/L in men, > 200mg/L in women of childbearing age, and> 300 mg/L in post-menopausal women,consider a liver biopsy. Biopsy of the liver

evaluates the accumulation and extent ofiron infiltration into tissues. A definitivediagnosis of HH can be made if hepaticiron concentration is greater than 80mmol/g dry weight.6

TreatmentThe primary treatment of HH is

phlebotomy or the removal of 1 U (500mL of blood) once or twice weekly untiliron deficiency anemia develops.Thereafter, normal iron status ismaintained by periodic phlebotomy,typically 3 to 5 U of whole blood per year.The frequency of phlebotomy is unique toeach patient and should be guided bymonitoring serum ferritin and maintenanceof a normal hemo-globin level.

Diet TherapyStrict dietary restrictions are not

indicated—patients don’t have to “go iron-free.” Reducing intake of iron-containingand iron-fortified foods and avoiding cast-iron cookware can avoid excess dietaryiron. Multivitamins without iron arepreferable and no more than the DRI forvitamin C is recommended. Avoid foodsand beverages that place an added stresson the liver, such as alcohol and rawseafood.

Role of the RDBecause many physicians are not

aware of the prevalence of HH, the dietitiancan be an invaluable resource. Invest-igating a patients’ family history for cluescan help identify the patient as a carrier. Adietitian who is alert to the clinical signsand symptoms of HH can recommend theappropriate lab tests to help the doctormake the correct diagnosis. Detecting andtreating HH early can make a vastdifference in the patients’ quality of life.

ScreeningCAP recommends screening for iron

overload with a transferrin saturation testin all persons 18 years of age or older aspart of routine medical care. Screening isalso advised in all persons, regardless ofage, who have one or more of the followingrisk factors: a family history of HH, anyof the clinical manifestations of ironoverload, and laboratory abnorm-alities.

Genetic TestingHH is an autosomal recessive disorder.

To develop the disorder, an individual must

inherit the defective gene on bothchromosomes. In 1996 the defective gene,dubbed the HFE gene, was discovered.Since the discovery of the HFE gene, DNAtesting has been done on an experimentalbasis.7 While some experts argue in favorof universal screening, several importantconcerns exist. As with all screening, thebenefits of screening for HH must bebalanced against its adverse effects, whichmay include complications of diagnosticprocedures (such as liver biopsy) and legal,social, and psychological problems (suchas discrimination, loss of insurancebenefits for a person with a known geneticcondition, and increased costs of healthcare or insurance). These risks need to beweighed against the psychological benefitof finding an explanation for symptoms,alleviating symptoms with treatment, andpreventing disease progression.

References1. Witte DL, Crosby WH, Edwards CQ, et al.Practice parameter for hereditaryhemochromatosis. College of AmericanPathologists. Clin Chim Acta. 1996; 245:139-200.2. Rouault TA. Hereditary hemo-chromatosis.JAMA. 1993; 269:3152-3154.3. McLaren C, Gordeuk VR, Looker AC, et al.Prevalence of heterozygotes for hemochromatosisin the white population of the United States. Blood.1995; 86:2021-2027.4. Bradley L, Haddow JE, Palomaki GE.Population screening for hemochrom-atosis:expectations based on a study of relative ofsymptomatic probands. J Med Screening1996;3:171-177.5. Adams PC, Valberg LS. Evolving expression ofhereditary hemochromatosis. Sem Liver Dis.1996;16:47-54.6. Powell LW, George DK, McDonnell SM,Kowdley KV. Diagnosis of hemo-chromatosis. AnnIntern Med. 1998;129:925-931.7. Burke W, Thomson E, Khoury MJ, et al.Hereditary hemochromatosis: gene discovery andits implications for population-based screening.JAMA. 1998;280:172-178.

Susan Moore, MS, RD is an educator andtechnical/consumer writer in the dietarysupplement industry and currently is theWestern Regional Trainer for Health FromThe Sun/Arkopharma, an East Coast-based dietary supplement company.Contact Susan at (714) 528-5936.

Supplements . . .(cont.)continued from page 1

of biotech crops becoming weedy pests isno greater than that for other crops. Andperhaps most comforting to those whohave heard the activist claims, thestatement: “The risks associated with plantvarieties developed using agriculturalbiotechnology are the same as those forsimilar varieties developed using classicalbreeding methods.”

References1. National Research Council. GeneticallyModified Pest-Protected Plants: Science andRegulation. Available at http://www4.nationalacademies.org/news.nsf. Accessed 5/30/00.2. International Consumers for Civil Society.Regulation of Agricultural Biotechnology in theUnited States: How the Process Works. Availableat http://www.icfcs.org/biotechreg.htm.Accessed 5/30/00.3. The World Is Still Safe for Butterflies. The WallStreet Journal. June 25, 1999.4. Gene-Altered Corn’s Impact Reassessed.The Washington Post. Nov. 3, 1999.5. Researcher Questions Nutritional Value ofGenetically Altered Crops. San FranciscoChronicle. July 26, 1999.6. “Royal Society rejects latest claims in Lancet onGM potatoes,” press release, Oct. 14, 1999.Available at http://www.royalsoc.ac.uk. Accessed5/31/00.

Channapatna S. Prakash is professor ofplant molecular genetics and the directorof the Center for Plant BiotechnologyResearch at Tuskegee University.He serves on The USDA AgriculturalBiotechnology Advisory Committee.Contact Dr. Prakash at [email protected].


Supplements . . .HomocysteinemiaJudy Shabert, MD, MPH, RD

Biochemical PhysiologyHomocysteine is a sulfur-containing

amino acid derived only from the essentialamino acid methionine. Abnormallyelevated blood homocysteine occurs fromgenetic abnormalities of enzymes thatrecycle methionine, such as nutritionaldeficiencies of specific vitamins and,frequently, a combination of genetic andnutritional interactions.

The production of homocysteine is anecessary step in the metabolic formationof methionine and cysteine. See Table onpage 10 for the enzymes and nutritioncofactors for these various reactions.

Homocysteinuria was proposed as arisk factor for atherosclerotic vasculardisease in 1969 by Kilmer McCully.1 Hepublished a report of an infant who had anautosomal recessive gene (two copies ofthe faulty gene are required to express thedisease) that led to abnormally highconcentrations of homocysteine in bloodand urine and who died of extensiveatherosclerosis. The cholesterol theory ofheart disease was popular at the time, andDr. McCully’s hypothesis was met withsharp criticism.2 However, over the next20 years, other investigators confirmedhis association of homocysteinuria andearly death from vascular disease.3,4

GeneticsIn the rare, classical presentation of

homocysteinuria, individuals who arehomozygous (have two faulty genes) fora defect in any of the methionine-regenerating enzymes produce excessivequantities of homocysteine. Theseenzymatic deficiencies result in severelyelevated blood homocysteine andhomocysteinuria with a characteristicsyndrome of mental retardation, detachedlens of the eyes, osteoporosis andatherosclerotic and /or thromboembolicevents. Individuals who are heterozygous(only one faulty gene) for cystathioninesynthase deficiency will have mild hyper-homocysteinemia. In people who areheterozygous for the classic 5,10-methylene-tetrahydrofolate reductasedeficiency, homocysteine will not beelevated. 5

PathologyMild hyperhomocysteinemia as a risk

factor for coronary heart disease in youngpeople was recognized in 1976.4 Theadverse effect of homocysteine on bloodvessels appears to be a graded response andis similar to that seen with increasingconcentrations of cholesterol. Thoseindividuals with increasing plasma levelsof homocysteine have more severevascular disease. In fact, in men with ahomocysteine concentration of 15.8 mcgmol/l compared to those with aconcentration within the normal range, therelative risk for vascular disease increasesthree-fold.6

DiagnosisThere are two methods for diagnosing

hyperhomocysteinemia. One method is toobtain a fasting homocysteine level. Theother method is to give an oral dose ofmethionine (0.1 g/kg body weight, called“methionine loading”) prior to obtainingthe serum homocysteine level.Approximately 50% of individuals whodemonstrate elevated homocysteine levelsfollowing methionine loading have normalfasting homocysteine levels. So, a normalserum homocysteine without amethionine-loading test does not rule outthis risk factor for cardiovascular disease.7

Individuals who do have post-loadingelevations in homocysteine have a relativerisk for cardiovascular disease of 13,compared to those with no elevation.5

Variant MTHFR mutationMost recently a common genetic defect

in 5,10-methylene-tetrahydrofolatereductase (MTHFR) has been recognized.8This mutation leads to a heat-labile formof MTHFR. Individuals homozygous forthis mutation do not have severehyperhomocysteinemia but maydemonstrate mild elevations in bloodhomocysteine. Mild hyperhomo-cysteinemia is associated with significantmorbidity, however, and in the generalpopulation the homozygous state for heat-labile MTHFR occurs in 1-in-20 (1:20)individuals. Its frequency increases inpeople with occlusive vascular disorders:coronary artery disease 1:5, peripheralvascular disease 1:3, and cerebrovasculardisease 1:4. Individuals who arehomozygous for MTHFR and also havelow serum folate concentrations are athighest risk for elevated homocysteine and,

presumably, for occlusive vasculardisease.9

Nutritional Expression of Genetic DefectHeterozygous individuals with heat-

labile MTHFR deficiency may havenormal serum homocysteine. However, ifserum folate is inadequate, hyper-homocysteinemia occurs. The relationshipbetween low serum folate and elevatedhomocysteine demonstrates the unmaskingof a genetic mutation when geneticindividuality requires nutrients greater thanthe Recommended Dietary Allowances.The genetic defect leading to hyper-homocysteinemia is unmasked whenfolate intake is inadequate. Numerousepidemiological studies have demon-strated this relationship for both folate andvitamin B6.

Other research demonstrated that in agroup of elderly people who had normalserum concentrations of B6, B12 andfolate, homocysteine was elevated.10

When the participants of the studyreceived eight intramuscular injections ofB6, B12 and folate over three weeks, serumhomocysteine normalized.

Dietitian’s RoleThe registered dietitian has a

significant role to play in this condition byhelping physicians understand theincidence and impact of homocysteinemiaand how it can be treated. Themeasurement of blood homocysteineconcentrations is not routine practice andthe methionine-loading test less so. Manyphysicians are unaware that genetic defectsof methionine are common in the generalpopulation. Furthermore, they sometimesdo not appreciate the impact of specificvitamins in lowering homocysteine levels.

References1. McCully KS. Vascular pathology ofhomocysteinemia: implications for thepathogenesis of arteriosclerosis. Am J Pathol.1969;56:111-128.2. Larkin M. Kilmer McCully: pioneer of thehomocysteine theory. Lancet. 1998;352:1364.3. Mudd SH, Skovby F, Levy HL, et al. The naturalhistory of homocysteinuria due to cystathionine-synthase deficiency. Am J Hum Genet. 1985;37:1-31.4. Wilcken DEL, Wilcken B. The pathogenesis ofcoronary artery disease. A possible role formethionine metabolism. J Clin Invest.1976:57:211-215.5. van der Berg, M, Boers GHJ. Homocysteinuria:what about mild hyperhomocysteinaemia?Postgrad Med J. 1996;72:513-518.

References continued on page 10


6. Stampfer MJ, Malinow MR, Willett WC, et al. Aprospective study of plasma homocyst(e)ine andrisk of myocardial infarction in US physicians.JAMA. 1992;268:877-881.7. Welch GN, Loscalzo J. Homocysteine andatherothrombosis. N Engl J Med. 1998;338:1042-1050.8. Rozen R. Molecular genetic aspects ofhyperhomocysteinemia and its relation to folicacid. Clin Invest Med. 1996;19:171-178.9. Ma J, Stampfer MR, Hennekens CH, et al.Methylenetetrahydrofolate reductasepolymorphism, plasma folate, homocysteine, andrisk of myocardial infarction in US physicians.Circulation. 1996;94:2410-2416.10. Naurath HJ, Joosten E, Riezler R, et al. Effectsof vitamin B12, folate, and vitamin B6 supplementsin elderly people with normal serum vitaminconcentrations. Lancet. 1995;346:85-89.

Judy Shabert, MD, MPH, RD, trained inobstetrics, gynecology and public health, is aclinical instructor at Harvard Medical Schoolin Boston, MA. She has, over the past 10years, returned to her first love—nutrition—where the basis of all health resides. ContactDr. Shabert at [email protected].

Overview of Homocysteine Pathway:1. Serine hydroxylase (requires B6)2. 5,10-methylene tetrahydrofolate reductase3. 5-methyltetrahydrofolate homocysteine methyltransferase (requires B12)

4. S-adenosylmethionine synthase5. Methyltransferase6. S-adenosylhomocysteine hydrolase

Members InThe News… Judy Shabert, author ofthe article Homocysteinemia inthis issue, was awardedthe 2000 John M. KinneyInternational Award for Nutritionand Metabolism for the paperentitled: Glutamine-AntioxidantSupplementation IncreasesBody Cell Mass in AIDS patientswith Weight Loss: aRandomized, Double-BlindControlled Trial. Nutrition1999;15:860-4. Judy and otherADA members who contributedto the article, CharmaineWinslow, RD (Florida), JanetLacey DrPH, RD (Boston) andDoug Wilmore, MD (honorarymember (Boston)) will bepresented their award in MadridSpain on Sunday, Sept 10.

7. Cystathionine b-synthase (requires B6)8. Cystathionase (requires B6)9. Betaine:homocysteine methyltransferase

8. Bertram, JS, Kolonel LN, Meyskens FL. Ratio-nale and strategies for chemoprevention of cancer inhumans. Cancer Res. 1987;47:3012-3031.

John S. Bertram, Ph.D. is Professor of Genet-ics and Molecular Biology at the John A. BurnsSchool of Medicine, University of Hawaii. Hisresearch focuses on the prevention of carcino-genesis with about 100 published scientificpapers in this area. Contact Dr. Bertram at theCancer Research Center of Hawaii, Universityof Hawaii, 1236 Lauhala St., Honolulu, HI96813.

Herbs. . .(cont.)continued from page 3

References continued from page 9


Functional Foods . . .(cont.)

the nutritional content of the food has beenchanged, or the product’s composition hasbeen substantially changed. Otherwise,these foods will have the same labels as allother foods.

FDA evaluates all new foods for thepresence of allergens. There are no foodscurrently on the market containing aller-gens transferred via biotechnology. Be-cause virtually all crop plants have beenmodified through plant breeding or bio-technology, the FDA does not require la-beling stating any declaration of processthat produced the food.

The American Dietetic Association’s(ADA) Position On Biotechnology

It is the position of ADA that biotech-nology has the potential to be useful in en-hancing the quality, nutritional value, andvariety of food available for human con-sumption and in increasing the efficiencyof food production, food processing, fooddistribution, and waste management.

ADA has just released the Biotechnol-ogy Resource Kit, which is a comprehen-sive peer-reviewed package of informationon the background, applications, safety andother issues related to food biotechnology.Educational resources and opposing viewsare also included. This kit is available fromADA’s Customer Service (800-877-1600ext. 5000) or through ADA’s Web site atwww.eatright.org.

ResourcesBiotechnology Resource Kit, The American DieteticAssociation; May 2000 (teaching tool).Food Biotechnology The International FoodInformation Council Foundation; October 1998(teaching tool).Busch F. The New Nutrition: From Antioxidants toZucchini. New York, NY: John Wiley and Sons; 2000.

Lori Holladay, MPH, RD is a consultantand writes articles and curriculum on avariety of nutrition topics for communityeducation programs and print media forFelicia Busch & Associates, NutritionCommunications Consultants.

Felicia Busch has been in private practicesince 1986 and is the author of The NewNutrition: From Antioxidants to Zucchini.She is treasurer of the NCC DPG andmedia spokesperson for ADA. Contact Lorior Felicia at [email protected] 651-645-4621 (fax).

Future Biotechnology BenefitsIn the near future expect food biotechnology to provide for:• reduced levels of natural toxins in plants;• simpler and faster methods to locate pathogens, toxins, and contaminants;• longer time before spoilage;• safer foods through reduction of allergenic proteins;• drought and flood tolerance;• heat and cold tolerance.

Food Crops currently produced through biotechnology:• soybeans• corn• canola• tomatoes• squash• potatoes• rice

New products that are currently being developed for release in thefuture include:• Oils, such as soybean and canola oils developed with more stearate to make margarine and shortening more healthful• Sweeter peas• Smaller, seedless melons for use as single servings• Bananas and pineapples that ripen more slowly• Peanuts with better protein balance• Fungus-resistant bananas• Tomatoes with more antioxidants• Potatoes with higher starch content so that they will absorb less oil when fried• Fruits and vegetables with more vitamin C and E• Garlic cloves with more allicin• Rice with more protein (using genes from pea plants)• Strawberries with more ellagic acid

Although food biotechnology is the hot topic today, considersome other benefits of the science of biotechnology:

• Medicines created from proteins that are naturally producedby the human body. These include FDA-approved medicines totreat diabetes, anemia, leukemia and many others.

• Vaccines consisting of the antigen only (unlike conventionalvaccines that use a weakened form of the virus) and thereforecannot transmit the virus itself. FDA has approved a biotech vac-cine for Hepatitis B.

• Diagnostics used to detect many diseases and conditions in-cluding HIV, hepatitis, and pregnancy.

• Gene therapy, which uses the genes themselves to treatinherited genetic disorders, has been used to treat severe com-bined immunodeficiency disease (SCID) or the “bubble boydisease.”

continued from page 5


Food Production Time Line 10,000 years8000 BC • The nomadic lifestyle was replacedby geographically stable communities thatgrew plants as crops. Seeds are saved forplanting in the next season.

1800 BC • Yeast is used to make beer, wineand to leaven bread. This is the first timepeople used microorganisms to create newfoods.

1865 • Mendel concludes from his experimentswith pea plants that unseen particles pass traitsfrom generation to generation.

1922 • Hybridized corn seed created bycrossbreeding two corn plants. This new cornhelps to account for a 600% increase in cornproduction in the US between 1930 and 1965.

1953 • Structure of DNA defined showinghow cells in all living things duplicate andpass genetic information from generation togeneration.

1986 • Biotechnology is used to create herbi-cide resistant soybean plants. Approved byUSDA, FDA and EPA by 1995 and commer-cialized in 1996.

1990 • Approval granted to the first food prod-uct modified by biotechnology- an enzymeused in cheese making.

1994 • FlavrSavr tomato the first food productenhanced by biotechnology available to con-sumers (slower ripening and longershelf life).

1997 • 18 crops improved through biotechnol-ogy have been approved by the US govern-ment.

Web site ResourcesThe American Dietetic Associationwww.eatright.org

Biotechnology Industry Organizationwww.bio.org

Council for Biotechnology Informationwww.whybiotech.com

Environmental Protection Agencywww.epa.gov

Food and Drug Administrationwww.fda.gov

International Food Information Councilhttp://ificinfo.health.org

United States Department of Agriculturewww.usda.gov

Approved US CropsSince the mid-1990s many different crops that have beenmodified for a variety of agronomic and functional traits havecompleted the regulatory process in the United States. Hereis a partial listing of those crops.

CROP TRAIT(s)Canola Herbicide tolerance, high laurate oilCherry Tomato Taste, color, textureCorn Insect protection, herbicide tolerancePapaya Virus protectionPotato Insect protectionSoybean High oleic oil, low saturated fat oil, low

linolenic oilSquash Virus protectionSugarbeet Herbicide toleranceSunflower High oleic oilTomato Altered ripening, thicker skin, modified

pectins

NUTRITION INCOMPLEMENTARY

CAREWeb site:

www.complementarynutrition.org

Member EML:

Contact Gretchen Forsellto be enrolled

([email protected])

Interested in contributingto the NCC Newsletter?

The following themes will becovered in upcoming issues.

Spring 2001-Allergies andfood intolerances

Summer 2001-Anti-Aging

Fall 2001-Interaction ofdietary supplements with

medications

For more information contactSarah Harding Laidlaw at

[email protected].

○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○

○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


Resources . . .Book ReviewGenetic Nutrition: Designing aDiet Based on Your FamilyHistory; Artemis P. Simopoulos, MD,Victor Herbert, MD, JD, and BeverlyJacobson; hardback, 335 pp; $22.00; ISBN0-02-611295-7: New York, NY:MacMillan Publishing Company, 1993.

One diet does not fit all because eachof us has our own genetic blueprint. Thisis the basic message the authors want toconvey in this book. Although intended forconsumers, dietetics and other healthprofessionals can benefit from theinformation provided. And, despite that itwas published 7 years ago, the informationremains relevant. With a greaterunderstanding of genetics resulting fromthe Human Genome Project, dieteticsprofessionals will need to have at least anoverview knowledge of genetics and itseffects on health.

Chapter one, “Your Genes and YourHealth,” provides just that type ofoverview. The authors guide you throughcell replication, review DNA in the cellnucleus and its role in genetic expression,and discuss types of genetic expression andgenetic transmission of diseases anddisorders. Our genetic heritage positionsus anywhere from being merelypredisposed to a medical condition tofrankly expressing a disorder. This chapteralso provides a review of how our humanhistory led to ethnic variations in theincidence of certain chronic diseases. Onestudy cited discusses the environmentaland genetic factors that cause some Finnishmen to have higher heart disease deathrates than Japanese men.

Chapter two details how to chart afamily medical history. A questionnaireand a diagram for charting this history areprovided.

Chapters three through ten discussfeeding your genes if you or your familyhistory includes obesity, heart disease,hypertension, diabetes, alcoholism, cancer,or food allergy. One chapter discusses thecautions of excessive iron in dietary intake.Because this book was published in 1993,the chapter on obesity does not containinformation on the link between insulin

Book ReviewGenetic Nutritioneering; Jeffery S.Bland, PhD, with Sara H. Benum, MA; pa-perback; 272 pages; $16.95; ISBN 0-87983-921-X; Lincolnwood, Illinois60646-1975; Keats, a division of NTC/Contemporary Publishing Group, Inc.;1999

Each individual has unique geneticcharacteristics. Some of these characteris-tics place a person at increased risk for spe-cific diseases. The premise of Dr. Bland’sbook is that inherited traits can be modi-fied through diet, nutritional supplementsand lifestyle to allow people to live longer,healthier lives.

Dr. Bland has spent his career educat-ing professionals on, and researching, thisapproach to disease management and

health. He holds a PhD in biochemistryfrom the University of California wherehe was a faculty member and worked withLinus Pauling, PhD at the Linus PaulingInstitute.

Whereas this book was written for thelay reader, it is an excellent first pass for awide spectrum of health professionals inunderstanding the complementary and al-ternative health approach to nutrition thatis being practiced in this country.

Chapter one explores the relationshipof one’s genes and the environment in de-termining health. It introduces the readerto Roger Williams, PhD who first de-scribed the concept of biochemical indi-viduality over 50 years ago.

Chapter two reviews the basics of ge-netic inheritance and, in a simple way, ex-plains how genes work. In chapter threethe book reports on foods that alter thegenetic expression of disease, such asphytochemicals in fruits and vegetablesand their ability to modulate the immunesystem.

The following chapter includes reportsthat illustrate the relationship of anindividual’s insensitivity to a food and dis-ease outcome. For example, lactose intol-erant people are more likely to developcataracts if they continue to drink milk intheir adult life. The concept of liver detoxi-fication is introduced. The ability of theliver to detoxify compounds is determinedgenetically but functionally expressedthrough toxins that are presented to it.

Chapters five through eleven discussnutrition and genetic factors thatinfluence aging, diabetes, arthritis, heartdisease, brain aging and cancer. The bookcites references to substantiate the ideaspresented in these chapters. However, thereis a lack of large scale, double blind, pla-cebo-controlled trials to support the rec-ommended nutritional supplementation.Despite this limitation, GeneticNutritioneering is an important, readablebook that builds on our understanding ofdietary choice and disease expression.

Reviewed by Judy Shabert, MD, MPH, RD.Dr. Shabert can be reached [email protected].

resistance and obesity. Interestingly, thehypertension chapter reads like aforerunner to the DASH (DietaryApproaches to Stop Hypertension) diet.

Chapter eleven provides suggestedmenus for various genetic tendencies. Themenus developed by several registereddietitians are based on USDA publicationsand the Food Guide Pyramid. Also offeredare the 1989 dietary guidelines and RDAs,both of which have been updated since thebook’s publication.

The greatest benefit dieteticsprofessionals can get from this book is anunderstanding of how genetics influencesour health. With this understanding, we canbecome more thorough in our patientassessments by investigating genetichistory and increase our effectiveness withappropriate medical nutrition therapy.Patients with higher levels of educationwould be able to benefit from the book’sinformation. Check your local library forthis book. You can then determine if youwant to add it to your own resource base.

One recommendation for this bookwould be to include the references for thestudies cited.

Reviewed by René Norman, RD, in privatepractice with Nutrition Consultants ofTulsa. Contact René at (918) 749-9077 orby fax (918) 749-4041.


The Human GenomeProject: Implicationsfor DieteticsPractitionersDavid H. Holben, PhD, RDIntroduction

How fitting that the 82nd AnnualMeeting and Exhibition of The AmericanDietetic Association (ADA) held inOctober, 1999, had the theme entitled, THEFUTURE IS NOW—DIETETICS 2000. Itis. Scientists, medical professionals, andindividuals from the media talk aboutgenetics, biotechnology, and molecularbiology on a daily basis. “Understandingthe basics of genetics, how nutrients andnutritional status influence geneexpression, and the relationship betweengenetics and nutrition in chronic diseasewill become increasingly important fordietetic professionals as the discoveries ofthe Human Genome Project (HGP)unfold….”1 Several authors have discussedgenetics issues related to dieteticspractice.2-9 This article summarizes theHGP and the Human Genome EducationModel Project II (HuGEM II) anddiscusses their relevance to dieteticsprofessionals.

What Is the Human Genome Project?Coordinated by the National Institutes

of Health (NIH) and the Department ofEnergy, the HGP is an internationalresearch effort that formally began in 1990to fully define the human genetic makeup(our “genome”). 10,11 The specific goals ofthis project are to: 1) characterize thegenomes of human and selected modelorganisms (Escherichia coli, the fruit fly,and the laboratory mouse) throughcomplete mapping and sequencing of theirgenetic material, i.e., DNA (there areapproximate 100,000 genes in humanDNA, which contains 3 billion chemicalbases); 2) store this information indatabases; 3) develop tools andtechnologies for genomic analysis; 4) trainscientists who will be able to utilize thetools and resources developed through theHGP to pursue biological studies that willimprove human health; and 5) examine theethical, legal, and social implications(ELSI) that may surface from this researchinto the human genome. The HGP is the

first large scientific undertaking to addressthe potential ELSI that may arise from thecharacterization of all of the genes inhumans.

What Is the Human GenomeEducation Model?12

HuGEM II is an initiative funded bythe NIH to provide educational trainingand resources to increase the knowledgeof and sensitivity to human genetics, theHuman Genome Project, and the ELSI ofgenetic testing and research for membersof seven collaberating professionalorganizations:• the American Dietetic Association,• the American Occupational Therapy Association,• the American Physical Therapy Association,• the American Speech-Language- Hearing Association,• the American Psychological Association,• the Council on Social Work Education• the National Association of Social

WorkersThe educational training includes severalseminars covering an orientation toHuGEM II and an overview of the HGPand its ethical, legal, and psychosocialissues provided for board members andnational staff members of the sevencollaborating professional organizations.“Educate the Leaders to Educate Others”workshops are held at national, regional,and state conferences of the collaboratingorganizations (basic human genetics andpriority topics of ethical, legal, and socialissues identified by the HuGEM II survey).And, a five-day continuing educationcourse, “Incorporating Genetics intoClinical Practice and Teaching” thatprovides 30 hours of instruction in humangenetics and genetic issues is held forhealth professional educators atGeorgetown University.

How Will the HGP Affect DieteticsPractice?

Genetic-related issues such as gene-environment interactions, gene therapy,and genetically engineered foods will haveprofound implications for the dieteticsprofession in the future and impact howwe provide medical nutrition therapy. TheHGP will undoubtedly change how wedetect, understand, and treat human

disease.1 Dietetics professionals must beproactive and seek out genetics resourcesto be effective practitioners. Gilbride hasreviewed how to find and use geneticsresources.9 Finally, Camp summarized thatdietetic professionals need to:• have a basic knowledge of genetics,• be comfortable with genetics

terminology,• have the knowledge to distinguish

between genetic and environmentalfactors of diseases when makingspecific recommendations aboutnutrient needs or changing behaviors,

• understand how an individual’sgenetic heritage influencesrequirements,

• be able to effectively work withfamilies with genetic conditions, and

• be an effective member of amultidisciplinary team.1

References1. Camp K. Genetics in clinical dietetic practice: apediatric perspective. Top Clin Nutr. 1999;14:6-21.2. Patterson RE, Eaton DL, Potter JD. The geneticrevolution: change and challengefor the dietetics profession. J Am Diet Assoc.1999;99:1412-1420.3. Isaacs JS. The impact of genetics research ondietetics practice. J Am Diet Assoc. 1999;99:1420.4. Tolstoi LG, Smith CL. Human Genome Projectand cystic fibrosis—a symbiotic relationship.J Am Diet Assoc.1999; 99:1421-1427.5. Maillet JO. Impact of genetic engineering on theprofession of dietetics. Top Clin Nutr. 1999;14:1-5.6. Luder E. Gene therapy for cystic fibrosis. TopClin Nutr. 1999;14:22-30.7. Hord NG. Dietary factors and geneticsusceptibilities in colorectal cancer risk: a briefreview. Top Clin Nutr. 1999;14:31-38.8. Stadler DD, Reeder AF, Strohbehn CH.Application of genetic engineering to foods. TopClin Nutr. 1999;14:39-50.9. Gilbride JA. Finding and using geneticsresources. Top Clin Nutr. 1999;14:51-57.10. National Human Genome Research Institute.The National Human Genome Research Institute.Available at http://www.nhgri.nih.gov/. AccessedApril 11, 2000.11. Department of Energy Office of Biological andEnvironment Research, Human Genome Program.Human Genome Project Information. Available athttp://www.ornl.gov/TechResources/Human_Genome/publicat/publications.html.Accessed April 11, 2000.12. Lapham EV. The Human Genome EducationModel Project II Web Site. Available at http://www.dml.georgetown.edu/hugem/. Accessed April11, 2000.

David H. Holben, PhD, RD is an assistantprofessor in the School of Human andConsumer Sciences at Ohio University.Formerly a pediatric dietitian whospecialized in caring for individuals withcystic fibrosis, he was selected in 1999 asone of ADA’s participants in the HuGEMII. Contact Dr. Holben at [email protected], 740/593-2875.

ReaDer REPORTS . . .


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ComplementaryCare forCardiovascularDisease: SeparatingFact From Fiction(6 CPE Credits)from the NCC/SCAN workshoppresented April 12, 2000 in Ohio.Includes 6 hours of lecture, allhandouts, and CPE questions andreporting form...........Price to be

The jointly developed and pre-sented NCC/SCAN cardiovascu-lar workshop. Learn the latest oncomplementary approaches tocardiovascular disease, including:

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ReaDer REPORTS . . .Preparing for theGenetics RevolutionTeresa Carithers, MHS, RD

For dietetic students and those justentering their professional careers, geneticsshould be viewed as an essential area ofstudy. More and more opportunities arebeing integrated into educationalexperiences due to the “diet-gene” or“nutrition-genetic” relationships that thisrapidly evolving science is bringing tolight. Students should take advantage ofevery educational opportunity to enhancetheir knowledge of genetics, especiallygenetic-nutrition relationships, andconsider specialization within an area ofgenetics, possibly becoming a geneticcounselor.

All this probably sounds exciting tothose just beginning their professionalpursuits, but what about those of us whoare not students any more, those of us whoare already “established” in our nutritionroles? Should we be concerned about theimpact of genetics on our careers as wellor is this just futuristic thinking? If youdon’t already know the answer to thisquestion, read the article recentlypublished in the Journal of The AmericanDietetic Association (J Am Diet Assoc.1999; 99:1412-1420) that describes therelationships between nutrition andgenetics and provides an overview of theimpact genetics will have on our clinicalpractice and our personal lives. ThisReaDer Reports column is provided in aneffort to relieve the panic that manyprofessionals experience when they firstencounter genetic information. Althoughmost find it intriguing, gaining a workingknowledge and becoming comfortablewith the information takes time and effort.

All of us are familiar with the statement“and duties as assigned.” My opportunityto work in genetics came suddenly and wasan addendum to a job assignment as anadministrative consultant to a public healthdepartment. Since then my work in thegenetics area has evolved into a trulyrewarding faculty level position within thedivision of medical genetics at theUniversity of Mississippi Medical Center.

Although the initial years were

challenging and sometimes stressful, theopportunity to work with individuals withinborn errors of metabolism and trainunder the close direction of a skilledgeneticist provided a great opportunity formy professional development and growth.Mutual respect for the role both thegeneticist and nutritionist could bring tothe table created a strong and successfulMD/RD team that has had a dramaticimpact on our state and greatly surpassedour initial expectations. My goal for thiscolumn is to share several “lessonslearned” that will help other dieteticsprofessionals faced with similarprofessional challenges.

• Become computer literate. Thisadvice may sound elementary, but it’samazing how many skilledprofessionals avoid becomingproficient with the computer. Geneticinformation can be accessed rapidly,but only if you know how to operatecomputer search engines with ease.Professionals not associated withcomputer networks can havesignificant access just through theirpersonal home computer.

• Find a genetics mentor. Ask toobserve a genetic clinic. Most geneticsprofessionals are quite willing to helpeducate and can direct you toopportunities that just don’t exist inthe library or local clinic. Many statesare beginning to offer geneticeducation courses for multi-disciplinary groups. Most colleges andmedical schools offer introductorygenetics or molecular biology courses.Taking the course for credit (beinggraded) really forces you to learn thecomplex principles. Self-studycontinuing education offerings areexciting, but it usually takes a greatdeal of self-discipline to review andretain the information over time.

• Focus initially on basic geneticsconcepts and principles. Manypeople make the mistake of focusingon specialized diagnostic information.Your understanding of concepts suchas the principles of inheritance,pedigree analysis, and variability ofexpression will be much morevaluable in the long term than learning

specialized diagnostic information ora few genetic facts.

• Focus on what’s of immediate useto you. Because of the complexity ofthe information, pace and focus yourlearning on what will help you themost day-to-day. If you work withpatients who have diabetes orcardiovascular disease, begin to studymulti-factorial diseases in general anddiabetes or cardiovascular disease inparticular. If you work with patientswith inborn errors of metabolism, thena study of autosomal recessive diseaseinheritance may be more worthwhile.If you don’t stay focused, you canwaste a lot of time on material thatyou may never need.

Below are resources that will be helpful inexpanding your exposure to genetics. Fromone who has “been there and done that,” Iencourage you to take the plunge. Best ofluck!Recommended ResourcesKhoury MJ, Beaty TH, Cohen BH. Fundamentals ofGenetic Epidemiology. New York, NY: OxfordUniversity Press; 1993.

Korf BR. Human Genetics: A Problem-BasedApproach. Cambridge, MA: Blackwell Science;1996.

Mueller RF, Young ID. Emery’s Elements of MedicalGenetics, 10th Ed. New York, NY: ChurchillLivingstone; 1998.

Patterson RE, Eaton DL, Potter JD. The geneticrevolution: change and challenge for the dieteticsprofession. J Am Diet Assoc. 1999; 99:1412-1420.

Seashore MR, Wappner RS. Genetics in PrimaryCare and Clinical Medicine,. Englewood Cliffs, NJ:Prentice Hall; 1996.

Thompson MW, McInnes RR, Huntington FW.Genetics In Medicine, 5th Ed. Philadelphia: W.B.Saunders Company; 1999.

Recommended Web sitewww.complementarynutrition.org

Teresa Carithers, MHS, RD is a doctoralcandidate and Instructor at the University ofMississippi Medical Center, Department ofPreventive Medicine, Division of MedicalGenetics. She is the State Nutrition Coordinatorfor individuals with inborn errors of metabolismand the Nutrition Investigator for the NHLBI-funded Jackson Heart Study. Contact Teresaat (601) 984-1900 (Secretary) or [email protected]


CPE Article . . .Genetics andNutrition: TheFuture is NowRuth M. DeBusk, RD, PhD

OVERVIEWThe central role of genetics in health

care is rapidly emerging. Dieteticsprofessionals need to understand howgenetics relates to health and disease andthe many connections among genes,nutrients, and disease development. Genescontain the information for makingproteins. Proteins, in turn, determine thestructure and function of the body and arethe basis for human individuality. Eachperson’s genes contain the same basicinformation but with enough individualvariation to result in unique differences inhow the body is put together and carriesout its activities. Metabolism, that complexprotein-based biochemical machinery,underlies our functional capability byproviding the vast number of metabolicproducts needed to sustain life. Mistakesin the genetic material result in mistakesin the metabolic machinery that result inmistakes in the production of metabolites.If a mistake occurs in a critical process,disease, and even death, can result.

Food plays a central role in thisinterrelationship of metabolism andfunction. It supplies the raw material formaking critical metabolic products, cansupply many of the products preformed,and can result in genes turning on or off sothat more or less of a product issynthesized. The genetic information mustbe expressed as a workable proteincomponent, and nutrition is a powerfulregulator and modulator of this wholeprocess. Nutrition, whether from food orsupplements, can potentially fill functionalgaps created by an individual’s geneticinformation and wire around geneticlimitations.

A simplistic view of this concept is theabsolute requirement of humans forvitamin C. We are genetic mutants forvitamin C; our genes do not produce theenzyme gulonolactone oxidase that’sneeded for vitamin C synthesis.1 Failureto supply vitamin C results in death. Thus,by supplying vitamin C, nutrition fills thebiochemical gap created by our genes and

enables us to live. Similarly, geneticlimitations result in requirements forcertain amino acids and fatty acids,biochemical gaps that must be filled by ourdiet. All humans share these geneticlimitations and nutritional requirements. Inaddition, each individual has his or her ownunique genetic limitations and nutritionalrequirements. It is these unique differencesthat will form the basis for gene-directednutrition therapy.

Examples of the Genetic-NutritionConnection

Many examples exist where the genescontain the potential for disease but dietand other lifestyle choices prevent theexpression of this potential.• The Pima Indians in Arizona and in

Sonora, Mexico share the samegenetic makeup, but the Arizonapopulation has the highest prevalenceof type 2 diabetes in the worldwhereas their Mexican counterpartsare lean and healthy.2,3

• Bouchard and colleagues showed withidentical twins that, although thegenetic predisposition existed forobesity, development of obesity wasnot a foregone conclusion.4 Further,genetic makeup appears to determinewhich obese individuals benefit fromparticular diet therapies and even fromphysical activity.5-7

• Individuals with gluten-sensitiveenteropathy have the geneticpredisposition but do not manifest thedisease if they do not eat gluten-containing foods.8 They still have thegenes that cause this disease, butnutrition prevents the expression ofthe disease.

• Individuals with a common geneticvariation in the 5,10-methyl-enetetrahydrofolate reductase gene arepredisposed to increased levels ofhomocysteine, a known risk factor forcardiovascular disease, yet do notdevelop elevated homocysteine levelsif folate is adequate.9-11

• Which apolipoproteinE variants(ApoE 2, 3 or 4) individuals haveaffects their risk for cardiovasculardisease and their response to dietarymanipulation.12 For example, thecommon advice to increase the dietarypolyunsaturated:saturated fat ratiobenefits men with the genotype ApoE

4/ApoE 3 (or “4/3”) but not womenwith the ApoE 3/2 genotype.13 Oatbran promotes a hypocholesterolemicresponse in those with the Apo E 3/3genotype but not in those with 4/4 or4/3.14

• The plant phytonutrients genistein andquercetin appear to work at the levelof gene expression to decrease the riskof prostate and liver cancer,respectively.15,16

• Many nutrients, vitamins, such asvitamin A and 1,25-dihydroxy vitaminD, and fatty acids bind to nuclearreceptors and affect geneexpression.17-19

• Genetic variability in components inthe renin-angiotension-aldosteronesystem have been correlated withhypertension and its response to low-salt diets.20

These are just a few examples. We canexpect many more as research continues.Clearly, failure to understand theunderlying genetics/ biochemistry/nutrition connection leads to a mismatchbetween our genes and the foods we eat,with potentially serious healthconsequences.

Genetic individuality leads tobiochemical individuality, which leads tonutritional individuality. This inter-relationship is so straight-forward, whyhas it taken so long to come to light? Allthe parts have been there; we simplyhaven’t understood how they fit together:which genes are involved, what their geneproducts are, and where these geneproducts fit into the metabolic machinery.The Human Genome Project will help tofill in these knowledge gaps. In time, wewill be able to look into the genes andfigure out which ones aren’t working in aparticular individual and what thebiochemical ramifications are.21-26 Withthis knowledge, we will have the basis forcustomizing nutrition therapyaccording to genetic limitations and fordeveloping rational biochemicalapproaches that address theselimitations. We need to begin now toincorporate these principles into thetherapies we develop for our clientsand the public policies we develop forpopulations. Science does not supporta one-size-fits-all approach nor theextrapolation of data from one population


as the basis for policy development foranother population.

The Challenge for Dietetics ProfessionalsDietetics professionals need to learn

key genetic concepts and practice applyingthem. We also need to understand thatscience has only begun to uncover specificexamples of how nutrition can be appliedin this way. The pace will soon snowballas a result of the rapid progress of theHuman Genome Project, which is predictedto fundamentally change the practice ofmedicine. Understanding which diseasesindividuals are predisposed to, how genesinteract with nutrients and medications, andwhat we can do to prevent future illnesswill allow health care practitioners of alldisciplines to target their therapies to thegenetically-determined unique needs of theindividual. We need to see personal healthas a continuum that ranges betweenwellness and illness. Genetics sets the upperand lower limits of our potential, but wherewe fall on that continuum depends on ourunique genetic makeup and the lifestylechoices we make, with nutrition beingpossibly the most critical choice.

In the forward to their book, GeneticNutrition, Artemis Simopoulos, MD, andher colleagues captured the key relationshipbetween genetics and nutrition succinctly:“Genetic factors determine susceptibility todisease, and environmental factors—ofwhich nutrition is one of the mostimportant—determine which geneticallysusceptible individuals will be affected.”27

The take-home message here is profound:Genetics is not destiny. Having “bad” genesdoes not necessarily doom us to a life ofdisease and disability. The information inour genes serves only to make us more orless susceptible to developing disorders thatrange from inconvenient to deadly.Nutrition therapy has the potential forintervening at strategic points, which canalter our genetic course and prevent theinformation in our genes from spellingdisaster for us.

FUNDAMENTAL GENETICCONCEPTS28-31

DNA: The Genetic MaterialDNA contains information. This

information directs the synthesis of all thelife-sustaining activities of the organism.DNA is made up of 4 chemical compoundscalled nucleotide bases: adenine (A),guanine (G), cytosine (C), and thymine (T).

The structures of these bases allow forweak hydrogen bonding between specificpairs, A pairs with T and G with C, to forma double helix. Picture a right-handedspiral staircase with the sugar-phosphatebackbone of the DNA forming the parallelrailings and the paired bases forming thesteps that connect the railings.

DNA is a language. It tells a story. Asthe text is read, an organized, logicaldescription unfolds as to how to make themyriad of proteins needed to build theorganism and support its functions. Likeany language, there’s an underlyingorganization: an alphabet that getsassembled into words, sentences, chapters,books and, ultimately, a completeencyclopedia of information. A, G, C, andT are the alphabet. These bases arearranged side-by-side to form a linearmolecule. Words are formed by reading 3bases at a time, a unit called a codon. Setsof three bases ultimately direct thepositioning of a particular amino acid intothe protein molecule being assembled.Each codon specifies one of the 20 aminoacids that make up proteins. Thus, DNA is“read” 3 bases (1 codon) at a time.

A gene is the set of sequential codonsrequired to synthesize a protein and isanalogous to a sentence. Like a sentence,a gene has a characteristic anatomy. Insteadof a subject, verb, and predicate, geneshave start, coding (informational), and stopsequences. DNA has many genes arrangedalong its length. Just as the total sentencecontent in a book is divided into chapters,DNA is subdivided into units calledchromosomes. And, just as a book is thesum total of all its chapters, the genome(“gene” + “chromosome”) is the sum totalof all the chromosomes containing all thegenes.

A fundamental principle of genetics isthat each cell’s nucleus contains thecomplete genome for the organism, eventhough all the information may not be usedby a particular cell type. Liver cells usedifferent subsections of geneticinformation than do heart cells or braincells. Think of the genome as a book; thebook in this case is an encyclopedia. Forus to learn something, we don’t need toread the whole encyclopedia; we just needto go to the section of interest and retrievethat specific information. Similarly, for acell to carry out a particular function, it

needs to “read” (translate) only certainsections of the total “book” (genome).

Another fundamental principle is thatthe language of DNA is common to allorganisms, whether microbes, plants, oranimals. Species differ in terms of what’sin their encyclopedias. The content isdifferent, but it’s all in the same languageand is decoded using the same basicmethods, which is why scientists can studythe fruit fly and uncover fundamentalprinciples that also apply to humans.

If all organisms within a species havebasically the same DNA, why don’t we alllook alike? Returning to the book analogy,think of individual differences as resultingfrom individual authors attempting to writethe same chapter for the encyclopedia. Ifwe give ten authors the same outline for achapter, they’ll write the sentences for thatchapter slightly differently to express thesame basic concepts. The meaning of manyconcepts will still be clear in spite of slightvariations. Other concepts will get lost inthe translation. Similarly, many genes canaccommodate slight variations and stillproduce a protein that’s functional. It may

The DNA Language• Alphabet = A, G, C, T for Adenine, Guanine,Cytosine, and Thymine

• Word = codon, a sequential arrangement of3 bases that ultimately translates into anamino acid molecule that is the building blockunit of proteins. DNA is "read" or "translated"3 bases at a time, one codon at a time

• Sentence = gene, which contains all theinformation needed to make a protein. Forthose proteins that are made up of morethan one polypeptide chain, two or moregenes are needed. Like a sentence, a genehas a characteristic anatomy. Instead of asubject, verb, and predicate, genes havestart, coding (informational), and stopsequences.

• Chapter = chromosome, a subunit of theDNA. To fit all the DNA into the nucleus of acell, it's divided into 46 packaging units calledchromosomes. Each chromosome containsmany genes arranged along its length.

• Book = genome (gene + chromosome).Like a book, which is the sum total of all itschapters, genome is the sum total of all thechromosomes containing all the genes in theorganism. Each cell's nucleus contains thecomplete genome.


doesn’t “read” the entire DNA just to makea particular protein; it transcribes only thegenes needed by the cell at a particulartime.

Within the coding region of a gene,interspersed in the information sequences,are sequences that are non-coding, thatdon’t translate into proteins. In molecularbiology terminology, DNA sequences thatcontain information that translates into theamino acid sequence of a protein are called“exons.” The intervening sequences arecalled “introns.” RNA polymerasetranscribes the entire gene into mRNA,both the coding (informational) and non-coding regions. Predictably, post-transcriptional processing has to occur. Theintrons are removed from the message, arun of adenines is attached, and the mRNAis transported to the cytoplasm fortranslation into protein.

In the cytoplasm, the mRNA attachesto ribosomal RNA and one codon(sequential sets of 3 RNA bases) at a timesystematically directs the assembly ofamino acid molecules into a protein. Theprotein may be ready to go at this pointor may require “post-translationalprocessing” before it is an active molecule,such as the addition of sugars or cleavageinto a smaller molecule. The finishedprotein then spontaneously assumes theconformation needed for that molecule tofunction. Familiar examples include thepost-translational cleaving of proenzymessuch as pepsinogen and trypsinogen andthe addition of a carbohydrate moiety toglycoproteins.

Thus, changes (called “mutations”) inthe DNA translate into changes in theprotein product. Changes in the codingregion are more likely to have harmfuleffects on function and lead to a diseasestate than changes in the interveningsequences.

Inheritance: Transmitting Genes to NewCells, New People

Cells are the foundational unit of thehuman body. Within a cell’s nucleus is thecomplete genome. To create new cells,genetic information must be passed fromthe original cell to the new or “daughter”cell. To continue a species, the informationin the DNA must be passed from parent tochild. From the pioneering geneticexperiments of Gregor Mendel, we

understand the mechanics of passing genesfrom one generation to the next. DNA isnot one long, continuous molecule inhumans. It’s divided into segments, called“chromosomes.” Each segment containsthousands of base pairs and, among thosebase pairs, are the informational sequencesthat make up the many genes. Humans areestimated to contain approximately80, 000- 100,000 genes.21

Humans have 23 distinct types ofchromosomes, which can be distinguishedby their physical characteristics, a processcalled “karyotyping”. Each chromosomehas a partner, one member of the paircoming from our mother and one from ourfather. Of the 23 pairs, one pair containsthe genes that determine our sex and iscalled the “sex chromosomes”: X and Ychromosomes for males, two X’s forfemales. The other 22 pairs are called“autosomes” and are numbered 1-22.

During growth and repair, cells divideto form new cells (a process calledmitosis). Both partners of a chromosomepair are duplicated and distributed to thenew cell so that each has a copy of all 46chromosomes. When an egg or sperm cellis formed, however, a special divisionprocess (called meiosis) insures that thegenetic material is not doubled when theegg and sperm combine. Only one memberof each chromosomal pair goes into an eggor sperm cell (23 chromosomes total) sothat, when these two unite to form the fetus,the normal number of 46 chromosomes isrestored. Which member of each pair, theone donated by the mother or the one fromthe father, ends up in the egg (or sperm) israndom and explains why children of thesame parents are each unique, their“phenotype”—how they look, act,function—is distinct from the parents andfrom each other because their underlyinggenes, their “genotypes”, are different.Further, meiosis has a special feature whereboth chromosomal partners physically pairand can exchange portions of their geneticmaterial, which further increases geneticdiversity. Genes that are physically locatednear each other tend to stay together duringthis genetic recombination and are said tobe “linked”.

Genotype vs. Phenotype/Dominancevs. Recessiveness

The genes are arranged along thelength of the chromosomes at specific

be as functional, less functional, or evenmore functional than the original version.Other genes cannot accommodate even aslight change. In molecular terms, changesare called “mutations” and are thecornerstone of evolution. Genes thatcannot accommodate change are said to be“highly conserved” and usually code forproteins that are critical to the functioningof the organism. Those genes that canaccommodate change exist in manyvariations (called “polymorphisms”).Polymorphisms generate the differencesbetween individuals within a species.Everyone in the species uses the same basicblueprint; they simply go about buildingand maintaining their houses slightlydifferently so that the end result reflectstheir individual characters.

The Molecular Biology of DNAThe information in DNA is in code and

needs to be decoded. Molecular biology isthe study of the decoding of the DNA, howthe sequence of bases is converted intoprotein components such as enzymes,hormones, messenger molecules,receptors and so on that are useful tothe cell. Essentially the point of theHuman Genome Project is to figure outwhat each gene codes for and how itsexpression is regulated.

Transferring the information intheDNA sequence into a protein requirestwo major steps: transcription andtranslation. Transcription “transcribes” theDNA sequence into an RNA sequence,which is in turn “translated” into an aminoacid sequence. In the nucleus the DNAdouble helix “unzips” and the enzymeRNA polymerase moves along one strandmatching bases in complementary pairingfashion to the linear sequence of bases inthe DNA. The RNA molecule that isformed is called messenger RNA or“mRNA”. RNA is similar to DNA exceptthat it pairs adenine with the base uracil(U) rather than with thymine.

Genes have a standard anatomy.Upstream from the informational region isa regulatory region where RNApolymerase binds (the “promoter region”)and where a variety of factors, includingnutrients, can bind to turn on and off theexpression of that gene. Then comes theinformational region (“coding region”),followed by a stop region. Like reading anencyclopedia, RNA polymerase


locations, called “loci”. There are twocopies of each gene, one on each memberof the chromosome pair and located at thesame position on the two chromosomes.The base sequence of the two copies is thegenotype for that particular gene; theexpression of those base sequences(translation into protein) is the phenotypefor that gene. Phenotypes can be dominantor recessive—genes themselves are notdominant or recessive; the effects theyproduce are.

The concept of dominance andrecessiveness used to be straightforward:one copy’s effects dominated the other, inan all-or-none fashion. Disease wasthought to result only when both copies ofthe gene were mutated (a “homozygousindividual”) and function was severelyimpaired. Genetic disease was, thereby,considered to be quite rare. So long as onenormal copy of that gene was present,some active protein was produced, severedysfunction was prevented and the disease,as it had been defined, was not evident. Asour level of technological sophisticationhas increased and we’ve learned what thegene product is and how to detect it, it’sbecome obvious that, in the carrierindividual (a “heterozygous individual”),one normal gene product and one mutantgene product are present and that suchindividuals have a functional level less thannormal but not severely dysfunctional.Increasing focus is now on detecting thecarrier individual and assessing whetherhaving less than 100% normal (fullyfunctional) gene expression impairsfunction and increases the risk ofdeveloping disease.

Mendelian InheritanceA trait may be inherited in 1 of 6 ways,

which corresponds to whether a gene is onan autosome, a sex chromosome, or onmitochondrial DNA and whether a mutantgene’s effect is dominant or recessive. The6 possibilities are: autosomal dominant,autosomal recessive, X-linked dominant,X-linked recessive, Y-linked dominant, ormitochondrial. Y-linked transmission fromone generation to the next isstraightforward and seldom elaborated on:males inherit whatever genes are on the Y-chromosomes of their fathers For thosegenes that are carried on mitochondrialDNA, inheritance is strictly maternal (seeMaternal Inheritance below).

Autosomal dominant means the geneis on one of the 22 autosomes and that thetrait is observable even though the secondcopy of the gene may be normal.Autosomal recessive means the trait is notobserved unless two abnormal copies ofthe gene are present. X-linked means thegene is on the X-chromosome. Whether atrait on the X-chromosome is dominant orrecessive is determined by its expressionin women, where two copies of the geneare present. Traits on the X-chromosomewill be expressed in men since only a singlecopy is present.

Clear detection of the mutantindividual can be difficult even whenthere’s a double dose of the mutant allelebecause the dysfunctional phenotype maynot be expressed fully. You would expect100% “penetrance”, that is, 100% of thetime when the double dose of the mutantallele is present, you would expect thedisease to be present. You don’t alwaysobserve 100% penetrance, however, forreasons we don’t yet understand butsuspect may be due to environment fillingin the genetic gaps. A related concept is“expressivity”. If different members of afamily all have the mutant gene but theirexpression of that gene takes differentforms, perhaps varying from mild to severedisease, the gene is said to exhibit variableexpressivity.

Clearly, gene expression is a complexprocess that varies with the particular geneand the environment in which it’sexpressed. Fully understanding diseasesthat are due to changes in a single gene isan ongoing challenge. Chronic diseasessuch as atherosclerosis, obesity, diabetes,and cancer are even more challengingbecause there are a number of genesinvolved (multigenic) and their expressionis strongly influenced by a number oflifestyle factors (multifactorial). At thisearly stage of understanding, scientists talkabout “genetic susceptibility” and“modifiable risk factors” in lieu ofidentifying which genes are involved, whatthey do, and how nutrition can influencetheir impact on health. Unraveling thecomplexity of chronic disease genes andthe factors that influence their expressionis a major goal of human geneticsresearchers, however, and the next decadeis expected to yield considerableinformation.

Maternal InheritanceAn exception to Mendel’s laws

regarding how traits are inherited is theinheritance of the DNA contained in themitochondria of each cell. Like the DNAin the cell’s nucleus, mitochondrial DNAis double-stranded but, unlike nuclearDNA, it’s circular and only a single copyexists so the concept of dominance/recessiveness does not apply. This DNAcodes for “housekeeping” proteins neededfor protein synthesis and for some of theproteins involved in energy metabolism,the key metabolic function of the mito-chondria. Changes in mitochondrial DNAcan cause diseases in the same waychanges in nuclear DNA affect function.What’s unique about mitochondrial DNAis that, when the egg and sperm unite, theegg donates the mitochondria. Ourmitochondrial DNA is inherited from ourmothers, a mode of transmission called“maternal inheritance.”

APPLICATIONSGenetic Techniques28-29

From genetic research have cometechnological advances that havebroadened the impact of genetics ondietetics beyond just diet therapy. Thediscovery of restriction endonucleases (akarestriction enzymes) provided the basis forthe development of genetic engineeringtechniques, which in turn gave rise tobiotechnology and its diverse clinical andfood science applications.

Restriction enzymes are produced bybacteria as a defense against foreign DNAinvading the cell and act like “molecularscissors” to cut the foreign DNA intofragments. Incubating an organism’s DNAwith a particular restriction enzyme resultsin a set of fragments that is characteristicand reproducible for that particular DNAand that enzyme. These fragments arecalled restriction fragment lengthpolymorphisms (RFLPs). Each person,except for identical twins, has a uniqueRFLP pattern that identifies them.RFLPs form the basis for theidentification technology known as DNAfingerprinting.

In a broader context, restrictionenzymes allow DNA to be cut-and-pastedand for pieces of DNA to be moved fromone organism to another. Since allorganisms share the same DNAlanguage,you can move words, sentences,


paragraphs from one book (genome) toanother. There are several applications ofthis technology:• human therapeutics where rare

human therapeutic products that solvea serious medical problem can besynthesized (ex. insulin, the clot-buster tPA)

• gene therapy whereby geneticlimitations can be repaired byreplacing the defective gene with acopy that restores normal function (ex.severe combined immunodeficiencydisease, hemophilia, growth of newblood vessels for the treatment ofcardiovascular disease),32-34 and

• agricultural applications wherebycrop yield and nutrient content can beimproved.

TAKE-HOME MESSAGEGenetics is central to nutrition and is

impacting dietetics professionals in everyaspect of dietetics, from clinical nutritionto public policy development to foodservice. The aspect that provides thegreatest leverage to us as a profession is inclinical nutrition and public policy.Genetics is the base; it determines thelimits of our personal health continuumbetween disease and wellness anddetermines whether we will be susceptibleto disease or to wellness. Nutrition ispotentially THE most powerful tool fortipping the balance to the wellness end ofthe continuum because it has the potentialfor filling the metabolic gaps caused byour genetic limitations. The dieteticsprofessional who understands theimplications of the client’s genetic historyand the underlying biochemistry is in aposition to develop effective nutritiontherapies and to possess a competency thatwill be in high demand within health careand that no other health care practitionercan provide. The potential for theprofession is enormous if we will takeaction now and prepare for the future,which is upon us.

Watch for further exploration of thesekey concepts in future issues of thenewsletter and on our Web sitewww.complementarynutrition.org.

References1. Groff JL, Gropper SS. Advanced Nutrition andHuman Metabolism, Third Edition. Belmont, CA:Wadsworth; 1999.2. Bennett PH. Type 2 diabetes among the PimaIndians of Arizona: an epidemic attributable toenvironmental change? Nutr Rev. 1999;57:S61-S54.

3. Valencia ME, Bennett PH, Ravussin E, et al. ThePima Indians in Sonora, Mexico. Nutr Rev. 1999;57:S55-S58.4. Bouchard C, Tremblay A, Despres JP, et al. Theresponse to long-term overfeeding in identicaltwins. N Engl J Med. 1990;322:1477-1482.5. Barsh GS, Farooqi IS, O’Rahilly S. Genetics ofbody-weight regulation. Nature. 2000;404:644-651.6. Chagnon YC, Perusse L, Weisnagel SJ, et al. Thehuman obesity gene map: the 1999 update. ObesRes. 2000;8:89-117.7. Martinez JA. Obesity in young Europeans:genetic and environmental influences. Eur J ClinNutr. 2000;54:S56-S60.8. Murray JA. The widening spectrum of celiacdisease. Am J Clin Nutr. 1999;69:354-365.9. Kang SS, Zhou J, Wong PWK, et al.Intermediate homocysteinemia: a thermolabilevariant of methylene tetrahydrofolate reductase.Am J Hum Genet. 1988;43:414-421.10. Jacques PF, Bostom AG, Williams RR, et al.Relation between folate status, a common mutationin methylene tetrahydrofolate reductase and plasmahomocysteine concentrations. Circulation.1996;93:7-9.11. Verhoeff BJ, Trip MD, Prins MH, et al. Theeffect of a common methylenetetrahydrofolatereductase mutation on levels of homocysteine,folate, vitamin B and on the risk of prematureatherosclerosis. Atherosclerosis. 1998;141:161-166.12. Simopoulos AP. Genetic variation and nutrition.Nutr Rev. 1999;57:S10-S19.13. Cobb MM, Teitlebaum H, Risch N, et al.Influence of dietary fat, apolipoprotein Ephenotype, and sex on plasma lipoprotein levels.Circulation. 1992;86:849-857.14. Uusitupa MIJ, Ruuskanen E, Makinen E, et al. Acontrolled study on the effect of beta-glucan-rich oatbran on serum lipids in hypercholesterolemicsubjects: relation to apolipoprotein E phenotype.J Am Coll Nutr. 1992;11:651-659.15. Davis JN, Kucuk O, Sarkar FH. Genisteininhibits NF-kappa B activation in prostate cancercells. Nutr Cancer. 1999;35:167-174.16. Kang ZC, Tsai SJ, Lee H. Quercetin inhibitsbenzo(a)pyrene-induced DNA adducts in humanHep G2 cells by altering cytochrome P-450 1A1gene expression. Nutr Cancer. 1999;35:175-179.17. DeLuca HF, Zierold C. Mechanisms andfunctions of vitamin D. Nutr Rev. 1998;S4-S10.18. Beato M, Herrlich P, Schutz G. Steroidhormone receptors: many actors in search of a plot.Cell. 1995:83:851-857.19. Mangelsdorf DJ, Thummel C, Beato M. et al.The nuclear receptor superfamily: the seconddecade. Cell. 1995:83:835-839.20. Laragh JH. Renin profiling for diagnosis, riskassessment, and treatment of hypertension. KidneyInt. 1993;44:1163-1175.21. Department of Energy Office of Biological andEnvironment Research, Human Genome Program.Human Genome Project Information. Available athttp://www.ornl.gov/TechResources/Human_Genome/home.html. Accessed May 16,2000.22. Collins FS, Jegalian KG. Deciphering the codeof life. Sci Am. 1999;281:86-91.23. Collins FS. The human genome project and thefuture of medicine. Ann NY Acad Sci.1999;882:42-55.24. Collins FS. Avoiding casualties in the geneticrevolution: the urgent need to educate physiciansabout genetics. Acad Med. 1999;72:48-49.25. Collins FS. Genetics: an explosion ofknowledge is transforming clinical practice.Geriatrics. 1999;54:41-47.26. Strausberg RL, Feingold EA, Klausner RD, etal. The mammalian gene collection. Science.1999;286:455-457.27. Simopoulos AP, Herbert V, Jacobson B.Genetic Nutrition: Designing a Diet Based on YourFamily Medical History. New York, NY:Macmillan Publishing Company; 1993.28. Lewin B. Genes VII. New York, NY: OxfordUniversity Press; 1999.

29. Snustad DP, Simmons MJ. Principles ofGenetics, 2nd Ed. New York, NY: John Wiley &Sons, Inc.; 1999.30. Horowitz M. Basic Concepts in MedicalGenetics. New York, NY: McGraw-HillCompanies; 2000.31. Thompson MW, McInnes RR, Huntington FW.Genetics In Medicine, 5th Ed. Philadelphia: W.B.Saunders Company; 1999.32. Cavazzana-Calvo M, Hacein-Bey S, de SaintBasile G, et al. Gene therapy of human severecombined immunodeficiency (SCID)-X1 disease.Science. 2000;288:669-672.33. Isner JM, Asahara T. Angiogenesis andvasculogenesis as therapeutic strategies forpostnatal neovascularization. J Clin Invest.1999;103:1231-1236.34. Kay MA, Manno CS, Ragni MV, et al.Evidence for gene transfer and expression of factorIX in haemophilia B patients treated with an AAVvector. Nature Genet. 2000;24:257-261.

Web site References:www.complimentarynutrition.org

Basic genetics:http://www.nhgri.nih.gov/DIR/VIP/—Office ofScience Education and Outreach of the NationalHuman Genome Research Institute; has a glossaryof genetics terms and also illustrations of many ofthe components and concepts

http://www.cdc.gov/genetics/resources/resources.htm—Centers for Disease Controland Prevention

Food biotechnology:http://www.infic.health.org—Institute for FoodInformation Council

Genetics and disease:http://www.hhmi.org/GeneticTrail—Howard Hughes Medical Institute

Human Genome Project:http://www.ornl.gov/TechResources/Human_Genome/home.html.

Ruth DeBusk, RD, PhD is a geneticist andclinical nutritionist who incorporatesgenetics and biochemistry into indi-vidualized nutrition therapies for herclients. She was on the genetics faculty atFlorida State University, co-developer ofa biotechnology company, and Chair of theFlorida Task Force on Biotechnology priorto going into private practice. Dr. DeBuskcan be reached at 850/562-3261 [email protected].


EditorSarah Harding Laidlaw, MS, RD, MPAAssociate EditorEsther Trepal, RD

SECTION EDITORSTherapiesMari Clements, MS, RD, CDESupplementsSusan Moore, MS, RDJudy Shabert, MD, MPH, RDHerbsJohn Westerdahl, MPH, RDWinston Craig, PhD, RDFunctional FoodsSusan Pitman, MA, RDPriscilla Connors, PhD, RDPoint/CounterpointRebecca Ephraim, RDReaDer ReportsDiana Noland, MPH, RDGerri French, MS, RDContinuing Professional EducationBarbara Knous, PhD, RDWeb siteRuth DeBusk, RD, PhD, EditorRick Hall, WebmasterDiane Rigassio, MS, RD, CDEAssociate EditorCathy Welsh, MS, RDAssistant WebMasterDonald Simon, MLS, MHA, RDLibrary ListDeralee Scanlon, RDHeads Up!

Editorial Staff . . .

Tuesday, October 172:00-3:30 pmBiotechnology: The Science and the Issues4:00-5:30 pmBiotechnology: Point/Counterpoint

Tuesday October 174:00- 5:30 pmComplementary Care in the Treatmentof Mood Disorder: Homeopathy andExercise Intervention (sponsored by theDDPD- DPG) presented by AmyRothenberg, ND and Lisa Dorfman, RD,MS

Wednesday October 184:00- 5:30 pmHerbal Medicine and Vitamin SupplementsRelevant to Multiple Sclerosis and otherNeurological Diseases

Thursday October 1910:00-11:30 amPills and Potions: Evaluating DietarySupplementsCholine and Canotenoids: The NextGeneration of Nutrition

Other Activities of Interest toNCC Members at FNCE

NCC at FNCESunday, October 158:00 am- 5:30 pmNCC Executive Committee MeetingAdams Mark Hotel, Plaza Court 81:00-5:00 pmSkill Building Workshop: BotanicalMedicine 101 for the Health CareProfessional presented by Tieraona LowDog, MD,AHGColorado Convention Center, Room A214

Monday, October 161:30 – 3 pmHealth Benefits of Soy Protein Throughoutthe Life Span; Pediatrics, Soy and ChronicDisease Management, and Adult Healthand Wellness.1:30 - 3 pmSymposium organized by The Office ofDietary Supplements of the NationalInstitutes of Health.Colorado Convention Center, Room A101-75:30- 8 pmNCC Business Meeting,/ReceptionAdams Mark Hotel, Plaza Ballroom D&E/Foyer

Tuesday, October 179:30 am -1:30 pmDPG ShowcaseExhibit Hall

Denver, Colorado

For more information on upcomingconferences on biotechnology andNatural Pharmacy go to: http://www.bioconferences.com

* Note: Schedule is subject to change.

THANK YOU to the reviewers ofthe CPE article for this issue:

Dr. Stephen C. HedmanUniversity of Minnesota-Duluth

Dr. Carolyn D. BerdanierUniversity of Georgia

Joan BurnsWaisman Center

University of Wisconsin-Madison

And thanks to all who made thisissue possible including reviewersBetsy Hornick, Dot Humm, EstherTrepal, and proofreaders SusanZabriskie, Elizabeth Thompson,and most of all, Ruth DeBusk.


CPE Questions- True or false

1. _____ Genetics is important forunderstanding health and disease and isbecoming a useful tool for dieteticsprofessionals.

2. _____ DNA is the genetic material forhumans and is found in the nucleus of each celland in the mitochondria.

3. _____ DNA is a double helix consisting ofa sugar-phosphate backbone and pairednucleotide bases that has encoded within it theinformation that directs the synthesis andfunction of the human body.

4. _____ The DNA code must be translatedinto proteins used to construct the frameworkof the body and its metabolic machinery.

5. _____ The DNA code consists of fournucleotide bases and it’s the linear sequence ofthese bases that determines the protein productinformation encoded within.

6. _____ A gene is a set of sequences thatcontains the information for a protein.

7. _____The information in the gene istranscribed directly into protein.

8. _____The base sequence of the messengerRNA is translated in units, sets of 3 consecutivebases, that correspond to one of the 20 aminoacids that are used to synthesize a protein.

9. _____Proteins are used by the body forstructural purposes and for functional(metabolic) purposes.

10._____Examples of metabolic proteins areenzymes, hormones, receptors, carriers andpumps, which play critical roles in cellularmetabolism.

11._____Changes in the genetic material aretransferred to the protein for which that genecodes and may affect the function of the protein.

12._____If function is negatively impacted, adisease may result.

13. _____ Each cell with a nucleus containsthe full genome for that individual.

14. _____The human genome consists of 23pairs of chromosomes: 22 pairs of autosomesand 1 pair of sex chromosomes, with onemember of each pair originating with theindividual’s mother (the maternal copy) and onemember with the father (the paternal copy).

15. _____Each chromosome contains manygenes along its length, genes have a specificlocation on a specific chromosome, and thelocation is the same for both members of thechromosome pair.

16. _____ Two copies of each gene are present,one on each member of a chromosome pair,including the sex chromosomes.

17. _____ The two copies of a gene may bepolymorphic, that is, they may have slightlydifferent base sequences and, thereby, code forslightly different proteins that may differ inability to carry out the function of that protein.

18. _____ Variations in genes, particularlypolymophisms, are responsible for thefunctional variation among individuals.

19. _____ New cells only originate fromexisting cells, and mitosis is the process of celldivision that duplicates the 46 chromosomesin the original cell and distributes them to eachnew cell.

20._____ Meiosis is a special division processwhereby the chromosomes are duplicated fromthe original cell but only one member of eachchromosome pair is distributed to the gamete(egg or sperm).

21._____It’s during meiosis that genes arerecombined into new combinations becausewhich member of the chromosome pair, thematernal or paternal copy, ends up in aparticular gamete is random.

22._____Genes that are physically closetogether are “linked” and tend to stay togetherwhen chromosomes are distributed intogametes.

23._____ “Genotype” refers to the DNAsequence of the gene; “phenotype” refers to thetrait (function) that’s produced upon translationof that DNA sequence.

24._____ Dominance and recessiveness referto phenotype and are not absolute terms butused to describe which allele prevailsfunctionally over the other in heterozygotes.

25._____ Most genes are actually co-dominantat the DNA level: both alleles are expressed butthe protein produced from one allele may beable to get the job done and mask theinadequacies of a less functional allele.

26._____ The phenotype may not be “fullypenetrant”, meaning that an individual mayhave the genotype that should manifest as adisease state but may not actually have diseasesymptoms.

27._____ Further, family members that havethe disease genotype may show a great deal ofvariability in how the disease is expressed.

28._____ Lifestyle choices, including nutritionchoices, may be impacting the penetrance andexpressivity of the phenotype.

29._____Nutrition, through its ability toinfluence the expression of the genes and itsability to supply needed metabolites, has thepotential to compensate functionally for faultygenes.

30._____Genetic technology has given rise tonew medical and agricultural applications,which have potential implications for thedietetics professional. A

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*This activity has been approved for 2 hours ofCPE credit. You will be notified if hours are notawarded.

Cost: $12 NCC members; $20 non-membersMake checks payable to: NCC-DPG #18Mail by 9/1/02 to:

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NCC’s Executive Committee 2000-2001 CONTACT INFORMATION2000-2001 CONTACT INFORMATIONChairCheryl R. Galligos MA RD118 CarefreeChatham, IL 62629-1510217-782-3300 (w)217-782-1235 (wfax)work: [email protected]: [email protected]

Chair-electRebecca J. Ephraim RD108 W. Grand AvenueChicago, IL 60610312-321-9700 (w)312-321-3655 (wfax) [email protected]

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SecretaryRosalyn Franta Kulik MS RD FADA16503 Cerrillo de AvilaTampa. FL 33513-1080813-960-1557 (w)813-960-4248 (fax)[email protected]

TreasurerFelicia L Busch MPH RD FADAFelicia Busch & Associates, Inc.1804 Lindig StreetSt. Paul, MN 55113-5538651-645-1234 (w)651-645-4621 (wfax)[email protected]

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