Feed the Brain

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Feeding the BrainHow oods ffect Children


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Feeding the rain

C. Keith Conners Ph .D .

P E R S E U S P U B L I S H I N GCambridge Massachusetts

HowFoods A f f e c tChildren


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Library ofCongressCataloging in Publication DataConners,C.Keith.Feeding thebrain:how foodsaffectchildren / C.KeithConners.

p. cm.Includesb ibliographicalreferencesandindex.ISBN0-7382-0620-21. Food allergy in childrenPsychological aspects. 2 Behavior disorders inchildrenNutritionalaspects,I.Title.

RJ386.5.C66 1989 89-160716I3.2'083dc20 CIP

Perseus Publishing booksarewailableatspecial discounts rbulkpurchases in theU.S.by corporations,institutions,mAotherorganizations.Formoreinformation please contacttheSpecialM arketsDepartmentat thePerseus Books Group,I CambridgeCenter,Cambridge, MA02142,orcall(800)255-1514 or(617)252-5291,ore-mail j.mccrafy@perseusbooks,cn

1 09 8 7 6 5 4 3

1989C. KeithConnersA member of the PerseusBooksGroupPublishedbyPerseus Publishing

AllrightsreservedNopartofthis book maybereproduced, stored in a retrievalsystem,ortransmittedin any form or by any rneans electronic, mechanical photocopying, microfilmingrecording, orotherwise,withoutwrittenpermission from the Publisher

Printed in the UnitedStatesofAmerica


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ref ce

The premise o this book is that what children eat can pro-foundly shape the course of the brain s growth, its functionsand its capabilities. Children s brains are actively changing, dy-namic structures, strongly influenced bywhat, howmuch, andwhenthey eat. Food nurtures the brain, providing key nutrientsand energy for growth. Food protects the brain, shutting outharmful threats from a toxic and polluted environment. Foodalertsas well ascalms brain activity. Food changes the moods ofthe brain, both through the pleasure it affords and by its chem-istry.

Foods, like drugs, are ultimately chemicals. Butthey aremore than that. Foodsare symbols, a parto f rituals, pathways tobody images, and vehicles through which love is expressed.Food ispartof human culture, habits, and lifestyles. Language,culture, and social environmentare intertwined withfood andthey powerfully affect brain growth in their own right. Theyinteractwithfood determining the course of the brain throughitsperilous journey from conception to adulthood.Important newunderstanding nowexists about the waysthat food changes behavior, mood, and mental proficiency inchildren;and how human behavior in turn affects nutrition. Butlittle of this information is available to parents, educators, andotherswho must decide how and what children should eat.

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goodconsumers,notjust offood but ofinformation.W e arguethat muchusefulinformationis prematurely dismissed by somescientistswith biased agendas. Butthere is also agood deal ofmisinformation too readily swallowedas if itwere fact.

This is not a diet book, nor a self-help book. But we doattemptto showhow one may learnforoneself, through experi-mentsathome, whether someo f theideasin the scientific litera-ture apply toone s own child. Science is nothing more than a setof rules, devised to prevent one fromkidding oneself and oth-ers, aboutsomeidea of how nature works. Muchofthis bookpresents the back-and-forth dialogue among scientists aboutfood and behavior. To the layreader, who wantsto know whatto donow,thesedebatesmayseemattimestoleadto a mystify-ing impasse. But we argue that the debates show us what tolook for in ourown, personal experiments,and how to use foodas a tool in optimizing mental and behavioral function inchildren.Iam grateful to Richard Wurtman, John Fernstrom, BonnieSpring, and Ernesto Pollitt for inspiration and helpful discus-sionsabout many of the issues in this book. Dan Raiten pro-vided me with many helpful suggestions and the benefitof aprofessionalnutritionist s perspective.

Grants from the National Institutes ofMental Health, Kel-logg s Foundation, General Foods, and theSugar Associationwere all helpful in my own research on sugar,breakfast, andbrain function in children. Without the unstinting support ofJames Egan, M.D., I would not have had the freedom or re-sources to pursue my interest in this subject.I am very grateful for the patience and encouragementofmyeditors,Linda Reganand Victoria Cherney, who ruthlesslypointed out the passive voice, dangling participles, and otherbad habits from a lifetime ofacademic writing.Finally I am especiallygrateful to mywife Karen Wells,forinsisting thatI eat the way I preachto others;and to my daugh-terKatie,fo rshowing mejusthow marvelousagrowing braincan be. C.Keith Conners

PREFACE


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ont nts

CHAPTER ONE Food, Mind and BehaviorBeliefsandEmotions about Food 1Food and the Brain 6Food and the World around Us 7ProblemsinStudying FoodandBehaviorBehaviorPatterns inChildren 16

CHAPTER T wo H yperactivity and A rtificial SweetenersA Case ofSevere Reaction toAspartarne 25T heNutraSweet Aspartame) Story 28A Controlled Case Study with Aspartame 38DietingandAspartame 47OtherControlled Trials of Aspartame in ChildrenSummary 52

C H P T E R T H R E E T he irst Meal of the DayDoes EatingBreakfastMatter? 55Supplementing Breakfast 57

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CONTENTS

Paying Attention 64Breakfast and Hyperactive Children 68Breakfast and Hypoglycemia 70Conclusions on Breakfast 71

CHAPTER FOUR Sugar and Its Effects onBehavior andMood 75What Is Sugar? 77Sugar Hyperactivity and Attention Deficits inChildren 79Dietary Intakeof Sugar and Behavior in Children 80Why Scientists Disagree about Sugar and Behavior 82T he Cause and Effect Problem 84Studying Sugar Effects by Adding It to the Diet 87Hormones Sugar and Breakfast 93Some Speculations about BrainGrowth and Sugar 94Are All Carbohydrates Equal? 97Summary 98

CHAPTER F IV Food and Violence 101Hyperactivity Aggression Alcohol and CriminalityDietand Killer Mice 105Hypoglycemia and Crime 106Societies T hatKill 108BloodSugar and Aggressive Fantasy in NormalAdults 111Hypoglycemia and ViolentO ffenders 114Dietand Aggression inPrison 118Conclusions 120

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CHAPTER Six Diet IQ andLearning 123Whatis IQ? 123Studying Foodand IQ in Children 128Malnutrition and IQ 13Mother s Dietand IQ in Her Children 132Dietand IQ in Young Children 134Diet and IQ in Older Children 136Tired Bloodand IQ 139Heavy Metal 144Nutrition and IQ: What Should We Do? 152

CHAPTER SEVEN Food Additivesand Food Allergies 157Food Additives 157Feingold sTheoryofFood Additivesand

Hyperactivity 158Food Allergy 176Adviceon Changing Behavior with Diet 184

CHAPTER EIGHT Megavitamins 187WhatAre Vitamins and Megavitamins? 188Orthomolecular Psychiatry and Biochemical

Individuality 189Megavitamins and Schizophrenia 192Megavitaminsand Hyperactivity 195ChildhoodAutism 204MentalRetardation 207WhereDo We GofromHere with Megavitamins?

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CONTENTS

C H A P T E R N i N E Eating Disorders andStressinChildren 211

EatingDisorders in Children 211TheExperienceofStress 221HowStress Affects the Bodyand Brain 223Foodand Stress 226StimulantDrugs Sugar and Protein 230Conclusions 232

C H A P T E R T E N Tracking Food Mood and BehaviorinChildren 235

ObservingandRating Children 235DoingExperimentsatHome 245

CHAP TER E L E V E N Conclusions 49Food Changes Brain Neurotransmitters 249Foods ProtecttheBrain 252Food and the Developing Brain 253Ideasand Emotions Control Nutrition 254TheScienceofFoodand Behavior 254

N O T E S

IN DE X

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Food Mind and Behavior

BELIEFS AND EMOTIONS ABOUT FOODThis book is about food and its relationship tobehavior andmentalprocessesinchildren. Everyone knowsandaccepts thatfoods are important to the functioningof thebody. Notevery-onebelieves that foodsaffectthemind however. Manypeoplefeel that aslong aschildren arewell-nourished what they eathas little relevanceto the waythey learn think feel and act.Itmay beeasy toaccept that foodscausecertain tr nsientchanges ofmental state suchaswhen discomfortor drowsinessfollows overeating when sedation ensues from imbibing alco-holic beverages orwhen our morning coffee makes us morealert. Most people can easily recognize these minor effects fromtheir own experience. It may also seem reasonable tobelievethat some very extreme nutritional conditions such as severeprotein malnutrition lead to failure ofbrain growth much aspoor nutritionstuntsthegrowthof thebody. utthereismoreto the food-mind connection than transient subtle changes orthe extremeeffects ofmajor nutritional deficiency.Foodhas profoundeffects on higher mental functions evenin well-nourished children eating ordinary foods in ordinaryamounts. Foodscanenhance problem-solving ability optimize

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alertness, andimprove moodandbehaviorinnormal children.Contrarily, foodscanalso impair children whose behaviorandlearning are already in trouble from other causes, hamperingtheir efforts toconcentrate and maintain self-control. Over anextended period, food affects basic intelligence through effectson brain growth and by altering the way the environmentchanges thedeveloping brain.Butsomescientists see the idea offood changingbehaviorasjust another popular fad.Ourcultureglorifiesnostrums andspecialdiets,promisingtoimprove everything fromlongevitytobeautyandsexual potency, Tabloids routinely announce secretdiets ormiracle foodsthat restore lost powers, increase IQ oreven enhance spiritual communications. Thereissomethingin-herently appealing, almost mystical,in the idea that Youarewhat youeat, Such beliefs seem to fulfill adeep need tohavesome control overone'sownmental functions, other thanthemore commonly acceptedand arduousmethods ofeduca-tionorpsychotherapy.Yet, moreoften than not, people adopt-ingthese ideas becomedisillusioned,untilthenextfadappears.The cycle of failed promises from bogus remedies eventuallyleads to skepticism.Scientific scrutinyofthese claims aboutthementaland be-havioral effects o foods is notalways dispassionate and objec-tive. Thereissomething aboutthesubject that seemstoprovokeinflamed debate. Sometimes scientists leamto be so skepticalabout fadsthattheyoverreactanddismiss llideasabout foodandbehavior out ofhand.Theresponse of theAmerican AcademyofPediatrics to astudy ofmegavitamins and mental retardation illustrates theemotions surrounding this issue.1In a 1981 article which ap-peared in the Proceed ings o f the Nat ional Academy o f Sc iences D r.RuthHarrell andcoworkers purported toshow that agroupof16retarded children had a 5- to10-point rise in IQ after ashortperiod ofnutritional supplementation with trace minerals and

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Therearesomeflaws in Dr.Kartell'sexperiment,but Dr.Rimlandhas caughtseveralerrors and misinterpretations by theAAPcommitteeitself. Inturn,heresponds with vehemencetowhatheseesasprofessional imperialismandentrenched con-servatism. Theargument has shifted from questions of fact toquestions ofmotives and professional bias. Wewill see otherexamples of the deep distrust between practitioners who believein the power ofdiet and scientists who regard it as fraud butwho then go on to display bias in their own handling of theissues,It isunderstandably difficult to remain cooland objectivewhen certain memberso f theprofessional community commer-ciallyexploit complexandunsubstantiated dietary routinesfo rcuring serious mental illnesses, with little or no evidence tosupporttheir schemes. For example, some practitioners chargelarge fees fo rdeveloping elaborate profilesofnutrients basedupon samples ofhuman hair, claiming thatthe rightbalanceof

Whatwehaveherec learlyis temper tantrumby agroupofpediatricians who find themselves unableto tolerate the frustra-tion resulting from the destruction o several o f their mostcherished beliefsbywell-designed and well-conducted research,Whata shock it must be to learn they have been wrong alltheseyears:first,mentally retarded children mbehelped;high potencynutritional supplementsc nbebeneficial. . . . Thelackofprofes-sional integrity and ofconcernfor the welfareo fretarded childrenand their familiesby the AAP isshameful. Comeon fellows,growup If you areskeptical,try thesupplementsonsomeofyourownpatients.3

OOD MIND ANDBEHAVIOR

megadoses ofvitamins (issues w ewill takeup indetaillater).2Thisstudywasroundly criticizedanddismissed by acommitteefrom theAmerican AcademyofPediatrics AAP). But Dr.Ber-nard Rimland,awell-known researcher onautismandmentalretardation, pointed out a half-dozen errors o freporting andinterpretation contained in the AAP's statement.He had thistosay:


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minerals will cure serious emotional problems. Perhaps suchaprofile ofminerals for aparticular individual isrelated to his orher mental health; the idea itselfis notunreasonable.But theexperiments needed to prove the truthof that idea have notbeen doneby thepeoplewhoproposed it.Untilothersdothatworkforthem,itseems reasonable thatthepractitioners shoulddesist intheir claims. Meanwhile, their operations only servetoincrease scientific skepticism.Amedical colleagueofmine recently toldme astory aboutapatient of his who perfectly illustrates the way fringe practi-tioners prey upon patients. The patient, a youngwoman hada problem with tension and fatigue unexplained by her doc-tors. She heard of a doctor who used diet to cure thetension-fatiguesyndrome. Thedoctortook ablood sampleand had itanalyzed by a company in the Midwest, at a cost of severalhundred dollars. Thereport prescribed acomplexseriesof di-etarychanges, supplements, mineral, and vitamin combinationswhich would take several monthstocomplete presumablyat averyhigh cost.What made the report interesting in the eyes of rnycol-league, however, was the disclaimer it contained at the end; Although the recommendations of this report arebackedbyscientificresearch, they still mustbeestablished byclinical cor-relations. In other words, Wehave toproceed by trial anderror atyourexpense, and don'tblameme ifitdoesn't work.

Some practitioners rely upon unproven methods ofdetect-ing food allergy, suchasplacing foods under the tongue andwatchingfor abehavioral reaction. Now, llergy is amuch mis-used term, and thoughit is a complexsubjectcovering a widearray ofbodily reactions thatareoftenhardto pindown, itdoeshave specific scientific meaning. As wewillsee in alater chap-ter, specificteststhat provoketheimmune systemcanverify thepresence oftrue allergy.But theadvocates ofdietary schemesfortreating allergy,who useunproven diagnostic methods, sel-

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dom feel the need for proven laboratory findings or criticalthinkingtosupporttheirtheories,relyinginsteadupon colorfulanecdotes to bolster their claims. Scientists learn to regard suchfrivolous claims with caution because thereareclear monetarymotives behind those making them. Skepticism is usually in-creased by theunwillingnessofthose makingtheclaimstocarryout thesupporting research necessarytodocument them.The individuality ofhuman responses to foods is also acause of skepticism that food alters mental functioning. Noteveryone reactstofoodsin thesameway.It maytherefore seemas though the effects of foods are random or inconsistent. Ifcertainfoodsalways changedacertain behaviororlearning abil-ity, then there would be no dispute. That there are importantindividual differences in the waychildren react tofood, how-ever, should be no more surprising thandifferencesin responsetodrugs.

Certainpsychoactive drugs drugs that affect mental pro-cessesandbehavior,suchas antidepressants andantipsychoticdrugs) have quite different even opposite effects dependinguponthegenetic makeupof thepersontakingthedrug. Drugsoften have quite different effects onnormal people and thosewith some biological dysfunction. For instance, some anti-depressants improve mood onlyinpeople withacertaintypeofdepressive illness,butthey havenoeffectsorevenunpleasanteffects innormal people. Foods, too actd ifferently onchildren,dependingupon their unique biochemical makeup,W ewill seethat the druglike specificity ofsome foodsonthe minds ofchildren is not just an analogy to psychoactivechemicals.Foodsaremadeup ofchemicals and, likedrugs,canproduce psychoactiveeffectswhich depend upon the chemistryoftherecipientand on theparticular circumstancesinwhichthefood iseaten.Butfringepractitioners exploit this idea, preciselybecauseitmakesithardto pindown dear-cut reactionstopar-ticular foods.

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Thereare certain nutrients designated as essential. Thisword has a specific meaning in nutrition: we must replenishthese chemicalsbyeating them, sincethebrainandbodydo notmanufacture them. For example, many of the brain's neuro-transmitterschemicalmessengersareeither essential aminoacidsfound inproteins orderived from essential amino acids.The functionsof thebrain therefore depend very muchoneat-ing protein foods withtheright amountof amino acidsinthemand ensuring their availabilityat the right time.Although not essential in this samesense, almostall thefuelfor thebrain s work comesfrom asugar knownasglucose,which the brain cannot manufacture. Glucose mustbe madefrom carbohydrates. (Thereisalsoaprocess called g lucomogene-sis which makesglucose from some proteins when carbohy-drates areunavailable.)Perhaps asmuchas 30 to 50 of thecalories consumed bychildren go to meet glucose energy requirements of thebrain.The body maintains a supply of glucose and other energysources (such asglycogen) whichisusually adequate to meetthe constant demandsof thebrain. Ifthis surplus poolofsugarbecomes depleted (ashappens,forexample, when thereis toomuch insulin), then even a fewminutes ofinsufficient glucosewill lead to faintness, unconsciousness, coma,and ultimately,death. Many foods we eat are quickly converted to bloodglucose, raising theblood sugar level.Thebrainmust receiveaconstant, accurate, steadyflow ofthis fuel inorderto survive.Sugar, therefore,hasoftenfiguredinspeculations about mentalillnessandbrain disorders. Wewill review evidence later show-ing that sugarcan actmuch like drugs on the brainand thatsugar interacts with drugs commonly used to treat children shyperactivity.Butiffoods like sugarand proteins doinfluencethe brain s

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basic energy supply and chemicalmessages (and therefore men-tal functioning and behavior), what prevents each meal fromradically upsetting ourmood oraltering our behavior in unpre-dictable, unpleasant, or even dangerous ways? And wouldn teach nneal be like blindly swallowing a bunch of psychoactivepills?Finally, would the human species evolve in a way thatallows foods to have amajor impact upon mental functioning?

Although the brain and body have evolved a highly elabo-rate system forprotecting the brain, there are special circum-stances which allowthe chemicals infoods to penetrate throughthe protective barriers of the brain, where they then interactwiththe brain s ownchemicals. Recentdiscoveries innutritionalresearch haveclarified some ofthese circumstances, which wewilldiscuss in detail later. Yes foodsare psychoactive, butonlyunder particular circumstances, and it is these circumstanceswhichwe must understand if we want to take advantageof thepossibilities for enhanced mental function and avoid the harm-ful consequences of eating the wrong food at the wrong time.

FOOD ND THEWORLD ROUNDUS

Not only are there special circumstances which permit aconnection between food and mental functioning, there are alsosubtle interactions between food and the environment, oftendisguisingthe connection offoodwith behavior. Eatingis not anisolated behavior that one engages in just to obtain sustenance.Rather it ishighly integrated with every aspect of our physical,cultural and social environment, and the effects offood dependto some extent on the environment.

Consider, for example, the question of the mental effectsofsevere protein malnutrition. Scientists have established thatduring certainperiods of early development, brain damage re-sults from inadequate protein intake. Butlong-term effects of

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such deprivation arequite different from onechild to another.Some children have much better functioning after early mal-nutritionthan others starvedto thesamedegree.They registerhigher IQs, and their behavioral deficits are fewer than otherchildren with similar early nutritional disadvantages. Whatac-counts fo rsuch inconsistency?Carefulstudyofchildren in theearly stages ofmalnutritionreveals that some mothers stopresponding totheirinfantsbe-causetheinfants have stopped sendingout thesignals mothersusually depend upon. Mothering becomes impaired when ababybecomeslistlessandapathetic,nolonger cries,and ceasesresponding to the mother by looking and smiling at her, whichwould encourage continued interaction. The lack o f mother-ingrocking soothing, talking, stimulatingin turn causesmore impairmento fbrain growth in thechild. Thereasons areno t wellunderstood; but the brain needs social stimulation inorderto grow,justas itneeds food.Without this socialnutri-tion, brain growth slows down even ifadequate caloriesareavailable.Similarly the fussy andirritable child, whose colic is theresulto fintolerancetocow's rnilk canturnamother against thechildand lead to a prolonged, hostile battle over feeding. Thisback-and-forthchainofeventsis anexampleo fwhat psycholo-gists call tr ns ction lism in child developmentthe intertwin-ingof child and parentresponses,so that both are causes andboth areeffects. Thechild'sbehavior causes the mother to reactin acertain way; thiseffectthemother'sreactionthencausesa further reaction in the child; and so on. When such systemsdevelop, they are often hard to disentangle. Thechild'sbe-haviorandemotional functioning m ayappearto be theresulto fparenting behaviors alone, whereasthechild's behaviorispartof awhole cycleofinfluences, including reactions to foods.Family an dcultural belief systems affect what, when, an dhow often certain foodsareeaten. Certain convictions, likethe

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beliefthat natural foods promote health, leadtoselective dietswhich can have unexpected consequences for mental func-tioninginchildren,as weshallseewhenwelookat therelation-shipbetween intelligenceanddiet. These beliefsarepartof ourculture and family life so their profound effects may go un-noticed and taken forgranted. Like the air webreathe, food issuch a familiarpartof ourenvironment thatwe m ay failtotakenoticeof ituntilitbecomes scarceorproduces sometoxic effect.

Theamount ofmoney people earn,where they live, andwhat theyeat are oftentied together. If you arewealthyyou areless likely toliveinpolluted environments. Then, even ifyourdiet is suboptimal, it might be oflittle consequence. On theother hand, because some foods have protective effectagainstpollutants, that same suboptimal diet might be hazardous toyourIQ if you arepoor andlivein anarea exposingyou totoxicchemicals. Here it is notjustthe lack of aparticular nutrientorfoodstuff that is the problem, but a lack which occurs in thepresence of anenvironmental hazard. Thus, we may overlooknutritional effects on brain function because the effects occuronly in aparticular environmental context.W e willdiscuss suchproblemswhen we look at the effects of heavymetals,such aslead, and their relation to diet and IQ.

PROBLEMS INSTUDYING FOOD AND BEH VIORMostpeople may not spot the flaws in studies purporting to

prove something aboutfoodandbehavior,or thelogicalflaws inthe counterarguments used for the other side. Ifeven reason-able scientists get caught up in biased and heated debates, howcan theordinary citizen expectto sift theevidence?Inthis book I try tospeak tothat citizen, not to scientistslockedinunresolved controversies. Laypersonsoften misunder-stand the goalsofscience, which concerns itself with general

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lawsapplying tolarge populations. Behavioral science, in partic-ular, deals with statistics and averages, not with individualcases.* Experiments on food and behavior with large groups ofchildren are especially difficult; manipulating and controllingdietsis hard, and there are ethical limits to what can be donein most experiments. As a result, many experiments remainflawed inconclusive,and difficult to interpret orreplicate.Even successful experiments resulting in support for a hy-pothesismay not tell us what we need to know.Parents andteachers usually want to know what to do about a p rt icul rchild, and an experiment seldom reveals which children areexceptionsto the general findings. Rather than waiting for reso-lutionof all the scientific squabbles, parents and teachers needto know what can be done now. Unlikescientists, parents don trequire certainty about general laws, but guidance about indi-vidualdecisions.

To some extent then, parents and teachers must becomeexperimenters themselves, because they cannot waitforresolu-tion of allconflicting evidence. There are many important ideasabout food and behavior testable at home by careful observa-tion. Scientistsmay conduct experiments orcarry out studies ongroupsof people, only tofind that the results are inconsistent,perhaps because there are too many variables out oftheir con-trol. Butmany important ide s tested by scientists are worthexploring with individual children in the home. The results ofhome experimentsm ay notsatisfyscientists who arelooking forgeneralizations that applyto large groups of children. Buttheymay unlock secrets of value for the one child we most careaboutourown.Before one begins experimenting with foods as a cause orBehavioralpsychologists often study individual animals, finding very preciselawsgoverning their behavior without resorting to statistics and averages. Buttheseanimals are usually genetically pure, and they live in controlled environ-ments impossible to achieve with humans.

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cure formisbehaviorandmental dysfunction,it simportanttobecome alerttosomeof the pitfallsofsuch experiments, wheth-er by scientists or ourselves as self-experimenting food con-sumers.Apersonal experience ofmine illustrates someofthesepitfalls.

Severalyears ago I was trying to find thetruth of atheorythatartificialcolorsand flavorscause childrento behyperactive.Thetheorywas firstput forth in1974by Dr.BenjaminFeingold,arespectedpediatric allergist,whoclaimed thatthebehaviorofmany hyperactive and learning-disabled children improvedwiththeintroductionof adietfreeofartificialcolors (suchas thered andyellow food dyes).Hesuspected that these chemicalshadsomethingincommon thataffected thebrain.Heobservedthat children sometimes improved in learning, sometimes inbehavior and sometimes inboth, when on adiet free of foodadditives.

Theapparent epidemicrise ofhyperac tivityin thepastfewdecadesappeared toFeingoldtocoincidew ithincreaseduse ofartificial flavors colors, andpreservatives in our food supply. Itwas theartificialcolors whichhemostsuspected,because theyhaveacertain chemical similarityto substances knowntopro-duce allergicresponses.Havingseenmany childrenin hisprac-ticewho showed dramatic improvement when placed on anadditive-free diet, Feingold assumed that the additives werecausingthecondition.But he hadnever doneacontrolled studyof the problem.Totest Feingold's contention experimentally,mycolleaguesand I selected children whose behavior markedly improvedwhen we put them on his diet. We randomly divided them intotw o groups. While keeping strictly to the diet, one group re-ceived daily challengesofchocolate cookies laced with artificialcolors, while the other received a placeboregular chocolatecookies withnoartificial colors.

This is atypeofstudy knownas double-blind, meaning

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that boththepatientand thedoctorare"Hind"towhich treat-ment is being given. Although both types of cookies containedchocolate, sugar,andotheringredients,onlyonecontained thesuspected offending agents, the artificialcolors.Since the twokinds of cookies looked and tasted alike, it was impossible forthesubjectsor the observers evaluatingtheresponsetohaveabias about the outcome. Parents who might believe that foodadditives caused the behavior were unawareofwhich typeofcookie their child received. Typical biases avoided by this meth-odwerethewishof thedoctorto see asignificanteffectand thewishof thesubjecttoaccommodate thedoctor,A7-year-old severely hyperactiveboy(whomwelater cametocallthe"cookie monster") improved remarkablywhileon theFeingold diet. He was the first subject we entered into thestudy. I became both concerned and excited when the patient'smother calledup the dayafter thechild receivedhis firstcookieand shouted at me, "Idon'tknow what you put in that cookie,but I amtakingmy son out of thestudy He hasgone berserkandbecomea monster.He got a knife slicedup ourcouch, tooka hammer to a neighbor's motorcycle, and has been runningaround likeawild man."A llafter onecookie

1 was"blind"towhich typeofcookiethechild received,butbecause the response was so much like the dramatic cases re-ported byFeingold, Iassumed atonce that the boy had eatenthe cookie with the artificial colors. A ssorry as I felt for thisfrightened mother, Icouldn't help feeling the excitementthatcomes witha newdiscovery. WhatifFeingoldwason thetrackof something important, and what if he had found a simpleexplanation for whythere are somany hyperactive, impulsive,aggressive,inattentive youngsters? Here was a boy with a se-vere disorder showing marked improvement whileon thedietand marked deterioration during his first double-blind chal-lenge.OfcourseIknew that suchresponsesneededverifying by

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manyother cases, utwhenthe first subjectreactedsodramat-ically and somuch likeFeingold'sdescription ofmany similarcases,myoriginal skepticism gaveway tohopesthatadiscoveryof great consequence had been made. Notonly wouldwe besolving a problemdefyingmany scientists overmanyyears, butthediscovery would provide asimple cure: simply omit thingsin foodwhich weren't necessaryin the firstplace.

Here was achild who precisely fit the picture described byFeingold in Msreports toCongress and medical societies anddecidedly met objective criteria for adiagnosis of thehyperac-tivitysyndrome. These werenotmere brat behaviorsbutdra-matic symptoms undeniably in the severely abnormal range.Thecauseof hyperactivity inchildrenhasbeenamystery longawaitingasolution. Perhapstheanswersto whysome childrenarehyperactive had been under our noses all along, hiding invarious thingsweeat.

Asitturned out, wedropped this particularboy from thestudy because we genuinely feared that the artificial colorsmightbehazardousto hismental health(to saynothing of hisfamily s and neighbors' safety). The scientists conducting thestudy thereforeopenedthesealed envelope containingthecodeofactiveandplacebo cookies with considerable excitement.Butalas, the cookie monster had received th eplacebo coo kie

This is not an isolated instance. During controlled studies Ihave experienced many such cases. Scientists are quite familiarwithsimilarepisodesproving thepowerof theplacebo, of hu-man wishfulthinking, or ofjust plain chance eventswhich hap-pen to coincide with the treatment.Butwhy had thisboyshownsucharemarkable improve-ment whileon thediet? Weretheapparent changes justaprod-uct of wishful thinking on his mother's part? Or did he pullhimselftogether inordertopleaseall theadults hopingforsomemiraculous cure?Was it areal behavior changeor only the reportof achange by parents eager to believe in Feingold's theory?

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More than likely, there is some truth to each of these specula-tions. It iseasy to see how hopeful parents might magnify asmall temporary change in the behavior of a child and howtheir behavior to the child mightfurtherencourage the child tochange.

Some scientists wondered whether all the extra personalattention received by children on Feingold s diet might havecaused real improvement in behaviors originating in the needforattention. Children whose bad behavior is just anattention-seeking mechanism are well known. The children on the dietbecame quite involved in selecting and preparing the foodsgaininga lot of attention from everyone athome and atschool.Everyone wasoptimistic about this treatment because of pub-licity about thediet. Hope and optimismforchangea repower-ful ingredients in most successful psychiatric treatments.W ecannot besure about any of these speculations, but I amsure that the cookiemonster s behavior was otcaused by theartificial colors. Episodes like these contribute to one s skepti-cism whenever a parent alleges that their child s behavior is adietary, not apsychological, problem.Even though the evidence to the naked eye seems unequiv-ocala dear association between a dietary and a behavioraleventwithoutthe placebo control and the double-blind exper-iment, dramatic cases likethe cookie monster s fool even themost experienced observers. I am ascientist, butlikemany par-ents, I w nted to believe in the effect of food additives on be-havior,and I was only tooready tobelieve itbased on asinglecase. Butfortunately, scientists have learned to protect them-selves from wishful thinking bydesigning safeguards, such astechniques likethedouble-blind control.

Even professional mental health workers and doctors, likeFeingold,are easily misled into believingin a food and behaviorconnection when there is none. One can easily understandFeingold s conviction and fervorabout this theory, for he had

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experienced many cases similar to the cookie monster s in hispractice.But the authorityofbeinga doctor, even a ery goodone, is insufficient as a basis foraccepting a scientific conclu-sion.Keeping a balance between healthy skepticism andopen-mindednessis therefore essential, both for the scientist and forthosepeople whosuspect foodsmight account for the aberrantbehaviorof their children or themselves.

There are other reasons to be cautious about the causalconnection between dietandbehavior. People often undertakeatreatment just when the symptoms reach their peak and areabout to subside. Parents in desperation, aftermany other fail-ures,mayenroll themselvesortheir childin adietary program,justas their own effortsresult in change for the better. Initiatinga special dietand then seeing these symptoms disappear couldmakeone a believer in the diet, when the changes simply reflectmotivating oneself to do something about the problem.

Bloodletting was a treatment forsickness forhundreds ofyears because the patients often got better anyway in spiteofthe treatment, not because of it. Of course, the surgeon wasalwayseager totake thecredit when health improved andwill-ing toforgetthecase when thepatient died. Asimple controlledtrial would have laid the issue to rest immediately. Folk wis-dom, such as hanging garlic aroundone s neck to relieve a cold,survives precisely because the symptoms usually goaway in afew days anyway. Many children have transient behavioral dis-turbances (stuttering, nail biting, nightmares, extreme shyness)whichgo away most of the time oftheir own accord.

There reimportant effects of foods on the way childrenbehave,learn, and feel but it isimportant toresist the tempta-tion to jump to conclusions without careful safeguards. In thecomingchapters we will see examples ofboth real and artifac-tual relationships between foodand behavior, and we will seethat such relationships are often a two-way street, in whichearingalters behavior,and behavior ofparent, child, and social

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communityshapeseating. Wewill seeexamplesof how foodenters into transactions between parents and children whichhave importantconsequences.Wewill seethat food and theenvironment aroundusbecome linkedinimportant ways worthunderstandingif we are tooptimize children's mentalandemo-tionalpotentialandprevent tragedies thatareavoidablebycom-monsense.

BEH VIORP TTERNSIN CHILDRENIf we are to understand the ways in which foods affect

mental processesand thebehaviorofchildren,weneedtoknowsomething about the majorbehavior patterns ofchildren, forthese patterns themselves reflectimportantaspectsof thecom-positionandchemistryof thebrain upon whichfoods act.

Whilebehavior patternsinchildrenare theproductofmanyinteracting forces, including social learning,thesepatterns arestrongly influencedbycertain aspects ofbrainfunction.There-fore these patterns can become an important clue to brain neu-rotransmittersystems. Neurotransmittersinturnare crucialinunderstanding how foods affect mental and behavioral pro-cesses.

ExternalizingChildrenOnebroad groupofchildren includes those whose prob-

lems are visible to the naked eye and mostly bother peopleexternalto the child (thus the label externalizing ). These chil-dren are abnormally intrusive and are easily noticed becausethey elicit strong reactionsfromothers,suchasannoyance, frus-tration, anger, or punishment. They are overactive, impulsive,andinattentive. They violate rulesandaresometimesdestrac-

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tive ofproperty or harmful topeople.Such children are oftenhappy-go-luckytypeswho areblissfullyunawareoftheir prob-lems. They seemto belackingininternal distressand arealwaysfocusedoutwardly (until they get older and their self-esteem hasbecome damagedbyconstant conflict with others).Ofcourse,allchildren areexternalizersatsome timesandnotothers,and incertain circumstances. Whether externalizingbehavioris normal or abnormaldependsboth upon the age andthesettingin which the behavior occurs. For example, it is nor-m alfor a 3- or4-year-old to runaround between mouthfuls atthe dinner tableor tostay seated onlyfor ashort time duringplay.This same behavior is deviant when it persists in a 10-year-old. The samerowdinessoraggressiveplay considered accept-ableon theplaygroundmay beabnormal whenitoccursin theclassroom.The level ordeg ree of thebehaviorisalso crucialin definingwhat isnormal for aparticular age and setting. A10-year-oldwho occasionally fidgets during the reading lesson is normal,but constant wriggling and fiddling with everything in sightcouldbe asignof anabnormal motor control system.Weunder-stand that impulsively running intothepathofoncoming carsisexpectable in young children, and so we take precautions toavoid it. But the same behaviorin ahyperactive 7-year-old isusuallyabnormalandevidenceofpoor impulse control.There are two major types ofexternalizing behavior pat-terns,thoughthe twotypesareoften seentogether invaryingdegrees inmany children.Hyperactive Children

One of the most common subtypes of externalizing be-havior disorders inchildrenishyperactivityalso knownas hy-perkineticsyndrome, minimal brain dysfunction MBD), at-tention deficitdisorder ADD), and bymanyother labels. The

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manylabelsare areflectionofth confusionandchanging viewsof the true nature ofthis problem. There areprobably manycausesforthis behaviorpattern,and it is onemostoften sus-pected as caused byfoods, foodadditives, toxic chemicals, or bylackofcertainmicronutrients(mineralsandvitamins that occurin tiny amounts).

Perhapsasmanyas 3 to 5% of allchildrenare sufficientlyhyperactive that they require some form of treatment. Thesechildren comprise most of the cases seen in mental healthclinics. Thesuccessful drug treatmentofhyperactive children(withstimulants like Dexedrine and Ritalin,forexample)hasserved tostrengthen thebelief that they suffer fromsome dys-function ofbrainprocesses,involvingtheneurotransmittersaf-fectedby thestimulants.

Forconvenience we will refer to this classofchildren ashyperactive, in recognition of the prominence of excessiveactivityin the earlier stages of thedisorder.But the term hyper-activity is somewhat misleading in that the symptom o exces-sive activity levelisonly partof amore complex picture, whichalso includes impulsiveandheedless behavior, poor concentra-tionor attention, and trouble relating well to other children. Anadditional complicationinabout halfofthese childrenislearn-ingdisabilities such aspoor reading, spelling,andarithmetic.Sometimes these learning problemsgetbetter with drug thera-py, suggesting that theyaresecondary effectsof thebehaviorproblemsofpaying attention and sitting still. Other times thelearning disabilitiespersist,andappearto reflect intrinsic dys-functionsin thebrain's learning centers.It is not dear whether hyperactivity is a true disease, asyndrome (collectionofsymptoms),orseveral different disor-ders with different causes.Butbecause thetrue conditioncanhavesevere long-term consequences for both the child and hisor herfamily,it isimportanttodistinguish itfrommere unrulybehavior stemmingfromlaxparentingoroverindulgence. There

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are children who superficially resemble truly hyperactive chil-drenbut whoprobably deservethelabelofordinary brats, Butunlikesuch children, hyperactive children have a more perva-sive inability to sitstill, to conform and to attend; and theirbasic behavior patterndoesnot change evenaftercorrecting thepoor parenting. Parenting skills may improve when the hyper-active childrespondswelltotreatment, showing that poor par-enting is sometimes the result, not the cause of misbehavior.Therefore,while poor parenting can make hyperactive childrenworse,it can also be the result of a child who does not respondto theordinary rules, rewards, andpunishmentsofsocialandfamily life.Somehaveevensuggestedthattheinabilitytoprofitfromrewardsinlearningis at theheartof thedisorder,prompt-ingthemtolinktheproblemto theneurotransmittersinvolvedin the brain's reward centers.ConductDisorders

Someexternalizing children are not hyperactive but are ag-gressive,antisocial, bullying, destructive, or in other ways likelytoviolateordinary socialproprietiesandrules. Whenthe nor-malnegativismand self-centerednessof the2-year-oldpersistsin the5-year-old, it may be asignof an opposi t ions disorder . It isasthough defianceofauthority becomesits owngoal. Truant-ing, stealing, fighting, and lyingmaybecome evident in suchchildrenasthey growolder.

Conduct disorders refers to apattern ofearly aggressive be-havior persisting into young adulthood, along withapatternofviolationofsocialauthority.Likehyperactivity, thereareproba-blyseveral forms ofconduct disorders, and also like hyperac-tivity thecontributionsofgenetic temperament, environment,andtraumatic insultsto thebrainmay allhavearoleincreatingthe pattern. Again, because certain neurotransmitters linkedwith aggressive behavior are also affected by diet, speculation

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about dietary therapy for conduct and aggressive disorders hasbeen rife.

Whilehyperactivity, conduct, and learning disorders mayalloccur quite separately insome children, it is notuncommonfor them tooverlap with each other within asingle child. Oftenone disorder causesanother, as when continual lack ofcontrolover behavior in the classroom eventually leads to learning fail-ure, or when learning failure eventually results in rebellious-ness, defiance, and oppositional behavior. Although thesebehavior patterns mayblend togetherintoavarietyofcombina-tions,theyare sufficiently distinctintheir natural history, out-come, and responsetotreatments that most professionals re-gard them as different disorders, requiring different causalexplanations.

Another broad classofproblemsarethoseinwhichit is thechildren who suffer more than those around them. Childrenwho areexcessively anxiousorfrightenedfor noapparent rea-son and who cryeasily and arevery afraid ofseparating fromtheirparents areexhibiting an internalizing disorder So are de-pressedchildren who aremelancholyandhopelessabout thefuture aswellaschildrenwho are notnotably anxiousor de-pressed but whowithdraw from allsocial contactand who areexceedingly shy and socially awkward, sometimes even with noapparentdesireto besociable.Manypeople readily accept that externalizing disorders inchildren mighthave abasis inbrain dysfunctions. After all, itwas the very similarity ofhyperactive children tobrain-dam-aged children that initiated such terms as minimal braindamage syndrome forsuch children. Butthey maydraw theline at the idea that anxiety,depression,and other internalizing

InternalizingDisorders

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conditions result fromchemical abnormalities in thebrain.Re-cent advances in human psychopharmacology and geneticsnonethelessshow that even theseapparently pure psychologi-calconditions have animportant connection with brain chem-istry.

One of theconditions most psychiatrists heldaspurely psy-chologicalfor alongtimewas theanxious,ritualisticbehaviorofthe hand-washing, frightened obsessive-compulsive. Thesepeoplehaveideasthey can't get out of their mind (obsessions)orrituals they must carryoutovera ndover (compulsions).Butrecent experiments with a new drug clomipramine)havepro-duced remarkable improvements insuch patients, even after alifetime ofsuffering. Brain imagingis a newtechnique inwhichX raysorradiation-labeled chemicals produce computer imagesof the brain's deep structures. Brain images ofthesepatientsrevealabnormal brain structures and patterns. Similarly, infu-sions of achemical called lactate have produced classic panicreactions in certain vulnerable people, exactly reproducingsymptoms ofanxietyand panic long believed to bepurelyso-cially acquired. These developments do not imply that braindysfunction ordisease causes allthese internalizing states. Butthey remindusthat almostallbehaviorhasimportant founda-tions inbiological functionsof thebrain. They encourage us toconsider alltypes ofbehavior, not just those most clearly at-tributable tobrain damage, aspossibly influencedby the foodsweeat.

These broad classes ofdisordersexternalizing and inter-nalizingprobably reflectvery basic aspects ofbrain organiza-tion. Just as work with drugs has revealed that drugs workdifferently depending upon the type of individual receivingthem, so the effects o foods m ay depend upon specific brainbehavior patterns. Much research workon both animalsandhumans now suggests thatthesebehavior patterns are stronglyinfluenced bygenetic factors and by thebrain's chemicalrnes-

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sengers theneurotransmitters.It is forthis reason thatit makessenseto ask howd ifferentbehavior patterns relate to the chemi-caleffects of foods weeat.In Chapter 2 wewill lookat a new classoffoods artificialsweeteners and theirpossibleroleinhyperactivity.Wewillseethat young children inparticularmay experience dramaticbe-havioral and personality changes from these new sweetenersthough the evidence remains tentative and scanty.In Chapter 3 we willsee how breakfast is ameal thatcanhave either verybeneficial orveryharmful effects on both nor-malchildrenandhyperactives.

Chapter4looksat theroleofsugarinhyperactive children.W ewillseethat common myths about sugarare partlytrueandpartlyfalse with sugar being eitherhelpful orharmful depend-inguponthetypeofchild thecontentsofmeals and thetimingofthesugardose.

In Chapter5 wewillseewhether sugar leadstoaggressionand violenceand whether special diets can affect criminality.W ewillturnacriticaleyetoward recent attemptstoalterthedietof criminals in hopes ofreducing their violent tendencies an ddiscusstheroleofsugarin aggressive behaviorof hyperactives.

Chapter6 deals withtheeffectoffoodson thegrowthof thebrain an d intellectual function. W e will discuss recent experi-ments showing that vitamin supplements increaseIQ in school-children and we will see that diet in pregnant mothers canaffect the IQ and cognitive skillsof their newborns.

Chapter7discussestheFeingold dietand food allergiesascausesofbehavior problemsinchildren. Again wewillseethatthe theory thatfood additives cause hyperactivity is partly truebut notentirelyso. Wewillexamine recent evidence that somedietshelpimprove the behavior of children with allergies.Chapter 8 examines the controversies and dangers sur-rounding the use of huge doses of vitaminsmegavitamin

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therapyandcritically discussestheevidence bothpro and confor itsuse.Chapter9 looksat the possible role o f diet in the way chil-dren react to stress, how certain foods may inoculate against

stress,and howstresscanleadtolife-threatening eating disor-ders.Finally, in Chapter10 we will present some simple meth-ods for carryingoutexperimentsin the homeand trackingchil-dren ssuspected reactionsto foods

Scientists are innately conservative, and in each chapter wewillsee that much controversy exists. But parents, teachers, andmental health professionals must make daily decisions aboutfood withchildren, and they need no twait fo rresolution of allcontroversies in order to make educated decisions and beknowledgeable consumers o f available remedies. Though ourknowledge is tentative and subject to revision as new dataemerge, prudent action regarding food management fo r chil-drencan o ftenbetakeninways that atleast will do noharmandatbest mayoptimizethechild sbehavior andmental function

Thus,we believe that foods do affect the mindso f childrenin many subtleand important ways.The foolish claimsof popu-lar culture and pseudo-science should not discourage us fromacknowledging the real connections between the chemicalsinfoods and the chemicals in the brains o f children.

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CH PTER TW OH yperactivity and rtificial

Sweeteners

Iwas skeptical when Jamie s mother calledme and said that her4-year-old son was totally out of control after drinking somecherryKool-Aid.Phone callslikethisoneoccuroften , andusu-ally the problem turns out to be much more commonplace thana reaction to food ordrink. Instead, the issues most often in-volve more familiarproblems in relationships between parentsand child, such as lack ofbalance between authority and nur-turance,poor parenting skills and lax discipline, or inappropri-ate modelsofbehavior in thehome. Butpeople willoften lookforeasy answers first,

However, Jamie s mother did not appear to be someoneavoiding hard choices; she had already investigated the problemlikeascientist. Sheobserved her son carefully and carried outsomeexperiments. She told me that during the summer Jamiedrank Kool-Aid forabout 3weeks, usually about three glasses aday 20 ouncesorso). Over this period oftimeshenoticed thathebecame increasingly erratic, with gradually escalating levelsof frustration, anger, and emotionality. He easily burst into

5

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tears, wasvery irritable, and had violent, unprovoked, angryoutbursts. Eventuallyhe had anepisodewhen hebecamesohyperactive thathe had to besentto hisroom,whereuponheproceeded tothrow himself againstawall, knockinghimself tothe floor, repeating this behavior until restrained. He was totallyout ofcontrol in a way she had notseen before.

Jamie's mother called her pediatrician, whoquestionedhercarefullyabout anythingthechild might have swallowed, think-ing that he may haveingestedsomepoison. Aftereliminatingseveral possibilities, his mother mentioned that the Kool-Aidwas new toJamie's diet.Apitcherwaskeptin therefrigeratorandJamiehad free accessto it. Thepediatriciansuggestedre-moving it, andafterdoing so Jamie's behaviorseemedto returntonormal overa10-day period.Themother, thinking logically,decided toreintroducethedrink, doubting that this seeminglybenign product could be the cause of herson'strouble.

However,thesecond timeJamiedranktheKool-Aid, with-inabout30minuteshebecame even more violent than beforeandcomplainedofsevere headache. Althoughtheepisode sub-sided withintheday, both motherandchildfeltfrightened,andthemother calledmeaskingforhelp.

She described him as usually a normal boy, a great baby, agood sleeper,and agood eater. TheKool-Aidepisodeswereaberrantandsuperimposeduponanotherwise normal pattern.Jamie was acute, well-nourished 4-year-oldwho was friendly,affectionate, and playful, withanendearing twinklein hiseye.Nevertheless, there were some subtle signs of potential prob-lemsinseveral areas.

Though Jamie was large at birth, weighing over l V zpounds,he was now a thin and wiry youngster, at only the 30thpercentile for weight (that is, 70 of children his age weighmore). His mother had gained a whopping 55 pounds duringpregnancy, which is twice the recommended amount. Thoughby nomeansaninevitable causeofhyperactivity,large weight

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gain and problems during pregnancy are sometimes part ot apicture contributing to asuspicion ofsome birth damage.

WhenI firstasked about Jamie'sbehavior, hismotherre-plied thaton the whole Jamie was a happy, bright, and pre-cocious boy.But as wetalked, itbecame apparent that Jamie'sbehaviorwas not perfect. Farfrom it; he w as avery active boy,goingall the time, One of thebest tip-offsthat hisactivitypattern was excessive came when his mother said, he acts likehe isdrivenby amotor. Afterperiods ofintense activity,Jamieappeared tosuddenly wind down; however, hewould haveanafternoon napevery day, somewhat unusualfor a4-year-old,

Though 4 years old, Jamie still showed the 2-year-old'scharacteristic pattern ofsaying no toeverything. Hecouldalsobequite aggressive, andaccordingto hismother,onocca-sion would beathisbrother to apulp. (This must have beenquiteanaccomplishment sincehisbrotherwas 3years older.)

There were also some indications ofproblems with parent-ingskills. Jamie's motherwas tender and solicitous withhimwhilethey werein thewaiting room,but sheadmitted thatsheoftenbecame exasperated withhim andmostly triedtomanagehim byyellingandscreaming,astrategy thatiseasyforparentsto fall into, but one thatisusually totally ineffective. Imadeanotetom yselfthatIwould havetorecommend some traininginparenting skills.Atfirst Ithought that Jamie's picturewasthatof aclassicalhyperkineticsyndrome. Jamie's mother had filled out a93-itemchecklist ofJamie's behavior, and all the majorcategories werewithinthenormal range exceptfor agroupofitems dealing withrestlessand impulsive behavior, such as blurting into conversa-tions and not waiting his turn; onthese,Jam iewas worse than90 ofchildren hisage. Jamie's mother hadchecked offon thesymptom list Jamie's explosive behavior and temper outburstsandhishabitofthrowing himself aroundandbreaking things.Similarly, he engaged in repetitive activities, had sudden

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mood shifts, and acted as if driven by amotor. Butwhen Iinterviewed the mother and went over each item she hadchecked, shesaid thevarious symptoms were severe only whenJam ie dra n k K oo l A id .Thus, thedrink seemed toexacerbate pat-ternsofresponse that were already there.

Moreover,Jamie's motor-driven behavior, sudden moodchanges, anddestructive outbursts only becameareal problemafter exposure toKool-Aidsweetened wi th a spar tame . This nowfamiliar artificialsweetenerhadonly recently become available,and because aspartame had a delicious sweetness without anaftertaste, itwould soonbegin toreplacelesspalatable sweet-eners like saccharin.

There were hintsofother problems withfood,though noth-ing conclusive. From the beginning there were some feedingproblems, and though such problems are not uncommon, theyseemed toreflect apatternoffoodintolerance.He hadconstantrhinitis stuffy nose) and diarrhea following formulafeedings,and he waseventually switched to acow's milkformula withalleviation of the symptoms. His mother had a suspicion,though notdocumentedby anallergist, that Jamiewasallergictoboth milk and molds. She herself could not eat apples,pears,peaches,orplums becauseofallergytopectin,andsaid thatshewasalso allergic to jelliedcandies,pollen, penicillin, and someother medicines.

THENUTRASWEET ASPARTAME) STORYLikemany scientific discoveries, aspartamewas theunin-

tended productofluck.Achemist workingon anulcer medicineinthe 1960s inadvertently licked the powder on his fingers andfound itpleasantlysweet,andunlike saccharin,it had no after-taste. WhenJamiewas just 2 years old, Searle Pharmaceuticalsintroduced this revolutionarynew artificial sweetener to the

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marketas atable-topsweetener,andthen duringthesame year first saw Jamie, in 1983, the Food and Drug AdministrationFDA)permitted its use as asweetener fordrinks. I w ascuriouswhy it took 20years for themanufacturerofaspartame to re-ceiveapproval to market it,Aspartame (trade names Equaland NutraSweet )wasoriginally approvedin1974by theFDA.Butanimalstudiesby aneuropathologist, D r.JohnOlney,suggested that aspartame might leadtobrain damage. Thisfind-ing caused suspension ofaspartame's approval by theFDA,which was sensitive to this issue, knowing that other sweet-eners,suchassodiumcyclamateandsaccharin,arecarcinogenic(cancer causing)inanimals.

Therewasalsoaquestionof howadequatetheexecutionofthe animalstudieswas. Searle's performance with several labo-ratorystudieson aspartame and other drugs had led the FDAcommissioner, D r.AlexanderM.Schmidt, to testifyearEer that recent investigations by the agency have raised questionsaboutSearle Laboratory's conduct ofanimal experiments andtheir reporting ofdata, 1 The FDAtherefore appointed asix-manteamofscientiststoevaluate Searle's animal data regardingaspartameand otherdrugs.Twoyears later, in 1976, the report of the scientists wasdamning: Searle madeanumberofdeliberate decisions whichseeminglywere calculatedtominimizethechancesofdiscover-ing toxicityand, or, toallayFD Aconcern. Thecommissionerofthe F D A had no choice but to tell Congress that Searle hadengaged in apatternofconduct which compromisesthescien-tific integrity of the studies, and heeven requested theU.S.JusticeDepartment to investigate whether Searle had concealeddataormadefalsestatements insupport ofaspartame.

The legal suit was eventually dropped, but meanwhile,over 80studiesquestioning aspartame's safety, most having todowith itscancer-causingpotential, hadaccumulated.By nowthe task ofindependently reviewing this mass ofdata was so

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large that Schmidt and the FDA decided not to waste morepublicfundson theissue,and the FDA andSearle agreedtohireanindependent research grouptoevaluatethe findings.How-ever,this group could review only15of the 80studies, and apublic board ofinquiry later appointed to do amore extensivereview also found the 140volumes of documentation over-whelmingandended up focusing on thesameset of 15studiesexaminedby the scientific panel. Although this review panelfoundno evidence that the sweetener was likelyto cause braindamage, they did find that they could not rule out the possibilitythataspartamecaused cancer,andthey recommended thattheFDAwithhold approval.

Despite this resounding defeat for aspartame's endorse-ment, Searlepersisted,and the dayaftertheRepublican admin-istration took office on January 21 1981, they petitioned forapprovalfrom thenewly appointed FD Acommissioner, ArthurHull Hayes. Hayes approved, and shortly thereafter resigned.Perhaps unfairly(considering hisdistinguishedrecord ofpublicservice), newspapers such as the Washington ostnoted that amonth after granting approval Hayes resigned, and that hebecame seniorscientificconsultant to the public relations agencythathasSearle'saccountforaspartame, Burson-Marsteller.It iseasyto see why onemight construe this sequenceofeventsasevidence of asinister government-industrial plot topromote a monumentally successful commercial venture. Thefactsdo notwarrant suchaconclusion.The FDA has tomakeareasonable judgment that protects the public interest fromharm,but italsohas toconsider thebenefitsof a newproductand notobstructitsavailability.Further researchhascontinuedtosuggest that aspartameis notcarcinogenic.Butwhatisstrik-ing about this whole episode is the narrow focus on physicalrisks with noattention paid topossible behavioralrisks.Behav-ioral toxicology hardly came intothediscussion atall.Much of the earlier concern about brain damage in new-

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boms and children arose because aspartame consists of twoamino acids (aspartic acid and phenylalanine) used in thebrain'sneurotransmlttersystems. Phenylalanine,likemany oth-eraminoadds,is essential, becauseitmustbeeateninordertoprovidethebrain withsufficientamountstoman ufactureitsbasic chemicalmessengers,the neurotransmitters. Inthis case,phenylalanineis a precursor used in the synthesis of the neu-rotransmitters dopamine andnorepinephrinetwo chemicalsthatw ewillhear much aboutinconnection with foods childrenandadults eat.In the condition called phenylketonuria PKU), one of theenzymes required to break down phenylalanine is missing atbirth,and as aresult, excessive amountsofphenylalanine accu-mulatein thebrain, eventually causing brain damageandvary-ingdegreesofmental retardation.One of the treatments forthis inborn metabolic error is adiet low in phenylalanine. Somescientiststherefore immediate-lyraisedthequestion whether aspartame mightposeathreattothose suffering from PKU orthose whohave someof thegenesnecessary for thediseasebut who do not have thediseaseitself.Fortunately,mostof theanimalandhumanstudiesappearedtoreassure scientists that aspartameinmoderatedosesposed nohazard forthesepopulations (though some worry on this pointpersists).Butapartfrombrain damageandcancer,asuddeninfluxofphenylalanine might affect beh v ior l functions of the brain. Tounderstand why, some technical backgroundisnecessary. Phe-nylalanineis onememberof aclassofamino acids (large neutralamino acids, or LNAA) that gain access to the brain onlyincompetition withoneanother. Since theyallhavetocompeteforaplace on the carrier molecules that transport themacross thebarrier from the peripheral blood supply into the brain itself,when many amino acids are eaten together (as usually happensin aprotein meal), they cancelout sothat none gains precedence

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inthe competition to enter the brain. Thus, when eating a ham-burger,phenylalanineistakeninalong with otherLNAAsuchas leucine, isoleucine, valine, tyrosine, and tryptophan. Thecompetition from these other ammo acids limits the accessofphenylalanineto thebrain.W eseldomeat singleamino acid protein, thoughw ecom-monly assume that protein refers to a single type of food.When drinking an aspartame-sweetened drink, however, thephenylalanine isheavily concentrated, and hence the r tio toother amino acids increases markedly. It isthis ratio whichfinallydetermines whichof themany substancesget to thebrainand towhatextent.Ahighratioof any oneamino acidto theothersgivesit acompetitive advantage fo rgettingto thebrain.Thebrain isnormally protected from asudden infusionofjust one amino acid by this competitive relationship amongthem.Most foodscontain manydifferentamino acids, sothatwhendigestingfoodthereis abalanced entryo f theamino acidsintothe brain. Only under unusual circumstances is itlikelythatasingletypeofamino acid gainssufficientprecedence thatit canovercome the competition for transport into the brain. Onemight consider thesystem similarto a lot ofpeopletryingto findseats on abus.Ordinarily people of allkinds will line up forseats. But if the local football orhockey teamhappened to arrive, theywould beoverrepresentedon thebusand get to theirdestinationat theexpenseof theordinary citizens.A m o n g the arguments often used for the safety of aspar-tame,isthattheincreasein theamountofphenylalaninein theblood followinga diet drink, or even several dietdrinks,isequalto orless than thephenylalanine increase after eatingaham-burgerorother protein-based meals.Butthereis a fundamentalfallacy inthis argument, for as wehave already noted, it is notthetotal amountin thebloodstreambut theconcentration com-pared with other amino acids that finally determines how muchgets into the brain.

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Considerable controversy centers on how much aspartameis sufficient tocause important changesin thebrain. Mostof theresearch on this question has involved laboratory rats. But ratsmetabolize phenylalanine quite differently than humans.Whereas rats convert phenylalanine in the liver to the aminoacid tyrosine, thisdoesnot happen with humans to anywherenear the same extent. Fundamental differences between theselaboratory animals and humans are so great that they callintoquestion manyof theconclusions regardingthe effects ofaspar-tameonhumans, especially regardinghowmuch increase thereis inbrainneurotransmittersfromeating aspartame.Anotherimportant point ignoredin the ratstudies isthattheamountsofaspartame getting to thebraincan bemarkedlyaltered bycertain dietary conditions. Dr.RichardWur tm an aleading researcher onthesequestions at MIT haspointedoutthat eating sugarorother carbohydratesat thesame timeas theaspartame for example, eating cookies along with the softdrink)compounds theproblem.O ne of theimmediateeffectsofeatingsugarorother carbohydratesis arapid insulinresponse.Insulinis the main counter-regulatory hormone which acts tokeep blood sugar within bounds. One of its effects is topurgethebloodstream ofmostof thecirculating amino acids. So theinsulin effectwould tend toreduce most of theamino acids atpreciselythetime whenthe liquidintakeofaspartamein adietdrinkis increasing the available phenylalanine, thus giving it aneven greater competitive advantage over other amino acids inthe fight toenter thebrain.

Another concern about aspartame has been its possibleeffects in producing convulsions or seizures. Scientists knowthat brain neurotransmitters which are dependent upon phe-nylalanine such as the neurotransmitters dopamine and nor-epinephrine) areimportant in theregulationofseizures. It hasbeen shown that animal brains treated with large doses of phe-nylalaninedevelop alower threshold forseizures provoked by

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certain seizure-causing substances. Since it is not possible toinvestigate this typeofproblem experimentallyinhumans, littledirectevidenceisavailable regardingtheeffectsofaspartameonseizuresinchildrenoradults,But scientists workingon aspartame, and the CenterforDisease Control apublic health agency inAtlanta), receivedmanyreportsof incidents involving headache and first-time sei-zures when aspartamewas first introduced. W ehave torecog-nizethat nynewly approved fooditemwillcause manysuchanecdotes to occur, but some are compelling enough that they atleast raise our concerns and suggest needed areas for furtherresearch.Forexample,oneletter receivedby Dr.Wu rtmanwas froma26-year-old registered nursewhogaveavery detailed clinicaldescription of herexperienceafter shebegan using aspartame.She wasusing6 to 10packetsa day ofEqual apowder versionofaspartame)andoccasional drinks withN utraSweet forabouta week when she began experiencing a left-temporal head-ache justabovethe left ear). That night she had amajor sei-zure.Theseizure beganin her righthandand marched in atypicalfashion through other partsof herbody.A fterhospitaliz-ation, she had manytests, allnormal.Nocausewas found forthe seizure.

Meanwhile, unawares, she continued usingEqu al.One daysheconsumed more thanherusual amountanddevelopedtheleft-temporal headacheagain. Thatnightat apartyshe had adrink of rum (probably not agood idea forsomeone prone toseizures) and while dancing she experienced anothermajorsei-zure, which waswitnessedby several doctors who were pres-ent. She continued having two to three headaches a week, andaboutamonth latershe had a1-ouncedrinkof rumwith guestsatdinnerandagainhad aseizure.Several interpretations of these incidents are possible,

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whichistypicalofmany such anecdotes.Was itjustthe rum in aseizure-prone individualthat triggeredtheattack,or was it thecombinationofexcessive aspartame intakeand therum,orjusttheaspartame alone?Wenoted earlier thatanecdotesareonlysuggestive,never proof, and the present case is no exception.Whatsetsthis account apartfrommost, however, is the carefuldescription ofdetails,madeby aprofessional observer, and therepeated close correlation ofsymptoms with excessive intakeofNutrasweet.

Although such anecdotes by themselves prove nothingabout theheadacheandseizure-causing roleofaspartame, labo-ratorystudieswith animals show that suchan effect is possibleOnemethodoftestingfor adrugeffect onseizurethresholdis togive a substance to an animal which isknown to lower thethreshold forseizures in that animal thatis,making seizuresmorereadilytriggered)andthen examinethe effect of thedrugonthat threshold.Onesuch agentismetrazol, whichinrats willlower their seizure threshold. Aspartame hasbeen shown tolower the level at whichmetrazol-induced seizures occur.Be-cause the levels of aspartame had to beveryhigh to produce theeffect most scientists concluded that it was unlikely to be apredisposingfactor in seizures forhumans.Butexperimental animals differ in somany waysfrom hu-mans that one cannot be sure that the same levels of theaminoacid cause similar effects in humans. What is ahigh level foranimalsm ay beverydifferent from thelevel requiredto produceaproblem in humans. One prominent scientist estimates that aslittleas15-20 mg per kg ofbody weight could lowertheseizurethreshold. For a 30-kgchildthismeans that threeor fourcansofsoda containing about 100 rng ofaspartame would reach thislevel of risk.Even that might seemto be anunlikely amountforverymany people toconsume.Butanother letterisworth quotinginsome detail, because

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ithighlights how easy it is for someyoungsters because of theirlifestyle, to usedietdrinkstoexcess thusexposing them selvestoenormousdosesofaspartame:

I suppose thebest way tosum up the past three yearsof my lifewould be tocall thema livinghell. I wastrapped in adeep darkand seeminglyendlessstateofdepressionthat neithermydoctorsnorIcould find reasonfor. Theonlyway toexplainthemagnitudeof myturmoil wouldbe tostart from thebeginning and thereforegive you aclear impression of my lifebefore and after aspartameentered it.Before aspartame was introduced to the public rny life hadbeen full and veryrewarding, I was a topstudent and very activeinalisportsandsocialactivities.Thehighlightofthoseyearsbeingwhen Icompeted in [World Championship games in Europe], Itwas just months after this e v e n t , . . that aspartame was intro-duced . . .intomydailylife. Thislowcalorie sugar substitutein-stantly became a success and the savior of teenage girls likemyself who were diet and health conscious. With this product inthe newdiet sodaswecoulddrinkasmuchas wewantedand nothaveto worry about our waistlines or possible health hazards tha tsaccharinwasreported tohave,Iwould drinkadiet sodatoquenchmythirstafter aworkoutand itsoon becamearegular routinefor me to opt for adiet drinkover all other drinks whenever possible. It soon became a well-known fact amongst my friends that 1 was a total addict of thedrinks.Afactw e alllaughedatbecause w ha t couldbe theharminsuchanaddiction?I t got to thepoint whereIwouldalwayshaveahug e bottleof the staff in my lockersothatIcould takeaswiginbetween classes. The teachers even kidded me that they shouldhave the stuff analyzed to see if it was spiked. They even docu-mented the fact bymentioningmy addiction toTab, Fresca andCoke (all diet drinks containing aspartame) in [class picturesj.Thelasttwoyearsofschool . . .wereradicallydifferent fromtheprevious years. Ibecame gradually m oreandmoredepressed.Many times unable to leave the house for classes or to see myfriends. Ibegan tolose interest in all extra-curricularactivities andrarelycould bring myself to do those things that I used to thrive onsuch as jogging, biking, dancing or just horsing around. Nothingwas FUNanymore.It's only now, four years later that I have learned about theside effects ofaspartame that I have realized the correlation be-tween the introduction ofaspartame intomy life and mygradual

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growing depression. Butbackinhigh school I had no ideawhy Iwas feeling the way Iwas. Ithonestlyseemedat the timethat theonlyenjoymentI wasgetting out of Me was acoldcan orbottleofdiet soda,I hadsomewhere alongthe linelosttheabiity toenjoyanything else.Itgot to thepoint wheremydaily rou tine consisted ofwatch-ing TV,eating,and theconsumptionof atleast10 to 15cansofdietsodas.Bat to add to theproblemIbegantogain weightbecauseofmyinactivityandpoor eating habits broughton by my depression.Inthose fewyearsI had gonefrom av ibrant outgoing person to alumpof flesh on the family-room couch.I tried many times to overcomemy depression bu t with noavail.Ijustcontinuedtodraincanafter canafter bottleafterbottleof the stuff hoping thatIwou ld somehow just snapoutof it. [Shethengoeson to describe her u nhe lpfu l experiences with aseriesofdoctors. After seeing a news report about aspartame she stoppeddrinkingit. Shecontinues:)Inconclusion I'd like to saythat since I've stopped using as-partame I have noticed an improvement in myattitude. WhenIfirst triedtostopuse Iexperienced shaking, nauseaand atremen-dous urge to h ave a diet drink. I wasn't able to stop immediately soIgraduallycutdownthenumberofcans eachdayuntilI had quitaltogether,. . . I have experienced other discomforts which I'mnotsure were causedbyaspartamebut . ..Iwilllist themforyou:a)acidicfeeling inchestand throat; chest pains;b)blurred vision;c)skin rash; d)headaches intemple area.Again,we cannot knowwhether thisis aresponse causedby aspartame or merely coincident with its use; the experi-

ment does not rule out many alternative explanations. Thepicture is a typical one for adolescent depression: inability toexperiencepleasure anymore, inactivity, hopelessness,and de-jected and sad mood. But this same story ofexcessive use withsimilar symptoms is one Ihaveheard from other teenagersandchildren.Itisalsostrikinghowmanyof the unsolicited letters containreferences to the last three symptoms this girl mentioned:blurred vision, skinrash,and temporalheadaches. These couldbecoincidence orinfluenceofpublic media (onenews reportorletter can spawn dozensof identical symptoms). Nevertheless,

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theaddictive quality of the experience stands out, suggestingthe possibility that gradually over time some important chemicaladjustmentstook place in the brain, much as happens with trueaddictivesubstances.

CONTROLLED C SESTUDYWITH SP RT ME

Now thatwehave learned somethingof thebackgroundofaspartame,it istimetoreturntoJamie s story. Though reluctantto furtherexposehim toaspartame,I hadlittle trouble persuad-ingJamie s mother to carry out a double-blind trial inorder tomore rigorously documentherson s aberrant response toaspar-tame. Her major concern was that continued exposure to thechemical might havedisastrous consequences, and in this sheproved to be partially correct, as we shall see.

Wesaw earlier how double-blind trials are usually carriedout on groups o subjects, onegroup receiving theactive ingre-dient, one the placebo. In the double-blind study of a singleperson,thetrial involves observations taken withthesame per-son receiving the drug and the placebo at different times, usu-ally some days apart. The drug and the placebo days are thencompared tocontrol days when neither agent isgiven,If areac-tion occurs on the days when the active ingredient is present,and not on the placebo or control days, it tends toconfirm thatthe reactionis due to theactive ingredient and not to randomeffects orplaceboeffects.Jamie s motherhadalready carriedoutasimilar experiment, using regularKool Aid.But,ofcourse, shewas not blind to the changes, and she could have been influenced by knowing which drink contained aspartame.

ForJamiewe had a ready-made drug andplacebo: regularKool Aid sweetened with sugar, and Kool Aidwith aspartame(NutraSweet). The two drinks were indistinguishable in tasteand color. Jamie s mother had said that his symptoms usually

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showed upaboutahalf hour after exposure, so westartedob-serving himoveraperiod ofabout1hour immediatelyafterhedranka6-ounceglassof thecherry-flavoredKool-Aid,with con-tinuing observations by hismother overthecourseof the dayafterthey left thelaboratory.W estudied Jamieon fourseparate occasions aboutaweekapart. For 10days his mother recorded his symptomaticbe-havior using abehavior checklist, as she had done when shefirst brought Jamie to the laboratory. InChapter 10 we willshow howparents and teacherscan usethis checklisttotrackth e effects offoods intheir ownchildren.)On 2later days hereceivedtheaspartame-flavoreddrink,and on 2daysthesugar-flavored drink. About 1 week separated each of the four visits,and inbetween, hismother continued recording his dailybe-havior. Our dietitian prepared the drinks and the order of ad-ministration without informing either thechid,parent, or ob-servers.W e set up twomethods toobserve Jamie. First, twopsy-chologists videotaped andobservedhim bycountingthenum-ber of times he engaged in aggressive, angry, or defiant be-havior. WeinstructedJamietoplay withtoysin theroomanyway he wished, while his mother sat over to the sidequietlywatching. After ahalfhouror so weinstructed Jamie's mothertogive various commands to put the toys away, clean up, andsoforth.Second, Jamie's motherfilled out thedaily checklistofhyperactive behaviorsat the end ofeach day.W ecould comparethesechecklistresponsestothousandsofparentsofnormal chil-drenofJamie's age.In onesense,nothing dramatic happened in the two ses-sions inwhich Jamie received th eartificially flavoreddrink.W esaw nowild,out-of-controldisplaysordestructive behavior.Butsomething was eginning tooccur. Duringthe aspartamedays,Jamie's levelofde fiantandnoncompliantbehaviorin thelabora-toryincreased from thenormal levelon regular Kool-Aidand

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Af te r we left Children's Hospital Jamie wasvery quiet (did notspeak) ll the wayhome and allthroughlunch. Hisgrandmothernoticed heseemed to beday-dreaming.He a te agood lunch,butseemednot to bewithit pre-occupied).Hestarted complainingofa headache (approx 2:30 p.m.) and was somewhat cranky andnasty. Heslept for 3hoursfor hisafternoon nap. Whenheawoke,he was not in the same disposition he wasearlier in theday.H ewoke upcryingandscreaming. Proceeded to findfaul twith every-thing. Refused to ea t dinner. Cried al l through the meal. Af te rdinner heplayedin thebasementbu tinstead ofplayinghestoodin themiddleof the floor andscreamedfor ihourat the top of hislungs. 1 put him to bedearly he wasrestless). Next morninghewas allsmiles.

CH FFER TWO

baseline dayssothat they were occurring over70 of thetime,amuch higher level than on the placebo days. On both of theaspartamedays,Jamie's mother marked many more hyperactivesymptomsoccurring later thatday.Thelevels reached the ab-normalrange, whereas oncontrol daysandplacebo days theywere entirelynormal.More interesting still are the informal comments that Ja-mie'smother wroteat the bottom of therating sheetson the twoaspartame days.On the first ofthese shewrote:

Therewasnothing else goingon that might accountfortheseunusualbehaviors.Jamieappearedtoshowsignsofexhaustionandirritability, muchas achild does when overtired. Insteadofhisoutgoing personality hebecame more withdrawn.Hishead-achewas a tell-tale sign that something had happened to hiscentral nervous system. Finally,whenhewokeup, and shouldhave fe l t refreshed, he was instead completely lackingincon-trols, asthough some basic capacityforrestraintorinhibition inthebrainhadbeen lost.In the intervening days his mother made comments likevery happyand sweet allday. OnJamie's second aspartameday(still double-blind), she said:

W henweleft thehospitalJamiesaidhe wasvery tired and had togo to the bathroom. W estopped at the restrooms as wewere


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leaving. W earrivedatm yparentsaround11:40 a.m.andJamieateeverything insight, but looked as though he werefalling asleep.His hands kept holding up hishead. After lunchhe had to go tothe bathroom again. Weleft myparents to gohome around 1:20p.m. andJamiewentto thebathroom again.He fellasleep in thecar5 m inutesbeforewe arrived home.When we arrived home he went to thebathroom againandsaidhe couldn't waittotakehisnap,he w as so tired. I put him tobed around 2:15p.m.(I wassurprisedhis bladder appeared to beworking overtime, as I'm tacky if he goes 2-3 timesaday, max-imum). I put him to bed withthe feeling thathewould sleepallafternoon since he appeared so tired.To my surprise, he neverslept.Iheardnoisesin hisroomat2:45(p.m.)andwhenIcheckedon him he was runningbackand forth from hisroomto hisbroth-er's and back again, runn ingincircles overandover again.As the afternoon wore on, he kept running and circlingandseemedto be everywhere-hetalkedso m uch and very fast Icouldhardly understand him. A t dinner time Jamie ate nothing andcouldn'tsitstilltoeat.Hekept ge ttingup and running full speedthrough thehouseand talkingfast and loud.I had ababy sitter comeat6:30 p.m. so Icouldgo to aclasswith my husband. Thesitter's first reaction to Jamie was: W howoundhimup? W ewere homeby10:30 p.m.and thesitter statedthatJamiewasvery argum entative w ithhisbrotherand waslikearubberband woundup tootight. W henshe put him to bed at9:00p.m. she said he almost collapsed into bed and fell asleep rightaway.Other signsof central nervous system disruption appear in

these notes: adisturbance ofappetite, sleep,and bladder con-trol. These are what psychiatrists call vegetativesigns, verybasic aspects of bodily function which are often impaired inpeople with serious mental illness such as majordepression.Such signs are thought toreflect very primitive biological func-tions regulatedby structures deepin the brain.A s tellingasthese vignettesmay be, theyare not conclu-sive.One still might have some doubts aboutthe roleofaspar-tame in Jamie's hyperactive behavior. Could it be possible, forexample, that these2 hyper days just happened to coincidewith2 baddaysin theup-and-down lifeof ahyperactive young-

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ster? Or could Jamie s mother have unconsciously guessed attheschedule, reporting biased observations because of her beliefin the aspartame connection? The 10-day period which she re-corded before the double-blind challenges was, of course, notblind. So perhaps she painted a rosy picture during those timesand simply guessed when Jamie received the aspartame. Theseare all possibilities, but considering the entire story, they seemimplausible.W e continued tofollowJarnieover succeeding months, andintermittentlyhis mother called with new episodes, each moreworrisome than the last. For instance, on Halloween (about 2weeksafter ourchallenges), Jamie went to aschool party wherehe accidentally drank some Swiss Miss hot chocolate (which theteacher thought was aspartame-free but later turned out notto be). Jamie w as sent home for screaming, kicking, cryinghysterically, being out of control, and threatening other kids.The same pattern reoccurred: hyperactivity, aggressiveness,intermittent somnolence, increased urine output, and slurredspeech.

Onanother occasion, Jamieand hismotherhadlunchat alocal family style restaurant and drank root beer, which theyknew to be naturally sweetened (one of the reasons they atethere). Later in the day the typical reaction occurred, with inces-sant talking, uncontrolled body movements, severe headache,and inability to stay asleep more than an hour at a time. Thisreaction continued through the following day, with almost nosleepover the 24-hour period. When Jamie s mother checkedback at the restaurant, the manager was very sheepish and con-cerned, because they had run out of theregular supply ofrootbeerand had taken the expedient oftemporarily using diet rootbeer purchased nearby, without notifying the customers of thechange. Insome respects, these serendipitous double-blind ex-periments are more convincing than thecarefullymanaged onesconducted in the laboratory.The most important aspect ofJamie s story is the progres-

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sivechangein hispersonality, whichseemedtooccuraftereachoftheseintermittentand terrifyingepisodes.Hebegantoshowsigns o fextremenervousness; he had nightmares and fearsoffallingasleepbecause the NutraSweet monster was going togethim.At onepointhedrewafrightening pictureo f themon-ster abouttodevourhim.

Television ads for NutraSweet now caused Jamie to feargoingtosleepand to bewithdrawnfor therestof theevening,One maywonder abouttheroleo fadultsinsensitizing Jamietothese fears but it seems unusual that a nonanxious and mildlyhyperactiveboyshould shift fromanexternalizing orientation toaninternalizing one. Jamiebegantoappear less likeahyperac-tiveboy and morelikea neurotic one.Eventually referred Jamie to a child psychiatrist whoworked with him over the next several months. Despite thistherapy, Jamie's depression and anxiety became progressivelyworse,and hisabilitytolearninschool becameimpaired Jam-ie's teacher reported that he was not the samehappy,confidentyoungsterwhostarted theyearandthathe wasmoreandmoretearful withdrawn, and afraid o fbeing touched. In many re-spects this course of events is so similar to the adolescent girlwho overindulged in diet drinks that we may well wonderwhetherasimilar processisoccurringinboth cases.Butunlikethe adolescent girl, Jamie did not have to take in large amountsofaspartame to triggerareaction.W e cannot be sure that aspartame began this disturbingcycle nor can we even becertain that the dramatic boutso fhyperactivity, sleeplessness, and excitability were directlylinked toNutraSweet. Onecould postulate that Jamiehas anearlyvariantofmanic-depressivedisorder, though such casesarevery rareinchildren Jamie's age. Possibly Jamie's mothersimply pinned the rap on the drinks, forgetting or minimizingthose hyperactive episodes that occurred when there was noartificialsweetenerin thevicinity.Asascientist,Ihavetoagree thatthesearepo ssi leinterpre-

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