The Diet Factor in ADHD

DOI: 10.1542/peds.2011-2199; originally published online January 9, 2012;Pediatrics

J. Gordon Millichap and Michelle M. YeeThe Diet Factor in Attention-Deficit/Hyperactivity Disorder

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The Diet Factor in Attention-Deficit/HyperactivityDisorder

abstractThis article is intended to provide a comprehensive overview of the roleof dietary methods for treatment of children with attention-deficit/hyperactivity disorder (ADHD) when pharmacotherapy has proven un-satisfactory or unacceptable. Results of recent research and controlledstudies, based on a PubMed search, are emphasized and compared withearlier reports. The recent increase of interest in this form of therapy forADHD, and especially in the use of omega supplements, significance of irondeficiency, and the avoidance of the “Western pattern” diet, make thediscussion timely.

Diets to reduce symptoms associated with ADHD include sugar-restricted,additive/preservative-free, oligoantigenic/elimination, and fatty acid sup-plements. Omega23 supplement is the latest dietary treatment withpositive reports of efficacy, and interest in the additive-free diet ofthe 1970s is occasionally revived. A provocative report draws atten-tion to the ADHD-associated “Western-style” diet, high in fat and refinedsugars, and the ADHD-free “healthy” diet, containing fiber, folate, andomega-3 fatty acids.

The literature on diets and ADHD, listed by PubMed, is reviewed withemphasis on recent controlled studies. Recommendations for the useof diets are based on current opinion of published reports and ourpractice experience. Indications for dietary therapy include medicationfailure, parental or patient preference, iron deficiency, and, when ap-propriate, change from an ADHD-linked Western diet to an ADHD-freehealthy diet. Foods associated with ADHD to be avoided and those notlinked with ADHD and preferred are listed.

In practice, additive-free and oligoantigenic/elimination diets are time-consuming and disruptive to the household; they are indicated only inselected patients. Iron and zinc are supplemented in patients withknown deficiencies; they may also enhance the effectiveness of stim-ulant therapy. In patients failing to respond or with parents opposed tomedication, omega-3 supplements may warrant a trial. A greater at-tention to the education of parents and children in a healthy dietarypattern, omitting items shown to predispose to ADHD, is perhaps themost promising and practical complementary or alternative treatmentof ADHD. Pediatrics 2012;129:1–8

AUTHORS: J. Gordon Millichap, MD, and Michelle M. Yee,CPNP

Division of Neurology, Children’s Memorial Hospital, andDepartment of Pediatrics, Northwestern University MedicalSchool, Chicago, Illinois

KEY WORDSadditive-free, attention, behavior, diet, elimination, hyperactivity,iron, ketogenic, oligoantigenic, omega-3, pediatrics, sucrose, zinc

ABBREVIATIONSADHD—attention-deficit/hyperactivity disorderEFA—essential fatty acidsEPD—enzyme-potentiated desensitizationIGg—immunoglobulin GLC—long chainPUFA—polyunsaturated fatty acids

Dr Millichap reviewed the literature; researched and selectedappropriate articles; and organized, drafted, and revised themanuscript in its final version. Nurse Practitioner Yee is clinicalassociate to the neurology clinic for attention-deficit/hyperactivity disorder. Yee assisted in the selection of articlesand references, collected the data for the table of vsupplements, read the manuscript, and made suggestions forrevision in its final form.

www.pediatrics.org/cgi/doi/10.1542/peds.2011-2199

doi:10.1542/peds.2011-2199

Accepted for publication Oct 5, 2011

Address correspondence to J. Gordon Millichap, MD, Division ofNeurology, Children’s Memorial Hospital, 2300 Children’s Plaza,Box 51, Chicago, IL 60614. E-mail: [email protected]

PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).

Copyright © 2012 by the American Academy of Pediatrics

FINANCIAL DISCLOSURE: The authors have indicated they haveno financial relationships relevant to this article to disclose.

PEDIATRICS Volume 129, Number 2, February 2012 1

STATE-OF-THE-ART REVIEW ARTICLE


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Theroleofdietanddietarysupplementsin the cause and treatment of attention-deficit/hyperactivity disorder (ADHD) inchildren is controversial, but the topiccontinues to interest parents and phy-sicians who prefer an alternative tostimulant medication or seek a comple-mentary therapy. Although prescriptionof medications for ADHD has shown asteady increase since their introductionin the 1960s, the popularity of variousdiets has risen and/or fallen in the sametime period, sometimes showing a Phoe-nicianrevival. In theselectionofa therapyfor ADHD, physicians generally prefer amedication of value proven by controlledtrial. Diets are more difficult to evaluate,and trials requiring elimination of cer-tain foods and dyes may need thesupervision of physician and dietician.

The list of proposed dietary treatmentsincludes sugar-restricted, additive- andsalicylate-free (Feingold diet), oligoanti-genic (elimination), ketogenic, megavita-min, and polyunsaturated fatty acidsupplements (PUFA) diets. The PUFA oromega-3 supplement is the latest di-etary ADHD treatment to receive posi-tive reports, whereas the additive-freeFeingold diet that enjoyed its initialpopularity in the 1980s shows an oc-casional, smoldering revival, especiallyin the United Kingdom, Europe, andAustralia. A recent provocative publi-cation from Australia, the Raine study,links ADHD in adolescents with a“Western-style” dietary pattern, high infat, refined sugars, and sodium and lowin fiber, folate, and omega-3 fatty acids.1

This review focuses on the literatureconcerning diets and ADHD selectedfrom a PubMed search. Results of re-cent research and controlled studiesare emphasized. Diet recommendationsin practice are based on the data pre-sented and on our experience in a neu-rology clinic for childrenandadolescentswith ADHD. In addition to pharmacother-apy, alternative and/or complementarymethods may warrant trial, including

a “healthy” diet pattern,1 eliminationof dyes or foodantigens, or omega-3 PUFAsupplementation.

OMEGA-3 AND -6 FATTY ACIDSUPPLEMENTS

Low levels of long-chain (LC) PUFA arereported in the plasma and red cellsof children with ADHD compared withcontrols.2,3 The potential mechanismsleading to abnormal essential fattyacid (EFA) levels in ADHD patients mayinclude reduced EFA intake, reducedconversion of EFA to LC-PUFAs andincreased metabolism of LC-PUFAs.4

These and other similar reports promp-ted trials of PUFA supplements in treat-ment of children with ADHD and learningproblems.

A frequently cited trial, the Oxford-Durham study,5 compared the effectsof dietary supplementation with omega-3 and omega-6 (in a ratio of 80% to20%) to placebo in 117 children withdevelopmental coordination disorder,one-third having symptoms of ADHD.Comparing the Conners’ Teacher Rat-ing Scale-L/ADHD scores, a reductionand improvement of.0.5 SD occurredduring the 3-month treatment phase,whereas no change was seen in theplacebo group (P, .0001). During a 3-to 6-month follow-up phase, a gain inreading was 3 times that expected, and

spelling advanced twice that expected.Incoordination, a common ADHD com-orbidity, was not benefited. No adverseeffects were reported.5 Although theprimary aim of this study directed to-ward alleviation of incoordination wasnot met, the results demonstrate a re-duction of symptoms of ADHD, an effectduplicated in other PUFA supplementtrials.6,7 However, some studies fail toshow a beneficial PUFA response,8,9

leading to the hypothesis of a geneti-cally impaired fatty acid metabolism insome ADHD patients.10,11

Reviewof 16studiesofPUFAblood levelsand PUFA dietary supplementation inchildren with ADHD found only isolatedreports from1995 to2006andaflurryofinterest from 2007 through 2011. Het-erogeneity of design and other factorsmay have influenced responses andresults: the type and dose of fatty acidemployed (omega-3 or omega-6 orcombination),methodofadministration,duration of treatment, and measure-ment of response.

On the basis of reports of efficacy andsafety,weusedosesof 300 to 600mg/dayofomega-3and30to60mg/dayofomega-6 FAS, continued for 2 or 3 months, orlonger if indicated. Table 1 lists a sampleof fatty acid supplements availableand the quantities of omega-3, -6, and -9in each. The wide variation in omega-3

TABLE 1 Omega Fatty Acid Supplements for Treatment of Children with ADHD

Supplement !mega-3 !mega-6 !mega-9

Nordic Gummy Bears (3) 82 mg(EPA 41 mg, DHA 27 mg, other 14 mg)

Nordic Fishes Chews (3) 136 mg(EPA 68 mg, DHA 45 mg, other 23 mg)

Nordic ProEFA (2 softgels) 565 mg 224 mg LA 244 mg OA(EPA 270 mg, DHA 180 mg, other 115 mg)

MegaRed Krill Oil (1 softgel) 90 mg(EPA 45 mg, DHA 27 mg)

Nutrigold (1 softgel) 380 mg 184 mg LA 100 mg OA(EPA 120 mg, DHA 80 mg, ALA 180 mg) 76 mg GLA

Nature Made 1200 mg soft gel 360 mg(EPA 180 mg, DHA 120 mg, Other 60 mg)

Oxford/Durham study5 732 mg daily(EPA 558 mg, DHA 174 mg)

60 mg GLA daily

ALA, a-linolenic acid; EPA, eicosapentaenoic acid; DHA, docosahexaenoic acid; GLA, g-linolenic acid; LA, linoleic acid; OA, oleicacid.

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content is noteworthy. As initial or add-on therapy, we have occasional reportsof improved school grades and less-ening of symptoms of ADHD, withoutoccurrence of adverse effects.Most parents are enthusiastic abouttrying thediet supplements, despiteourexplanation of only possible benefit andlack of proof of efficacy. In almost allcases, for treatment to be managedeffectively, medication is also required.Additional controlled studies of PUFAare warranted, including larger num-bersofpatientswithdifferentageranges(young and older children), as well asvarious doses of omega-3 and omega-6fatty acid, monitored with blood levels.Subjects with andwithout EFA deficiencyshould be distinguished. We agree withother investigators12 that althougha linkexists between low LC-PUFA and ADHD,the beneficial effects of omega-3 andomega-6 supplements are not clearlydemonstrated.

ADDITIVE AND SALICYLATE-FREE(FEINGOLD) DIET

The history of the Feingold diet is wellknown to physicians who practiced inthe 1970s.13 Amelioration of symptomswas claimed in .50% of hyperactivechildren treated. The enthusiasm gen-erated by the media led to parentaladvocacy groups, necessitating federallysupported scientific trials. Controlledstudies failed to confirm the effective-ness of the diet to the extent claimed.14,15

Nevertheless, a small subgroup ofpreschool children responded ad-versely to additives and preservativesadministered as a challenge.16 An oc-casional child might react adversely todyes and preservatives in foods andmight benefit from their elimination.

Interest in additives in relation to ADHDhas waned in the United States. In thedecade 1979–1988, a PubMed searchlists 20 pertinent articles; in the 2decades from 1990 through 2010, only2 are recorded. Articles appearing in

2010–2011 point to a renewed interestin food additives and ADHD.17–19 In thelatest article,19 referring to 35 years ofresearch on dietary sensitivities andADHD symptoms, a literature reviewshows that of children with suspectedsensitivities, 65% to 89% react whenchallenged with 100 mg of artificialfood colors. In addition to being sensi-tive to these additives, some childrenare sensitive to common nonsalicylicfoods, and cosensitivity is more therule than the exception. A trial combi-nation antigen- and additive-free dietmay be appropriate therapy for chil-dren with sensitivities to food antigensor allergens and to dyes.20,21 Atopicchildren with ADHD have a significantlyhigher response rate to a multiple-itemelimination (foods, artificial colorings,and preservatives) diet than does anonatopic group.22

According to the Feingold diet,13 foodsto be avoided include apples, grapes,luncheon meats, sausage, hot dogs, andcold drinks containing artificial flavorsand coloring agents. Red and orangesynthetic dyes are especially suspect, aswell as preservatives, butylated hydro-xytoluene and butylated hydroxyanisole.Foods permitted include grapefruit,pears, pineapple, and bananas, beefand lamb, plain bread, selected cereals,milk, eggs, and vitamins free of coloring.A parent wishing to follow this dietneeds patience, perseverance, and fre-quent evaluation by an understandingphysician and dietician. The samedegreeof patience and follow-up is requiredwith the oligoantigenic (elimination)diet for ADHD.

OLIGOANTIGENIC(HYPOALLERGENIC/ELIMINATION)DIET

An oligoantigenic diet eliminates mostknown sensitizing food antigens orallergens. Foods often found to be al-lergenic include cow’s milk, cheese,wheat cereals, egg, chocolate, nuts, and

citrus fruits. Examples of hypoallergenicfoods include lamb, potato, tapioca, car-rots, peas, and pears. Skin tests for al-lergic reactivity to foods are unreliable,and elimination diets are required totest for specific food intolerances. Anearly controlled trial of an oligoanti-genic diet in 76 hyperkinetic childrenfound that symptoms improved in 62(82%), and normal behavior was ach-ieved in 22 (29%).23 The diet consistedof 2 meats (lamb and chicken), 2 car-bohydrates (rice and potatoes), 2 fruits(banana and apple), vegetables andcalcium and vitamins for 4 weeks. A sub-sequent double-blind study, using a “fewfoods” elimination diet, reported improve-ment in 76% patients and worsening ofbehavior ratings and cognitive tests af-ter provoking food challenge.24

The term “elimination diet” is now morepopular than “oligoantigenic,”withPubMedlisting 14 articles under the former and4 using the latter title, the majority fromthe United Kingdomand Europe. Interestin the oligoantigenic/elimination diethas increased, but studies have pro-vided mixed opinions of efficacy. A par-tial benefit of the diet was demonstratedin a small cohort of 21 children testedwith both subjective and objectivemeasures.25 The effect was significantfor subjective, but not objective, mea-sures. The oligoantigenic diet may in-fluence only certain dimensions of theADHD syndrome.

A more favorable effect followed a fewfoods elimination diet (containing rice,turkey, pear, and lettuce) in 40 children,36 boys and 4 girls, aged 3 to 7 years,diagnosed with ADHD.26 Twenty-fivepatients (62%) showed an improvementin behavior of$50%, 9 (23%) withdrewfrom the study, and 10 (25%) had im-proved parent and teacher ratings. Inthis controlled study, the eliminationdiet resulted in a statistically signifi-cant decrease in symptoms of ADHD.

The effectiveness of the diet is demon-stratedbya larger randomizedcontrolled


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trial in an unselected group of 100 chil-dren27 in the Impact of Nutrition on Chil-dren with ADHD study in the Netherlands.This study consisted of an open-labelphase (phase 1; 5 weeks of a restrictedelimination diet or healthy control diet)followed by a double-blind crossover,challenge phase (phase 2). Respondersto challenge with high- or low immuno-globulin (Ig) G foods showed an increaseof 20.8 points on the ADHD rating scale(P , .0001) and an 11.6 increase of aConners’ Score (P , .0001). After thechallenge, relapse of ADHD symptomsoccurred in 19 of 30 (63%) children, in-dependent of the IgG blood levels.

The utility of IgG blood tests is unsup-ported, but the effectiveness of a super-vised, restricted elimination diet is anindication of the influence of foodon ADHD. For some investigators,however, the role of the elimination dietin the treatment of ADHD remainsuncertain.28,29 The report generated crit-icism that the study did not permit theunqualified recommendation of dietarytreatment in all childrenwith ADHD,30 anda placebo effect could not be excluded.31

The diagnosis of food sensitivity is com-plex, time-consuming, and sometimestoo burdensome for patient, family, andphysician. In selected patients with dili-gent parents, a short 2- to 3-week periodof restricted elimination diet is justified.In patients benefited by the diet, re-stricted foodsare introducedeachweek,1 at a time, until the offending item oritems are identified. Improvements inbehavior may be delayed for 10 days to 2weeks, and food preferred and con-sumed most is often the offending item.

FOOD ANTIGEN DESENSITIZATION

Terms used for food intolerance in-clude “food sensitivity,” “food allergy,”or “food hypersensitivity,” and “psycho-logically determined food aversions.”32

Food allergy was investigated by a trialof enzyme-potentiated desensitization(EPD) in 40 children with food-induced

hyperkinetic behavior disorder.33 Of 20who received active EPD treatment, 16became tolerant of provoking foodscompared with 4 of 20 taking placebo(P, .001). EPD permitted children to eatfoods previously known to provoke symp-toms. Food allergy is a possible mecha-nism of the hyperkinetic syndrome, andresearch involving the influence of foodtriggers could inform clinicians on via-ble alternative and/or supportive im-munotherapy.34

SUGAR, ASPARTAME, AND ADHD

Parentsof childrenwithADHD frequentlyreport aworseningofhyperactivity afteran excessive ingestion of candy or dietsoda. Isolated reports support theparents’ observations, but the majorityof controlled studies fail to demonstratea significant adverse effect of sucroseor aspartame. A PubMed search for“sugar, aspartame, and ADHD” listed 8articles, dated 1984 through 1995. In acontrolled trial involving preschool andschool-age children described by parentsas sensitive to sugar, diets high in su-crose or containing aspartame and freeof additive had no effect on children’sbehavior or cognitive function.35 This ar-ticle provoked much correspondence,mainly critical of the negative conclusion.

The authors’subsequent meta-analysisof 16 reported studies, identifiedthrough Medline and PsychINFO data-bases, concluded that sugar does notusually affect the behavior or cognitiveperformance of children, but a smalleffect on subsets of children cannot beruled out.36 In preschool boys aged 2 to6 years rated by parents as “sugarresponders” and “nonresponders,”neither acute sugar loading nor aspar-tame increased activity level or aggres-sion, but the daily sucrose intake andtotal sugar consumption correlatedwithduration of aggression.37 Inattentionwasincreased after sugar intake, but notaspartame or saccharine. The sugarand placebo challenges were given

with a breakfast high in carbohydrate,a possible reason for the adverse effectof the sucrose challenge.38 The hyperac-tive response is blocked if a proteinmealis ingested before or with the sugar.39

Reactive Hypoglycemic Responseto Sugar Load

An alternative explanation for sugar-induced cognitive impairment andinattention may be a reactive hypogly-cemia. Compared with adults, childrenare more vulnerable to the effects ofhypoglycemia on cognitive function. Ameasure of cognitive function usingauditory evoked potentials was signif-icantly reduced when blood glucosewas lowered,75 mg/dL in children butwas preserved in adults until the levelfell to 54 mg/dL.40 Aspartame used asa control had no adverse effects onbehavior or cognition in children withattention-deficit disorder.41 The avoidanceof rapidly absorbed sucrose-containingfoods in young children may preventdiet-related exacerbations of ADHD.

In a study of adolescents with insulin-dependent diabetes mellitus, mildhypoglycemia (60 mg/dL) caused a sig-nificant transient decline in performanceof a battery of cognitive tests, whereashyperglycemia had no effect.42 Thefrontal cortex, known to be involvedin the control of attention, was morehighly activated than other brain regionsduring acute hypoglycemia.43 Childrenwith food-induced ADHD show an in-crease in b activity in frontotemporalareas during EEG topographic map-ping of brain electrical activity afteringestion of provocative foods.44

Sugar and the EEG

The effects of sugar and especially hy-poglycemiaon theEEGhavebeenstudiedsince the late 1930s.45,46 Lowbloodsugarlevels are associated with an impair-ment of the normal electrical activityof the cerebral cortex. A deficiencyof glucose to the brain causes the



appearance of slow rhythms in the EEG,with fall in the dominant a frequencyand appearance of u and finally d fre-quency. It is not surprising that a sugarload would cause an increase in fasterb rhythms in the EEG.44 An electrophys-iologic approach, using EEG biofeedback(neurofeedback), in support of a possi-ble relation between sugar and symp-toms of ADHD requires additional study.However, studies of EEG biofeedback inthe treatment of ADHD provide mixedresults and possible benefit, with im-provement in only selected attentionalbrain functions.47

In practice, the link between sugar andhyperactive behavior is so universalin the opinion of parents of childrenwith ADHD that no controlled study orphysician counsel is likely to changethis perception. Parents will continue torestrict the allowance of candy for theirhyperactive child at Halloween in thebelief that this will curb the level of ex-uberant activity, an example of the Haw-thorne effect. The specific type of therapyor discipline may be less important thantheattentionprovidedby the treatment.21

The Ketogenic Diet and ADHD

The ketogenic diet, a diet high in fatcontent and low in carbohydrate, wasintroduced for the treatment of epi-lepsy in 1921.48 The mechanism is stillunclear, but metabolic balance studiesin children with absence seizures showthat the antiepileptic effect of the dietis correlated closely with a negative bal-ance of sodium and potassium.49 The re-introduction of carbohydrate to the diet isassociated with recurrence of spike-and-wave epileptiform discharges in the EEG.In 65 children with intractable seizures,treatment with the ketogenic diet waseffective in control of seizures at 1-yearfollow-up, and developmental quotients,behavior, attention, and social function-ing were significantly improved.50

Childrenwith epilepsy frequently exhibitsymptoms of ADHD, and children with

ADHD have a high frequency of epilep-tiform discharges in the EEG.51 Animalsreceiving a ketogenic diet show a re-versible decrease in activity level.52 TheEEG, of value in prediction of a sustainedanticonvulsant effect,53 may also proveindicative of a behavioral response tothe ketogenic diet.

IRON DEFICIENCY AND ADHD

Iron deficiency is associated with anumber of neurologic disorders, in-cluding breath-holding, restless legsyndrome, and febrile seizures. A reportof low serum ferritin in children withcognitive and learning disorders54

prompted the inclusion of a serum fer-ritin level in the battery of laboratorytests obtained on patients attending ourneurology clinic for ADHD. In our hos-pital laboratory, the range of controlserum ferritin levels is 300 ng/mL witha lowof 22 ng/mL inmales and 10 ng/mLin females. In 68 consecutive patients(aged 5–16 years; 54 male, 14 female),themean serum ferritin level in patientswith ADHD was 39.9 ng/mL and was notdifferent from control subjects. Twelve(18%) patients had values ,20 ng/mLthat were considered abnormal andsuggestive of iron deficiency withoutanemia, and a similar number had levels.60 ng/mL and were not iron deficient.A comparison of clinical characteristicsof the low-ferritin and high-ferritingroups disclosed no significant differ-ence in severity or frequency of ADHD andcomorbid symptoms or response to drugtherapy. In this patient cohort, a causativerole for low serum ferritin and iron de-ficiency in ADHD was not confirmed.55

In an earlier study of the effects of ironsupplements in ADHD children in Israel,a significant increase in serum ferritinlevels (25.9–44.6 ng/mL) was associ-ated with a significant decrease in theConners’ Parent Rating Scale but not inthe Teachers’ Rating Scales.56 In laterstudies of children with ADHD in France,the proportion with low (,30 ng/mL)

and very low (,15 ng/mL) serum fer-ritin levels was greater than that of ourpatients in the United States: 84% ver-sus 32%.57 Low serum ferritin levelswere correlated with more severe ADHDsymptoms measured with Conners’Parent Rating Scale and greater cogni-tive deficits. A trial of iron supplemen-tation found improvements in behaviorrating scales, but this finding did notreach significance.58

A threshold effect may be important inthe evaluation of a proposed causativerole of iron deficiency in ADHD, and ad-ditional controlled studies are probablywarranted. The unusually low ferritinlevels (mean: 18.4 ng/mL; 23% partic-ipants ,7 ng/mL) encountered in a re-cent study of ADHD children in Iowa Citymay explain the observed correlationwith ADHD symptomscores.59 Lowserumferritin was correlated with baseline in-attention, hyperactivity, and impulsivityand also with the dose of amphetaminerequired to optimize a clinical response.Serum ferritin and iron supplementationas potential predictor or intervention tooptimize stimulant therapy is a novel in-dication for additional study of iron de-ficiency and ADHD.

ZINC DEFICIENCY AND ADHD

Published reports of the role of zinc inADHD show low zinc levels in serum, redcells, hair, urine, and nails of affectedchildren.60 Most reports are from theMiddle Eastern countries, Turkey andIran, areas with suspected endemic zincdeficiency. Two placebo-controlled trials,one of zincmonotherapy and the other ofzinc supplementation of methylpheni-date, report significant benefit.61,62

In one study involving children in theUnited States, low serum zinc levelscorrelated with parent/teacher-ratedinattention but not with hyperactivity/impulsivity.63 Zinc supplements enhancedthe benefit from d-amphetamine; theoptimal dose of stimulant was 37%lower with zinc than with placebo.64




Zinc is a cofactor for metabolism ofneurotransmitters and fatty acids andalso regulates dopamine metabolisminvolved in ADHD. The relationship ofzinc to EFA supplements and stimulantsevaluated in treatment of ADHD foundthat the d-amphetamine response waslinear with zinc nutrition. Fatty acidsmay benefit ADHD by improving orcompensating for borderline zinc nu-trition.65 Although zinc supplementsare of value in treatment of Middle East-ern children with ADHD associated withendemic zinc deficiency, the incorpo-ration of zinc in the therapy of ADHD in theUnited States is less well defined.

OTHER ALTERNATIVE DIETARYTHERAPIES FOR ADHD

The concept of orthomolecular (“rightmolecule”) medicine and megavitamintherapy refers to the use of a combina-tion of nutrients and minerals alleged toprovide the optimum molecular environ-ment for the mind. The treatment, sub-sequently advocated for children withhyperactivity, as well as for mental re-tardation and Down’s syndrome,66 is ofunproven value.

In a double-blind crossover study ofmegavitamin therapy in 41 childrenwith ADHD, no significant improvementwas demonstrated in behavior scores,and25%weremoredisruptive (P, .01).67

Serum transaminase levels exceededthe upper limits of normal in 42%children while receiving vitamins.Megadoses of some vitamins are notwithout danger of hepatotoxicity, andtheir efficacy is unconfirmed. Mineralanalyses, especially iron and zinc,may be warranted in children with

ADHD and learning disorders, butthe need for adequate controls andblood levels is emphasized. Treat-ment based on inaccurate measure-ment techniques may lead to adversereactions.21

“HEALTHY” DIET PATTERN INPREVENTION AND TREATMENT OFADHD

In the Australian Raine study, the re-lationship between dietary patterns andADHD was examined in a population-based cohort of live births followed toage 14.1 Two major dietary patternswere identified as “Healthy” and “West-ern,” according to foods considered themain contributors. (Table 2) The West-ern dietary pattern associated with anADHD diagnosis contains higher intakesof total fat, saturated fat, refined sugars,and sodium and is deficient in omega-3fatty acids, fiber, and folate. The Healthydiet pattern, not associated with ADHDdiagnosis, is rich in fish, vegetables,fruit, legumes, and whole-grain foods. Ahigher risk of having an ADHD diagnosis,inattentive or combined types, is ob-served for boys compared with girls.The major specific foods in a Westerndiet are also contributory to an in-creased tendency to obesity amongnonmedicated ADHD children andadolescents.68

The relationship between a Westerndietary pattern and ADHD may be me-diated by other factors, such as poorfamily functioning and emotional dis-tress, leading to a craving for fat-richsnack foods. Whatever the specificcause, a modification of the child’s di-etary pattern may offer an alternative

method of treatment of ADHD and lessreliance on medications.

SUMMARY AND CONCLUSIONS

Various alternative therapies for ADHDare offered as substitutes or supple-ments to medication and behavioraltreatments. The evaluation of claims fortherapies in a disorder such as ADHD,without a single,well-definedcause, is ascientific challenge requiring controlsand appropriate neuropsychologicaltesting. The indications for diet therapyinclude the following: (1) medicationfailure or adverse reaction, (2) parentor patient preference, (3) symptoms orsigns of mineral deficiency, and (4) theneed to substitute an ADHD-free healthydiet for an ADHD-linked diet.1 Diet is oneenvironmental etiology of ADHD that isamenable to modification.69

Oligoantigenic,elimination, andadditive-free diets are complicated, disruptive tothe household, and often impractical, ex-cept for selected patients. Supplementaldiet therapy is simple, relatively inexpen-sive, and more acceptable to patient andparent. Public education regarding ahealthy diet pattern and lifestyle to pre-vent or control ADHD may have greaterlong-term success.

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“ADHD-associated”Foods to Avoid

“Healthy” Foods:Preferred

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Red meat VegetablesProcessed meats TomatoCrisps, potato chips Fresh fruitHigh-fat dairy products Whole grainsSoft drinks Low-fat dairy products

Based on Howard AL et al.1



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DOI: 10.1542/peds.2011-2199; originally published online January 9, 2012;Pediatrics

J. Gordon Millichap and Michelle M. YeeThe Diet Factor in Attention-Deficit/Hyperactivity Disorder

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