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ATTENTION DEFICIT, HYPERACTIVITY, AND LEARNING DISORDERS: A Scientific Appraisal of Dietary Therapies* by J. Gordon Millichap, MD, FRCP, Professor Emeritus, Northwestern University Medical School; Pediatric Neurologist and Director, Attention Deficit Disorder Clinic, Division of Neurology, Children’s Memorial Hospital, Chicago, Illinois; and member of NOHA’s Professional Advisory Board. ADHD, or attention deficit hyperactivity disorder, is a syndrome commonly encountered in children and adolescents, and occasionally in adults. It is often associated with learning disabilities, resulting in a child’s failure to achieve the expected level of academic performance based on estimates of intelligence. At least one child in every classroom and approximately 3 to 5% of the school age population are inattentive or abnormally overactive in behavior.
The causes of ADHD are diverse and often undetermined; both genetic and environmental factors have been invoked. Anomalies of brain development, premature birth, anoxic brain injury (involving lack of oxygen), encephalitis, toxic lead and cocaine exposures, and PCBs and other contaminants of our food and water supplies are sometimes uncovered as associated and potential causes. One of the earliest references to a hyperkinetic behavior syndrome may be traced to an encephalitic illness associated with the World War 1 influenza epidemic of 1918. The link to viral and sometimes head trauma causes for ADHD led to the concept of a brain damage or neurobiologic syndrome, a theory subsequently supported by recent MRI (magnetic resonance imaging) and brain metabolism studies. Unfortunately, a recent National Institutes of Health consensus development conference on ADHD (Novemer 16-18, 1998) ignored the neurologic basis for the syndrome and chose to emphasize the psychiatric approach. The influence of dietary factors, sucrose, aspartame, food additives and preservatives, on behavior and learning is of special concern to some parents, but has provoked skepticism and controversy among members of the medical profession. The evaluation of claims for therapies in a disorder such as ADHD, having no single, well-defined cause, presents a scientific challenge, requiring controls and appropriate measurement techniques, including the identification of subgroups that can respond to particular treatments. Children with ADHD are inattentive and distractible (ADHD - inattentive type) or hyperactive (H) and impulsive (I) (ADHD - HI type). Many are both inattentive and hyperactive (ADHD - combined type).
Medications, such as methylphenidate (Ritalin®) are of proven value in 80% of patients, diagnosed with ADHD, but their widespread use and potential side effects have sparked criticism by the media, influencing parents to turn to alternative methods of treatment, mainly behavior modification and diet. Scientific proof of a cause and effect, linking food items to the ADHD syndrome, is difficult to establish, and many reports are anecdotal and flawed by the author’s biased opinion. Unfortunately, remedies are often published before they have been subjected to rigorous scientific evaluation by recognized experts. Parents, in their efforts to find help, may be confused by enthusiastic claims for novel treatments and may be persuaded to try unproven remedies. Most are without physical harm to the child, but may consume time, energy, and finances of the families involved. Why are parents sometimes convinced that scientifically unproven treatments are effective in their child? There are two reasons. First, the methods of scientific study may be at fault. The use of groups of children with ADHD may fail to recognize positive effects in individuals, and evaluations by teacher and parent questionnaires may be insensitive to the measurement of small responses. The scientific method may not be as smart as a mother’s intuitive observations. An example of the failed scientific study in detection of behavioral changes observed by parents is the response of occasional children to sugar and chocolate deprivation and the omission of dyes in the diet. A second reason for a parent’s enthusiasm for a certain treatment is the so-called "Hawthorne" or indirect effect. The specific type of therapy may be less important than the attention provided by the treatment. An example of the Hawthorne effect is the benefit that appears to follow sensory and perceptual motor training programs. Children may show improvements in learning and behavior after enrollment in these exercises, but according to some experts, the effects may be indirect and non-specific. (Hynd and Cohen, 1983). Of all the alternative therapies proposed for the treatment of ADHD, diet and dietary supplements have demanded the most attention and caused major controversy. In the following question and answer sections, the separation of fact and fantasy about diet and behavior will be attempted by referral to the current scientific literature and results of controlled investigations. What are the various diets or diet supplements advocated in the treatment and prevention of ADHD and learning disorders? A list of dietary treatments proposed for ADHD and learning disorders includes the following:
For most of these diets and supplements, both positive and negative results have been reported. It may be concluded that some children are responsive to one or another of the diets, but the demonstration of significant effects in a group of children as a whole may defy the available scientific method. What is the evidence for and against a sugar-restricted diet for ADHD? FOR: Studies in favor of a sugar-restricted diet include the following: At Colorado State University, 30 preschool children (20 boys and 10 girls, mean age 7 years, 2 months) received a breakfast of high sucrose content (50 grams), low sucrose (6 grams), or aspartame (122 milligrams), randomly selected, 5 days on each, using a double-blind control design. On measures of cognitive function, girls made significantly less errors on a learning task performed 30 minutes following the low-sugar content breakfast when compared to the high-sugar meal, whereas boys were unaffected. On an Abbreviated Conners Teacher Rating Scale completed before lunch, both boys and girls were more active in behavior after the high-sugar meal compared to a low-sugar intake. Prior to the study, approximately 50% of the children were considered behaviorally sensitive to sugar, based on parent and teacher questionnaires (Rosen, L. A., et al, 1988). At the Children’s Hospital, Washington, DC, the adverse effects of sugar in children with ADHD were demonstrated only if the challenge dose of sucrose was taken after a high carbohydrate breakfast. The hyperactive response could be prevented by a high protein breakfast. (Conners C. K., personal communication, 1987).
The beneficial and protective effects of a protein diet are correlated with neuroendocrine changes and blocking of serotonergic (increased serotonin, a hormone and neurotransmitter) effects of sugar on behavior and attention. Diets low in protein and high in carbohydrates have been found to cause increase spontaneous activity in animal studies. For reviews of the effects of dietary nutrients and deficiencies on brain biochemistry and behavior, see Yehuda, S. (1986,1987). At the Schneider Children’s Hospital, New York, the effects of sugar in a sample of young hyperactive boys with ADHD were similar to those observed by Conners. Inattention, measured by a continuous performance task, was increased following a sucrose drink given with a breakfast high in carbohydrate, but not after a drink containing aspartame (Wender, E. H., and M. V. Solanto, 1991). Inattentiveness may be benefited by the restriction of sucrose at the morning meal, by avoidance of a high carbohydrate breakfast, or by providing a protein-containing, balanced meal. At Yale University School of Medicine, New Haven, Connecticut, the immediate and delayed (3-5 hours) effects of a glucose load on plasma glucose and epinephrine (a neurotransmitter) levels were compared in 25 healthy children and 23 young adults. A late fall in plasma glucose (reactive hypoglycemia) stimulated a rise in epinephrine, twice as high in children compared to adults; and hypoglycemia symptoms (shakiness, sweating, weakness, or rapid pulse) occurred in children but not in adults. A measure of cognitive function by auditory-evoked potentials, which was significantly reduced when glucose levels fell to 75 milligrams per deciliter (mg/dl) in children, was preserved until the level fell to 54 mg/dl in adults (Jones, T. W., et al, 1995). Children are more vulnerable to a glucose load and the effects of hypoglycemia on cognitive function and behavior than are adults. The avoidance of rapidly absorbed glucose or sucrose-containing foods in young children might prevent diet related exacerbations of ADHD. A balanced diet of protein, fat, and complex carbohydrates should limit a sudden fall in glucose levels after a meal, and should avoid symptoms related to the epinephrine-hormonal response.
At the University of Pittsburgh School of Medicine, mild hypoglycemia (60 mg/dl) caused a significant decline in performance on a battery of cognitive tests in a study of adolescents with insulin-dependent diabetes mellitus, whereas hyperglycemia (high blood sugar) had no effect. (Gschwend S., et al, 1995). This study in diabetics supports the theory that a delayed fall in blood sugar following a high-sucrose load can have an adverse effect on learning. A sugar-restricted diet may benefit children with ADHD. At Otto-von-Guericke University, Magdeburg, Germany, the effects of hypoglycemia on cognition were studied using event-related, brain-potential (ERP) measures and reaction times. Compared to base-line readings, measures of selective attention, choice of response, and reaction time were delayed during hypoglycemia; and responses were slow to recover after normal blood sugar levels were restored. The frontal cortex, known to be involved in the control of attention, was more highly activated than other brain regions during acute hypoglycemia (Smid H., et al, 1997). This electrophysiological approach to the study of effects of sugar levels on learning also demonstrates an adverse effect of hypoglycemia, supporting a possible relation between sugar and symptoms of ADHD. AGAINST: Studies failing to demonstrate either an adverse effect of sugar or a difference between sugar-containing and sugar-restricted meals were as follows: At the University of Toronto, Ontario, Canada, the frequency of minor- and gross-motor behaviors, measured by "actometer" readings and video-taped observations, was significantly less in 9-10 year-old normal children after the consumption of a sucrose drink than after a drink containing aspartame. Different responses might occur in ADHD children. At Vanderbilt University, Nashville, Tennessee, 25 normal preschool children (3 to 5 years of age) and 23 school-age children (6 to 10 years old), described by their parents as sensitive to sugar, received a diet high in sucrose or an aspartame substitute for three-week periods. Measures of behavior and cognitive performance showed no significant differences between the groups. Neither sucrose nor aspartame caused a worsening of behavior or impairment of learning in normal or alleged sucrose-sensitive children (Wolraich, M, L., et al, 1994).
It may still be argued that individual children are sensitive to sugar or aspartame, but adverse effects are difficult to document by limited trial periods in children selected for specific studies.
PARTIALLY FOR AND AGAINST: Some studies provided conflicting results, as follows: At the National Institute of Mental Health, Bethesda, Maryland, 18 boys aged 2-6 years, rated by parents as "sugar responders," and 12 male playmates, rated as "non-responders," received single doses of sucrose, glucose, aspartame, or saccharin in a randomized, double-blind design. Parent and teacher ratings of activity levels and aggression failed to show differences between substances for either the alleged "responders" or "non-responders," No parent differentiated between sugar and artificial sweetener trials. Whereas acute sugar loading did not increase aggression or activity in preschool children, the daily sucrose intake and total sugar consumption correlated with duration of aggression for the alleged sugar-responsive group (Krnesi, M. J. P., et al, 1987). At the Schneider Children’s Hospital, New York, boys with ADHD and oppositional disorder and age-matched control subjects received either sucrose or an aspartame drink with a breakfast high in carbohydrate. Measures of aggressive behavior were unchanged by either sucrose or aspartame; but inattention, measured by a continuous performance task, was exacerbated in the ADHD group following sugar, but not with aspartame (Wender, E. H., and M. V. Solanto,1991).
It follows that the avoidance of sucrose might benefit inattentiveness in the ADD child. Should aspartame and diet sodas be restricted in ADHD children? The Food and Drug Administration (FDA) and the manufacturer claim that aspartame (Nutrasweet®) and diet drinks are safe, except for children with phenylketonuria (a hereditary inability to metabolize phenylalanine, one of the components of aspartame). Despite these claims, consumer groups and some scientists issue warnings of reported side effects and brain disorders related to the widespread ingestion of aspartame in dietary beverages and foods. Researchers in the Department of Psychiatry and Biostatistics, Washington University Medical School, St Louis, have proposed a link between the increasing rate of brain tumors and the introduction of aspartame in the diet in the 1980s (Olney, J. W., et al, 1996). A review of earlier studies from equally prestigious universities, published following peer review in recognized medical journals, has concluded that aspartame can precipitate migraine headaches and exacerbate electroencephalogram (EEG) abnormalities in children with epilepsy. (Millichap, J. G., 1991, 1994, 1997). Studies failing to support a ban on aspartame in children with ADHD include reports from Schneider Children’s Hospital, New York, (Wender, E. H. and M. V. Solanto, 1991); Vanderbilt University, Nashville, Tennessee (Wolraich, M. L., et al), 1994); and the University of Toronto, Ontario, Canada (Saravis, S., et al, 1990).
A study at Yale University School of Medicine, showing mixed results in 15 ADHD children, found no significant differences between aspartame (a single morning doses before school for 2 weeks) and placebo on various measures of cognition, behavior, and monoamine (e.g., the neurotransmitters, serotonin, dopamine, and norepinephrine) metabolism, but a significant increase in activity level following aspartame based on Teacher Ratings (Shaywitz, B. A., et al, 1994). Until more evidence is available, specifically in ADHD children, Nutrasweet® containing drinks and foods should probably be restricted in the diets of children with ADHD, epilepsy, or headaches. What is the current medical opinion of the additive and salicylate-free diet in ADHD? After sugar, additives and preservatives have attracted the interest of parents of children with ADHD more than most items in the diet. The Feingold additive-free diet was introduced in 1975, with the publication of a book entitled Why Your Child Is Hyperactive. Without documentation by controlled studies, the author claimed success in more than 50% of hyperactive children treated. The enthusiasm generated as a result of premature and widespread publicity stimulated the necessity for Federally organized and supported scientific trials. Controlled studies in two major universities failed to provide convincing evidence for the efficiency of the additive-free diet to the extent claimed by Dr. Feingold (Conners, C. K., et al, 1976; Harley, J. P., et al, 1978). Nevertheless, a small subset of younger pre-school children appeared to respond adversely to additives when presented as a challenge. It was concluded that an occasional child might react adversely to dyes and preservatives in the diet and might benefit from elimination of these additives. The interest in additives in relation to ADHD among parents and neurologists in the United States has waned, but in England, Europe, and Australia, the avoidance of foods containing additives is of widespread concern and their relation to behavior continues to be investigated. In a study of the prevalence of food-additive intolerance in the UK, 7% of 18,000 respondents to questionnaires reported reactions to additives, and 10% had symptoms related to aspirin. A preponderance of additive-related behavioral and mood reactions occurred in children, boys more than girls (Young, E., et al, 1987). At the Royal Children’s Hospital, Victoria, Australia, of 55 hyperactive children included in a 6-week, open trial of the Feingold diet, 47% showed a placebo response and 25% were identified as likely reactors to additives (Rowe, K. S., 1988). In a larger group of 200 hyperactive children, 150 reported behavioral improvements on a diet free of synthetic colorings. A subsequent double-blind, placebo-controlled, 21-day challenge study of 34 suspected reactors indentified 24 with a significant behavior change that varied in severity with the dose of tartrazine synthetic colorings. Extreme irritability, restlessness, and sleep disturbance rather than attention deficit were the common behavioral patterns associated with the ingestion of food colorings (Rowe, K. S. and K.. J. Rowe, 1994).
The number of reactors to the synthetic dye, tartrazine, identified in this Australian study, is significant and contrasts markedly with the isolated cases reported in earlier studies in the United States. Children with ADHD complicated by irritability, restlessness, and sleep disturbance may be benefited by an additive-free diet. The strict Diagnostic and Statistical Manual (DSM) criteria for the diagnosis of ADHD and an inappropriate behavioral rating scale, omitting irritability and sleep disturbance, may have failed to identify some reactors to food additives in previous studies of the diet. In Australia, the Feingold hypothesis is still alive, and in the United States, further interest in the use of the additive-free diet may be warranted (Millichap, J. G., 1993). What are the foods omitted and those permitted in the additive-free and salicylate-free diet? According to the Feingold diet, foods to be avoided included apples, grapes, luncheon meats, sausage, hot dogs, jams, gum, candies, gelatin, cake mixes, oleomargarine and ice creams, cold drinks and soda pop containing artificial flavors and coloring agents. Medicines containing aspirin were also excluded. Red and orange synthetic dyes were especially suspect, as well as preservatives, BHT and BHA, found in margarine, some breads and cake mixes, and potato chips.
Foods permitted included the following: grapefruit, pears, pineapple and bananas; beef and lamb; plain bread, selected cereals, milk, eggs, home-made ice cream, and vitamins free of coloring. Labels and packages require checking to avoid offending additives; and a dietitian should be consulted to ensure that the caloric content and food items are adequate for growth and metabolism. A parent wishing to follow this diet needs patience, perseverance, and the frequent monitoring by an understanding physician.
What is the oligoantigenic diet for ADHD? An oligoantigenic diet is one that eliminates all but a few known, sensitizing food antigens or allergens. Foods most commonly found to be allergenic include cow’s milk, cheese, wheat cereals, egg, chocolate, nuts, and citrus fruits. Skin tests of allergic reactivity to foods are unreliable; and elimination diets are required to test for specific food intolerances.
A combination of the antigen- and additive-free (AAF) diet is sometimes advised in suspected additive-reactive and allergy-prone children (Millichap, J. G., 1986). If improvements in behavior are not evident after three to four weeks, alternative methods of treatment are considered. At the Alberta Children’s Hospital and Learning Center, Calgary, Canada, a 4-week trial of an AAF elimination diet in 24 hyperactive pre-school boys, aged 3.5 to 6 years, was associated with significant improvements in behavior in 42% and lesser improvements in 12%, when compared to baseline and placebo-control periods of observation (Kaplan, B. J., et al, 1989). The diet eliminated artificial colors and flavors, chocolate, monosodium glutamate, preservatives, and caffeine; it was low in sucrose. It was dairy-free if an allergy to milk was suspected. At the Universitatskinderklinik, Munchen, Germany, and the Allergy Unit, London, UK, a controlled trial of desensitization by intradermal food antigen injection found 16 of 20 hyperactive children became tolerant toward provoking foods, compared with 4 of 20 who received placebo injections. After desensitization, children with food-induced ADHD were able to eat the foods previously found to cause reactions, especially chocolate, colorings, cow’s milk, egg, citrus, wheat, nuts, and cheese (Egger, J., et al, 1992). These controlled studies lend support to the theory of food allergies and additives as a potential precipitating cause of ADHD in some patients. What are the effects of the ketogenic diet for epilepsy and fatty acids on ADHD? Some children with epilepsy are also hyperactive; and a high-fat/low-carbohydrate (ketogenic) diet is occasionally used in treatment, particularly when seizures are resistant to antiepileptic drugs (AEDs). In addition to seizure control, an added benefit of the ketogenic diet is a noticeable improvement in hyperactive behavior, attentiveness, and cognitive abilities. With better seizure control, the doses of AEDs known to impair behavior and learning can often be reduced. For reviews of the effects and mechanisms of the ketogenic diet, see Progress in Pediatric Neurology, I and II (Millichap, J. G., 1991 and 1994).
Studies of fatty acid supplements in the treatment of children and adults with dyslexia have provided some interesting, preliminary results. Low serum levels of docosahexaenoic (DHA) and arachidonic acids are reported in hyperactive children with dyslexia (Mitchell, E. A., et al, 1987). In adults with dyslexia, improvements in dark adaptation and reading ability followed treatment with DHA supplements (Stordy, B. J., 1995). Studies of the importance of DHA in vision and brain function have often been reported in NOHA NEWS See, for example:
Other fatty acid containing supplements of unproven efficacy include the lecithins, which are essential in many tissues. What are the rationale and risks of "orthomolecular" and megavitamin therapy for ADHD and learning disorders? The terms orthomolecular psychiatry and megavitamin therapy are now used synonymously to describe a theory and treatment of mental illness. The term orthomolecular, very simply stated, means "right molecule." The concept was adopted by Nobel Prize winner, Dr. Linus Pauling, in 1968. He proposed a treatment of mental disease, principally schizophrenia, using megadoses of niacin (vitamin B3), ascorbic acid (vitamin C), other vitamins, the minerals—zinc and manganese, and cereal-free diets. This combination of nutrients was thought to provide the optimum molecular environment for the mind. The treatment was subsequently advocated for children with hyperactivity, for mental retardation, and Down’s syndrome (Cott, A., 1972).
In my own practice, an open trial of Vitamin B complex (Becotin®) in ten children with ADHD failed to demonstrate effects on pre- and post-trial measures of behavior and psychological function. A double-blind, controlled study was not considered warranted based on these preliminary results (Millichap, J. G., 1986). Biological subgroups of children with autistic and hyperactive behavior may be amenable to treatment with megavitamins and minerals but, for the most part, practitioners of orthomolecular-megavitamin therapy have failed to convince colleagues of the validity of their claims. Furthermore, megadoses of some vitamins are not without danger. For example, pyridoxine (vitamin B6), in doses of 100 milligrams or above, can cause peripheral neuropathy if continued for prolonged periods (Millichap J. G, 1997). What is the basis for mineral and trace element treatment of ADHD? The theory of trace element and mineral deficiency as a cause of ADHD and learning disabilities was proposed on the basis of hair analyses and a report of lower than normal values for several minerals. Caution in the interpretation of hair analyses is important, since environmental and seasonal factors, age, sex, and infection can affect mineral concentrations in hair samples, in addition to dietary factors. (Millichap, J. G., 1991). Trace elements such as zinc, copper, manganese, iron, selenium, copper, and fluorine can cause disease either as a result of a deficiency state or when consumption is in excess of normal requirements. Toxicity may result from food additives or adulteration, or from inadvised prescription or nonprescription medicines. The recognition of symptoms and signs of chronic, low-level, trace-element exposure is often difficult and the interactions between minerals are poorly understood (Millichap, J. G., 1993).
At the Dyslexia Institute, Staines, Middlesex, and the Hornsby Learning Centre, London, UK, an association between dyslexia and low concentrations of zinc in sweat analyses has been demonstrated in a study of 26 children, aged 6 to 14 years, attending for treatment. Hair analyses showed no differences in zinc concentrations but higher concentrations of copper, lead, and cadmium were present, when compared to control, normal readers. Measurement of zinc in sweat was a more useful guide to clinical zinc deficiency than hair or serum analyses. The authors theorize that zinc deficiency in the mother might predispose to developmental dyslexia (Grant E. C. G., et al, 1988). Mineral analyses, especially zinc, may be warranted in children with learning disorders, but the need for adequate controls and appropriate specimen collection is emphasized. Treatment based on inaccurate measurement techniques may lead to toxicity. Other therapies? In addition to dietary methods of treatment, other alternative therapies for ADHD and learning disorders have included behavior modification and family counseling, biofeedback techniques, optometric visual training, sensory integrative therapy, central auditory training, and music, especially Mozart. Scientific studies have provided some support for the use of these therapies as part of the multimodal management of ADHD. CONCLUSION: Dietary management should be complementary, not an alternative therapy for ADHD. A parent of a child with ADHD should embrace recommended therapies of proven value, including medications such as Ritalin®, when used conservatively. Adverse reactions to stimulant drugs may by avoided by careful attention to dosage and frequent monitoring of the response by a physician. Of the various alternative methods of management of ADHD proposed, diet is perhaps the most important and the most neglected. Doctor Theodore TePas, NOHA Professional Advisory Board member, in his excellent article on ADHD (NOHA NEWS, Fall 1996), stresses the need for an increased interest of physicians in the dietary and nutritional aspects of learning and behavior.
Despite problems with proof of efficacy and the rigors of some dietary restrictive regimens, the potential adverse effects of certain food items and additives should not be ignored. By attention to the diet as complementary to proven medications, not as alternative therapy, a more favorable long-term outcome may be expected. Furthermore, the necessity for substitution of more toxic or experimental therapies may be avoided. Shakespeare’s Hamlet has appropriate advice for doctors treating ADHD, given by Polonius to Laertes, and paraphrased as follows:
BIBLIOGRAPHY AND REFERENCES Conners, C. K., et al, "The effects of sucrose on children with attention deficit," In: Diet and Behavior, Lubbock, Texas, Texas University Press, 1984. Cott, A., "Megavitamins: The orthomolecular approach to behavioral disorders and learning disabilities," Academic Therapy, 7:245, 1972. Egger, J., et al, "Controlled trial of hyposensitization in children with food-induced hyperkinetic syndrome," Lancet, 339:1150-3, 1992. Feingold, B. F., Why Your Child Is Hyperactive, New York, Random House, 1975. Grant, E. C. G., et al, "Zinc deficiency in children with dyslexia: concentrations of zinc and other minerals in sweat and hair," British Medical Journal, 296:607-9, 1988. Gschwend, S., et al, "Effects of acute hyperglycemia on mental efficiency and counterregulatory hormones in adolescents with insulin-dependent diabetes mellitus," Journal of Pediatrics, 126:178-84, 1995. Harley, J. P. et al, "Hyperkinesis and food additives: Testing the Feingold hypothesis," Pediatrics, 61:818-28,1978. Harley, J. P. et al, "Synthetic food colors and hyperactivity in children. Double- blind challenge experiment," Pediatrics, 62:975-83, 1978. Hynd, G., and M. Cohen, Dyslexia. Neuropsychological Theory, Research, and Clinical Differentiations, New York, Grune and Stratton, 1983. Jones, T. W., et al, "Enhanced adrenomedullary response and increased susceptibility to neuroglycopenia: Mechanisms underlying the adverse effects of sugar ingestion in healthy children," Journal of Pediatrics, 126:171-7, 1995. Kaplan, B. J., et al, "Dietary replacement in preschool-aged hyperactive boys," Pediatrics, 83:7-17, 1989. Krnesi, M. J. P., et al, "Effects of sugar and aspartame on aggression and activity in children," American Journal of Psychiatry, 144:1487-90, 1987. Millichap, J. G., Nutrition, Diet, and Your Child’s Behavior, Springfield, Illinois, Charles C. Thomas, 1986. Millichap, J. G., Environmental Poisons in Our Food, Chicago, PNB Publishers, 1993. Millichap, J. G., Progress in Pediatric Neurology I, II, & III, Chicago, PNB Publishers, 1991, 1994, &1997. Millichap, J. G., and N. M. Millichap, Dyslexia As the Neurologist and Educator Read It, Springfield, Illinois, Charles C. Thomas, 1986. Mitchell, E. A., et al, "Clinical characteristics and serum essential fatty acid levels in hyperactive children," Clinical Pediatrics, 26:406-11, 1987. Olney, J. W., et al, "Increasing brain tumor rates: Is there a link to aspartame?" Journal of Neuropathology and Experimental Neurology, 55:1115-23, 1996. Pauling, L., "Orthomolecular psychiatry," Science, 160:265, 1968. Platel, H., et al, "The structural components of music perception. A functional anatomical study," Brain, 120:229-43, 1997. Rosen, L. A. et al, "Effects of sugar (sucrose) on children’s behavior," Journal of Consulting Clinical Psychology, 56:583-9, 1988. Rowe, K. S., "Synthetic food colorings and ‘hyperactivity’: A double-blind crossover study," Australian Pediatrics, 24:143-7, 1988. Rowe, K. S., and K. J. Rowe, "Synthetic food coloring and behavior: A dose response effect in a double-blind, placebo-controlled, repeated-measure study," Journal of Pediatrics, 125:691-8,1994. Saravis, S., et al, "Aspartame effects on learning, behavior and mood," Pediatrics, 86:75-83, 1990. Sarnthein, J., et al, "Persistent patterns of brain activity: An EEG coherence study of the positive effect of music on spacial-temporal reasoning," Neurological Research, 19:107-16, 1998. Shaywitz, B. A., et al, "Aspartame, behavior, and cognitive function in children with attention deficit disorder," Pediatrics, 93:70-5, 1994, Smid, H. G. O. M., et al, "Differentiation of hypoglycemia induced cognitive impairments. An electrophysiological approach," Brain, 120:1041-56,1997. Stordy, B. J., "Benefit of docosahexaenoic acid supplements to dark adaptation in dyslexics," Lancet, 346:385, 1995. Wender, E. H., and M. V. Solano, "Effects of sugar on aggressive and inattentive behavior in children with attention deficit disorder with hyperactivity and normal children." Pediatrics, 88:960-6, 1991. Wolraich, M. L., et al, "Behavior and cognitive performance of children unaffected by sucrose or aspartame," New England Journal of Medicine, 330:301-7,1994. Yehuda, S., "Brain biochemistry and behavior," Nutrition Reviews, Supplement, 44:1-250, May, 1986. Yehuda, S., "Brain biochemistry and behavior,:"International Journal of Neuroscience, 35: 21-36, 1987. Young, E., et al, "Prevalence of food additive intolerance in the UK," Journal of the Royal Society of Medicine, 21:241-7, 1987. ___________ *Dr. Millichap has selected and adapted material and references for this article from his new book, Attention Deficit Hyperactivity and Learning Disorders: Questions and Answers , PNB Publishers, P. O. Box 11391, Chicago, Illinois,1998, 253 pages, ISBN 0-9629115-4-2, soft cover, $14.95) Article from NOHA NEWS, Vol. XXIV, No. 1, Winter 1999, pages 5-10. |