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Volume 38, No. 2

Attention Deficit, Hyperactivity, and Learning Disorders: A Scientific Appraisal of Dietary Therapies

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:

  • Sugar-restricted diet.
  • Additive and salicylate-free diet.
    (Some foods contain salts of salicylic acid.)
  • Oligoantigenic diet (eliminates
    many sensitizing food allergens and antigens).
  • Ketogenic diet (High fat/low carbohydrate
    diet causes ketones to appear in the urine.).
  • Fatty acid supplements.
  • Orthomolecular and megavitamin
    therapy.
  • Mineral and trace element treatment.

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:

"Fish, Oils, and Vision", Fall 1987; "Breast Milk
Enhances Intelligence," (DHA, which is accumulated in large amounts
in the brain and retina, is in breast milk and not in formula.), Summer
1992; "Food: The Driving Force of Evolution," (The "neural"
fatty acids are emphasized. One quote: "The most polyunsaturated
fatty acid (docosahexaenoic acid, from the omega 3 family) makes up
60 per cent of the structure of the photo receptors in the eye. One
part of this structure can send ‘10,000 signals approximately every
1/25 of a second to the corresponding network of brain cells.’ (IBM
and Apple take notice!)"), also, "Stalking the Essential
Fatty Acids," Fall 1991; "Food for Thought," (Both
DHA and arachidonic acid are essential for the evolution of the human
brain.), Summer 1995.

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:

Those drugs thou hast, and their adoption tried,

Grapple them to thy soul with hoops of steel;

But do not dull thy palm with entertainment

Of each new-hatch’d, unfledged remedy.


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.

BIBLIOGRAPHY AND REFERENCES

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attention deficit," In: Diet and Behavior, Lubbock, Texas,
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Cott, A., "Megavitamins: The orthomolecular approach to behavioral
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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:
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Gschwend, S., et al, "Effects of acute hyperglycemia on mental efficiency
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Harley, J. P. et al, "Hyperkinesis and food additives: Testing the
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Hynd, G., and M. Cohen, Dyslexia. Neuropsychological Theory, Research,
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Jones, T. W., et al, "Enhanced adrenomedullary response and increased
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Millichap, J. G., and N. M. Millichap, Dyslexia As the Neurologist
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Platel, H., et al, "The structural components of music perception.
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Rosen, L. A. et al, "Effects of sugar (sucrose) on children’s behavior,"
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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
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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, Winter 1999

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