Hyperactivity, attention deficit and other so called mental disorders of childhood may simply be an outcome of poor nutrition.

One of the biggest growth areas in medicine, particularly in America, is the problem child. Instead of “hard to handle”, his symptoms now go by a variety of masterful medical euphemisms hyperactivity, attention deficit, hyperkinesis, minimal brain damage, minimal cerebral dysfunction and, Attention Deficit Hyperactivity Syndrome. These labels, all redolent of serious organic pathology, are shorthand for the type of child who just cannot sit still, cannot concentrate, has a difficult time settling down to eat or sleep, cannot adapt to new situations, overreacts to new stimuli and, through his unpredictable, impulsive and often destructive behaviour, makes life a hell on earth for every other member of the family.

The standard therapy for hyperactivity, particularly in America, is drugs central nervous stimulants like methylphenidate (Ritalin), which have a paradoxical effect on children. Instead of hyping them up, stimulants in general (including caffeine) drug them into a calmed, soporific state. And now the most recent tack taken by medicine is to blame it on genes. One recent study (New England Journal of Medicine, 8 April 1993) concluded that hyperactive children have something in their makeup that causes them to have a “generalized resistance” to thyroid hormone. In other words, they’re restless because their thyroid gland isn’t regulating properly.

In 1973 the late American pediatrician and allergist Ben Feingold introduced the then ground breaking theory that foods containing salicylates, aspirin like substances such as artificial colours and artificial flavours, were mainly responsible for hyperactivity. He found that reducing a child’s intake of sugar or artificial additives or locating possible allergies could help. Although study after study backs Feingold’s theories, many standard medics still label his approach a fad and are happier to reach for the prescription pad and sentence a small child to many years of stupefying, potentially addictive medication.

What the standard medical approach fails to consider is that hyperactivity doesn’t stem from a single cause. Dr Sidney M Baker, director of the Gesell Institute of Human Development in New Haven, Connecticut, who has worked with many learning disabled and hyperactive children, emphasizes that short attention spans and impulsive, restless behaviour are indicative of “individual chemical imbalance” anything from nutritional shortages to constant exposure to allergens or food additives, a situation often exacerbated by the typical American or British child’s constant consumption of “altered, adulterated, sweetened, fatty and refined foods”. Anyone faced with a hyperactive child, says Dr Baker, has to do a great deal of detective work with a trained practitioner to find out both what is lacking and what the child might be getting too much of.

Dr Melvyn R Werbach, assistant clinical professor at University of California at Los Angeles’ School of Medicine, has spent years studying the effect of nutrition on a variety of so called mental illnesses, including childhood hyperactivity. In his book Nutritional Influences on Mental Illness (Third Line Press, Tarzana, CA) he has compiled a source book of all clinical research published on nutritional influences on hyperactivity, among other disorders. The following is a summary of his findings (noted with full medical references). Keep in mind that these findings are meant to be a sourcebook, not a treatment manual. Any readers wishing to use nutritional therapy should work in tandem with a trained professional, who will carefully consider a patient’s dietary history, discover nutritional deficiencies, and perform relevant lab tests before initiating treatment.

It seems that sugar itself isn’t so much the culprit as sugar ingested in place of a well balanced meal. C Keith Conners, director of behavioural research in the department of psychiatry at the Children’s Hospital National Medical Center in Washington, DC, was the first to suggest that the effect of sugar is modified by the foods consumed along with it. Conners and his cohorts found that when sugar is consumed alone, the effects are different from when it is consumed along with protein or starch or as part of a well balanced meal. The combination of sugar and starch in the absence of substantial protein (a combination found, for example, in children’s’ sweetened breakfast cereals) increased deviant behaviour, not only in children who were mentally disturbed, but also in normal children.

In one of Conners’ studies, three groups of hyperactive children between 8 and 13 received either a high carbohydrate breakfast, a high protein breakfast or no breakfast. On different days, children in each group also received a non nutritive orange drink sweetened with aspartame or sucrose. Children who received the high carbohydrate breakfast with the sucrose drink did significantly worse than controls on a recognition test, while those eating the high protein meal did substantially better than any other group (New Medical Science, December 1987).

Conners’ conclusion: hyperactive children may benefit from a high protein, low carbohydrate, sugar free diet.

Two other observational studies showed that hyperactive children process food more rapidly than others, are smaller than normal children and hence may need more protein than most (American Journal of Clinical Nutrition 39: 520-24, 1984)

In another study of children aged 4-7, the higher the ratio of carbohydrates to protein in their diets, the greater the destructive, aggressive and restless behaviour (J Consult Clin Psychol 48: 760-9, 1980).

Leo Galland, American nutritional expert on the diets of children, suggests that you cut all sugar out of your hyperactive child’s diet other than 4 oz of fruit juice and two pieces of fresh fruit a day.

Before trying drugs, first rule out food sensitivities and food additives. One study (The Lancet: 1: 540-5, 1985) showed that 62 out of 76 overactive children (that is, 82 per cent) treated with an elimination diet improved, and the behaviour of 21 more than a third became entirely normal. The most common offenders were invariably artificial colours and preservatives.

These results were confirmed in a double blind study of 10 hyperactive children, matched against 10 controls. Both were given a commercial orange drink, but the hyperactive group’s contained tartrazine. After 24 hours, there was a significant increase in urinary zinc in the hyperactive children receiving tartrazine, suggesting that the artificial colorant may bind with the zinc, causing more of it to be excreted. Furthermore, only the hyperactive children had any changes in behaviour or emotion. Four had severe reactions (two developed eczema and one asthma after 30-45 minutes), and five, moderate reactions (NI Ward et al, J Nutr Med 1: 51-57, 1990).

Other foods besides additives can provoke hyperactive like symptoms. Another experimental double blind study tested 13 hyperactive children against a matched set of 13 controls with 40 different food and inhalant allergens. The salicylates caused the greatest frequency of responses (80 per cent), while sugar, corn, beef and egg caused 25-30 per cent of responses, and cat hair and house dust, another 25 per cent (Int J Biosocial Res 4: 40-2, 1983).

Finally, another double blind study of 24 nonasthmatic children diagnosed as hyperactive found that 17 had allergic nasal symptoms or skin problems; 17, skin reactions to dust and pollen; and nine, a marked increase in activity after taking food dye. After an elimination diet, parents noted a moderate to marked improvement in 12 children for at least 12 weeks among 11, indefinitely (J Learn Disabil 11(6): 383-88, 1978).

Once you have ruled out food sensitivities, look to one of a number of nutritional deficiencies. In Werbach’s view, one important double blind, controlled study has confirmed the findings of a number of uncontrolled trials, suggesting that the symptoms of some hyperactive children are due to a deficiency of brain serotonin, the brain hormone which keeps us calm. Giving such children vitamin B6, or pyridoxine, which is required for the conversion of tryptophan to serotonin, has been shown to increase whole blood serotonin levels and in several studies, to be more effective than placebo.

In this controlled study (published in Biol Psychiatry 14 (5): 741-51, 1979) six hyperactive children with low whole blood serotonin experienced an increase in these levels after being given B6. The vitamin was more effective than methylphenidate in decreasing hyperactivity. Also, unlike the drug, the benefit of B6 continued after patients were switched to a placebo, suggesting that the B6 supplement corrected a deficiency.

“In all fairness, a related study, finding no benefit from B6 on hyperactivity, did appear as a letter to the editor in the New England Journal of Medicine four years later (309(21): 1328-9, 1983),” writes Dr Werbach.

“. . .However, its subjects were hyperkinetic children with normal blood serotonin levels, so the study did nothing to disprove the hypothesis that pyridoxine may benefit hyperkinetic children with low blood serotonin. ”

Dr Werbach cautions that megadoses of B6 can have adverse effects. He recommends starting with low dosages (50 mg of pyridoxine is a low dose for adults) of pyridoxal-5-phosphate, the “active coenzyme” form of vitamin B6, and then gradually raise the dosage, depending on changes in blood serotonin levels and behavioural response.

Besides vitamin B6, hyperactive children may be deficient in other nutrients or reacting to an excess exposure to toxic materials like lead (see box, right). The solution to your child’s problem behaviour may only be a matter of some careful detective work to locate the possible culprit or culprits.

Adapted from Nutritional Influences on Mental Illness by Dr Melvyn R Werbach (available for $44 from Third Line Press, 4751 Viviana Drive, Tarzana, CA 91356-5038 Tel: 818 996 4727 .

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