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 A Role for Food Intolerance in Childhood Migraine  
 
The following is one in an ongoing series of columns entitled Dr. Galland's Integrated Medicine by . View all columns in series

(6) Because valid dietary testing requires that a food substance be absorbed through the usual pathway at the usual rate, each food must be tested in the form in which it is normally consumed.

Based on these principles, Egger, Carter and Soothill developed a standard diagnostic protocol and used it for two trials. In the first they studied childhood migraine 45, in the second hyperkinetic syndrome/attention deficit disorder46. All stages of the work were carried out while the children lived at home. The response of children to the diagnostic diet and reintroduction of foods were first determined by open experiment. The initial oligoantigenic diet was followed for four weeks. It consisted of one meat (chicken, lamb or turkey), one starch (potatoes or rice), one fruit (apples, pears or bananas), one vegetable from the brassica family, sunflower oil, a multivitamin, calcium and mineral water. The results were assessed by parents at home and by doctors during visits to the clinic. At the conclusion of the open phase of the trials, each child was considered to be food-intolerant if he remained symptom-free on the oligoantigenic diet and relapsed with addition of specific foods. To be included in the second phase, each child had to remain symptom-free by avoiding only those foods to which he was thought to be reactive. In phase two, the results of the open trial were tested in a double-blind, placebo-controlled cross-over experiment. One food to which the child had reacted in the open trial was consumed daily for a week, in a disguised form, indistinguishable from placebo, in quantities which the child would normally eat. The base in which the foods were hidden consisted of rice flour, carrot or banana, caramel, onion and salt or cane sugar and citric acid. Accuracy of blinding was assessed by the investigators. Only 5% of parents were able to correctly separate placebo and active challenge food by taste or smell. Most parents were unable to distinguish one substance from another and 12% guessed incorrectly.

The migraine study involved 40 boys and 48 girls, aged 3 to16, with headaches occurring at least once a week for six months to eleven years (mean 3.73 years), associated with two of the following symptoms: pallor, photophobia, dizziness, nausea, abdominal pain, visual disturbances or focal neurologic deficits. Classical migraine was the diagnosis in 39, common migraine in 49. During the open trial, 78 children (89%) became symptom-free and 4 children greatly improved. Relapse with refeeding of specific foods occurred in 90% of the responders. The interval between exposure and provocation varied from one hour to one week but averaged two to three days. The number of foods which provoked headache ranged from one to twenty-four. The frequency with which specific foods provoked headache is shown in Table 1. Forty children were selected for the double-blind placebo-controlled crossover study, the results of which are summarized in Table 2. This trial confirmed 65% of the food reactions identified in the open trial, using the strictest criteria available for clinical studies. Considering the total group of 88 children with severe and frequent migraine, 52% were shown to be intolerant of specific foods in this experiment. It is of note that when children were maintained on a dietary regime devoid of provoking foods, they were also resistant to other, non-specific triggers which had previously been thought to activate migraines, such as emotional distress, physical activity and temperature change.

When the trial of children with attention deficit disorder produced similarly dramatic results, the findings were challenged by Professor P. J. Graham in the Department of Psychiatry at Great Ormond Street and Dr. Eric Taylor, Head of Child Psychology at the Maudsley Hospital. A second study involving hyperkinetic children was instituted at Great Ormond Street, with the sceptical participation of Graham and Taylor, and the results of the first study were confirmed47.

Table 2. Results of double-blind placebo-controlled
cross-over trial, 40 children, one food each
(Egger et al, Lancet 1983)

Trigger

A-P P-A Total
Neither food 2 6 8
Active food 14 12 26*
Placebo food 0 2 2*
Both foods 1 3 4

Soothill's group also studied 36 children with refractory epilepsy, half of whom suffered from migraine and half of whom did not. None of the children Nvith epilepsy alone responded to diet but 89% of the children with both epilepsy and migraine showed improvement in both sezures and headaches during the oligoantigenic diet48. The strong association between reactions to cow's milk and cow's cheese but not sheep cheese was interpreted by the authors as indicating an allergic mechanism rather than a biochemical mechanism.

Four other studies performed in children have since found a positive effect of oligoantigenic diets in migraine, although none attempted to confirm their findings with a double-blind placebo-controlled followup49-52. In all studies, long term improvement in frequency mid severity of headache was achieved by those children who complied with the specific food elimination diet., but compliance was often difficult. In some cases, re-exposure after prolonged avoidance (e.g. two years) was no longer associated with provocation of symptoms, indicating a loss of sensitivity.

HYPOSENSITIZATION FOR FOOD-INDUCED MIGRAINE

In 1992. Egger, McEwen an J. Stolla completed a double-blind placebo-controlled trial of immunologic hyposensitization for children with food-induced migraine at Universitatskinderklinik, Munich (unpublished results). Children with frequent severe migraine were initially selected by the methods used in the study of diet and pediatric migraine at Great Ormond Street, ie freedom from headache during the oligoantigenic diet period and provocation of headache upon exposure to individual foods. Participation in the hyposensitization trial was offered to children who fulfilled these criteria but for whom a safe diet was unacceptably restricted. The active treatment consisted

of an intradermal injection of food antigens mixed with the enzyme beta-glucuronidase, a technique developed by McEwen called Enzyme-Potentiated Desensitization (EPD)53. A parallel. study of EPD in food-sensitive hyperkinetic children was conducted at the same time; the protocols were the same in both trials54.

Forty children took part in the double-blind placebo-controlled trial of hyposensitization for migraine, each receiving an injection of placebo or active material every eight to ten weeks for a total of three injections. Provoking foods were

Table 3
Enzyme-potentiated densensitization for childhood migraine, response to double-blind, placebo-controlled trial
EPD Placebo
Food tolerant 16 5
Still reactive 2 10
Inconclusive 0 1
Dropped out 2 4
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 About The Author
Leo Galland, M.D. has received international recognition as a leader in the field of Nutritional Medicine for the past 20 years. A board-certified internist, Dr. Galland is a Fellow of the......moreLeo Galland MD, FACN
 
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