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More light on migraine
fd Cormrr. Joxicol. Vol. 19. pp. 393 to 403. 1981 printed in Great Britain
Wl5-6264i81/030393-I lSO2.00,U Pcrgamon Press Lid
ABSTRACTS AND COMMENTS FOOD AND FOOD ADDITIVES More light on migraine Monro, J., Brostoff, J., Car%, C. & Zilkha, K. (1980). Food allergy in migraine. Study of dietary exclusion and RAST. Lancer II, 1. Food allergy is considered by many to be a cause of migraine, and the study cited above adds to the evidence that has accumulated in support of this theory. In the first phase of the study, 47 patients with severe migraine were given rotation and elimination diets for 2 yr. Of the 33 patients who completed the study, migraine-provoking foods were identified for 23, no dietary factors were found in six cases,and in four, food factors were suspected but eliminating them from the diet did not help. In the 23 subjects for whom migraine-provoking foods were identified, the elimination of those foods from the diet resulted in relief from the migraine within 2 wk. The relief was usually complete. At the end of the phase, tests were carried out for specific IgE antibodies to foods using radioallergosorbent tests (RAST). A good correlation was observed between high RAST values and the foods identified by the elimination diets in the 23 patients, although RAST values to other foods were higher than normal. All six patients for whom dietary factors were not detected showed low RAST values. The foods tested were milk, cheese, eggs, chocolate, tea, coffee, fish, shellfish, wheat, rice, tomato, apple and orange, and it was found that patients were generally allergic to more than one food group (usually three). In the second phase of the study the predictive value of RAST was investigated in 26 patients. Foods with the highest RAST titre were eliminated from the patients’ diets. Only three of the subjects failed to benefit from the elimination diets. A group of ten patients was challenged with identified migraineinducing foods after pretreatment with oral sodium cromoglycate. One was completely protected by 4OOmgsodium cromoglycate daily for 7 days before challenge, eight were partially protected by 800 or 1600mg daily, and one remained unprotected (but also did not keep to his diet). It is suggested that the initial specificallergic reaction in the gut may increase mucosal permeability, which in turn allows food antigens,complexes or mediators to be absorbed, provoking the migraine syndrome.
Within a period of 1 month, methaemoglobinaemia was diagnosed in a group of nine infants in an Israeli paediatric ward. Whereas typical neonates have methaemoglobin levels in the blood some two to five times the normal adult figure of I%, the average level in these nine, who were all 6-15 weeks old was 18%. All the infants had recently recovered from a bout of acute gastroenteritis and had as a precaution been fed Hyprovit, a brand of soya-bean product formulated for babies with milk allergy or lactose and sucrose intolerance. Replacing the Hyprovit with cows’ milk or other infant formulas led to a rapid return to normal methaemoglobin levels. Although Hyprovit had been sold in Israel for about 1Oyr without any reported toxicological problems, the. fact that signs of methaemoglobin returned in those particular infants with its reintroduction into the diet strongly suggestedthat it was the cause of the observed effects. In an attempt to confirm these suspicions, a number of the components of the Hyprovit, including soya-bean concentrate, vitamins and minerals were given separately to some of these infants and to several other babies of the same age group, but this produced no toxic effects. Enquiries to the suppliers of the fatty component, soya-bean oil, revealed a recent change in the oil’s antioxidant to a BHABHT-propyl gallate mixture. On ethical grounds, the investigators could not justify feeding the soya-bean oil containing this mixture to infants; however as no further casesof methaemoglobinaemia were reported once these antioxidants were removed from the Hyprovit, they felt the circumstantial evidence of guilt was sufficient. Of the three antioxidants, propyl gallate was favoured as the specific causative agent, because the structurally related pyrogallol had been implicated as a methaemoglobinaemic agent by an earlier report (Konrady, Arch. Tox. 1936, 7, 179). Although the affected infants were shown to have a fully functional methaemoglobin-reductase systemreduced diphosphopyridine nucleotide diaphorase in the red blood cells was in the normal range-the fact that haem iron of foetal haemoglobin is known to be susceptible to oxidation could well predispose the newborn to methaemoglobinaemia. Furthermore, it has long been known that neonates have a lower metabolic capability than do older infants and therefore xenobiotics requiring metabolism prior to excrePremature antioxidant ingestion tion could be present for a relatively long period in Nitzan, M., Volovitz, B. & Topper, E. (1979). Infantile the blood. Both these factors may explain why two methemoglobinemia caused by food additives. C/in. older babies (each about 6 months old) at the hospital Toxicol. 15, 273. in question did not develop overt signs of toxicity Methaemoglobin, formed when the iron of haemo- when fed the suspect soya-bean preparation. [British babies should be protected from a fate globin is oxidized to the ferric state, cannot interact with oxygen, and its presencein the blood is therefore similar to that which befell these Israeli infants. The potentially life-threatening. The paper cited above UK food additive regulations do not permit the use of describesan outbreak of toxic methaemoglobinaemia BHA, BHT or the gallates in food specifically desigamongst hospitalized infants. nated for babies.] 393
Wl5-6264i81/030393-I lSO2.00,U Pcrgamon Press Lid
ABSTRACTS AND COMMENTS FOOD AND FOOD ADDITIVES More light on migraine Monro, J., Brostoff, J., Car%, C. & Zilkha, K. (1980). Food allergy in migraine. Study of dietary exclusion and RAST. Lancer II, 1. Food allergy is considered by many to be a cause of migraine, and the study cited above adds to the evidence that has accumulated in support of this theory. In the first phase of the study, 47 patients with severe migraine were given rotation and elimination diets for 2 yr. Of the 33 patients who completed the study, migraine-provoking foods were identified for 23, no dietary factors were found in six cases,and in four, food factors were suspected but eliminating them from the diet did not help. In the 23 subjects for whom migraine-provoking foods were identified, the elimination of those foods from the diet resulted in relief from the migraine within 2 wk. The relief was usually complete. At the end of the phase, tests were carried out for specific IgE antibodies to foods using radioallergosorbent tests (RAST). A good correlation was observed between high RAST values and the foods identified by the elimination diets in the 23 patients, although RAST values to other foods were higher than normal. All six patients for whom dietary factors were not detected showed low RAST values. The foods tested were milk, cheese, eggs, chocolate, tea, coffee, fish, shellfish, wheat, rice, tomato, apple and orange, and it was found that patients were generally allergic to more than one food group (usually three). In the second phase of the study the predictive value of RAST was investigated in 26 patients. Foods with the highest RAST titre were eliminated from the patients’ diets. Only three of the subjects failed to benefit from the elimination diets. A group of ten patients was challenged with identified migraineinducing foods after pretreatment with oral sodium cromoglycate. One was completely protected by 4OOmgsodium cromoglycate daily for 7 days before challenge, eight were partially protected by 800 or 1600mg daily, and one remained unprotected (but also did not keep to his diet). It is suggested that the initial specificallergic reaction in the gut may increase mucosal permeability, which in turn allows food antigens,complexes or mediators to be absorbed, provoking the migraine syndrome.
Within a period of 1 month, methaemoglobinaemia was diagnosed in a group of nine infants in an Israeli paediatric ward. Whereas typical neonates have methaemoglobin levels in the blood some two to five times the normal adult figure of I%, the average level in these nine, who were all 6-15 weeks old was 18%. All the infants had recently recovered from a bout of acute gastroenteritis and had as a precaution been fed Hyprovit, a brand of soya-bean product formulated for babies with milk allergy or lactose and sucrose intolerance. Replacing the Hyprovit with cows’ milk or other infant formulas led to a rapid return to normal methaemoglobin levels. Although Hyprovit had been sold in Israel for about 1Oyr without any reported toxicological problems, the. fact that signs of methaemoglobin returned in those particular infants with its reintroduction into the diet strongly suggestedthat it was the cause of the observed effects. In an attempt to confirm these suspicions, a number of the components of the Hyprovit, including soya-bean concentrate, vitamins and minerals were given separately to some of these infants and to several other babies of the same age group, but this produced no toxic effects. Enquiries to the suppliers of the fatty component, soya-bean oil, revealed a recent change in the oil’s antioxidant to a BHABHT-propyl gallate mixture. On ethical grounds, the investigators could not justify feeding the soya-bean oil containing this mixture to infants; however as no further casesof methaemoglobinaemia were reported once these antioxidants were removed from the Hyprovit, they felt the circumstantial evidence of guilt was sufficient. Of the three antioxidants, propyl gallate was favoured as the specific causative agent, because the structurally related pyrogallol had been implicated as a methaemoglobinaemic agent by an earlier report (Konrady, Arch. Tox. 1936, 7, 179). Although the affected infants were shown to have a fully functional methaemoglobin-reductase systemreduced diphosphopyridine nucleotide diaphorase in the red blood cells was in the normal range-the fact that haem iron of foetal haemoglobin is known to be susceptible to oxidation could well predispose the newborn to methaemoglobinaemia. Furthermore, it has long been known that neonates have a lower metabolic capability than do older infants and therefore xenobiotics requiring metabolism prior to excrePremature antioxidant ingestion tion could be present for a relatively long period in Nitzan, M., Volovitz, B. & Topper, E. (1979). Infantile the blood. Both these factors may explain why two methemoglobinemia caused by food additives. C/in. older babies (each about 6 months old) at the hospital Toxicol. 15, 273. in question did not develop overt signs of toxicity Methaemoglobin, formed when the iron of haemo- when fed the suspect soya-bean preparation. [British babies should be protected from a fate globin is oxidized to the ferric state, cannot interact with oxygen, and its presencein the blood is therefore similar to that which befell these Israeli infants. The potentially life-threatening. The paper cited above UK food additive regulations do not permit the use of describesan outbreak of toxic methaemoglobinaemia BHA, BHT or the gallates in food specifically desigamongst hospitalized infants. nated for babies.] 393