IN 1952, Osmond and Smythies and Harley-Mason suggested the possibility of a disturbance in transmethylation in schizophrenia.20 Subsequently, Hoffer and his associates administered niacin and niacinamide to chronic schizophrenic patients in the hope that these methyl acceptors would competitively inhibit other methylations. The clinical improvements which they saw14 have not been confirmed.Pollin et al22 administered large doses of 1methionine and ordinary doses of iproniazid to chronic schizophrenic patients to learn whether possible increases in amounts of methylated amines would potentiate a schizophrenic process. The monoamine oxidase inhibitor (MAOI) was expected to slow amine catabolism, and it was felt that the methionine load might favor the formation of methylated compounds15 by way of S-adenosylmethionine, shown by Cantoni6 to play a crucial role in biological transmethylations. They reported that 4 of their 12 patients demonstrated a
PARK LC, BALDESSARINI RJ, KETY SS. Methionine Effects on Chronic SchizophrenicsPatients Treated With Monoamine Oxidase Inhibitors. Arch Gen Psychiatry. 1965;12(4):346–351. doi:10.1001/archpsyc.1965.01720340018003
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