Methionine Effects on Chronic Schizophrenics: Patients Treated With Monoamine Oxidase Inhibitors

Introduction  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