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April 1965

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

Author Affiliations

From the Johns Hopkins University, Assistant Professor of Psychiatry (Dr. Park); and from the Laboratory of Clinical Science, National Institute of Mental Health (Dr. Baldessarini); and National Institute of Mental Health, National Institutes of Health, US Department of Health, Education, and Welfare, Chief, Laboratory of Clinical Science. (Dr. Kety).
Rubel, Durell, and Kety, unpublished observations.
Dr. Albert A. Kurland, Director of Research, Department of Mental Hygiene, Maryland, cooperated in this study. Mr. Kenneth McCusker and Mrs. Kester Johnson of the Spring Grove Research Staff gave assistance.
Hoffman-LaRoche, Inc., supplied the medications.

Arch Gen Psychiatry. 1965;12(4):346-351. doi:10.1001/archpsyc.1965.01720340018003

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

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