Abstract
IT HAS been proposed that schizophrenia is a consequence of metabolic abnormalities associated with endogenous production of psychotogenic compounds. The original hypothesisi noted the chemical similarity between adrenaline and mescaline, and postulated an abnormal methylation of adrenaline as the source of the psychotoxin. Since then, methylation processes have been implicated by a number of studies: the controversial finding of dimethoxyphenethylamine (DMPEA) in the urine of schizophrenics;2 the similarity of many psychotomimetic compounds to known methylated metabolites of norepinephrine;s the differential metabolism of the methoxyl groups of DMPEA;4 the claimed improvement of schizophrenics after administration of the methyl acceptor nicotinamide;s and exacerbation of the disease by administration of the methyl donor methionine.617 The involvement of aromatic amines in affective disorders has recently been reviewed,8 although methylation reactions have not been strongly implicated. Since the major methyl donor for methylation processes within the body is methionine, we decided to study an aspect of the metabolism of the S-methyl moiety of this compound in patients with schizophrenic and affective disorders.
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