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Related Experiment Videos

Methylation hypothesis.

R J Baldessarini, G Stramentinoli, J F Lipinski

    Archives of General Psychiatry
    |March 1, 1979
    PubMed
    Summary
    This summary is machine-generated.

    L-Methionine supplementation did not affect behavior in humans or increase blood S-adenosylmethionine levels. The study found no support for the methylation hypothesis in treating psychotic disorders.

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    Area of Science:

    • Biochemistry
    • Neuroscience
    • Pharmacology

    Background:

    • The methylation hypothesis proposes that altered methylation processes contribute to psychotic disorders.
    • S-adenosylmethionine (SAMe) is a key methyl donor, and L-methionine is its precursor.

    Purpose of the Study:

    • To investigate the effects of L-methionine and S-adenosylmethionine on methylation processes in biological systems.
    • To evaluate the validity of the methylation hypothesis in the context of idiopathic psychotic disorders.

    Main Methods:

    • Administration of L-methionine and S-adenosylmethionine to humans, rats, and rabbits.
    • Measurement of S-adenosylmethionine levels in blood and liver.
    • Assessing the methylation of levodopa and production of dimethyltryptamine.

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  • Investigating the role of methyl acceptors and S-adenosylhomocysteine.

    • Main Results:

    • L-methionine did not alter behavior or blood SAMe in humans; it significantly increased rat liver SAMe.
    • High doses of methionine or SAMe had minimal impact on levodopa methylation in rodents.
    • Methionine and SAMe decreased dimethyltryptamine production in rabbit lungs, potentially via S-adenosylhomocysteine inhibition.
    • S-adenosylhomocysteine strongly inhibited dopa methylation in rats.

    Conclusions:

    • The study's findings do not support key predictions of the methylation hypothesis for psychotic disorders.
    • The observed clinical worsening effects of methionine in schizophrenia remain unexplained by these results.