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Biol Psychiatry. 1998 Jul 15;44(2):141-3.

Schizophrenia and impaired homocysteine metabolism: a possible association.

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  • 1Department of Psychiatry, Columbia University, New York, New York, USA.



An increased risk of both schizophrenia and neural tube defects was observed in a birth cohort exposed to famine during early gestation. Neural tube defects have been related to a folate-sensitive genetic defect in homocysteine metabolism. If this were also true for schizophrenia, then cases with low folate (LF)--and only these cases--should have increased homocysteine levels compared with controls.


We compared homocysteine levels of schizophrenia cases and normal controls with low folate (LF) and without low folate (non-LF). Low folate was defined by the bottom tertile for controls.


In the LF group (6 cases, 8 controls), mean homocysteine was 10.7 microM in cases compared with 7.7 microM in controls (p = .03). In the non-LF group (11 cases, 16 controls) mean homocysteine did not differ for cases and controls.


These pilot data are compatible with the hypothesis that a folate-sensitive defect in homocysteine metabolism contributes to cases of schizophrenia.

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