Schizophrenia and impaired homocysteine metabolism: a possible association

Abstract

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