| Elevated prenatal homocysteine levels as a risk factor for schizophrenia. | |
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MedLine Citation:
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PMID: 17199052 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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CONTEXT: Elevated prenatal homocysteine level is a plausible risk factor for schizophrenia because of its partial antagonism of N-methyl-D-aspartate receptors under physiologic glycine concentrations and its association with abnormal placental function and pregnancy complications. OBJECTIVE: We examined whether elevated maternal levels of homocysteine during the third trimester were associated with adult schizophrenia risk. DESIGN: Nested case-control study of a large birth cohort, born from 1959 through 1967 and followed up for schizophrenia from 1981 through 1997. SETTING: Population-based birth cohort and health plan. PARTICIPANTS: Cases (n = 63) were diagnosed with schizophrenia and other spectrum disorders (mostly schizophrenia and schizoaffective disorder). Controls (n = 122) belonged to the birth cohort; had not been diagnosed with a schizophrenia spectrum or major affective disorder; and were matched to cases on date of birth, sex, length of time in the cohort, and availability of maternal serum samples. MAIN MEASURES: Archived maternal serum samples were assayed for homocysteine levels during pregnancies of cases and matched controls. RESULTS: In a model that tested for a threshold effect of third-trimester homocysteine levels, an elevated homocysteine level was associated with a greater than 2-fold statistically significant increase in schizophrenia risk (odds ratio, 2.39; 95% confidence interval, 1.18-4.81; P = .02). CONCLUSIONS: These findings indicate that elevated third-trimester homocysteine levels may be a risk factor for schizophrenia. Elevated third-trimester homocysteine levels may elevate schizophrenia risk through developmental effects on brain structure and function and/or through subtle damage to the placental vasculature that compromises oxygen delivery to the fetus. If future studies both replicate this association and support a causal link, then the use of folic acid supplementation would merit evaluation as a strategy for prevention of schizophrenia in offspring. |
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Authors:
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Alan S Brown; Teodoro Bottiglieri; Catherine A Schaefer; Charles P Quesenberry; Liyan Liu; Michaeline Bresnahan; Ezra S Susser |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Archives of general psychiatry Volume: 64 ISSN: 0003-990X ISO Abbreviation: Arch. Gen. Psychiatry Publication Date: 2007 Jan |
Date Detail:
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Created Date: 2007-01-02 Completed Date: 2007-02-28 Revised Date: 2012-05-11 |
Medline Journal Info:
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Nlm Unique ID: 0372435 Medline TA: Arch Gen Psychiatry Country: United States |
Other Details:
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Languages: eng Pagination: 31-9 Citation Subset: AIM; IM |
Affiliation:
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College of Physicians and Surgeons of Columbia University and New York State Psychiatric Institute, 1051 Riverside Drive, New York, NY 10032, USA. asb11@columbia.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Case-Control Studies Child Child of Impaired Parents / statistics & numerical data Cohort Studies Female Homocysteine / blood*, metabolism, physiology Humans Maternal-Fetal Exchange / physiology Pregnancy Pregnancy Trimester, Third / blood Prenatal Exposure Delayed Effects* Psychotic Disorders / epidemiology, etiology, metabolism Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors, blood Risk Factors Schizophrenia / epidemiology*, etiology, metabolism |
| Grant Support | |
ID/Acronym/Agency:
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1K02 MH 65422-01/MH/NIMH NIH HHS; 1R01 MH 63264-01A1/MH/NIMH NIH HHS; K02 MH065422/MH/NIMH NIH HHS; N01 HD 13334/HD/NICHD NIH HHS; N01 HD 63258/HD/NICHD NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Receptors, N-Methyl-D-Aspartate; 454-28-4/Homocysteine |
| Comments/Corrections | |
Comment In:
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Arch Gen Psychiatry. 2007 Aug;64(8):980-1
[PMID:
17679645
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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