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Schizophrenia Bulletin Advance Access originally published online on July 17, 2008
Schizophrenia Bulletin 2008 34(6):1083-1094; doi:10.1093/schbul/sbn080
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© The Author 2008. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Gene-Environment Interaction and Covariation in Schizophrenia: The Role of Obstetric Complications

Vijay A. Mittal2,4, Lauren M. Ellman3 and Tyrone D. Cannon1,2,4
2 Department of Psychiatry and Biobehavioral Sciences, University of California Los Angeles, Los Angeles, CA
3 Department of Psychiatry, Columbia University, New York, NY
4 Department of Psychology, University of California Los Angeles, Los Angeles, CA

1 To whom correspondence should be addressed; Department of Psychology, University of California Los Angeles, 1285 Franz Hall, Los Angeles, CA 90095-6968; tel: 310-206-8765, fax: 310-794-9740, e-mail: cannon{at}psych.ucla.edu.

While genetic factors account for a significant proportion of liability to schizophrenia, a body of evidence attests to a significant environmental contribution. Understanding the mechanisms through which genetic and environmental factors coalesce in influencing schizophrenia is critical for elucidating the pathways underlying psychotic illness and for developing primary prevention strategies. Although obstetric complications (OCs) remain among the most well-documented environmental indicators of risk for schizophrenia, the pathogenic role they play in the etiology of schizophrenia continues to remain poorly understood. A question of major importance is do these factors result from a genetic diathesis to schizophrenia (as in gene-environment covariation), act additively or interactively with predisposing genes for the disorder in influencing disease risk, or independently cause disease onset? In this review, we evaluate 3 classes of OCs commonly related to schizophrenia including hypoxia-associated OCs, maternal infection during pregnancy, and maternal stress during pregnancy. In addition, we discuss several mechanisms by which OCs impact on genetically susceptible brain regions, increasing constitutional vulnerability to neuromaturational events and stressors later in life (ie, adolescence), which may in turn contribute to triggering psychosis.

Keywords: schizophrenia / obstetric complications / gene-environment interaction / covariation / hypoxia / infection / stress / rGE / G x E


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