Schizophrenia Bulletin Advance Access originally published online on August 20, 2008
Schizophrenia Bulletin 2008 34(6):1095-1105; doi:10.1093/schbul/sbn101
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Psychosocial Stress and Psychosis. A Review of the Neurobiological Mechanisms and the Evidence for Gene-Stress Interaction
2 Department of Psychiatry and Neuropsychology, EURON, South Limburg Mental Health Research and Teaching Network, Maastricht University Medical Centre, PO Box 616, 6200 MD Maastricht, The Netherlands
3 University Psychiatric Center Catholic University Leuven, Leuvensesteenweg 5173070 Kortenberg, Belgium
4 National and Kapodistrian University of Athens, Eginition Hospital, 74 Vas SofiasAvenue, Athens 11528, Greece
5 University Mental Health Research Institute, Athens, Greece
6 Division of Psychological Medicine, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK
7 School of Psychological Sciences, University of Manchester, Manchester, UK
1 To whom correspondence should be addressed; tel: +31-43-36-85-372, fax: +31-43-36-88-689, e-mail: ruud.vanwinkel{at}sp.unimaas.nl.
This article presents evidence suggesting that psychosocial stress may increase risk for psychosis, especially in the case of cumulative exposure. A heuristically useful framework to study the underlying mechanisms is the concept of "behavioral sensitization" that stipulates that exposure to psychosocial stress—such as life events, childhood trauma, or discriminatory experiences—may progressively increase the behavioral and biological response to subsequent exposures. The neurobiological substrate of sensitization may involve dysregulation of the hypothalamus-pituitary-adrenal axis, contributing to a hypothesized final common pathway of dopamine sensitization in mesolimbic areas and increased stress-induced striatal dopamine release. It is argued that, in order to reconcile genetic and environmental influences on the development of psychosis, gene-environment interactions may be an important mechanism in explaining between-subject differences in risk following (cumulative) exposure to psychosocial stress. To date, most studies suggestive of gene-stress interaction have used proxy measures for genetic vulnerability such as a family history of psychosis; studies investigating interactions between molecular genetic measures and psychosocial stressors are still relatively scarce. Preliminary evidence suggests that polymorphisms within the catechol-O-methyltransferase and brain-derived neurotrophic factor genes may interact with psychosocial stress in the development of psychosis; however, extensive further investigations are required to confirm this.
Keywords: schizophrenia / sensitization / ethnicity / trauma / urbanicity / cannabis / gene-environment interaction
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