Article

Social defeat: risk factor for schizophrenia?

Utrecht University, Utrecht, Utrecht, Netherlands
The British Journal of Psychiatry (Impact Factor: 7.34). 09/2005; 187:101-2. DOI: 10.1192/bjp.187.2.101
Source: PubMed

ABSTRACT The hypothesis that chronic and long-term experience of 'social defeat' may increase the risk for schizophrenia is proposed. This increased risk may result from sensitisation of the mesolimbic dopamine system and/or increased baseline activity of this system. Data supporting the social defeat hypothesis are presented.

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    • "This model suggested that PTSD symptom clusters (avoidance, arousal, and re-experiencing) could have both direct effects on psychosis symptoms and indirect effects through traumatic sequelae such as substance abuse, re-traumatization, and interpersonal difficulties. Other models have attempted to explain these trauma–psychosis associations (Bentall & Fernyhough, 2008; Selten & Cantor-Graae, 2005). Cognitive models suggest that there may be numerous casual routes to the development and maintenance of psychotic symptoms such as adverse experiences, social marginalization, and the experience of childhood trauma (Garety, Kuipers, Fowler, Freeman, & Bebbington, 2001; Morrison, 2001; Morrison et al., 2003). "
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    ABSTRACT: Objective Previous research has identified an association between traumatic experiences and psychotic symptoms. Few studies, however, have explored the underlying mechanisms and contingent nature of these associations in an integrated model. This study aimed to test a moderated mediation model of negative childhood experiences, associated cognitive processes, and psychotic experiences within a context of adolescent loneliness.DesignCross-sectional survey.MethodsA total of 785 Northern Irish secondary school adolescents completed the survey. A moderated mediation model was specified and tested.ResultsChildhood experiences of threat and subordination were directly associated with psychotic experiences. Analyses indicated that peer victimization was a mediator of this effect and that loneliness moderated this mediated effect.ConclusionA new model is proposed to provide an alternative framework for assessing the association between trauma and psychotic experience in adolescence that recognizes loneliness as a significant contextual moderator that can potentially strengthen the trauma–psychosis relationship.Practitioner pointsModerated mediation analyses poses an alternative framework to the understanding of trauma–psychosis associationsAdolescent loneliness is a vulnerability factor within this associationData are based on a Northern Irish sample with relatively low levels of lonelinessCross-sectional data cannot explore the developmental course of these experiences in adolescence.
    03/2015; DOI:10.1111/bjc.12077
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    • "Accordingly ASD prevalence increases in children born at higher latitudes (Grant and Soles, 2009) and in infants from migrant mothers with dark skin compared to offspring from lighter skinned migrants (Dealberto, 2011). This later finding is reminiscent of the epidemiological data showing increased risk of schizophrenia in offspring from darkskinned migrants (Cantor-Graae and Selten, 2005). Finally, further indirect support comes from one study showing autistic boys have unexplained reductions in metacarpal bone thickness (Hediger et al., 2008). "
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    Frontiers in Neuroendocrinology 07/2012; 34(1). DOI:10.1016/j.yfrne.2012.07.001
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    • "Social interest may be diminished by anxiety and impaired social memory after CSD [74]. Social stress can affect susceptibility to schizophrenia [75] [76], possibly through sensitization of the mesolimbic dopamine system. For example, CSD in male Long–Evans rats produce dopaminergic hyperactivity in the mesocorticolimbic tract [77], which could be similar to the hyperdopaminergic observed in patients with schizophrenia [78]. "
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    ABSTRACT: DISC1 (Disrupted-in-schizophrenia 1) is a strong candidate susceptibility gene for psychiatric disease that was originally discovered in a family with a chromosomal translocation severing this gene. Although the family members with the translocation had an identical genetic mutation, their clinical diagnosis and presentation varied significantly. Gene-environment interactions have been proposed as a mechanism underlying the complex heritability and variable phenotype of psychiatric disorders such as major depressive disorder and schizophrenia. We hypothesized that gene-environment interactions would affect behavior in a mutant Disc1 mouse model. We examined the effect of chronic social defeat (CSD) as an environmental stressor in two lines of mice carrying different Disc1 point mutations, on behaviors relevant to psychiatric illness: locomotion in a novel open field (OF), pre-pulse inhibition (PPI) of the acoustic startle response, latent inhibition (LI), elevated plus maze (EPM), forced swim test (FST), sucrose consumption (SC), and the social interaction task for sociability and social novelty (SSN). We found that Disc1-L100P +/- and wild-type mice have similar anxiety responses to CSD, while Q31L +/- mice had a very different response. We also found evidence of significant gene-environment interactions in the OF, EPM and SSN.
    Behavioural brain research 05/2012; 233(2):337-44. DOI:10.1016/j.bbr.2012.05.037
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