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      Evidence that the wider social environment moderates the association between familial liability and psychosis spectrum outcome

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          Abstract

          Familial liability to both severe and common mental disorder predicts psychotic disorder and psychotic symptoms, and may be used as a proxy in models examining interaction between genetic risk and the environment at individual and contextual levels.

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          Most cited references27

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          The environment and schizophrenia.

          Psychotic syndromes can be understood as disorders of adaptation to social context. Although heritability is often emphasized, onset is associated with environmental factors such as early life adversity, growing up in an urban environment, minority group position and cannabis use, suggesting that exposure may have an impact on the developing 'social' brain during sensitive periods. Therefore heritability, as an index of genetic influence, may be of limited explanatory power unless viewed in the context of interaction with social effects. Longitudinal research is needed to uncover gene-environment interplay that determines how expression of vulnerability in the general population may give rise to more severe psychopathology.
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            Strauss (1969) revisited: a psychosis continuum in the general population?

            Although dichotomously defined for clinical purposes, psychosis may exist as a continuous phenotype in nature. A random sample of 7076 men and women aged 18-64years were interviewed by trained lay interviewers with the Composite International Diagnostic Interview (CIDI). Those with evidence of psychosis according to the CIDI were additionally interviewed by psychiatrists. For the 17 CIDI core psychosis items, we compared a psychiatrist's rating of hallucinations and/or delusions (Clinical Psychosis; sample prevalence 4.2%) with three other possible positive CIDI ratings of the same items: (i) symptom present, but not clinically relevant (NCR Symptom; sample prevalence 12.9%); (ii) symptom present, but the result of drugs or somatic disorder (Secondary Symptom; sample prevalence 0.6%); (iii) symptom appears present, but there is a plausible explanation (Plausible Symptom; sample prevalence 4.0%). Of the 1237 individuals with any type of positive psychosis rating (sample prevalence 17.5%), only 26 (2.1%) had a DSM-III-R diagnosis of non-affective psychosis. All the different types of psychosis ratings were strongly associated with the presence of psychiatrist-rated Clinical Psychosis (NCR Symptom: OR=3.4; 95% CI: 2.9-3.9; Secondary Symptom: OR=4.5; 95% CI: 2.7-7.7; Plausible Symptom: OR=5.8; 95% CI: 4.7-7.1). Associations with lower age, single marital status, urban dwelling, lower level of education, lower quality of life, depressive symptoms and blunting of affect did not differ qualitatively as a function of type of rating of the psychotic symptom, were similar in individuals with and without any CIDI lifetime diagnosis, and closely resembled those previously reported for schizophrenia. Presence of any rating of hallucinations was strongly associated with any rating of delusions (OR=6.7; 95% CI: 5.6-8.1), regardless of presence of any CIDI lifetime diagnosis. The observation by Strauss (1969. Hallucinations and delusions as points on continua function. Arch. Gen. Psychiatry 21, 581-586) that dichotomously diagnosed psychotic symptoms in clinical samples are, in fact, part of a continuum of experiences, may also apply to the general population. The boundaries of the psychosis phenotype may extend beyond the clinical concept of schizophrenia.
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              Gene-environment interactions in schizophrenia: review of epidemiological findings and future directions.

              Concern is building about high rates of schizophrenia in large cities, and among immigrants, cannabis users, and traumatized individuals, some of which likely reflects the causal influence of environmental exposures. This, in combination with very slow progress in the area of molecular genetics, has generated interest in more complicated models of schizophrenia etiology that explicitly posit gene-environment interactions (EU-GEI. European Network of Schizophrenia Networks for the Study of Gene Environment Interactions. Schizophrenia aetiology: do gene-environment interactions hold the key? [published online ahead of print April 25, 2008] Schizophr Res; S0920-9964(08) 00170-9). Although findings of epidemiological gene-environment interaction (G x E) studies are suggestive of widespread gene-environment interactions in the etiology of schizophrenia, numerous challenges remain. For example, attempts to identify gene-environment interactions cannot be equated with molecular genetic studies with a few putative environmental variables "thrown in": G x E is a multidisciplinary exercise involving epidemiology, psychology, psychiatry, neuroscience, neuroimaging, pharmacology, biostatistics, and genetics. Epidemiological G x E studies using indirect measures of genetic risk in genetically sensitive designs have the advantage that they are able to model the net, albeit nonspecific, genetic load. In studies using direct molecular measures of genetic variation, a hypothesis-driven approach postulating synergistic effects between genes and environment impacting on a final common pathway, such as "sensitization" of mesolimbic dopamine neurotransmission, while simplistic, may provide initial focus and protection against the numerous false-positive and false-negative results that these investigations engender. Experimental ecogenetic approaches with randomized assignment may help to overcome some of the limitations of observational studies and allow for the additional elucidation of underlying mechanisms using a combination of functional enviromics and functional genomics.
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                Author and article information

                Journal
                applab
                Psychological Medicine
                Psychol. Med.
                Cambridge University Press (CUP)
                0033-2917
                1469-8978
                December 2012
                April 16 2012
                : 42
                : 12
                : 2499-2510
                Article
                10.1017/S0033291712000700
                22717152
                721a42bc-4a6a-4fd1-907f-4e1af5dbb67e
                © 2012

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