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In contrast to studies on poor social functioning outcomes in individuals with schizophrenia that tend to focus on environmental explanations (for example, marked changes to social policy and socioeconomic disparities), a shared genetic etiology between schizophrenia and socioeconomic deprivation would imply that such associations are, at least partly, due to genetic confounding.We adopted multiple genetically informed designs to address the following aims: Statistics Sweden maintains all nationwide Swedish longitudinal registries with routinely gathered governmental data.Proponents of the social causation interpretation have proposed a number of hypotheses postulating that the development of schizophrenia results from early exposure to adverse neighborhood stressors, accumulated over time, particularly in individuals with genetic liabilities.In contrast, the drift interpretation suggests that the association goes in the opposite direction; namely that psychotic patients tend to gradually undergo downward social mobility (or to ‘drift’) into deprived neighborhoods following employment difficulties associated with experiencing psychotic-like symptoms and declining cognitive functioning.We used the Total Population Register to identify all individuals born in Sweden between 19 and linked their data with the Multi-Generation Register to identify all biological full and half siblings in the sample and generate family pedigree structures.Censoring information on mortality and migration dates was obtained from the Cause of Death and Migration Registries, respectively.Neighborhood characteristics data were aggregated from the Total Population Register, census registries, as well as the National Crime Register, which includes all criminal convictions in lower general court in Sweden since 1973.
Large-scale, eco-epidemiological studies that simultaneously account for individual, familial and social contextual determinants are therefore integral in clarifying underlying mechanisms.
To test the social drift hypothesis, we used three complementary genetically informed Swedish cohorts.
First, we used nationwide Swedish data on approximately 760 000 full- and half-sibling pairs born between 19 and quantitative genetic models to study genetic and environmental influences on the overlap between schizophrenia in young adulthood and subsequent residence in socioeconomically deprived neighborhoods.
Although the correlation between schizophrenia and neighborhood deprivation was moderate in magnitude (r=0.22; 95% CI: 0.20–0.24), it was entirely explained by genetic influences. Moreover, the association between polygenic risk for schizophrenia and neighborhood deprivation was statistically significant (R=0.15%, P=0.002).
Our findings are primarily consistent with a genetic selection interpretation where genetic liability for schizophrenia also predicts subsequent residence in socioeconomically deprived neighborhoods.