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Chunk #15 — Discussion

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Genetic predisposition to schizophrenia associated with increased use of cannabis.
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These results highlight the blurring between behavioural phenotypes and environment, and have wider implications for how we perceive supposedly environmental risks for disease. Individuals select their own environments based on their innate and learned preferences, and have their environments react to their own behaviour. Further, parents pass down both genes and environment to their children. All of these can contribute to gene-environment correlation, particularly with respect to behavioural traits. Several studies have shown that supposedly environmental risk factors such as urbanicity, religiosity, and stressful life events have heritable components to them41–43. The existence of heritability for supposedly environmental risk factors does not mean they are inevitable, only that causality is more complicated to discern. Future studies will need to explore the matching of cases and controls on environmental risk variants in order to fully disentangle causation. This can be supplemented exploring the generating of polygenic risk scores for environmental risk factors, and their role in predicting disease status. The wider availability of genetic data in richly phenotyped samples should allow for the integration of genetics into an epidemiological framework, and so the discovery of gene-environment correlations where they exist.