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Chunk #29 — 5. Non-Additive Genetic Mechanisms involved in SUD — 5.1 Gene-Environment Interplay

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The genetic epidemiology of substance use disorder: A review.
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In comparison to GxE studies of alcohol use disorder, there are far fewer studies of GxE for nicotine dependence, cannabis use disorder or opioid addiction. Twin smoking studies (Kaprio, 2009) report increased genetic influence on adolescent smoking in the presence of low parental monitoring. Further, a study of nicotine dependence in adults ages 25–44 reported a significant interaction between adolescent parental monitoring and a variant of the alpha 5 neuronal nicotinic acetylcholine receptor subunit (CHRNA5, rs16969968); genetic risk was reduced in participants with high levels of parental monitoring (Chen et al., 2009). This variant was also identified as having a significant interaction with increasing exposure to peer smoking (Johnson et al., 2010). Additionally, the influence of genetic risk variants as measured by a PRS for smoking was increased in individuals who experienced more traumatic events in their lifetime. Further, genetic risk for smoking was reduced in individuals who lived in neighborhoods with high social cohesion (Meyers et al., 2013). Therefore, the magnitude of genetic variance on smoking may increase as the environment is less enriched, either through reduced parental monitoring or through low social cohesion.