Gene-Environment Interplay and Substance Use: A Review of Recent Findings

Abstract

Substance use problems are chronic and common public health problems. We review recent studies that implicate genetic and environmental factors in their etiology. Although findings are mixed with respect to specific genotypes, some patterns are evident. For example, exposure to peers or parents who engage in high rates of substance use tends to exacerbate genetic diatheses or eliminate the protective effects of certain genotypes. We discuss reasons for mixed findings and highlight the need for translational research to advance understanding of gene function as well as new methods for using genomewide data in biologically relevant pathways.

Tobacco and cannabis use in college students are predicted by sex‐dimorphic interactions between MAOA genotype and child abuse

“…To the best of our knowledge, although G × E interactions are posited to play a central role in the pathogenesis of cannabis and tobacco use, very few studies have examined these mechanisms with most analyses focusing on serotonergic and dopaminergic genes. 138 From this perspective, our recent analyses underscore the importance of gender as a factor in these analyses. In addition to MAOA, only very few genes have been shown to interact with environmental factors to influence the risk for psychopathology in a sex-dimorphic fashion.…”

“…These limitations notwithstanding, our data point to sex‐dimorphic G × E interactions in shaping the vulnerability for tobacco and cannabis use in college students. To the best of our knowledge, although G × E interactions are posited to play a central role in the pathogenesis of cannabis and tobacco use, very few studies have examined these mechanisms with most analyses focusing on serotonergic and dopaminergic genes . From this perspective, our recent analyses underscore the importance of gender as a factor in these analyses.…”

A genome-wide association study of cocaine use disorder accounting for phenotypic heterogeneity and gene–environment interaction

“…Variation in measurements among studies is a well-recognized problem in data aggregation. 17 The 3 non-replicated loci and the 6 loci without data for replication could represent falsepositive findings from GWAS, especially those for which there was no previous evidence supporting their potential involvement in the biological processes contributing to CUD. Nonetheless, among the 7 loci for which replication data were available, 4 were GWS either in replication or after combining results from the 2 analytic phases through meta-analysis, so they are worthy of further investigation.…”

“…In addition, multiple studies have shown that the genetic risk for developing a substance use disorder can be moderated by environmental factors such as stressful life events, neighbourhood stability, religiosity and peer drug use. [12][13][14][15][16][17][18] Thus, the statistical power of genome-wide association studies (GWAS) to identify the genetic variation contributing to the risk of substance use disorders is limited by the extent to which environmental effects and phenotypic heterogeneity are unaccounted for.…”

Interaction between ADH1B*3 and alcohol‐facilitating social environments in alcohol behaviors among college students of african descent

“…Protective effects of alcohol metabolism gene variants have been strongest in low-risk environments, remitting in high-risk peer or stressful family environments, 20,21 but see also Meyers and colleagues 22 . For example, carriers of another protective ADH1B variant, ADH1B*2 , were at lower risk for experiencing symptoms of alcohol use disorder than non-carriers, only when exposed to low levels of childhood adversity.…”