genetic influences on alcohol use were stronger when social support was higher for women, and the opposite was found for men. Differences in G×E findings across studies could be attributed to differences in genetic methodology, sample design, and measurement of constructs. By using a molecular genetic design, we characterized a specific dimension of genetic risk (i.e., alc-PRS), whereas twin studies quantify overall latent genetic influences. It is possible that high social support buffers genetic risk in relation to a particular developmental outcome, while also providing a context for the overall genetic predisposition to be expressed (rather than being suppressed). Future research is needed to replicate our findings and further understand the role of social support in moderating molecular genetic influences on alcohol use outcomes. Furthermore, we note that there was a small negative correlation between alc-PRS and family support and friend support. Although the present study focused on examining G×E effects, we note that these gene-environment correlation (rGE) processes may also underlie polygenic influences on alcohol use. Future research is warranted to examine rGE in addition to G×E processes to further understand mechanisms linking genetic risk and social support to alcohol use outcomes.
