We use the term environment to broadly refer to community- or societal-level factors like per capita alcohol consumption, drinking norms, and alcohol outlet density, as well as social network factors like peer relationships and family circumstances (e.g., childhood abuse/neglect). This conceptualization of the environment is consistent with a multi-level perspective on health7,8 and risk behavior including substance use9 in that we emphasize contexts in which individuals are embedded, including peer groups, organizations, physical and social spaces, and the broader culture. This multi-level perspective is reflected in the model presented here (See Figure 1) as a means of organizing environmental exposures across three spheres of influence: social network, community, and societal. Additionally, we categorize these environments under two central mechanisms, social control and trigger, that are thought to modify genetic predisposition to AUD and that have previously been the focus of GxE studies. Earlier literature (e.g. Dick & Kendler10, Shanahan & Hofer11, and Sher et al.12) offers a solid place to start in identifying examples of environmental social controls and triggers important to AUD, although issues relevant to specific racial/ethnic groups
