There has been some debate as to whether it is important to establish a link between an environmental exposure and the neurobiological changes associated with the psychiatric disorder being studied60. We do not weigh in on that here; existing literature provides an examination of proposed pathways of environmental exposure to neurobiological functioning and the association with alcohol use, relapse, and recovery (e.g., Koob & Volkow, 201661; Seo & Sinha, 201562). Research on neurobiological changes is more consistently linked to social triggers like stress and trauma, but social control influences, such as those studied by Brody and colleagues26–30, may offer actionable targets for intervention. Here, we contend that for G–E studies of AUD, environmental conditions should be logically associated with changes in both exposure to alcohol and levels of drinking (see Figure 1). This could mean that an environmental feature increases risk for greater alcohol exposure and a resultant escalation of drinking, or it may be protective and decreases drinking. Such conditions can occur at the social network, community, and societal levels, but identification of plausible mediating mechanisms from higher-order (community
