et al.20 and Sartor et al.21 reported, respectively, an enhanced association of the ADH1B risk variant and a reduced association of the ADH1B protective variant with AUD under adverse childhood conditions. These studies are complemented by evidence suggesting strong main effects of these stressors on AUD, including robust evidence for adverse effects of early child abuse and parental loss on alcohol outcomes in adulthood22–24. Additional indicators of environmental stress may be relevant moderators of genetic influences, including at community and societal levels. Boardman et al.8 suggest a reframing of the ‘environment’ in studies of G–E relationships to include macro-level factors that characterize where people live and work when assessing their exposure to risks and resources. One potential trigger for AUD is neighborhood disadvantage, which has consistently been associated with illicit drug use, and in some studies has also shown associations with heavy drinking and AUD25. Later we return to a discussion of neighborhood disadvantage as an environmental variable that may be relevant to studies of AUD and G–E relationships for ethnic/racial minority populations.
