The reasons for the disparities in drinking and alcohol-related problems between AA and EA are not fully understood (Hasin & Grant, 2015; Zapolski et al., 2014). Studies have suggested that both environmental and genetic factors contribute to these differences (K. G. Chartier et al., 2014). Relevant to the current study, there is evidence for differential heritability of problem drinking in EA and AA (Sartor et al., 2013). Genome-wide association studies (GWAS) of alcohol-related phenotypes have also identified variants that are only significant in AA or EA (Kranzler et al., 2019; Lai, Wetherill, Bertelsen, et al., 2019; Lai, Wetherill, Kapoor, et al., 2019; Walters et al., 2018). For example, different functional single nucleotide polymorphisms (SNP) in ADH1B, the gene encoding the main alcohol-metabolizing enzyme in liver, have been linked to alcohol dependence in various populations partially due to their population specific allele frequencies: rs2066702 in AA and rs1229984 in EA (Bierut et al., 2012; Edenberg & McClintick, 2018; Walters et al., 2018). Polimanti and colleagues studied functional variants in 24 genes related to alcohol dependence and found frequencies of these variants to vary between AA and EA (Polimanti, Yang, Zhao, & Gelernter, 2015).
