Previous linkage studies have located genetic variants associated with MaxDrinks on chromosomes 2, 4, and 7 in European Americans (EAs)(Saccone et al., 2000, Saccone et al., 2005), and chromosomes 12 and 18 in a study of Irish affected sibpairs (Kuo et al., 2006). Consistent with gene-based association studies for AD, the strongest and most consistent signals for MaxDrinks in European-ancestry populations are located on ADH1B, a gene that encodes an alcohol dehydrogenase, a key enzyme in alcohol metabolism (Macgregor et al., 2009, Bierut et al., 2010). A functional single nucleotide polymorphism (SNP) at ADH1B, rs1229984 (A>G Arg48His), has been associated with MaxDrinks in Asian, Israeli, Australian, and European American populations (Bierut et al., 2012, Macgregor et al., 2009, Meyers et al., 2013), with the His48 allele conferring a protective effect against heavy consumption (i.e., lower MaxDrinks). This variant is uncommon in individuals of African descent and has not been found to be associated with MaxDrinks in AA samples; however, another functional variant rs2066207 with similar functional effects associated with AD diagnostic traits in AA samples (Edenberg et al., 2006). Gene-based
