ADH1A is expressed at lower levels in liver than ADH1B or ADH1C, and is barely expressed in other adult tissues (Figure 2). ADH1A is expressed early in fetal development, and may play a role there (Smith et al., 1971). Coding variations are essentially non-existent, with none having an allele frequency of 1% or above in any population studied (Lek et al., 2016). The lack of coding variants and low level of expression in adults suggests that variations in ADH1A are not likely to play major roles in affecting risk for alcoholism. There is nominal evidence that several SNPs are associated with AD (Edenberg et al., 2006, Kuo et al., 2008) but that is likely due to LD with SNPs in ADH1B.
