As AUD has a large genetic component, specific risk-conferring genes may be captured through variance in single nucleotide polymorphisms (SNPs) in candidate genes which, in turn, serve as determinants of alcohol consumption and response to alcohol as a pharmacological agent itself (for review see3). As an example, in a genome-wide association study using a sample of individuals of Asian ancestry, Quillen et al. reported that SNPs found in the aldehyde dehydrogenase (ALDH2) region are strongly associated with both flushing response and daily maximum drinks.4 Similarly, genetic variance not only affects response to alcohol, but can affect response to pharmacotherapies. A study conducted by Kiefer et al., in a sample largely comprised of individuals of European ancestry, found that a SNP in the gene for GATA-binding protein 4 (GATA4), rs13273672, believed to be important in embryogenesis and regulation of myocardial differentiation and function,5, 6 was associated with relapse and more importantly, with response to acamprosate.7 Individuals homozygous for the G allele were more likely to relapse to heavy drinking by the end of the treatment period compared to A/A or A/G individuals. This is just one example of how certain genetic alleles influence pharmacologic response to AUD medications (recently reviewed by8).
