Alcohol misuse is a common and costly human behavior, accounting for 3.3 million deaths worldwide in 2012 (World Health Organization, 2014) and over $220 billion in annual economic tolls in the US alone (Bouchery et al., 2011). Alcohol-related outcomes are influenced by genetic factors: the heritability of alcohol use disorder (AUD) was estimated at 0.50 in a meta-analysis of twin studies (Verhulst et al., 2015), and recent genome-wide association studies of alcohol consumption and symptoms have reported SNP-based heritabilities of 0.13 (Clarke et al., 2017) and 0.12 (Sanchez-Roige et al., 2017), respectively. Variation in genes involved in alcohol metabolism (e.g., alcohol and aldehyde dehydrogenases) is known to impact liability to problems (Edenberg, 2007) and consumption (Jorgenson et al., 2017); there is support for a role of genes outside of this metabolic pathway as well (Schumann et al., 2011; Schumann et al., 2016). However, much remains unclear about the mechanisms underlying genetic influences on alcohol outcomes, necessitating further study and consideration of precursors in addition to the outcomes themselves.
