Both alcohol consumption and AUD (as well as other indices of problematic drinking, e.g., the problem subscale of the Alcohol Use Disorders Identification Test (AUDIT-P) (Sanchez-Roige et al., 2017)) are heritable. Twin studies suggest that additive genetic factors contribute to 40–70% of the variance in alcohol consumption and AUD (Heath & Martin, 1994; Prescott & Kendler, 1999; Verhulst et al., 2015). The degree to which there is overlap in the genetic factors contributing to alcohol consumption vs. AUD is less clear from twin data (Agrawal, Lynskey, Heath, & Chassin, 2011; Dick, Meyers, Rose, Kaprio, & Kendler, 2011; Grant et al., 2009; Kenneth S Kendler, Myers, Dick, & Prescott, 2010), but recent genome-wide association studies (GWAS) have estimated this overlap using Linkage Disequilibrium Score Regression (LDSC (Bulik-Sullivan et al., 2015)). Based on GWAS of both alcohol consumption (N=112, 117) (Clarke et al., 2017) and DSM-IV alcohol dependence (N=14,904 cases and 37,944 controls) (Walters et al., 2018), common variants explain, in aggregate, between 9–13% of the variance in these phenotypes (i.e., SNP heritability) and the estimated genetic correlation between them ranges from rg = 0.37 – 0.70 (Walters et al., 2018).
