Genetic factors can impact on risk for AAD symptoms at a wide range of levels and are likely to share genetic influences on alcohol consumption measures, partly (Whitfield et al. 2004) or (almost) entirely (Grant et al. 2009; Kendler et al. 2010). Genetic influences include those on alcohol metabolism by the ADH and ALDH gene cluster (Edenberg et al. 2006; Luo et al. 2006; Kuo et al. 2008; Macgregor et al. 2009; van Beek et al. 2010), the level of response to alcohol (Schuckit et al. 2004) and neurotransmitters related to the reward system that interact directly and indirectly with ethanol (e.g., dopamine, and GABA) (Enoch 2008; Smith et al. 2008; Munafo et al. 2007). Genetic influences on AAD also act via general predispositions to abuse licit and illicit psychoactive drugs (Kendler et al. 2007; Agrawal et al. 2008), predispositions toward externalizing behaviors in general (Cerda et al. 2010) and the tendency to self-select into environments where alcohol is widely available and its misuse socially condoned (Kendler et al. 2007; Gillespie et al. 2007). In addition, genetic factors for AAD
