Studies of whether the relationship between candidate genes and alcohol use outcomes is moderated by childhood adversity (G×E interaction) have largely focused on genes affecting neuronal pathways (Young-Wolff et al., 2011). For example, in youths, the higher risk serotonin transporter promoter “s” variant together with childhood adversity (maltreatment) increases risk for early-onset alcohol use (Brody et al., 2007; Kaufman et al., 2006). Similarly, in women, the monoamine oxidase A risk allele was associated with alcoholism, but only among those experiencing childhood adversity (sexual abuse (Ducci et al., 2008)). Another study suggested that a variant in the DRD2/ANKK1 region is associated with alcohol problems among individuals exposed to stress (Madrid et al., 2001). While these studies are all important, the neuronal pathways underlying substance phenotypes remain to be elucidated, while the relationship of alcohol metabolizing liver enzymes to alcohol consumption is better understood. Therefore, investigating the effects of interaction between childhood adversity and ADH1B on heavy alcohol consumption and related alcohol disorder phenomena could more specifically address how adversity moderates direct gene effects on alcohol use and disorders.
