AUDs develop via complex processes beginning with (1) drinking initiation, followed by (2) regular consumption, progressing to (3) heavier and potentially maladaptive consumption, culminating in (4) AUD criteria. Twin studies indicate that each of these steps is influenced by shared and unique environmental and genetic risk factors (Dick & Kendler, 2012b; Slutske et al., 1998). Childhood adversity increases risk for earlier age of initiation (Kilpatrick et al., 2000), most likely due to associated risk factors, such as increased access to alcohol and poor parental monitoring (Young-Wolff et al., 2011). As one transitions to regular consumption followed by heavier alcohol consumption, genes directly affecting alcohol metabolism (e.g. ADH1B) become increasingly relevant (Kendler et al., 2011). For example, ADH1B-rs1229984 can impact alcohol consumption through a physiological response to alcohol metabolism, potentially leading individuals with the protective A allele to drink less regularly or heavily, even after exposure to other strong risk factors such as childhood adversity. Furthermore, regular heavy consumption provides alcohol to the brain, where alcohol exerts its addictive effects via a cascade of biochemical actions, mainly encoded by neuronal genes
