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 (Heinz et al., 2003), which promote the progression to experiencing AUD criteria. Childhood adversity may also lead to psycho-biological changes that promote maladaptive coping strategies, such as stress-related drinking, and heighten sensitivity to genetic predispositions (Enoch, 2011), further increasing risk for heavier consumption and AUDs. Longitudinal studies should formally assess the exact roles of childhood adversity, ADH1B and other genes in this progression, as such relationships are beyond the scope of this study.
