For decades, candidate gene studies were used to determine the contribution of specific genes that increase risk for AUD. Candidate gene studies tended to focus on genes that influenced pharmacokinetic and pharmacodynamic (e.g. dopaminergic, glutamatergic and opioid signaling systems) factors. Larger genetic studies have generally not replicated the findings from candidate gene studies (10). One exception to this are the genes encoding ethanol metabolizing enzymes, particularly alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), which have repeatedly been shown to have the largest impact on alcohol consumption and risk for AUD (7).
