areas, a key component to understanding alcohol’s effect on the brain can be found in variation both within and across biological mechanisms that regulate ethanol concentration and intercellular communication among neurons. Studies have demonstrated that the liver enzymes, alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) regulate the degradation of alcohol into acetate. Pharmacogenetic research has also shown that variation within ADH and ALDH genes alters a person’s risk for developing alcohol problems (Alcohol_Alert, 2007). For instance, of the seven genes that code for different forms of ADH (clustered on chromosome 4q), variants within the genes encoding the hepatic forms, ADH1B and ADH1C, have been related to alcohol dependence. The ADH1B*2 alleles has also been shown to protect against alcoholism in males and females of different ethnic origins (Lorenzo et al., 2006; Toth et al., 2010). Koob and Volkow’s review of the neurobiology of drug addiction highlights several circuits that mediate the ‘binge/intoxication’, ‘withdrawal/negative affect’, and ‘preoccupation/anticipation (craving)’ stages of the addiction cycle. These stages have been linked to specific neural networks. For example, in regards to the Binge/Intoxication Stage, the acute reinforcing effects of alcohol are hypothesized to invoke the release of dopamine in the nucleus accumbens through its actions
