individual responds to repeated alcohol use over time. Based on the body of literature across humans and animals, AD is likely to involve neuronal circuits involved in the Binge/Intoxication, Withdrawal/Negative Affect, and Preoccupation/Anticipation stages of the addiction cycle (Koob and Volkow, 2010); see Figure 1. In fact, neurotransmitter systems, such as dopamine, glutamate, opioid, serotonin, and γ-aminobutyric acid (GABA) systems, as well as stress response circuits (Neuropeptide-Y and Corticotropin-Releasing Factor) and appetite regulating systems are key to alcohol’s effects (Hillemacher, 2011). For instance, studies demonstrate that opioid antagonists suppress alcohol drinking (Rosner et al., 2010) and that gamma-aminobutyric acid A receptors (GABAA) mediate the rewarding effects of alcohol (Koob, 2004) and alcohol consumption (Rewal et al., 2012; Tabakoff et al., 2009). Given the role of each of these metabolic and neuronal pathways in alcohol use and addiction, they are regarded as candidate pathways for genetic studies of alcohol. It is believed that individual differences in the genetic code of these and other candidate molecules will provide insight into the risk for AD. Unfortunately, the extant body of animal and human research on alcohol has also demonstrated that alcohol, as a drug, is not specific in its effects, but rather casts
