Two primary models have been proposed to describe the relationship of alcohol response and AUD risk, the low level of response (LLR) model and the differentiator model (DM) (Morean and Corbin, 2010). The LLR model proposes that individuals who experience decreased sensitivity to alcohol intoxication are at greater risk for AUD. In early longitudinal studies linking LLR and AUD risk, LLR was determined using the SHAS (Schuckit and Smith, 2000), which is primarily sensitive to the sedative and negative subjective effects of alcohol (Ray et al., 2016). In contrast, the DM addresses a broader range of alcohol effects. As reviewed by King et al. (2011), the DM proposes greater risk is associated with increased sensitivity to alcohol’s positive and stimulant effects on the ascending limb of the BAC curve, as well as decreased sensitivity to alcohol’s sedative and negative effects on the descending limb. DAT1 A9 and OPRM1*G carriers, who showed higher SHAS scores and greater negative effects of alcohol when compared to other genotype subgroups, would be at lower risk for AUD based on both the LLR and DM
