In terms of theoretical models, the data provide the most support for the modified differentiator model (16), because higher stimulation and lower sedation during peak BrAC at an intoxicating dose of alcohol were predictive of the increase over time in AUD symptoms. These effects were not predictive when measured during rising and declining BrAC limbs, which may be due to greater variability in responses at those temporal phases as compared with the peak BrAC interval at 60 minutes. Historically, the low-level response model has been widely accepted, with less intense alcohol effects assumed to be the mechanism for risk of development of AUD above and beyond known risk factors such as FH (9). However, as we previously suggested (5), a paradigm shift to greater emphasis on reward sensitivity in the development of AUD is now of paramount importance in the alcohol field. Although not explicitly stated, the lower-level response model does not apply across the spectrum of subjective alcohol responses but appears rather to focus on alcohol’s impairing and sluggish effects. At peak BrAC, the only low-level response that predicted
