Finally, the results did not support sensitization theory, as heavy drinkers with progressive AUD subjects maintained but did not further increase their already heightened sensitivity to stimulation. Motivational reward (wanting) was persistently elevated in heavy drinkers with both intermediate and high AUD symptoms. Thus, incentive sensitization, i.e., an increase in alcohol’s incentive salience (wanting), was not evident over the interval tested, and hedonic reward (liking) also remained elevated in heavy drinkers with high AUD. Putting these data together, it is possible that neither tolerance nor sensitization processes were observed because they may have taken place earlier in the drinking history of these young adults, or responses approached ceiling or floor effects for what can be observed in the controlled laboratory environment. It is also possible that behavioral and objective biomarkers in animal models (locomotion, tail flick, conditioned incentive procedures, etc.) do not directly translate to subjective responses and the progression of human AUD. While objective biomarkers in animal models are well-developed, human subjective responses and clinical phenomena are crucial to our understanding of the processes affecting addiction propensity.
