Differential sensitivity to the acute effects of alcohol, particularly reduced sedation-like effects and enhanced stimulation-like effects (here simplified as ?low sensitivity;? LS), is known to be a potent risk factor for alcohol abuse, dependence, and drinking-contingent adverse consequences. However, at present relatively little is known concerning the specific psychological mechanisms through which LS promotes problematic drinking. The research proposed here is aimed at testing a novel translational hypothesis, based in the incentive sensitization theory of addiction, linking LS with specific psychological and neurobiological processes that both promote craving and motivation for alcohol and facilitate heavy drinking. The proposed research will use a combination of laboratory-based measures to gauge attention to, motivation for, and incentive value of alcohol- related cues (alcohol cue-reactivity; ACR) and ecological momentary assessments (EMA) of ?real-world? drinking and related experiences. Participants will be young drinkers (ages 18-20 years) recruited from the community, permitting investigation of a novel, theory-driven model of risk for problematic drinking during a critical developmental period for alcohol involvement (emerging adulthood). Using a variety of recruitment channels, we will screen potential participants to obtain information about their level of alcohol sensitivity (as determined using validated questionnaires) and drinking patterns. A target sample of 420 emerging adults (70 males and 70 females in each of three sensitivity terciles) will be invited to participate in a laboratory session during which four tasks will be used to evaluate ACR: (1) a visual dot-probe detection task assessing involuntary capture of attention by alcohol cues; (2) an alcohol approach-avoidance task evaluating implicit approach bias elicited by alcohol cues; (3) amplitude of the P3 event-related potential elicited by alcohol cues, assessing incentive value for alcohol; and (4) an olfactory cue exposure task measuring self-reported craving for alcohol. Following this laboratory session, participants will begin a 21-day EMA period during which they will use a smartphone app to record alcohol cue exposure, alcohol craving, drinking behaviors, and adverse consequences of drinking in their natural environments. Participants will complete an online follow-up survey one year after the laboratory session. The research will permit us to (a) characterize how individual differences in alcohol sensitivity relate to neurobehavioral and self-report measures of incentive sensitization processes; (b) investigate how LS relates to drinking behavior, ACR, craving, and problems in young drinkers' natural environments; and (c) evaluate empirical associations among alcohol sensitivity, laboratory endophenotypes, ecologically assessed drinking experiences, and problematic drinking outcomes. This approach will produce a unique and rich dataset, findings from which will help fill critical gaps in extant knowledge about the etiology of LS-related risk for AUD.
Problematic drinking, particularly among young adults, represents a significant public health concern for both the drinkers themselves and for those whom their drinking impacts. Results of this research will provide new insights by clarifying how an established alcoholism risk factor is translated into problematic alcohol use through basic brain processes and drinking-related decisions and behaviors.
