Aim: Impulsivity is a robust predictor of alcohol use in adolescence. There is little evidence on the causal mechanisms through which it influences drinking or how they are affected by key social and genetic risk factors. This study investigated the moderating effect of polygenic risk for alcohol use disorder on alcohol consumption after the experimental induction of an impulsive state.

Procedures: 120 adolescents (50% female) of legal drinking age (18-21) provided saliva for genetic analysis before undergoing an Experimental Paradigm to Investigate Impulsive Consumption (EPIIC). EPIIC involved exposure to 1 of 3 experimental manipulations to increase impulsivity (reward cue exposure, mood induction, ego depletion). Participants then completed a laboratory drinking task alone or with a heavy-drinking confederate.

Hypothesis: Polygenic risk would strengthen the increase in alcohol consumption observed after the induction of an impulsive state, particularly in the reward cue exposure condition.

Statistical Analyses: Two-level multilevel regression. Polygenic risk score constructed from the results of independently published large-scale genome wide association studies (GWAS) and meta-analyses.

Results: Polygenic risk significantly moderated the effect of reward cue exposure on laboratory drinking, such that higher polygenic risk was associated with greater impulsivity-induced alcohol consumption (p = .03). Polygenic risk was not associated with greater consumption in the control (non-impulsive state) condition, nor did it moderate the influence of a heavy-drinking peer on consumption.

Conclusion: Findings provide preliminary evidence that, in adolescence, genetic risk for alcohol misuse involves a unique susceptibility to reward-related impulsivity, rather than general disinhibition or negative mood-related impulsivity. The new EPIIC paradigm can provide novel insights that could be used to help identify new targets for intervention.