The purpose of this study is to determine how adults who binge drink are differentially affected by a simulated alcohol binge and reduction of serotonin synthesis. Unlike moderate social drinking, binge drinking involves engaging in episodes of heavy drinking separated by periods of abstinence. Many college students engage in binge drinking, which has been the focus of the majority of research. But, most binge drinkers are not college students and those who continue binging behavior beyond the college years are an understudied group. One mechanism that may be important to understanding alcohol binging is a "loss of control" of alcohol intake, which is hypothesized to be a fundamental process that distinguishes individuals who engage in binge drinking from those who engage in moderate social drinking. Alcohol's effects on binging behaviors may be related, in part, to underlying mechanisms of serotonergic dysregulation and behavioral impulsivity. But, the effects of alcohol consumption and serotonin dysregulation on behavioral impulsivity among binge drinkers beyond college age have not been tested. Here, Binge (n = 48) and Non-Binge (n = 48) drinkers, ages 24 to 34, will be recruited from the community and studied while sober and during a simulated alcohol binge after reductions in serotonin synthesis to determine how these conditions affect laboratory-measured impulsivity. Three unique measures of impulsivity will be used to assess group differences at multiple time points before, during, and after a simulated alcohol (or placebo) binge procedure. The 4 primary experimental conditions include alcohol or placebo administered after L-tryptophan Depletion (reduced serotonin synthesis) and after L- tryptophan Balanced Control (maintained serotonin synthesis).
The aims of this study are to determine: (1) whether a simulated alcohol binge increases impulsivity in binge drinkers more than moderate drinkers;and (2) to what extent reductions in serotonin synthesis affect impulsivity in both binge and moderate drinkers, and how these reductions affect alcohol-induced impulsivity during a simulated binge. A secondary aim is to determine how changes observed in impulsivity after an initial "priming" dose of alcohol relate to subsequent choices for consuming additional alcohol. This secondary aim includes assessment of group differences in measures of impulsivity prior to and after a "priming" dose of alcohol, followed by a session of ad libitum alcohol consumption.
These aims are designed to examine how "loss of control" (i.e., impulsivity) is affected by alcohol and by an individual's underlying biological state (i.e., reduced serotonin synthesis), which have been proposed as contributing to binging episodes. The innovation and clinical significance of this study is that it combines methodologies in novel ways to examine an understudied population and address gaps in the literature that exist between animal models and epidemiological characterizations of binge drinking. In doing so, we will clarify the role of mechanisms hypothesized as contributing to the maintenance of a binge episode.
This study addresses critical gaps in understanding how alcohol and individual differences in underlying biological states affect behavioral processes involved in binge alcohol drinking. This study will yield data to clarify the role of impulsive behavior and serotonin function as mechanisms that contribute to the maintenance of an alcohol binge-drinking episode. With this understanding, we can develop treatments aimed at disrupting such mechanisms using cognitive-behavioral and pharmacological strategies.