ALCOHOL STIMULATION AND SEDATION IN BINGE DRINKERS

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Binge drinking continues to be a major problem in young adults in the United States. Persons who are chronic, heavy alcohol drinkers (i.e., consume 5+ drinks/occasion on a weekly or more frequent basis) not only incur greater consequences and adverse effects if they maintain hazardous drinking levels, but are also at increased risk for progression to Alcohol Dependence. Little is known about the individual response factors, such as acute response to ethanol, in these early-age heavy drinkers (HDs) compared to light drinkers (LDs). The majority of laboratory research in this area has examined persons at high risk by virtue of a positive family history of alcoholism (FH+), with mixed results on their relative sensitivity and/or tolerance to the effects of alcohol. Given the multiple etiologies and complexities of alcohol use disorders, it is important to broaden the range of risk factors examined in alcohol challenge paradigms. Our prior data suggest that heavy drinkers show greater sensitivity to alcohol-induced stimulation and less sensitivity to alcohol sedation compared to light drinkers. Therefore, our goal in Study 1 is to replicate and extend these findings of differential acute alcohol response in early-stage heavy binge drinkers versus light drinkers. In the proposed within-subjects study, the effects of alcohol will be measured through subjective, objective, and performance domains during two alcohol sessions (0.4 and 0.8 g/kg) and a placebo session. In addition, we will examine the role of drinking history as a risk factor, along with other potential risk factors, to develop a predictive model for acute alcohol response characteristics (subjective stimulation, sedation, and objective/performance response). Study 2 will further extend this model by conducting a prospective study in the same subjects to examine the role of acute alcohol response to future alcohol-related behaviors and consequences. We hypothesize that those persons who show increased sensitivity to alcohol reinforcement, as measured by euphoria and stimulation, and less alcohol-induced sedation during the testing session will exhibit significantly greater signs of subsequent heavy drinking, as measured by heightened alcohol quantity, frequency, binge episodes, and early alcohol-related consequences.