Jessica Weafer1,2, K Luan Phan3, Harriet de Wit4. 1. Department of Psychiatry and Behavioral Neuroscience, University of Chicago, MC3077, 5841 S. Maryland Ave., Chicago, IL, 60637, USA. jweafer@uky.edu. 2. Department of Psychology, University of Kentucky, 171 Funkhouser Dr., Lexington, KY, 40506, USA. jweafer@uky.edu. 3. Department of Psychiatry and Behavioral Health, The Ohio State University, 1670 Upham Drive, Columbus, OH, USA. 4. Department of Psychiatry and Behavioral Neuroscience, University of Chicago, MC3077, 5841 S. Maryland Ave., Chicago, IL, 60637, USA.
Abstract
RATIONALE AND OBJECTIVE: Poor inhibitory control is a well-established risk factor for alcohol use disorder (AUD). Similarly, greater sensitivity to the stimulant effects and less sensitivity to the sedative effects of alcohol are also strongly linked to risk for AUD. Traditionally, these two risk factors have been considered to be orthogonal, and thus they have been studied independently. However, recent evidence from animal and human studies suggests that they may be related. The current study examined the relationship between inhibitory control and subjective responses to alcohol in a sample of healthy young adults. METHODS:Moderate social drinkers (N = 69) first completed the stop signal task to assess inhibitory control. They then participated in four sessions in which they received an oral dose of ethanol (0.8 g/kg) or placebo in alternating order, providing self-report measures of stimulation and sedation on the Biphasic Alcohol Effects Scale (BAES) at regular intervals. RESULTS: Linear mixed effects models showed that poor inhibitory control was associated with greater stimulation and less sedation following alcohol compared with placebo. CONCLUSION: These findings provide the first direct evidence that individuals with poor inhibitory control experience greater sensitivity to the rewarding, stimulant effects of alcohol, and less sensitivity to the negative, sedative effects. These findings suggest that inhibition and subjective response to alcohol are not independent risk factors, and that together they constitute a heightened profile of risk for AUD.
RCT Entities:
RATIONALE AND OBJECTIVE: Poor inhibitory control is a well-established risk factor for alcohol use disorder (AUD). Similarly, greater sensitivity to the stimulant effects and less sensitivity to the sedative effects of alcohol are also strongly linked to risk for AUD. Traditionally, these two risk factors have been considered to be orthogonal, and thus they have been studied independently. However, recent evidence from animal and human studies suggests that they may be related. The current study examined the relationship between inhibitory control and subjective responses to alcohol in a sample of healthy young adults. METHODS: Moderate social drinkers (N = 69) first completed the stop signal task to assess inhibitory control. They then participated in four sessions in which they received an oral dose of ethanol (0.8 g/kg) or placebo in alternating order, providing self-report measures of stimulation and sedation on the Biphasic Alcohol Effects Scale (BAES) at regular intervals. RESULTS: Linear mixed effects models showed that poor inhibitory control was associated with greater stimulation and less sedation following alcohol compared with placebo. CONCLUSION: These findings provide the first direct evidence that individuals with poor inhibitory control experience greater sensitivity to the rewarding, stimulant effects of alcohol, and less sensitivity to the negative, sedative effects. These findings suggest that inhibition and subjective response to alcohol are not independent risk factors, and that together they constitute a heightened profile of risk for AUD.
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