Journal article
E. Burnette, E. Grodin, Joseph P. Schacht, L. Ray
Alcoholism, clinical and experimental research, 2020
Alcoholism, clinical and experimental research, 2020
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APA
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Burnette, E., Grodin, E., Schacht, J. P., & Ray, L. (2020). Clinical and neural correlates of reward and relief drinking. Alcoholism, Clinical and Experimental Research.
Chicago/Turabian
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Burnette, E., E. Grodin, Joseph P. Schacht, and L. Ray. “Clinical and Neural Correlates of Reward and Relief Drinking.” Alcoholism, clinical and experimental research (2020).
MLA
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Burnette, E., et al. “Clinical and Neural Correlates of Reward and Relief Drinking.” Alcoholism, Clinical and Experimental Research, 2020.
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@article{e2020a,
title = {Clinical and neural correlates of reward and relief drinking.},
year = {2020},
journal = {Alcoholism, clinical and experimental research},
author = {Burnette, E. and Grodin, E. and Schacht, Joseph P. and Ray, L.}
}
Abstract
BACKGROUND Alcohol use disorder (AUD) is heterogenous. One approach to parsing this heterogeneity is to phenotype individuals by their underlying motivation to drink, specifically drinking for reward (i.e. positive reinforcement) or for relief (i.e. negative reinforcement/normalizing). Reward- vs. relief-motivated behavior is thought to be associated with a shift from ventral to dorsal striatal signaling. The present study examined whether reward and relief drinking were differentially associated with other clinical characteristics and with alcohol cue-elicited activation of the ventral and dorsal striatum.
METHODS Non-treatment-seeking heavy drinkers (N=184; 61 female, 123 male) completed the UCLA Reward, Relief, Habit Drinking Scale (RRHDS) and the Reasons for Heavy Drinking Questionnaire (RHDQ), to categorize drinking motivation. Measures of alcohol use, alcohol problems, mood, and craving were also collected. A subset of participants (N=45; 17 female, 28 male) also completed a functional neuroimaging alcohol cue reactivity task.
RESULTS RRHDS-designated relief/habit drinkers scored lower than reward drinkers on the RHDQ Reinforcement subscale (p=0.04) and higher on the RHDQ Normalizing subscale (p=0.004). Relief/habit drinkers also demonstrated greater AUD severity on a host of clinical measures. Relief/habit drinkers displayed higher cue-elicited dorsal striatal activation compared to reward drinkers (p=0.04), while ventral striatal cue-elicited activation did not significantly differ between groups.
CONCLUSIONS Our findings support and extend the differentiation of reward from relief/habit-motivated drinking and suggest that differences in dorsal striatal response to conditioned alcohol cues may underlie this distinction. Elucidating neurobiological and clinical differences between these subtypes may facilitate treatment matching and precision medicine for AUD.
