Heavy drinking is the third leading cause of preventable death in the U.S. and is the second leading cause of
disability among adults aged 24-44, however, there are two important gaps in current knowledge: 1) the
mechanisms underlying less severe forms of AUD, like problem drinking (PD), are poorly understood, as are 2)
the mechanisms underlying behavior change in PD, including both spontaneous (non-treatment) behavior
change and behavior change that results from brief interventions (BI), which are particularly effective in PD .
Here, we address the first gap by positing that PD have heightened incentive salience to alcohol cues
(reactivity) and impaired ability to regulate incentive salience (regulation), compared to social drinkers (SD).
We will test this hypothesis at a neural and behavioral level in the lab using functional MRI (fMRI) and in the
natural environment ecological momentary assessment (EMA). We address the second gap by positing that
whereas spontaneous behavior change in PD depends primarily upon the reactivity processes, behavior
change in response to a BI depends primarily upon regulation processes. To these ends, we will recruit 100
PDs and 50 social drinkers (SD). At baseline, all participants will complete two weeks of EMA, perform an
alcohol regulation of craving (ROC) task during fMRI scanning, and then complete 3 more weeks of EMA. The
ROC task provides behavioral and fMRI measures of reactivity (e.g. increased ventral striatum activity and
reports of cue-induced alcohol craving) regulation (e.g. control-related prefrontal activity and diminished
craving). The analyses will test for group differences in baseline neural and environmental measures of
reactivity and regulation. Next, PDs will be randomized to receive either a BI immediately or to receive the BI
after 6 months, after outcomes are measured (the delayed intervention control, or DIC group). Both BI and DIC
groups will complete an EMA protocol for the three weeks following assignment. Drinking outcomes will be
assessed at 3 and 6 months. We expect that relative to SDs, PDs will show heightened neural measures of
reactivity (e.g. elevated ventral striatum (VS) activation to alcohol cues in passive viewing conditions), and
reduced neural measures of regulation (e.g. reduced activity in prefrontal control regions during regulation
conditions) (Aim 1). In parallel, PDs will report higher levels of reactivity and lower levels of regulation in EMA
measures, compared to SD, which will be correlated with fMRI measures (Aim 2). We predict that in the BI
group, reduction in alcohol use will be moderated by the functioning of neural systems for regulation (e.g.
dorsolateral PFC), whereas in the DIC group a persistence of alcohol use will be moderated by the functioning
of neural systems for reactivity (e.g. VS) (Aim 3). Finally, we predict that in the BI group, changes in alcohol
use will be mediated by changes in EMA measures of regulation and predicted by pre-treatment indices of
regulation in the ROC task, whereas in the DIC group, changes in alcohol use will be mediated by changes in
EMA measures of reactivity and predicted by pre-treatment measures of reactivity in the ROC task (Aim 4).