Craving, cortisol and behavioral alcohol motivation responses to stress and alcohol cue contexts and discrete cues in binge and non-binge drinkers.

Alcohol use disorders are associated with high craving and disruption of stress biology, but their role in behavioral alcohol motivation is less clear. We examined the effects of craving and cortisol responses on behavioral alcohol motivation to stress, alcohol cue and neutral-relaxing context cues, in addition to discrete alcohol cues, in demographically matched binge/heavy (BH) and moderate (MD) social drinkers. Subjects participated in a 3-day laboratory experiment of provocation by three personalized guided imagery contexts and discrete alcohol cues followed by the 'alcohol taste test' (ATT) to assess behavioral motivation, as measured by ATT intake. Post-ATT alcohol effects on craving and cortisol responses were also examined. Results indicate BH consumed significantly more alcohol than MD in the ATT. Stress and alcohol cue contexts, relative to neutral, led to significantly greater ATT intake across both groups, which also correlated positively with self-reported alcohol use in past 30 days. Stress and alcohol context and discrete alcohol cues each significantly increased alcohol craving, more so in the BH than MD, and significantly predicted greater ATT intake in BH only. The BH showed significantly lower cortisol responses than MD overall and blunted cortisol responses to cues predicted significantly greater ATT intake in the stress condition for BH and in the alcohol cue condition for MD. Higher ATT intake predicted greater cortisol response and higher craving post-ATT, and these effects were moderated by group status. In sum, findings suggest a role for sensitized context-induced craving and blunted cortisol responses in increased behavioral motivation for alcohol.

Stress vulnerability and alcohol use and consequences: From human laboratory studies to clinical outcomes.

It is well known that vulnerability to stress is a risk factor for alcohol use disorder (AUD). Chronic alcohol use can result in neuroadaptations in cortico-striatal pathways and hypothalamic pituitary adrenal (HPA) axis function that are manifested in altered behavioral and cognitive control functions contributing to alcohol craving, compulsive motivation, consumption, and consequences. This symposium brings together studies utilizing novel approaches to help improve our understanding of stress - past, acute, and chronic - on alcohol seeking and consumption and related outcomes using a combination of human laboratory models, neuroimaging, and clinical measures. Examining factors that determine vulnerability as well as resilience to stress are of particular interest in the study of AUD because, in addition to increasing our understanding of the risk factors for AUD, such knowledge can be used to develop more effective treatments. Dr. Stangl presented a novel human experimental model that demonstrates, for the first time, stress-induced increases in alcohol self-administration in binge drinkers using a guided imagery paradigm combined with intravenous alcohol self-administration (IV-ASA). Dr. Blaine presented data demonstrating that glucocorticoid response to stress drives compulsive alcohol motivation and intake in binge/heavy drinkers. Dr. Plawecki presented data examining sex differences in the effect of two distinct stress paradigms - mood induction and abstinence - on IV-ASA in moderate drinkers. Dr. Schwandt presented clinical data providing a new perspective on the relationship between childhood trauma and AUD by suggesting possible underlying mechanisms that confer resilience, rather than vulnerability, to severe early life stress exposure.