Elevated ad libitum alcohol consumption following continuous theta burst stimulation to the left-dorsolateral prefrontal cortex is partially mediated by changes in craving.

Previous research indicates that following alcohol intoxication, activity in prefrontal cortices is reduced, linking to changes in associated cognitive processes, such as inhibitory control, attentional bias (AB), and craving. While these changes have been implicated in alcohol consumption behaviour, it has yet to be fully illuminated how these frontal regions and cognitive processes interact to govern alcohol consumption behaviour. The current preregistered study applied continuous theta burst transcranial magnetic stimulation (cTBS) to examine directly these relationships while removing the wider pharmacological effects of alcohol. A mixed design was implemented, with cTBS stimulation to right and left dorsolateral prefrontal cortex (DLPFC), the medial orbital frontal cortex (mOFC) and Vertex, with measures of inhibitory control, AB, and craving taken both pre- and post-stimulation. Ad libitum consumption was measured using a bogus taste task. Results suggest that rDLPFC stimulation impaired inhibitory control but did not significantly increase ad libitum consumption. However, lDLPFC stimulation heightened craving and increased consumption, with findings indicating that changes in craving partially mediated the relationship between cTBS stimulation of prefrontal regions and ad libitum consumption. Medial OFC stimulation and AB findings were inconclusive. Overall, results implicate the left DLPFC in the regulation of craving, which appears to be a prepotent cognitive mechanism by which alcohol consumption is driven and maintained.

Intoxication without anticipation: Disentangling pharmacological from expected effects of alcohol.

BACKGROUND: The pharmacological effects of alcohol on executive function, craving and subsequent alcohol-seeking have been well documented. Yet, insufficient methodological controls within existing alcohol administration paradigms have meant that the relative importance of alcohol's pharmacological and anticipatory effects remains in need of further elucidation. AIM: The objective of this study is to disentangle alcohol's pharmacological effects from its anticipatory effects on alcohol-related cognitions and subsequent consumption. METHODS: Inhibitory control, attentional bias and craving were assessed pre- and post-consumption in 100 participants who were randomly allocated to one of four beverage conditions in a two by two design: (1) alcohol aware (alcohol with participant knowledge (pharmacological/anticipation effects)), (2) alcohol blind (alcohol without participant knowledge; in a novel grain alcohol masking condition (pharmacological/no anticipation effects)), (3) placebo (no alcohol but participants were deceived (anticipation/non-pharmacological effects)) and (4) pure control (no alcohol with participant knowledge (no anticipation/non-pharmacological effects)). RESULTS: Findings suggest that the pharmacological effects of alcohol result in greater inhibitory control impairments compared with anticipated effects. Anticipatory but not the pharmacological effects of alcohol were found to increase attentional bias. Both pharmacology and anticipation resulted in increased craving, though higher levels of craving were observed due to alcohol's pharmacology. Furthermore, alcohol pharmacology resulted in heightened ad libitum consumption; however, anticipation did not. Changes in craving partially mediated the relationship between initial intoxication and subsequent drinking, while inhibitory control impairments did not. CONCLUSIONS: Successive alcohol consumption appears driven primarily by the pharmacological effects of alcohol which are exerted via changes in craving.

The Effects of Placebo and Moderate Dose Alcohol on Attentional Bias, Inhibitory Control and Subjective Craving.

AIMS: Previous research indicates that acute alcohol intoxication and placebo can inhibit people's control over consumption behaviour and heighten attentional bias (AB) towards alcohol-related stimuli and craving. We designed a study to disentangle anticipated from pharmacological effects of alcohol in order to gain a clearer view of their relative contributions to alcohol consumption. METHODS: In a within-participants design (moderate alcohol dose, placebo and control), and over a minimum 2-week period, participants completed a battery of questionnaires and cognitive tasks, followed by a bogus taste task to measure ad libitum consumption. RESULTS: Both alcohol preload and placebo resulted in cognitive and psychological changes, including impaired inhibitory control, heightened AB and craving. However, ad libitum consumption only increased following alcohol and not placebo. Furthermore, inhibitory control impairments did not mediate the relationship between initial intoxication and ad libitum consumption, and findings indicate that increases in craving may mediate this association. CONCLUSION: Psychological processes such as craving may be more important in driving consummatory behaviour relative to transient changes in cognitive processes, such as inhibitory control.