Previous research indicates that alcohol intoxication impairs inhibitory control and that the right dorsolateral prefrontal cortex (rDLPFC) is a functional brain region important for exercising control over thoughts and behaviour. At the same time, the extent to which changes in inhibitory control following initial intoxication mediate subsequent drinking behaviours has not been elucidated fully. Ascertaining the extent to which inhibitory control impairments drive alcohol consumption, we applied continuous theta burst transcranial magnetic stimulation (rDLPFC cTBS vs. control) to isolate how inhibitory control impairments (measured using the Stop-Signal task) shape ad libitum alcohol consumption in a pseudo taste test. Twenty participants (13 males) took part in a within-participants design; their age ranged between 18 and 27 years (M = 20.95, SD = 2.74). Results indicate that following rDLPFC cTBS participants’ inhibitory control was impaired, and ad libitum consumption increased. The relationship between stimulation and consumption did not appear to be mediated by inhibitory control in the present study. Overall, findings suggest that applying TMS to the rDLPFC may inhibit neural activity and increase alcohol consumption. Future research with greater power is recommended to determine the extent to which inhibitory control is the primary mechanism by which the rDLPFC exerts influence over alcohol consumption, and the degree to which other cognitive processes may play a role.
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.
In the absence of any pharmacological effects of alcohol, social and environmental context have an interactive impact on shaping consumption.
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.
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.
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