Rationale: The relationship between inhibitory control and alcohol consumption is well established, with research suggesting that impaired inhibitory control is associated with heightened alcohol consumption (e.g. Christiansen, Cole, Goudie, & Field, 2012) . Furthermore, it has been demonstrated that acute alcohol intoxication results in inhibitory control impairments and it is suggested that these impairments mediate subsequent alcohol consumption (c.f. Field, Wiers, Christiansen, Fillmore, & Verster, 2010) . However, alcohol intoxication has widespread neuro- and psychopharmacological effects (c.f. Koob & Volkow, 2010; Koob, 2014) . Aims: Therefore, the current study aimed to investigate the specific relationship between acute impairments of inhibitory control and subsequent alcohol consumption. Design: Transcranial Magnetic Stimulation (TMS) was used in a within-participants design to stimulate the right dorsolateral pre-frontal cortex (rDLPFC), in order to impair inhibitory control. Participants underwent TMS in two experimental sessions, once to the rDLPFC and once to the Vertex (control). Measures: A measure of inhibitory control was taken using the Stop-Signal task at baseline and both post-stimulations. Subsequent alcohol consumption was measured in the laboratory using a bogus taste task. Hypotheses: It was predicted that stimulation to rDLPFC would result in significantly impaired inhibitory control and increased ad libitum alcohol consumption, and inhibitory control impairments would mediate the relationship between stimulation and consumption. Results: TMS stimulation to the rDLPFC resulted in impaired inhibitory control compared to both control stimulation and baseline. Moreover, ad libitum consumption was significantly greater in the rDLPFC stimulation condition compared to control and this consumption was associated with acute impairments in inhibitory control. However, impairments in inhibitory control did not mediate this association. Conclusions: Findings suggest that inhibitory control may not be the central mechanism controlling alcohol consumption, and other cognitive mechanisms may play a more determinant role. Wider implications and further research are discussed.
Co-Authors
Dr. Rebecca Monk, Edge Hill University Dr. Adam Qureshi, Edge Hill University Dr. Stergios Makris, Edge Hill University Prof. Derek Heim, Edge Hill University
Conflicts of interest:
No conflict of interest
