Citation

Blanco-Ramos J, Cadaveira F, Folgueira-Ares R, Corral M, Rodríguez Holguín S. Int. J. Environ. Res. Public Health 2019; 16(22): e16224550.

Affiliation

Department of Clinical Psychology and Psychobiology, Universidade de Santiago de Compostela, 15782 Santiago de Compostela, Spain.

Copyright

(Copyright © 2019, MDPI: Multidisciplinary Digital Publishing Institute)

DOI

10.3390/ijerph16224550

PMID

31752082

Abstract

Binge drinking is a common pattern of alcohol consumption in adolescence and youth. Neurocognitive dual-process models attribute substance use disorders and risk behaviours during adolescence to an imbalance between an overactivated affective-automatic system (involved in motivational and affective processing) and a reflective system (involved in cognitive inhibitory control). The aim of the present study was to investigate at the electrophysiological level the degree to which the motivational value of alcohol-related stimuli modulates the inhibition of a prepotent response in binge drinkers. First-year university students (n = 151, 54 % females) classified as binge drinkers (n = 71, ≥6 binge drinking episodes, defined as 5/7 standard drinks per occasion in the last 180 days) and controls (n = 80, <6 binge drinking episodes in the last 180 days) performed a beverage Go/NoGo task (pictures of alcoholic and nonalcoholic drinks were presented according to the condition as Go or NoGo stimuli; Go probability = 0.75) during event-related potential recording. In binge drinkers but not controls, the amplitude of the anterior N2-NoGo was larger in response to nonalcohol than in response to alcohol pictures. No behavioural difference in task performance was observed. In terms of dual-process models, binge drinkers may require increased activation to monitor conflict in order to compensate for overactivation of the affective-automatic system caused by alcohol-related bias.

Language: en

Keywords

Go/NoGo; adolescence; alcohol consumption; binge drinking; dual-process model; event-related potentials; neurocognitive; response inhibition