Aims: Adolescence is usually the time when individuals first drink alcohol and this has been associated with relatively weak or immature inhibitory control. This review examines the changes on brain development and inhibitory function that take place during adolescence and youth as well as the relationship between inhibitory control and alcohol use at this early age. Methods: Narrative review of the chief studies related to (a) the development of inhibitory control during adolescence, (b) the deficits in the inhibitory ability in alcohol use disorders and (c) the effects of acute alcohol intake and binge drinking on inhibitory control in adolescents and young adults. Results: Inhibitory control processes are developing during adolescence and youth. Poor inhibitory functions may predispose the individual to alcohol misuse. Likewise, acute and binge alcohol drinking may impair the inhibitory control and compromise the ability to prevent or stop behaviour related to alcohol use. Conclusion: Poor inhibitory control can be both the cause and the consequence of excessive alcohol use. Adolescence and young adulthood may be a particularly vulnerable period due to (a) the weak or immature inhibitory functioning typical of this stage may contribute to the inability of the individual to control alcohol use and (b) alcohol consumption per se may alter or interrupt the proper development of inhibitory control leading to a reduced ability to regulate alcohol intake. Further longitudinal research is needed to evaluate the interaction between inhibitory control dysfunction and alcohol use in both situations.
Aims: The objective of this study was to examine brain activity related to visual attention processes in youths who had maintained a binge drinking (BD) pattern of alcohol consumption for >2 years. Methods: The participants were 57 university students (26 binge drinkers: BDs) with no personal or family history of alcoholism or psychopathological disorders in first-degree relatives. Event-related potentials (ERPs) were recorded while participants performed a visual oddball task (twice within a 2-year interval). The latency and amplitude of the P3b component of the ERPs were analysed. Results: The P3b amplitude was larger in young BDs than in aged-matched controls at both evaluation times, and the difference was more pronounced after 2 years of maintenance of a BD pattern of consumption. The larger P3b amplitude was associated with an earlier onset of regular drinking and with a greater quantity and intensity of consumption. Conclusions: These findings suggest that young BDs exhibit anomalies in neural activity involved in attentional/working memory processes, which increase after 2 years of maintenance of BD. This anomalous neural activity may reflect underlying dysfunctions in neurophysiological mechanisms as well as the recruitment of additional attentional/working memory resources to enable the binge drinkers to perform the task adequately.