Young binge drinkers appear to show abnormal brain activity as measured by event-related potentials during response execution and inhibition which may represent a neural antecedent of difficulties in impulse control.

No abstract

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.

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.

Binge drinking or heavy episodic drinking is a high prevalent pattern of alcohol consumption among young people in several countries. Despite increasing evidence that binge drinking is associated with impairments in executive aspects of working memory (i.e. self-ordered working memory), processes known to depend on the mid-dorsolateral prefrontal cortex (Brodmann areas 46 and 9), less is known about the impact of binge drinking on prefrontal gray matter integrity. Here, we investigated the effects of binge drinking on gray matter volume of mid- dorsolateral prefrontal cortex in youths. We used voxel-based morphometry on the structural magnetic resonance images of subjects reporting a persistent (at least three years) binge drinking pattern of alcohol use (n = 11; age 22.43±1.03) and control subjects (n = 21; age 22.18±1.08) to measure differences in gray matter volume between both groups. In a region of interest analysis of the mid-dorsolateral prefrontal cortex, after co-varying for age and gender, we observed significantly larger gray matter volume in the left mid-dorsolateral prefrontal cortex (Brodmann areas 46 and 9) in binge drinkers in comparison with control subjects. Furthermore, there was a significant positive correlation between left mid-dorsolateral prefrontal cortex volume and Self-Ordered Pointing Test (SOPT) total errors score in binge drinkers. The left mid-dorsolateral prefrontal cortex volume also correlated with the quantity and speed of alcohol intake. These findings indicate that a repeated exposure to alcohol −that does not meet criteria for alcohol dependence− throughout post-adolescent years and young adulthood is linked with structural anomalies in mid-dorsolateral prefrontal regions critically involved in executive aspects of working memory.

Adolescence is a period of ongoing brain maturation characterized by hierarchical changes in the functional and structural networks. For this reason, the young brain is particularly vulnerable to the toxic effects of alcohol. Nowadays, binge drinking is a pattern of alcohol consumption increasingly prevalent among adolescents. The aim of the present study is to evaluate the evolution of the functional and anatomical connectivity of the Default Mode Network (DMN) in young binge drinkers along two years. Magnetoencephalography signal during eyes closed resting state as well as Diffusion Tensor Imaging (DTI) were acquired twice within a 2-year interval from 39 undergraduate students (22 controls, 17 binge drinkers) with neither personal nor family history of alcoholism. The group comparison showed that, after maintaining a binge drinking pattern along at least two years, binge drinkers displayed an increased brain connectivity of the DMN in comparison with the control group. On the other hand, the structural connectivity did not show significant differences neither between groups nor over the time. These findings point out that a continued pattern of binge drinking leads to functional alterations in the normal brain maturation process, even before anatomical changes can be detected.

Binge Drinking (BD) is a pattern of intermittent intensive alcohol intake which has spread among young adults over the last decades. Adolescence constitutes a critical neuromaturation period in which the brain is particularly sensitive to the effects of alcohol. However, little is known about how BD affects the brain activity. This study aimed to characterize the brain's functional organization in BD and non-BD young population by means of analyzing functional connectivity (FC) and relative power spectra (PS) profiles measured with magnetoencephalography (MEG) during eyes-closed resting state. Our sample composed 73 first-year university students (35 BDs and 38 controls). Results showed that the BD subjects displayed a decreased alpha FC in frontal-parietal regions, and conversely, an enhanced FC in the delta, theta and beta bands in fronto-temporal networks. Besides the FC differences, the BD group showed a decreased PS within alpha range and an increased PS within theta range in the brain's occipital region. These differences in FC and PS measurements provide new evidence of the neurophysiological alterations related to the alcohol neurotoxicity and could represent an initial sign of an anomalous neural activity caused by a BD pattern of alcohol consumption during youth.

It is well known that alcohol impairs response inhibition and that adolescence is a critical period of neuromaturation where cognitive processes such as inhibitory control are still developing. In recent years, growing evidence has shown the negative consequences of alcohol binge drinking on the adolescent and young human brain. However, the effects of cessation of binge drinking on brain function remain unexplored. The objective of the present study was to examine brain activity during response execution and inhibition in young binge drinkers in relation to the progression of their drinking habits over time. Event-related potentials (ERPs) elicited by a Go/NoGo task were recorded twice within a 2-year interval in 57 undergraduate students (25 controls, 22 binge drinkers, and 10 ex-binge drinkers) with no personal or family history of alcoholism or psychopathological disorders. The results showed that the amplitude of NoGo-P3 over the frontal region correlated with an earlier age of onset of regular drinking as well as with greater quantity and speed of alcohol consumption. Regression analysis showed that NoGo-P3 amplitude was significantly predicted by the speed of alcohol intake and the age of onset of regular drinking. The group comparisons showed that, after maintaining a binge drinking pattern for at least 2 years, binge drinkers displayed significantly larger NoGo-P3 amplitudes than controls, whereas ex-binge drinkers were in an intermediate position between the two other groups (with no significant differences with respect to controls or binge drinkers). These findings suggest that binge drinking in young people may impair the neural functioning related to inhibitory processes, and that the cessation of binge drinking may act as a brake on the neurophysiological impairments related to response inhibition.