A retrospective analysis of psychosocial risk factors modulating adolescent alcohol binge drinking.

BACKGROUND/AIMS: Adolescent alcohol binge-induced hospital admissions (BIHAs) are an increasing problem in Europe. We investigated whether psychosocial factors (e.g., drinking situations, drinking occasions and neighborhood unemployment) are associated with particularly risky patterns of alcohol or substance use. METHOD: We performed a systematic retrospective chart review of all the respective cases in 2003-2008 (n = 586; age range: 12-17 years) from both pediatric hospitals in the city of Dresden, Germany. RESULTS: The vast majority of adolescent BIHAs were associated with drinking together with peers at weekend parties. Compared to this 'typical' drinking pattern, adolescents drinking 'atypically' (i.e., drinking either alone, to cope or despite the fact that the next day was a school/work day) more often had already used alcohol and illegal substances before and were more often diagnosed with substance use disorders and other mental disorders prior to BIHA. The unemployment rate in the patients' neighborhood was positively related to the incidence proportion of adolescent BIHAs in the respective subdistricts (r(s) = 0.61). CONCLUSION: Adolescent atypical drinking may indicate an increased risk for the development of alcohol and substance use disorders. This information is quickly accessible and can alert clinicians to initiate psychosocial aftercare; their infrastructure should address the strong relation between BIHA probability and neighborhood unemployment rates.

Alcohol-induced impairment of inhibitory control is linked to attenuated brain responses in right fronto-temporal cortex.

BACKGROUND: A self-enhancing loop between impaired inhibitory control under alcohol and alcohol consumption has been proposed as a possible mechanism underlying dysfunctional drinking in susceptible people. However, the neural underpinnings of alcohol-induced impairment of inhibitory control are widely unknown. METHODS: We measured inhibitory control in 50 young adults with a stop-signal task during functional magnetic resonance imaging. In a single-blind placebo-controlled cross-over design, all participants performed the stop-signal task once under alcohol with a breath alcohol concentration of .6 g/kg and once under placebo. In addition, alcohol consumption was assessed with a free-access alcohol self-administration paradigm in the same participants. RESULTS: Inhibitory control was robustly decreased under alcohol compared with placebo, indicated by longer stop-signal reaction times. On the neural level, impaired inhibitory control under alcohol was associated with attenuated brain responses in the right fronto-temporal portion of the inhibition network that supports the attentional capture of infrequent stop-signals and subsequent updating of action plans from response execution to inhibition. Furthermore, the extent of alcohol-induced impairment of inhibitory control predicted free-access alcohol consumption. CONCLUSIONS: We suggest that during inhibitory control alcohol affects cognitive processes preceding actual motor inhibition. Under alcohol, decreased brain responses in right fronto-temporal areas might slow down the attentional capture of infrequent stop-signals and subsequent updating of action plans, which leads to impaired inhibitory control. In turn, pronounced alcohol-induced impairment of inhibitory control might enhance alcohol consumption in young adults, which might promote future alcohol problems.