Binge Drinking: Current Diagnostic and Therapeutic Issues

International audienceThe concept of binge drinking (BD) refers to patterns of heavy episodic alcohol consumption, with BD primarily occurring among adolescents and young adults. Several official definitions of BD have been proposed, in particular by the World Health Organization, the National Institute on Alcoholism and Alcohol Abuse, and the Substance Abuse and Mental Health Services Administration. Nevertheless, none of these definitions address the psychosocial and medical consequences of the type of alcohol use seen in BD. In practice, BD can thus correspond to either hazardous or harmful use of alcohol (HUA), while the episodic nature of heavy drinking in BD means that it does not meet the criteria for `alcohol dependence'. This diagnostic differentiation is important because it determines which type of intervention is recommended. Psychosocial, rather than pharmacological, interventions are recommended as first-line treatment for adults with HUA, while pharmacological treatment is recommended for alcohol dependence; however, HUA appears to be associated with much poorer outcomes in adolescents, which could thus warrant early use of pharmacotherapy in this patient group. For HUA, and especially in adolescents, there is currently a severe lack of data regarding the efficacy and safety of the different drugs that have been approved for adults with alcohol dependence. Various guidelines propose the use of drugs for some types of BD but that use remains off-label and empirical, which raises important safety and ethical concerns. Future research on BD should systematically assess the criteria for HUA to better differentiate its subtypes with actual consequences and better address the heterogeneity of BD in terms of both clinical profiles and outcomes. Regarding pharmacotherapy, some national guidelines have recommended nalmefene for `mild' dependence or second-line treatment for HUA, but such recommendations are not supported by evidence. Only naltrexone has been investigated in HUA but not in adolescents. More clinical trials should be conducted among adolescents with BD and HUA criteria to determine the most appropriate use of drugs in this particularly vulnerable population of subjects

GluN2B Subunit of the NMDA Receptor: The Keystone of the Effects of Alcohol During Neurodevelopment

International audienceThe glutamatergic system plays a central role in both the acute and chronic effects of ethanol. Among all the glutamate receptors the ionotropic NMDA receptors are crucial because of their role in synaptic plasticity. A large body of evidences suggests that short-term and long-term effects of ethanol may change synaptic plasticity via an alteration of the expression of the GluN2B subunit, one constitutive element of the NMDA receptor. The present review is focusing on the role of the GluN2B subunit after ethanol exposure during early life (in utero and adolescence) and also at adulthood. The roles of other NMDA subunits are also discussed in the context of the increasing evidence that the ratio of the different subunits, such as GluN2A-to-GluN2B, seems to better reflect the effects of ethanol and to explain how ethanol exposure can have short lasting and long lasting effects on synaptic plasticity, cognitive processes and some of the ethanol-related behaviors

Substance-use disorders in later life

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Corrélats neuro-anatomiques de la pratique du binge-drinking: résultats de l’étude Européenne Alcobinge

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Sex difference in the vulnerability to hippocampus plasticity impairment after binge-like ethanol exposure in adolescent rat: Is estrogen the key?

International audienceBinge drinking during adolescence induces memory impairments, and evidences suggest that females are more vulnerable than males. However, the reason for such a difference is unclear, whereas preclinical studies addressing this question are lacking. Here we tested the hypothesis that endogenous estrogen level (E2) may explain sex differences in the effects of ethanol on hippocampus plasticity, the cellular mechanism of memory. Long-term depression (LTD) in hippocampus slice of pubertal female rats was recorded 24 h after two ethanol binges (3 g/kg, i.p., 9 h apart). Neither the estrous cycle nor ethanol altered LTD. However, if ethanol was administered during proestrus (i.e., at endogenous E2 peak), LTD was abolished 24 h later, whereas NMDA-fEPSPs response to a GluN2B antagonist increased. The abolition of LTD was not observed in adult female rats. Exogenous E2 combined with ethanol replicated LTD abolition in pubertal, prepubertal female, and in pubertal male rats without changes in ethanol metabolism. In male rats, a higher dose of ethanol was required to abolish LTD at 24-h delay. In pubertal female rats, tamoxifen, an antagonist of estrogen receptors, blocked the impairing effects of endogenous and exogenous E2 on LTD, suggesting estrogen interacts with ethanol through changes in gene expression. In addition, tamoxifen prevented LTD abolition at 24 h but not at 48-h delay. In conclusion, estrogen may explain the increased vulnerability to ethanol-induced plasticity impairment seen in females compared with males. This increased vulnerability of female rats is likely due to changes in the GluN2B subunit that represent a common target between ethanol and estrogen

The genetics of alcoholic liver disease: better patient group definition is required.

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Hétérogénéité des déterminants du comportement de binge drinking : arguments en faveur d’une typologie

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Efficacy of psychedelics in animal models of binge drinking and alcohol use disorder

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