An early onset of drinking has been associated with greater likelihood of subsequent alcohol use or alcohol use disorders (AUD), a finding that prompted educational and public policy efforts to impede or at least delay the age of first use of alcohol. Yet, it is not clear if these two events (i.e., first alcohol use and increased probability of later alcohol use) are linked in a causal chain. Some claim that both are manifestations of a third factor (e.g., pre-existing psychopathology) whereas others suggest that an early onset of alcohol use only heightens risk of AUD in those already at risk for these disorders, for instance due to chronic stress exposure or because of exhibiting a positive family history of alcohol problems. Animal (mostly rodent) models have been used to shed light upon these issues and, among other important findings, have suggested that an early onset of drinking can alter normal developmental trajectories of brain systems responsible for alcohol’s effects.
Moreover, it is not clear which drinking milestone (e.g., sipping, drinking a full glass, getting intoxicated) is the key factor in the association between early alcohol use and subsequent engagement in heavy alcohol use or heightened likelihood of AUD. Substantial attention has been recently devoted to binge drinking, a pattern of heavy alcohol use frequently defined as drinking 4-5 drinks (women/male, respectively) in a short time frame, approximately 2 hours or less. Binge drinking seems to be more common in adolescents than in adults, and several animal models of this pattern of drinking have been developed. These pre-clinical models allowed an important boost to the field, providing a benchmark to assess potential therapeutic strategies to diminish the effect of an early onset of alcohol use, or to study its behavioral and neurobiological underpinnings.
With this Research Topic we aim at bringing together different aspects of the field that assesses the effects of an early onset of alcohol use. Contributions addressing the prevalence and consequences of such early onset are welcomed, as well as those that address molecular aspects of this exposure or interventions aimed at reducing its consequences. Particularly important will be contributions that, either via pre-clinical or clinical approaches, aim at scrutinizing the mechanism underlying the putative promoting effect of an early age of alcohol use onset on subsequent alcohol use or AUD.
An early onset of drinking has been associated with greater likelihood of subsequent alcohol use or alcohol use disorders (AUD), a finding that prompted educational and public policy efforts to impede or at least delay the age of first use of alcohol. Yet, it is not clear if these two events (i.e., first alcohol use and increased probability of later alcohol use) are linked in a causal chain. Some claim that both are manifestations of a third factor (e.g., pre-existing psychopathology) whereas others suggest that an early onset of alcohol use only heightens risk of AUD in those already at risk for these disorders, for instance due to chronic stress exposure or because of exhibiting a positive family history of alcohol problems. Animal (mostly rodent) models have been used to shed light upon these issues and, among other important findings, have suggested that an early onset of drinking can alter normal developmental trajectories of brain systems responsible for alcohol’s effects.
Moreover, it is not clear which drinking milestone (e.g., sipping, drinking a full glass, getting intoxicated) is the key factor in the association between early alcohol use and subsequent engagement in heavy alcohol use or heightened likelihood of AUD. Substantial attention has been recently devoted to binge drinking, a pattern of heavy alcohol use frequently defined as drinking 4-5 drinks (women/male, respectively) in a short time frame, approximately 2 hours or less. Binge drinking seems to be more common in adolescents than in adults, and several animal models of this pattern of drinking have been developed. These pre-clinical models allowed an important boost to the field, providing a benchmark to assess potential therapeutic strategies to diminish the effect of an early onset of alcohol use, or to study its behavioral and neurobiological underpinnings.
With this Research Topic we aim at bringing together different aspects of the field that assesses the effects of an early onset of alcohol use. Contributions addressing the prevalence and consequences of such early onset are welcomed, as well as those that address molecular aspects of this exposure or interventions aimed at reducing its consequences. Particularly important will be contributions that, either via pre-clinical or clinical approaches, aim at scrutinizing the mechanism underlying the putative promoting effect of an early age of alcohol use onset on subsequent alcohol use or AUD.
