Binge drinking and the differential influence of ethanol on cognitive control subprocesses: a novel field of neurotoxicology

Stock, Ann-Kathrin; Beste, Christian · 2014 · Crossref

DOI: 10.1007/s00204-013-1172-8

archive: archived pipeline: cataloged verified

Get this paper ↗ (DOI — opens at the source; we link to it, we don't host it)

Summary

This guest editorial addresses the growing prevalence of binge drinking, particularly among young people in Western cultures, and the resulting neurotoxicological concerns. Binge drinking is defined as consuming alcohol with the primary intention of reaching marked intoxication, characterized by a blood alcohol concentration of at least 0.8 ‰. This pattern differs from traditional alcoholism through its irregularity and the young age of consumers. Because the prefrontal cortex (PFC) undergoes development and maturation during adolescence and emerging adulthood, binge drinking before age 24 likely poses greater harm to executive functioning than consumption in later life stages. The authors highlight a critical gap in current research: while the adverse effects of chronic alcohol abuse are well-documented, there is a marked scarcity of studies investigating the acute effects of heavy, binge-like intoxication. This shortage hinders the ability to logically link acute intoxication effects to long-term consequences. The paper examines the neurobiological mechanisms underlying these effects. Acute alcohol intoxication alters several neurotransmitter systems, notably downregulating glutamatergic neurotransmission while enhancing signaling via GABA, dopamine, serotonin, and opioid peptides. These changes are expected to impact executive functions mediated by fronto-striatal loops, including response inhibition, task selection, task switching, and response monitoring. The authors argue against the assumption that alcohol causes a global, unspecific dampening of cognition. Instead, they propose that ethanol differentially influences distinct cognitive subprocesses, depending on the specific transmitter systems and neural circuits involved. To support this hypothesis, the authors reference their recent investigation into the acute effects of binge-like ethanol intoxication on task switching in young healthy humans. Their study demonstrated specific changes in both behavioral and neurophysiological measures, confirming that not all cognitive subprocesses are equally altered by ethanol. This finding suggests that executive deficits during pronounced intoxication result from disruptions in specific subsets of cognitive subprocesses rather than a uniform decline in higher-order cognition. The significance of this work lies in its potential to clarify how alcohol-related deficits develop and are maintained. The authors conclude that future research must investigate the development of these deficits through elaborate comparisons of behavioral and cognitive changes across acute intoxication, acute withdrawal, regular binge drinking, and long-term alcohol abuse. A key challenge is determining whether the deterioration of cognitive subprocesses follows a linear dose-effect relationship with blood alcohol concentrations or if certain processes decouple from this relationship based on their underlying neurobiological systems. Understanding these specific mechanisms is essential for linking acute intoxication effects to the long-term cognitive impairments observed in chronic alcohol abuse.

Provenance

The full processing record for this entry. Every stage of this paper's journey through the pipeline is logged — what ran, with which tool and model, how many attempts it took, and when it last completed.

Summary generated by qwen3.6-27b-prismaquant on 2026-06-25; verification: verified.

Topics

Ranked by relevance to this paper. Hover a topic for its definition.

• alcohol