Rationale <p>The relationship between alcohol misuse and aggression has long intrigued clinical and preclinical researchers. While acute alcohol use is well known to promote aggression, converging evidence indicates a more complex, bidirectional association. Both behaviors often arise from shared genetic, neurobiological, and environmental vulnerabilities and can mutually increase risk, creating a vicious spiral in which alcohol misuse and aggression reinforce one another over time.</p> Objective <p>This review synthesizes epidemiological, clinical, and experimental findings to establish an integrated framework linking alcohol misuse and aggression, while introducing a translational perspective connecting human and animal research.</p> Results &amp; conclusions <p>The relationship between alcohol misuse and aggression can be conceptualized through two complementary models. In the first, alcohol use facilitates aggression: acute intoxication disrupts executive control and heightens emotional reactivity, while chronic exposure induces neuroadaptations that sensitize individuals to aggression-promoting effects and may elevate aggression during abstinence. In the second, aggression increases vulnerability to alcohol misuse: longitudinal studies reveal that aggressive traits, emotional dysregulation, and externalizing psychopathology frequently precede problematic drinking. These pathways are influenced by shared dysfunctions within prefrontal–limbic circuits involved in emotion regulation and impulse control. Despite progress in modeling alcohol-induced aggression, little research addresses how aggressive phenotypes contribute to alcohol misuse, representing an important translational gap. Overall, this relationship is best understood as a dynamic, bidirectional system rooted in overlapping neurobehavioral mechanisms. By integrating clinical findings with preclinical models, this framework highlights targets for mechanistic investigation and the development of tailored therapeutic strategies.</p>

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Decoding the bidirectional links between alcohol misuse and aggression: toward a unified translational framework

  • Nicholas M. Russell,
  • Micah D. Frier,
  • Marco Bortolato,
  • Regina A. Mangieri

摘要

Rationale

The relationship between alcohol misuse and aggression has long intrigued clinical and preclinical researchers. While acute alcohol use is well known to promote aggression, converging evidence indicates a more complex, bidirectional association. Both behaviors often arise from shared genetic, neurobiological, and environmental vulnerabilities and can mutually increase risk, creating a vicious spiral in which alcohol misuse and aggression reinforce one another over time.

Objective

This review synthesizes epidemiological, clinical, and experimental findings to establish an integrated framework linking alcohol misuse and aggression, while introducing a translational perspective connecting human and animal research.

Results & conclusions

The relationship between alcohol misuse and aggression can be conceptualized through two complementary models. In the first, alcohol use facilitates aggression: acute intoxication disrupts executive control and heightens emotional reactivity, while chronic exposure induces neuroadaptations that sensitize individuals to aggression-promoting effects and may elevate aggression during abstinence. In the second, aggression increases vulnerability to alcohol misuse: longitudinal studies reveal that aggressive traits, emotional dysregulation, and externalizing psychopathology frequently precede problematic drinking. These pathways are influenced by shared dysfunctions within prefrontal–limbic circuits involved in emotion regulation and impulse control. Despite progress in modeling alcohol-induced aggression, little research addresses how aggressive phenotypes contribute to alcohol misuse, representing an important translational gap. Overall, this relationship is best understood as a dynamic, bidirectional system rooted in overlapping neurobehavioral mechanisms. By integrating clinical findings with preclinical models, this framework highlights targets for mechanistic investigation and the development of tailored therapeutic strategies.