Influence of stress associated with chronic alcohol exposure on drinking.
paper
Cited
Public
- Authors
- Becker, Howard C
- Year
- 2017
- Journal
- Neuropharmacology
- PMID
- 28431971
- DOI
- 10.1016/j.neuropharm.2017.04.028
- PMCID
- PMC5497303
Stress is commonly regarded as an important trigger for relapse and a significant factor that promotes increased motivation to drink in some individuals. However, the relationship between stress and alcohol is complex, likely changing in form during the transition from early moderated alcohol use to more heavy uncontrolled alcohol intake. A growing body of evidence indicates that prolonged excessive alcohol consumption serves as a potent stressor, producing persistent dysregulation of brain reward and stress systems beyond normal homeostatic limits. This progressive dysfunctional (allostatic) state is characterized by changes in neuroendocrine and brain stress pathways that underlie expression of withdrawal symptoms that reflect a negative affective state (dysphoria, anxiety), as well as increased motivation to self-administer alcohol. This review highlights literature supportive of this theoretical framework for alcohol addiction. In particular, evidence for stress-related neural, physiological, and behavioral changes associated with chronic alcohol exposure and withdrawal experience is presented. Additionally, this review focuses on the effects of chronic alcohol-induced changes in several pro-stress neuropeptides (corticotropin-releasing factor, dynorphin) and anti-stress neuropeptide systems (nocicepton, neuropeptide Y, oxytocin) in contributing to the stress, negative emotional, and motivational consequences of chronic alcohol exposure. Studies involving use of animal models have significantly increased our understanding of the dynamic stress-related physiological mechanisms and psychological underpinnings of alcohol addiction. This, in turn, is crucial for developing new and more effective therapeutics for treating excessive, harmful drinking, particularly stress-enhanced alcohol consumption. This article is part of the Special Issue entitled "Alcoholism".
Stress Influences on the Progression of Alcohol Addiction.When drinking is first initiated and regulated, alcohol and stress interact in a complex manner. Stress may promote alcohol consumption via glucocorticoid interactions with brain reward systems and, for some individuals, the anxiolytic (stress-alleviating) effect alcohol may influence motivation to drink. Continued heavy drinking results in fundamental changes in brain function. Under assault from continued alcohol exposure, the brain engages a host of adaptations in brain reward and stress systems that contribute to the perpetuation of excessive levels of drinking. Stress associated with heavy bouts of drinking and repeated failed attempts at abstinence fuel progressive dysregulation of these brain systems beyond normal homeostatic limits, setting the stage for a persistent dysfunctional (allostatic) state. This is characterized by exaggerated neuroadaptations that manifest as reduced reward processing, a blunted neuroendocrine stress response, engagement of extra-hypothalamic stress (e.g., CRF, dynorphin) and anti-stress (e.g., nociceptin, NPY, oxytocin) systems, and heightened autonomic nervous system (sympathomimetic) function. Collectively, these changes contribute to a persistent negative emotional (affective) state along with compromised executive function that renders individuals ill-equipped to exert appropriate behavioral control over alcohol consumption, as well as appropriately respond to stressful events that may provoke return to excessive drinking.
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