The DOI matches its Crossref record; 134 of the 134 references it cites were found in a registry or an index.
Alcohol, stress, and glucocorticoids: From risk to dependence and relapse in alcohol use disorders
Open accessAbstract
In this review, we detail the clinical evidence supporting the role of psychological and physiological stress in instrumental motivation for alcohol consumption during the development of mild to moderate alcohol use disorders (AUDs) and in the compulsive, habitual alcohol consumption seen in severe, chronic, relapsing AUDs. Traditionally, the study of AUDs has focused on the direct and indirect effects of alcohol on striatal dopaminergic pathways and their role in the reinforcing effects of alcohol. However, growing evidence also suggests that alcohol directly stimulates the hypothalamic pituitary adrenal (HPA) axis and has effects on glucocorticoid receptors in extrahypothalamic, limbic forebrain, and medial Prefrontal Cortex (PFC) circuits, which contribute to the development of AUDs and their progression in severity, chronicity, and relapse risk. Evidence indicates HPA axis, glucocorticoid, and PFC dysfunction during protracted withdrawal and under high arousal conditions in those with severe AUDs, and novel evidence is also emerging to suggest HPA axis dysfunction with binge/heavy drinking, which is associated with motivation for alcohol in non-dependent individuals. Specifically, alcohol-associated alterations in HPA axis responses to stress and alcohol cues may serve as interoceptive physiological signals and facilitate conditioning mechanisms to influence alcohol motivation. Thus, this dysfunction may serve as a potential biomarker of both risk and of relapse. Based on this emerging data, we conceptualize and present early evidence for treatment targets that may improve PFC function and/or normalize HPA axis functioning and may be beneficial in the treatment and relapse prevention of AUDs. Finally, we suggest that individual differences in alcohol-related pathophysiology in these circuits may modulate treatment and recovery response, thereby supporting the need for building personalized medicine algorithms to understand and treat AUDs. This article is part of the Special Issue entitled "Alcoholism".
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“Chronic activation of the HPA axis causes sustained cortisol to increase and altered stress responses, which is a common occurrence in substance addiction [35].”
From The Impact of Social Media & Technology on Child and Adolescent Mental Health (2025) · cites this paper as [35]
Experimental — accuracy not yet measuredIn the citing paper
“Both chronic stress and long-standing alcohol use promote PFC dysfunction [172].”
From Food Addiction and Psychosocial Adversity: Biological Embedding, Contextual Factors, and Public Health Implications (2020) · cites this paper as [172]
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Drawbacks to strengthening neural salience encoding: a link between cortisol and risky drinkingPreprint
Harris, B. B., Sinha, R., & Goldfarb, E. V. (2024) · doi:10.31234/osf.io/kht4d · Cited by 2
“Finally, cortisol effects on brain and behavior can differ based on drinking history ( Blaine and Sinha, 2017 ).”
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“…(Cinar et al., 2008; Pedersen et al., 2023; Subramaniam et al., 2019), exercise habits (Caplin et al., 2021), diet (Tomiyama et al., 2010), recent infections (Alzahrani et al., 2021), and alcohol, including recency of use and family history (for a review, see Blaine & Sinha, 2017).”
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Metadata
- Authors
- Blaine, S. K., & Sinha, R.
- Affiliations
- Yale University (US)
- Corresponding author
- Sinha, Rajita
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2017-08
- Volume
- 122
- Pages
- 136-147
- ISSN
- 0028-3908 (ISSN-L)
- PMC
- PMC5479733
- OpenAlex
- W2583762848
- Cited by
- 257
- References
- 133
- Citations by year
- 2026: 21 · 2025: 20 · 2024: 25 · 2023: 35 · 2022: 38 · 2021: 30 · 2020: 39 · 2019: 13 · 2018: 29 · 2017: 7
- FWCI
- 3.19
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Neuropharmacology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Alcoholism (R01-AA13892, R01-AA020504)
- Alcohol Abuse at the National Institutes of Health (R21-AA025277)
- Topics
- Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- alcoholism, stress, glucocorticoids, hypothalamic-pituitary-adrenal axis, relapse, drinking motives, binge drinking, prefrontal cortex, alcohol withdrawal, alcohol cue reactivity, interoception, conditioning, biomarkers, personalized medicine, treatment goals
- MeSH terms
- Alcohol Drinking, Alcoholism, Animals, Brain, Glucocorticoids, Humans, Hypothalamo-Hypophyseal System, Pituitary-Adrenal System, Recurrence, Stress, Physiological, Stress, Psychological, Prefrontal Cortex
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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