Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (732 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A primary, chronic disease with genetic, psychosocial, and environmental factors influencing its development and manifestations. The disease is often progressive and fatal. It is characterized by impaired control over drinking, preoccupation with the drug alcohol, use of alcohol despite adverse consequences, and distortions in thinking, most notably denial. Each of these symptoms may be continuous or periodic. (Morse and Flavin for the Joint Commission of the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine to Study the Definition and Criteria for the Diagnosis of Alcoholism: in JAMA 1992;268:1012-4)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Alcohol Addiction; Addiction, Alcohol; Alcohol Dependence; Dependence, Alcohol; Alcoholic Intoxication, Chronic; Chronic Alcoholic Intoxication; Intoxication, Chronic Alcoholic; Alcohol Abuse.
Where it fits in the MeSH classification
- Broader topics
- Alcohol-Related Disorders
- See also
- Alcohol Deterrents; Alcoholics Anonymous; Psychoses, Alcoholic; Temperance
Research landscape
PubMed indexes 83,999 records tagged with the MeSH heading “Alcoholism” (counts retrieved 2026-10-31). 8,827 of them (10.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 46,852 records.
Reviews account for 9,219 records (11.0%) and meta-analyses for 519. Randomized controlled trials number 3,115 (3.7%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 46,852 |
| 2000-2009 | 13,668 |
| 2010-2019 | 14,652 |
| 2020 onward | 8,827 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 9,219 | 11.0% |
| Meta-analyses | 519 | 0.6% |
| Randomized controlled trials | 3,115 | 3.7% |
Method: PubMed query "Alcoholism"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in psychiatry and psychology
Research on mental health and behaviour relies on questionnaires, interviews and rating scales rather than physical measurements, so how a condition was defined and measured shapes every result. Many studies are observational or small, placebo responses can be large, and findings in one group or culture may not carry over to another. Nothing on this page is advice about diagnosis or treatment; anyone worried about their mental health should talk to a qualified clinician. Check how outcomes were measured, who took part and how long they were followed.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Tirzepatide reduces alcohol drinking and relapse-like behaviours in rodents | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41506148 · DOI · PMC12808897 |
| Central amygdala single-nucleus atlas reveals chromatin and gene transcription dynamics in human alcohol use disorder | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41554730 · DOI · PMC12905162 |
| SWI/SNF complexes modulate gene expression and the development of physical dependence to ethanol | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41527326 · DOI · PMC12796780 |
Tirzepatide reduces alcohol drinking and relapse-like behaviours in rodents [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundAlcohol use disorder (AUD) remains a major public health problem, with few effective medications currently available.
- Closing excerpt
- Thaynnam A Emous held an international internship scholarship from the São Paulo Research Foundation (FAPESP), Process Number #2023/18470-5, while conducting research at the University of Gothenburg.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (277 words)
BackgroundAlcohol use disorder (AUD) remains a major public health problem, with few effective medications currently available. However, peptides of the gut-brain axis appear to offer promising therapeutic targets for AUD as they influence the mesolimbic reward circuitry.MethodsHere, we examined the effects of tirzepatide, a long-acting dual glucagon-like peptide-1 receptor (GLP-1R) and glucose-dependent insulinotropic polypeptide receptor (GIPR) agonist approved for diabetes and obesity, using behavioural assays (locomotor activity and conditioned place preference), alcohol intake paradigms (intermittent access two-bottle choice, drinking in the dark and the alcohol deprivation effect), and molecular analyses (microdialysis, electrophysiology and proteomics) in rodents.FindingsFirst, tirzepatide effectively attenuated the rewarding properties of alcohol, measured through locomotor stimulation, conditioned place preference, and accumbal dopamine release (P InterpretationTogether, our findings suggest tirzepatide modulates alcohol-related behaviours through reward-related mechanisms while also affecting physiological consequences associated with long-term alcohol use. Given tirzepatide's established clinical use and the consistency of effects observed here, these results support further investigation for treating AUD and associated complications.FundingThe study is supported by grants from the Swedish Research Council (2023-2600, 2020-00559, 2020-01463, 2024-03054), LUA/ALF (723941 & 1005347) from the Sahlgrenska University Hospital, Alcohol Research Council of the Swedish Alcohol Retailing Monopoly (FO2024-0048), National Institutes of Health (NIH) (P50 AA010761 & U01 AA014095), U.S. Department of Veterans Affairs Office of Research and Development (BLR&D I01BX000813 & IK6BX006299), Herbert & Karin Jacobssons Foundation (2024-Forskning-225), Adlerbertska Research Foundation (2024-791), Wilhelm & Martina Lundgren's Research Foundation (2024-SA-4698), Åke Wibergs Foundation (M24-0216), Swedish Diabetes Foundation (DIA 2024-898) and Mary von Sydow Foundation (2024-36 & 2024-185). Thaynnam A Emous held an international internship scholarship from the São Paulo Research Foundation (FAPESP), Process Number #2023/18470-5, while conducting research at the University of Gothenburg.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41506148 · DOI · PMC12808897
Central amygdala single-nucleus atlas reveals chromatin and gene transcription dynamics in human alcohol use disorder [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Regulation of gene expression is a highly coordinated process in both the healthy and pathological brain with unique patterns across a multitude of cell types.
- Closing excerpt
- Finally, we also perform cell type-specific fine mapping for AUD GWAS to prioritize variants within functional genomic elements.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (161 words)
Regulation of gene expression is a highly coordinated process in both the healthy and pathological brain with unique patterns across a multitude of cell types. Here we present a multi-omic single nucleus study of ~175,000 nuclei from 50 donors with alcohol use disorder (AUD) and control donors without AUD, profiling cell type specific gene expression and chromatin accessibility in the human central amygdala. We identify all major CNS cell types and neuronal subtypes and find inhibitory neurons are particularly affected by AUD. We find high numbers of differentially expressed genes (DEGs) including GABRA2, GRM8, and NCAM1 and show significant enrichment for AUD risk genes within these DEGs. We identified 51,431 cell type-specific, disease associated candidate cis-regulatory elements including an interneuron-associated set of chromatin loops at the AUD risk gene CALN1. Transcription factor footprinting identified Kruppel-like factors upstream of AUD GWAS genes and DEGs. Finally, we also perform cell type-specific fine mapping for AUD GWAS to prioritize variants within functional genomic elements.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41554730 · DOI · PMC12905162
SWI/SNF complexes modulate gene expression and the development of physical dependence to ethanol [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundLong exposure to ethanol causes the development of physical dependence, which causes withdrawal symptoms when ethanol is removed.
- Closing excerpt
- Together, these results suggest a model in which modulation of lipid membrane composition may be one mechanism for the development of physical dependence on ethanol.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (294 words)
BackgroundLong exposure to ethanol causes the development of physical dependence, which causes withdrawal symptoms when ethanol is removed. We exploited the rapid development of physical dependence in Caenorhabditis elegans (C. elegans) to examine the ethanol-induced transcriptional changes that correspond with physical dependence and withdrawal effects.MethodsAfter an 18-h exposure to an intoxicating concentration of ethanol, we observe the development of physical dependence; withdrawal from ethanol causes an increase in their preference for thicker parts of a bacterial lawn, a behavior we term withdrawal-induced bordering (WIB). We performed transcriptional analysis to identify genes whose expression changes correlate with WIB.ResultsWe found that WIB is transient, resolving within 6 h of removal from ethanol, suggesting it is driven by short-term gene expression changes. We identified 1870 genes with differential expression immediately after ethanol exposure but not after 6 h of withdrawal; these are candidate mediators of WIB. We found that the SWI/SNF chromatin remodeling complex, known to be important in the response to acute ethanol exposure, is required for normal WIB. Loss of swsn-9 attenuated but did not eliminate WIB, suggesting that there are swsn-9-dependent and swsn-9-independent components of WIB. Regulation of 1031 ethanol-responsive genes requires swsn-9. WIB phenocopies reduced npr-1 activity, and two genes implicated in the npr-1 signaling pathway, jmjc-1 and dod-24, were transiently regulated after extended ethanol exposure. dod-24 mutants have attenuated WIB.ConclusionsExtended exposure to ethanol causes the development of transient physical dependence in C. elegans, and the SWI/SNF complex is involved in this process. Genes involved in fatty acid metabolism were regulated over the WIB timecourse, and dod-24, which is involved in temperature sensitivity, is required for normal WIB. Together, these results suggest a model in which modulation of lipid membrane composition may be one mechanism for the development of physical dependence on ethanol.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41527326 · DOI · PMC12796780
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Age at onset of mental disorders worldwide: large-scale meta-analysis of 192 epidemiological studies [4]
- Research article Alcohol and depression [5]
- Research article Widespread and sustained cognitive deficits in alcoholism: a meta-analysis [6]
- Research article Effectiveness of brief alcohol interventions in primary care populations [7]
- Research article Lysergic acid diethylamide (LSD) for alcoholism: meta-analysis of randomized controlled trials [8]
- Research article Cognitive-behavioral treatment with adult alcohol and illicit drug users: a meta-analysis of randomized controlled trials [9]
References
- Edvardsson CE, Adermark L, Gottlieb S, Alfreji S, Emous TA, Gouda Y, et al.. Tirzepatide reduces alcohol drinking and relapse-like behaviours in rodents. . 2026. PMID 41506148 · DOI · PMC12808897
- Lee CY, Hwang A, McRiley D, Lee J, Thibodeau G, Duman C, et al.. Central amygdala single-nucleus atlas reveals chromatin and gene transcription dynamics in human alcohol use disorder. . 2026. PMID 41554730 · DOI · PMC12905162
- Mathies LD, Blackwell GG, Davies AG, Bettinger JC. SWI/SNF complexes modulate gene expression and the development of physical dependence to ethanol. . 2026. PMID 41527326 · DOI · PMC12796780
- Solmi M, Radua J, Olivola M, Croce E, Soardo L, Salazar de Pablo G, et al.. Age at onset of mental disorders worldwide: large-scale meta-analysis of 192 epidemiological studies. Mol Psychiatry. 2022. PMID 34079068 · DOI · PMC8960395
- Boden JM, Fergusson DM. Alcohol and depression. Addiction. 2011. PMID 21382111 · DOI
- Stavro K, Pelletier J, Potvin S. Widespread and sustained cognitive deficits in alcoholism: a meta-analysis. Addict Biol. 2013. PMID 22264351 · DOI
- Kaner EF, Beyer FR, Muirhead C, Campbell F, Pienaar ED, Bertholet N, et al.. Effectiveness of brief alcohol interventions in primary care populations. Cochrane Database Syst Rev. 2018. PMID 29476653 · DOI · PMC6491186
- Krebs TS, Johansen PØ. Lysergic acid diethylamide (LSD) for alcoholism: meta-analysis of randomized controlled trials. J Psychopharmacol. 2012. PMID 22406913 · DOI
- Magill M, Ray LA. Cognitive-behavioral treatment with adult alcohol and illicit drug users: a meta-analysis of randomized controlled trials. J Stud Alcohol Drugs. 2009. PMID 19515291 · DOI · PMC2696292
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.