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 (457 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 clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages.
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, Ethyl; Ethyl Alcohol; Grain Alcohol; Alcohol, Grain; Absolute Alcohol; Alcohol, Absolute.
Where it fits in the MeSH classification
- Broader topics
- Alcohols
- Narrower topics
- Blood Alcohol Content; Ethamoxytriphetol; Ethanolamines; Ethylene Chlorohydrin; Mercaptoethanol; Phenylethyl Alcohol; Trifluoroethanol
- See also
- Alcoholic Beverages
Related concepts
- Alcoholic Beverages
Research landscape
PubMed indexes 126,206 records tagged with the MeSH heading “Ethanol” (counts retrieved 2026-10-31). 17,444 of them (13.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 56,061 records.
Reviews account for 8,259 records (6.5%) and meta-analyses for 414. Randomized controlled trials number 3,610 (2.9%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 56,061 |
| 2000-2009 | 23,379 |
| 2010-2019 | 29,322 |
| 2020 onward | 17,444 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 8,259 | 6.5% |
| Meta-analyses | 414 | 0.3% |
| Randomized controlled trials | 3,610 | 2.9% |
Method: PubMed query "Ethanol"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
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 |
|---|---|---|---|---|
| Innate immune sensing of dietary alcohol ignites inflammation to drive alcohol-related disease | 2026 | Research article Design not recorded in structured metadata | 7 | cc by PMID 41961937 · DOI · PMC13068059 |
| Hydroxytyrosol Bioavailability: Unraveling Influencing Factors and Optimization Strategies for Dietary Supplements | 2025 | Review article Design not recorded in structured metadata | 7 | cc by PMID 41010464 · DOI · PMC12473018 |
| Neurotoxicity of Chronic Alcohol Exposure: Mechanistic Insights, Cellular Disruption, and Emerging Therapeutic Strategies | 2025 | Review article Design not recorded in structured metadata | 5 | cc by PMID 41516173 · DOI · PMC12786252 |
Innate immune sensing of dietary alcohol ignites inflammation to drive alcohol-related disease [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Alcohol consumption has short- and long-term impacts on physical and mental health.
- Closing excerpt
- These findings reveal a mechanism by which alcohol and interferon converge to induce ZBP1-dependent inflammatory cell death and liver pathology, providing mechanistic insight and highlighting potential therapeutic targets for alcohol-related disease.
- 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 (149 words)
Alcohol consumption has short- and long-term impacts on physical and mental health. Although multiple host and environmental factors contribute to alcohol-related disease, the innate immune sensors that detect toxic signals from alcohol remain poorly defined. Here, we show that alcohol cooperates with sterile- or infection-induced interferon signaling to drive inflammatory cell death, cytokine release, and liver injury in humans and mice. We identified the pattern recognition receptor Z-DNA binding protein 1 (ZBP1) as a key innate immune sensor mediating pyroptosis, apoptosis, and necroptosis in response to combined ethanol and interferon stimulation. While interferon elevated ZBP1, ethanol suppressed adenosine deaminase acting on RNA 1 (ADAR1) expression. Together, interferon and ethanol activated JNK signaling to promote Z-RNA formation, triggering ZBP1. These findings reveal a mechanism by which alcohol and interferon converge to induce ZBP1-dependent inflammatory cell death and liver pathology, providing mechanistic insight and highlighting potential therapeutic targets for alcohol-related disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41961937 · DOI · PMC13068059
Hydroxytyrosol Bioavailability: Unraveling Influencing Factors and Optimization Strategies for Dietary Supplements [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Hydroxytyrosol (HT) is a major phenolic compound in olives and extra virgin olive oil (EVOO), known for its antioxidant, anti-inflammatory, and cardiometabolic properties.
- Closing excerpt
- Further well-designed human studies are needed to guide the development of nutraceutical formulations capable of replicating the health benefits of EVOO beyond its natural matrix.
- 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 (187 words)
Hydroxytyrosol (HT) is a major phenolic compound in olives and extra virgin olive oil (EVOO), known for its antioxidant, anti-inflammatory, and cardiometabolic properties. The European Food Safety Authority (EFSA) has approved a health claim for the protection of LDL particles from oxidative damage only when HT is consumed within EVOO, which limits its direct use in supplements or functional foods. Since its biological effects depend on absorption, distribution, metabolism, and excretion (ADME), understanding how formulation and delivery strategies influence bioavailability is essential. HT is mainly present as secoiridoid derivatives in EVOO, whereas in supplements, it often appears in its free form, potentially affecting its metabolic fate. This review summarizes human studies on HT bioavailability from EVOO, isolated supplements, and enriched foods, and examines how matrix type, chemical modifications of HT, and advanced delivery systems, such as emulsions, encapsulation, and vesicular carriers, modulate absorption and metabolism. The gut microbiota is highlighted as an emerging factor in HT biotransformation, although its role remains underexplored. Further well-designed human studies are needed to guide the development of nutraceutical formulations capable of replicating the health benefits of EVOO beyond its natural matrix.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41010464 · DOI · PMC12473018
Neurotoxicity of Chronic Alcohol Exposure: Mechanistic Insights, Cellular Disruption, and Emerging Therapeutic Strategies [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Chronic alcohol exposure induces complex pathophysiological changes in the central nervous system (CNS), contributing to the onset and progression of neurodegenerative disorders.
- Closing excerpt
- A comprehensive understanding of these processes is critical for the development of neuroprotective interventions aimed at mitigating alcohol-related cognitive and functional decline.
- 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 (121 words)
Chronic alcohol exposure induces complex pathophysiological changes in the central nervous system (CNS), contributing to the onset and progression of neurodegenerative disorders. This review integrates recent findings on ethanol-induced neurotoxicity, focusing on key mechanisms including oxidative stress, protein misfolding, mitochondrial dysfunction, calcium dysregulation, neuroinflammation, and epigenetic alterations. We further discuss the detrimental impact of ethanol metabolism particularly its neurotoxic intermediates such as acetaldehyde and salsolinol on neuronal integrity. Special emphasis is placed on glial cell activation, blood-brain barrier disruption, and dysregulation of survival pathways such as PI3K/Akt/mTOR. Finally, we highlight promising therapeutic strategies targeting these molecular and cellular disruptions. A comprehensive understanding of these processes is critical for the development of neuroprotective interventions aimed at mitigating alcohol-related cognitive and functional decline.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41516173 · DOI · PMC12786252
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 Effect of alcohol use on the adolescent brain and behavior [4]
- Research article Pathophysiological Aspects of Alcohol Metabolism in the Liver [5]
- Research article Analgesic Effects of Alcohol: A Systematic Review and Meta-Analysis of Controlled Experimental Studies in Healthy Participants [6]
- Research article Alcohol and Immediate Risk of Cardiovascular Events: A Systematic Review and Dose-Response Meta-Analysis [7]
- Research article Association between alcohol consumption and the risk of incident type 2 diabetes: a systematic review and dose-response meta-analysis [8]
- Research article Caffeic Acid and Diseases-Mechanisms of Action [9]
References
- Jang Y, Bae H, Oh S, Yu G, Bae H, Nguyen MQ, et al.. Innate immune sensing of dietary alcohol ignites inflammation to drive alcohol-related disease. . 2026. PMID 41961937 · DOI · PMC13068059
- Jordán M, García-Acosta N, Espartero JL, Goya L, Mateos R. Hydroxytyrosol Bioavailability: Unraveling Influencing Factors and Optimization Strategies for Dietary Supplements. . 2025. PMID 41010464 · DOI · PMC12473018
- Gołaszewski P, Wawrzyniak A, Kłosowicz M, Burbelka A, Balawender K. Neurotoxicity of Chronic Alcohol Exposure: Mechanistic Insights, Cellular Disruption, and Emerging Therapeutic Strategies. . 2025. PMID 41516173 · DOI · PMC12786252
- Lees B, Meredith LR, Kirkland AE, Bryant BE, Squeglia LM. Effect of alcohol use on the adolescent brain and behavior. Pharmacol Biochem Behav. 2020. PMID 32179028 · DOI · PMC7183385
- Hyun J, Han J, Lee C, Yoon M, Jung Y. Pathophysiological Aspects of Alcohol Metabolism in the Liver. Int J Mol Sci. 2021. PMID 34071962 · DOI · PMC8197869
- Thompson T, Oram C, Correll CU, Tsermentseli S, Stubbs B. Analgesic Effects of Alcohol: A Systematic Review and Meta-Analysis of Controlled Experimental Studies in Healthy Participants. J Pain. 2017. PMID 27919773 · DOI
- Mostofsky E, Chahal HS, Mukamal KJ, Rimm EB, Mittleman MA. Alcohol and Immediate Risk of Cardiovascular Events: A Systematic Review and Dose-Response Meta-Analysis. Circulation. 2016. PMID 26936862 · DOI · PMC4783255
- Li XH, Yu FF, Zhou YH, He J. Association between alcohol consumption and the risk of incident type 2 diabetes: a systematic review and dose-response meta-analysis. Am J Clin Nutr. 2016. PMID 26843157 · DOI
- Pavlíková N. Caffeic Acid and Diseases-Mechanisms of Action. Int J Mol Sci. 2022. PMID 36614030 · DOI · PMC9820408
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 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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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.