The DOI matches its Crossref record; 128 of the 128 references it cites were found in a registry or an index.
Alcohol in Moderation, Cardioprotection, and Neuroprotection: Epidemiological Considerations and Mechanistic Studies
Open accessAbstract
In contrast to many years of important research and clinical attention to the pathological effects of alcohol (ethanol) abuse, the past several decades have seen the publication of a number of peer‐reviewed studies indicating the beneficial effects of light‐moderate, nonbinge consumption of varied alcoholic beverages, as well as experimental demonstrations that moderate alcohol exposure can initiate typically cytoprotective mechanisms. A considerable body of epidemiology associates moderate alcohol consumption with significantly reduced risks of coronary heart disease and, albeit currently a less robust relationship, cerebrovascular (ischemic) stroke. Experimental studies with experimental rodent models and cultures (cardiac myocytes, endothelial cells) indicate that moderate alcohol exposure can promote anti‐inflammatory processes involving adenosine receptors, protein kinase C (PKC), nitric oxide synthase, heat shock proteins, and others which could underlie cardioprotection. Also, brain functional comparisons between older moderate alcohol consumers and nondrinkers have received more recent epidemiological study. In over half of nearly 45 reports since the early 1990s, significantly reduced risks of cognitive loss or dementia in moderate, nonbinge consumers of alcohol (wine, beer, liquor) have been observed, whereas increased risk has been seen only in a few studies. Physiological explanations for the apparent CNS benefits of moderate consumption have invoked alcohol’s cardiovascular and/or hematological effects, but there is also experimental evidence that moderate alcohol levels can exert direct “neuroprotective” actions—pertinent are several studies in vivo and rat brain organotypic cultures, in which antecedent or preconditioning exposure to moderate alcohol neuroprotects against ischemia, endotoxin, β‐amyloid, a toxic protein intimately associated with Alzheimer’s, or gp120, the neuroinflammatory HIV‐1 envelope protein. The alcohol‐dependent neuroprotected state appears linked to activation of signal transduction processes potentially involving reactive oxygen species, several key protein kinases, and increased heat shock proteins. Thus to a certain extent, moderate alcohol exposure appears to trigger analogous mild stress‐associated, anti‐inflammatory mechanisms in the heart, vasculature, and brain that tend to promote cellular survival pathways.
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“a protective effect of light to moderate drinking has some biological plausibility 212, but evidence on this is inconsistent.”
From The relationship between different dimensions of alcohol use and the burden of disease—an update (2017) · cites this paper as [212]
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1 retracted
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Metadata
- Authors
- Collins, M. A., Neafsey, E. J., Mukamal, K. J., Gray, M. O., Parks, D. A., Das, D. K., & Korthuis, R. J.
- Affiliations
- San Francisco General Hospital (US)
- Venue
- Alcoholism: Clinical and Experimental Research
- Publisher
- Wiley
- Published
- 2009-01-22
- Volume
- 33
- Issue
- 2
- Pages
- 206-219
- ISSN
- 0145-6008 (ISSN-L)
- 1530-0277
- PMC
- PMC2908373
- OpenAlex
- W2111348890
- Cited by
- 235
- References
- 128
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 8 · 2023: 5 · 2022: 11 · 2021: 7 · 2020: 9 · 2019: 16 · 2018: 9 · 2017: 13 · 2016: 14 · 2015: 11 · 2014: 17 · 2013: 24 · 2012: 16
- FWCI
- 2.38
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Alcoholism Clinical and Experimental Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5r01aa011723-03)
- National Institute on Alcohol Abuse and Alcoholism (R01AA013568, AA 11135, AA014945, R01AA011135, R01AA014945, AA013568, AA 13361, AA 011723, F31AA013361)
- National Institute of Diabetes and Digestive and Kidney Diseases (P01DK043785)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Health Sciences › Medicine › Clinical Neurology › Alcoholism and Thiamine Deficiency
- Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
- Keywords
- moderate drinking, cardioprotection, neuroprotection, coronary artery disease, ischemic stroke, dementia, cognitive decline, anti-inflammatory mechanism, adenosine receptors, protein kinase C, nitric oxide synthase, heat shock proteins, cerebral ischemia, amyloid-beta, gp120, reactive oxygen species, signal transduction
- MeSH terms
- Resveratrol, Alcohol Drinking, Ethanol, Animals, Antioxidants, Cardiotonic Agents, Cardiovascular Diseases, Central Nervous System Depressants, Dementia, Humans, Nitric Oxide, Protein Kinase C, Stilbenes, Neuroprotective Agents
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