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
RETRACTED: Redox regulation of resveratrol-mediated switching of death signal into survival signal
Das, S., Khan, N. I., Mukherjee, S., Bagchi, D., Gurusamy, N., Swartz, H. M., & Das, D. K. (2007) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2007.09.008 · Cited by 46 · cited 2×
“Whether resveratrol is the essential component that is responsible for much of the cardioprotective effects of wine or the alcohol that is present in wines and is responsible for cardioprotection remains under considerable debate, but there is no doubt that resveratrol may protect the heart in many ways (Das et al., 2…”
Self-citationRetractedThe pathogenesis of atherosclerosis: a perspective for the 1990s
Ross, R. (1993) · Nature · doi:10.1038/362801a0 · Cited by 10,618 · cited 2×
“In patients with cardiovascular risk factors such as hypercholesterolemia, hypertension, or aging (Zeiher et al., 1993), endothelial dysfunction predisposes to the development of structural vascular changes (Ross, 1993) and may play a critical role in acute MI and sudden death.”
Global prevalence of dementia: a Delphi consensus study
Ferri, C. P., Prince, M. J., Brayne, C., Brodaty, H., Fratiglioni, L., Ganguli, M., Hall, K. S., Hasegawa, K., Hendrie, H. C., Huang, Y., et al. (2005) · The Lancet · doi:10.1016/s0140-6736(05)67889-0 · Cited by 5,336 · cited 2×
“…that cardiovascular disease and stroke are 2 of the top 3 leading causes of mortality in developed countries and, according to a Lancet review (Ferri et al., 2005), new cases of dementia are being diagnosed about every 7 seconds worldwide, it seems imperative that as much as possible is…”
Rimm, E. B., Williams, P., Fosher, K., Criqui, M., & Stampfer, M. J. (1999) · BMJ · doi:10.1136/bmj.319.7224.1523 · Cited by 1,360 · cited 17×
“These include dose-dependent associations of alcohol with lower risk of CHD but higher risk of hemorrhagic stroke throughout a recommended range of drinking, an increased risk of ischemic stroke with heavier drinking, and an emerging but somewhat variable association with lower risk of dementia.”
InfluentialAlcohol consumption and mortality among middle-aged and elderly U.S. adults
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“Heavy alcohol consumption has long been associated with vascular as well as myocardial complications (Klatsky, 1996), whereas, as discussed earlier in this summary, several epidemiological studies suggest an inverse association between longterm moderate alcohol consumption and the risk of CHD and MI (Thun et al., 1997…”
‘Ischemic tolerance’ phenomenon found in the brain
Kitagawa, K., Matsumoto, M., Tagaya, M., Hata, R., Ueda, H., Niinobe, M., Handa, N., Fukunaga, R., Kimura, K., Mikoshiba, K., et al. (1990) · Brain Research · doi:10.1016/0006-8993(90)90189-i · Cited by 1,090 · cited 2×
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Alcohol Consumption and Risk of Stroke
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Alcohol and coronary heart disease: a meta-analysis.
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Roles of Drinking Pattern and Type of Alcohol Consumed in Coronary Heart Disease in Men
Mukamal, K. J., Conigrave, K. M., Mittleman, M. A., Camargo, C. A., Stampfer, M. J., Willett, W. C., & Rimm, E. B. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa022095 · Cited by 811 · cited 9×
“In the CHS and HPFS, alcohol intake correlates well with HDL-C levels, with coefficients of 0.25 to 0.35.”
InfluentialSelf-citationIschemic tolerance and endogenous neuroprotection
Dirnagl, U., Simon, R. P., & Hallenbeck, J. M. (2003) · Trends in Neurosciences · doi:10.1016/s0166-2236(03)00071-7 · Cited by 791 · cited 1×
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Cited by
Sorted by citations
The relationship between different dimensions of alcohol use and the burden of disease—an update
Rehm, J., Gmel, G. E., Gmel, G., Hasan, O. S. M., Imtiaz, S., Popova, S., Probst, C., Roerecke, M., Room, R., Samokhvalov, A. V., et al. (2017) · Addiction · doi:10.1111/add.13757 · Cited by 1,204
The relation between different dimensions of alcohol consumption and burden of disease: an overview
Rehm, J., Baliunas, D., Borges, G. L. G., Graham, K., Irving, H., Kehoe, T., Parry, C. D., Patra, J., Popova, S., Poznyak, V., et al. (2010) · Addiction · doi:10.1111/j.1360-0443.2010.02899.x · Cited by 1,174
“Other mechanisms for the cardioprotective effect of light to moderate consumption have been discussed [116,128] but, based on current knowledge, appear to play less prominent roles in explaining the beneficial effects of regular light to moderate drinking.”
Natural products as a source of Alzheimer's drug leads
Williams, P., Sorribas, A., & Howes, M.-J. R. (2011) · Nat. Prod. Rep. · doi:10.1039/c0np00027b · Cited by 404
Effects of moderate beer consumption on health and disease: A consensus document
de Gaetano, G., Costanzo, S., Castelnuovo, A. F. D., Badimón, L., Bejko, D., Alkerwi, A., Chiva‐Blanch, G., Estruch, R., Vecchia, C. L., Panico, S., et al. (2016) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2016.03.007 · Cited by 295
Neuroinflammation, Neurodegeneration, and Depression
Hurley, L. L., & Tizabi, Y. (2012) · Neurotoxicity Research · doi:10.1007/s12640-012-9348-1 · Cited by 268
“Epidemiological studies show trends that light to moderate drinkers have reduced risk of dementia and cognitive decline in comparison to non-drinkers (reviewed Collins et al. 2009).”
Background
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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