Document Type

Article

Disciplines

Cardiology | Medicine and Health Sciences

Abstract

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 beneficial effects of light-moderate, non-binge 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 non-drinkers have received more recent epidemiological study. In over half of nearly 45 reports since the early 1990’s, significantly reduced risks of cognitive loss or dementia in moderate, non-binge consumers of alcohol (wine, beer, liquor) have been observed, whereas increased risk has been seen in only 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.

Comments

Alcohol Clin Exp Res. Author manuscript; available in PMC 2010 July 22. Published in final edited form as: Alcohol Clin Exp Res. 2009 February; 33(2): 206–219. Published online 2008 November 19. doi: 10.1111/j.1530-0277.2008.00828.x.

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