The authors state that 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, 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.
Further, 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, non-binge 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’’ actionspertinent are several studies in vivo and rat brain organotypic cultures, in which antecedent or preconditioning exposure to moderate alcohol neuroprotects against ischemia, endotoxin, b-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.
Professor R Curtis Ellison comments: This is an excellent review of current data on how alcohol consumption is associated with coronary artery disease, stroke, and dementia. It provides brief summaries of epidemiologic studies, but focuses especially on experimental evidence for a variety of mechanisms by which alcohol, as well as resveratrol, relate to disease. These mechanisms include intracellular signaling pathways, nitric oxide pathways, inflammation, and additional processes involving neuroprotection.
A figure from the paper, copied below, summarises proposed cardio-protective and molecular targets of alcohol and resveratrol. The data presented provide evidence that moderate drinking reduces the risk not only of coronary disease but possibly also reduces the risk of cognitive decline/dementia. Recent experimental studies suggest that alcohol-related anti-inflammatory heat shock proteins, and protein kinase changes in the brain bear similarities to those elucidated in heart, particularly with respect to PKC - and quite likely other signal transduction kinases.
Source: Collins MA, Neafsey EJ, Mukamal KJ, Gray MO, Parks DA, Das DK, Korthuis RJ. Alcohol in moderation, cardioprotection, and neuroprotection: Epidemiological considerations and mechanistic studies. Alcohol Clin Exp Res 2009;33:206219.