While the physiological damage and social havoc created by alcohol abuse and dependency are well-known, it is also true that light-to-moderate drinking has certain health benefits. This mini-review summarizes a roundtable discussion held at the July 2007 annual meeting of the Research Society on Alcoholism in Chicago, Illinois.
Results will be published in the February 2009 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
"Alcohol abuse, often in combination with poor nutrition, is responsible for a great deal of permanent organ damage, and that includes the brain," explained Michael A. Collins, professor of biochemistry at Loyola University Chicago and corresponding author for the research roundtable. "In fact, studies of alcoholics over the years sometimes indicate that brain damage can develop earlier than liver damage, but it simply is not recognized because there are common clinical lab tests for liver disease but not for subtle cognitive impairment."
Conversely, Collins added, human studies have indicated that mild or moderate social consumption of alcohol can have beneficial effects on the cardiovascular state and cognitive function. "Alcohol in low to moderate concentrations appears to promote cytoprotective cellular mechanisms," he said, "which might explain some of these epidemiological findings. It seemed important to bring researchers together in this roundtable, in part to inform the research community about these emerging mechanisms."
Some of the key points discussed were:
- Alcohol appears to have a complex relationship with cardiovascular and neurovascular diseases. These include dose-dependent associations with a lower risk of coronary heart disease (CHD), a higher risk of hemorrhagic stroke throughout a range of drinking, a higher risk of ischemic stroke with heavier drinking, and a possible lower risk of dementia or cognitive decline with aging.
"We need greater insight into how cells in the adult brain and heart, in response to moderate alcohol exposure, are able to achieve a relatively protected state with respect to certain insults or cytotoxins," said Collins. "Knowing more about these mechanisms might allow us to design 'non-addictive' molecules that trigger key cytoprotective biochemical steps, for example. This achievement, however small, potentially could have a significant impact, since - worldwide - heart disease is the major killer, and a new case of dementia from all causes is estimated to develop every seven seconds or so."
- Experimental studies with rodents and cultures indicate that moderate alcohol exposure can promote anti-inflammatory processes involving adenosine receptors, protein kinase C (PKC), nitric oxide synthase, and heat shock proteins that may underlie cardioprotection.
"Like many chemicals that we ingest, alcohol is sort of a classic double-edged sword," said Collins. "With respect to 'inflammation,' alcohol in high binge amounts, either directly or through its metabolism, appears to trigger increases in a number of inflammatory players in many cells that include free radicals and inflammatory protein molecules such as cytokines. These are probably responsible for much of the organ damage of alcoholism."
Yet alcohol in low to moderate amounts seems to do the opposite. "It increases other factors that are typically anti-inflammatory in their effects" said Collins. "After moderate alcohol exposure, we find higher levels of cellular 'heat shock' proteins which are well known to be neuroprotective. Of further relevance to the question of aging-dependent cognitive loss is how this alcohol neuroprotection is exerted against beta-amyloid, a neuroinflammatory protein abnormally increased in Alzheimer's disease and likely underlying the progressive dementia."
- Additional evidence suggests that alcohol may even help lower the risk for dementia via "preconditioning" mechanisms, that is, inducing neuronal survival pathways through its selective activation of PKC and focal adhesion kinase enzymes, the focal adhesion complex, and stabilization of the cytoskeleton.
Alcoholism: Clinical & Experimental Research (ACER) is the official journal of the Research Society on Alcoholism and the International Society for Biomedical Research on Alcoholism. Co-authors of the ACER paper, "Drinking and Alcohol-Related Harm among New Zealand University Students: Findings from a National Web-Based Survey," were: Edward J. Neafsey of the Department of Cell Biology, Neurobiology & Anatomy at Loyola University Chicago Stritch School of Medicine; Kenneth J. Mukamal of the Division of General Medicine and Primary Care at Beth Israel Deaconess Medical Center in Boston; Mary O. Gray of the Division of Cardiology at San Francisco General Hospital; Dale A. Parks of the Center for Wine and Cardiovascular Health at the University of Alabama; Dipak K. Das of the Cardiovascular Research Center at the University of Connecticut School of Medicine; and Ronald J. Korthuis of the Department of Medical Pharmacology and Physiology at the University of Missouri School of Medicine. The research and roundtable discussion was funded by the National Institutes of Health, the Loyola University Neuroscience Institute, and the Alcohol Beverage Medical Research Foundation.
Michael A. Collins, Ph.D.
Loyola University Chicago Stritch School of Medicine
Alcoholism: Clinical & Experimental Research