Alcohol heart protection may not be down to inflammatory markers
exert cardioprotective effects in some, but in elderly men at least
the mechanism of action does not seem to be down to a reduction in
inflammatory markers as previously thought.
Although alcohol has been implicated in worsening some other chronic diseases and the overall effect of drinking on survival is not clear, some studies have shown that light to moderate drinking may reduce the risk of heart disease. The effect was thought to be somehow connected with inflammation, since reduction in levels of C-reactive protein and interleukin-6 circulating in the blood were seen to drop.
But the current study, which the researchers claim is the first with the specific aim of investigating the impact of inflammation on the relationship between alcohol consumption and health-related outcomes, found that these markers did not seem to be linked to heart disease incidence. This leads to the suspicion that some other, as yet unidentified mechanism may be at play.
Researchers led by Cinzia Maraldo, MD, at the University of Florida recruited 2487 adults without heart disease and aged between 70 and 79 years. The participants answered questions about disease diagnostics, medication and drinking habits during an initial interview, with telephone follow-up every six months and clinical examination every year.
Alcohol consumption was classified by number of drinks in a typical week over the past year. The categories were: former; never or occasional (less than one); light to moderate (one to seven); and heavier (more than seven).
Over a five-and-a-half year follow up, 397 participants had died and 383 experienced a cardiac event. Light to moderate drinkers were seen to have a 26 per cent lower risk of death over all and a 30 per cent lower risk of cardiac events, compared to those who drank never or rarely.
Heavy drinkers were seen to be more likely to die or have a cardiac event than never or rare drinkers.
They also conducted stratified analyses to determine whether the alcohol effect was modified by inflammatory marker levels - although this was only possible in men due to the low number of events in women.
IL-6 and CRP levels were categorized as high level (above the median) and low level (below the median).
Among the high IL-6 level light to moderate drinkers, a significantly lower risk of all cause mortality and cardiac events was observed than in never and occasional drinkers. But in low IL-6 level men, light to moderate alcohol consumption was not associated with any significant risk reduction, while heavier alcohol consumption significantly increased all-cause mortality.
There did not seem to be any link between CRP levels and health-related outcomes of alcohol consumption.
The researchers said that they controlled for many potentially confounding variables, including social and lifestyle indicators and a number of established cardiovascular risk factors, but nonetheless the study had several weaknesses. These include self-reporting of alcohol consumption using questionnaires, the inability to differentiate between different drink types, the 'snapshot' nature of the study looking at drinking patterns at one point in time, and the relatively small number of cardiac events.
"The mechanisms underlying the cardioprotective effect of light to moderate alcohol intake are complex and not completely understood," wrote the researchers in the July 24 issue of the Archives of Internal Medicine (Vol. 166, No. 14).
"Although our findings confirm the association between alcohol intake and cardiovascular risk factors, the present study suggests that the protective effect of light to moderate alcohol consumption may not be mediated by its beneficial effects on lipids and inflammatory profile."
"Further studies are needed to explore this possibility and to clarify ethanol anti-inflammatory and molecular effects."
In the meantime, they stressed that, as with any medical advice, alcohol consumption recommendations should be based on evaluation of an individual's risks and benefits, in the context of treatment and control of established cardiovascular risk factors.
