Moderate Drinking Protective After MI, Stroke in 'Flawed' Study

Megan Brooks

July 27, 2021

People with established cardiovascular disease (CVD) might not need to quit drinking to prevent a repeat CVD event, new research suggests, although quantity matters (less is better) and teetotallers should not start drinking to prevent a repeat event, researchers say.

The study, which involved original data and meta-analysis, showed that drinking up to 105 g of alcohol a week — equal to less than six British pints of beer or just over one bottle of wine — could be associated with a decreased risk for heart attack, stroke, angina, or death in patients with CVD.

Study investigator Chengyi Ding, however, cautioned that the findings might "overestimate" the reduced risk for recurrent CVD events for moderate drinkers.

"This is due to the under-representation of heavy drinkers and the categorization of former drinkers, who may have quit drinking due to ill health, as nondrinkers in some of the datasets included in the analyses," Ding, PhD student, Department of Epidemiology and Public Health, University College London, told | Medscape Cardiology.

"Major Flaw"

This is a "major flaw that biases the study toward finding benefits" of moderate alcohol consumption, Richard Saitz, MD, MPH, who wasn't involved in the study, told | Medscape Cardiology.

Saitz, professor, Boston University Schools of Medicine and Public Health, noted that in the few studies that excluded people who quit drinking because of illness, the effects of drinking were "attenuated."

"It is honestly tiresome that investigators continue to do these studies and journals continue to publish them even though they continue to have the same flaws," Saitz commented.

"The bottom line" — based on work by others who used appropriate methods — is that alcohol in low amounts is "unlikely to provide cardiovascular or mortality benefits," Saitz added.

The study was published online on July 26 in BMC Medicine.

Among healthy adults, light to moderate drinking has been reported to have cardioprotective effects in a J-shaped manner; however, it's unclear whether this is true in adults with pre-existing heart disease.

To investigate further, Ding and colleagues conducted a meta-analysis of results from three major British cohorts and 12 published studies. They examined alcohol consumption in relation to repeat CVD events (MI, stroke, angina) and death in 48,423 adults.

Relative to current nondrinking, alcohol intake was associated with all assessed outcomes in the familiar J-shaped manner, with the greatest risk reduction at 7 g/day for all-cause mortality (relative risk [RR], 0.79; 95% CI, 0.73 - 0.85), at 8 g/day for CV mortality (RR, 0.73; 95% CI, 0.64 - 0.83), and at 6 g/day for CV events (RR, 0.50; 95% CI, 0.26 - 0.96). The risk reductions remained significant up to 62, 50, and 15 g/day, respectively.

The upper alcohol intake limit for lower risks for death and CVD events was about 105 g/week, which is lower than that recommended in most current secondary prevention guidelines, the researchers note.

There was no evidence of elevated risk among heavy drinkers, but this was potentially due to selections and under-representation of heavy drinkers in the studies analyzed, they say.

"That there was no negative effect of heavy drinking — yet we know heavy use is harmful — is not reassuring regarding the methodology," Saitz observed.

It's also interesting, he said, that the associations between alcohol use and lower risk for CVD and overall mortality are the same. "What could be the mechanism, especially since alcohol causes cancer? Alcohol is protective for everything? This nonspecific effect is a sign that the associations are not real," Saitz cautioned.

"The totality of the literature on this subject suggests that alcohol in low amounts is carcinogenic, and it is unlikely to lower the risk of heart disease or death," Saitz added.

"For certain, no one should begin drinking for health reasons, and the safest amounts (as with any carcinogen) are the lowest amounts or none — since there is no solid evidence for cause and effect for alcohol and mortality beyond associations in flawed studies that inadequately adjust for confounding factors or for those who stop drinking due to illness," Saitz said.

This study was supported by the Economic and Social Research Council, the National Institute for Health Research (NIHR), UK Medical Research Council, British Heart Foundation, and the NIHR Cambridge Biomedical Research Centre at the Cambridge University Hospitals NHS Foundation Trust. Ding has no relevant disclosures. Coauthor Steven Bell, PhD, is a member of the editorial board for BMC Medicine. Saitz has no relevant disclosures.

BMC Med. Published online July 26, 2021. Full text

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