Coffee drinkers, perk up: Regular consumption was not linked with a heightened risk for cardiac arrhythmias, even in those genetically predisposed to sluggish caffeine metabolism, researchers reported.
In a prospective cohort study of U.K. Biobank participants, each additional cup of coffee was associated with a 3% lower risk of incident arrhythmia (adjusted HR 0.97, 95% CI 0.96-0.98) at a mean follow-up of 4.5 years, according to Gregory Marcus, MD, MAS, of the University of California San Francisco, and co-authors.
Also, small reductions were observed for atrial fibrillation and/or flutter (HR 0.97, 95% CI 0.9 to 0.98), as well as supraventricular tachycardia (HR 0.96, 95% CI 0.94-0.99), they wrote in JAMA Internal Medicine.
And a pair of “distinct interaction analyses,” which used a caffeine metabolism-related polygenic score of seven genetic polymorphisms and CYP1A2 rs762551 alone, respectively, did not show “any evidence of effect modification… A mendelian randomization study that used these same genetic variants revealed no significant association between underlying propensities to differing caffeine metabolism and the risk of incident arrhythmia,” the authors noted. However, they cautioned that “there may be other genes, such as those related to arrhythmia risk, that may yet modify this association.”
Overall, the data “suggest that common prohibitions against caffeine to reduce arrhythmia risk are likely unwarranted,” adding that their findings were in sync with previous research, such as studies from Brazil and Portugal, that showed no link between coffee consumption and increased tachyarrhythmias.
The debate over the health pros and cons of coffee have been brewing for some time, with much of the discussion focusing on the role of caffeine metabolism and arrhythmic risk, but Marcus and co-authors noted that a review of 201 meta-analyses “found that moderate consumption of coffee is likely more beneficial than harmful to health.” They offered some potential mechanisms for coffee’s observed antiarrhythmic effects in their study, such as its prolongation of left atrial effective refractory periods, blocking of adenosine receptors, antioxidant and anti-inflammatory properties, and catecholaminergic properties.
However, while the current study may bring joy to all java junkies, the results “should not be taken as proving that coffee is an antiarrhythmic,” and “this distinction is of paramount importance,” cautioned Zachary Goldberger, MD, MS, of University of Wisconsin-Madison, and Rodney Hayward, MD, of the University of Michigan in Ann Arbor Healthcare System, in an invited commentary accompanying the study.
They pointed out that “the study sample was limited to patients who did not have a formal prior diagnosis of arrhythmia. As such, it remains unclear if coffee consumption could aggravate atrial or ventricular ectopy.”
In addition, coffee intake was self-reported at a single time point, which can lead to recall bias, they noted, with potential “subsequent and substantial changes in coffee consumption… including reductions due to new signs or symptoms (i.e., patients with palpitations may avoid coffee).”
As for the mendelian randomization analysis, it was centered on caffeine, and not coffee exposure, Goldberger and Hayward emphasized, so it’s “important to recognize the distinction between coffee and caffeine. Caffeine is only one element of coffee, which contains other bioactive compounds such as diterpene alcohols and chlorogenic acids.”
For the time being, healthcare providers “can reassure patients that there is no evidence that drinking coffee increases the risk for developing arrhythmias. This is particularly important for the many patients with benign palpitations who are devastated when they think, or are told, that they have to stop drinking coffee,” Goldberger and Rodney Hayward said, adding that for the latter patients, coffee consumption—and contending with any ill effects because of it—will be a personal choice and not a medical one.
According to a March 2020 report from the National Coffee Association, seven of 10 people in the U.S. reporting drinking coffee every week, while 62% drink coffee daily, and the average person reports downing a little over three cups a day.
The U.K. Biobank included >500,000 participants, with a median coffee consumption of two cups daily per day. The authors included 386,258 participants (mean age 56, 52.3% women, >90% White) who did not have a prior diagnosis of arrhythmia. They noted that coffee drinkers were more likely to be White, older, and male, as well as reporting more peripheral artery disease, cancer, smoking, and alcohol drinking.
Study limitations included a lack of data on the type of coffee consumed—brewed, espresso, other coffee-based products—or consumption of other non-coffee, caffeinated beverages. As for changes in coffee consumption over time, the authors conceded that their study was done “with an assumption that the coffee consumption reported at baseline was sufficiently indicative of consumption that persisted during the study,” but that “previous studies have demonstrated consistent answers regarding coffee consumption over time.”
Finally, the impact of coffee intake on arrhythmia risk, which is generally considered immediate versus long-term, was assumed to be constant over time, but that is “challenging to prove,” and the 4-year follow-up may not have been long enough, they noted.
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Neither habitual coffee consumption nor genetically mediated differences in caffeine metabolism was linked with a heightened risk of cardiac arrhythmias.
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Be aware that the study results should not be seen as proof that coffee is an antiarrhythmic.
Shalmali Pal, Contributing Writer, BreakingMED™
The UK Biobank is supported by the Wellcome Trust, the Medical Research Council, the UK Department of Health, the Scottish Government, the Welsh Assembly Government, the British Heart Foundation, and Diabetes United Kingdom, Northwest Regional Development Agency, Scottish Government.
Marcus reported relationships with, and/or support from, Baylis, Medtronic, Eight Sleep, Johnson & Johnson, and InCarda. A co-author reported support from the NIH.
Goldberger and Hayward reported no relationships relevant to the contents of this paper to disclose.
Cat ID: 2
Topic ID: 74,2,730,2,192,925
