Summary: Contrary to popular belief, moderate coffee consumption does not increase the risk of cardiac arrhythmias or other heart health problems. Researchers found daily coffee consumption was associated with a 3% lower risk of certain cardiac conditions. Findings add to the growing body of evidence that coffee consumption can help reduce the risk of several health problems including Parkinson’s disease and some cancers.
Source: UCSF
In the largest study of its kind, an investigation by UC San Francisco has found no evidence that moderate coffee consumption can cause cardiac arrhythmia.
In fact, each additional daily cup of coffee consumed among several hundred thousand individuals was associated with a 3 percent lower risk of any arrhythmia occurring, including atrial fibrillation, premature ventricular contractions, or other common heart conditions, the researchers report. The study included a four-year follow-up.
The paper is published July 19, 2021, in JAMA Internal Medicine.
“Coffee is the primary source of caffeine for most people, and it has a reputation for causing or exacerbating arrhythmias,” said senior and corresponding author Gregory Marcus, MD, professor of medicine in the Division of Cardiology at UCSF.
“But we found no evidence that caffeine consumption leads to a greater risk of arrhythmias,” said Marcus, who specializes in the treatment of arrhythmias. “Our population-based study provides reassurance that common prohibitions against caffeine to reduce arrhythmia risk are likely unwarranted.”
While some professional societies suggest avoiding caffeinated products to lower the risk for arrhythmia, this connection has not been consistently demonstrated – indeed, coffee consumption may have anti-inflammatory benefits and is associated with reduced risks of some illnesses including cancer, diabetes, and Parkinson disease.
In the new study, UCSF scientists explored whether habitual coffee intake was associated with a risk of arrhythmia, and whether genetic variants that affect caffeine metabolism could modify that association. Their investigation was conducted via the community-based UK Biobank, a prospective study of participants in England’s National Health Services.
Some 386,258 coffee drinkers took part in the coffee research, with an average mean age of 56 years; slightly more than half were female. It was an unprecedented sample size for this type of inquiry.
In addition to a conventional analysis examining self-reported coffee consumption as a predictor of future arrhythmias, the investigators employed a technique called “Mendelian Randomization,” leveraging genetic data to infer causal relationships.
As those with the genetic variants associated with faster caffeine metabolism drank more coffee, this analysis provided a method to test the caffeine-arrhythmia relationship in a way that did not rely on participant self-report and should have been immune to much of the confounding inherent to most observational studies.
With a mean four-year follow up, data were adjusted for demographic characteristics, health and lifestyle habits.
Ultimately, approximately 4 percent of the sample developed an arrhythmia. No evidence of a heightened risk of arrhythmias was observed among those genetically predisposed to metabolize caffeine differently. The researchers said that higher amounts of coffee were actually associated with a 3 percent reduced risk of developing an arrhythmia.
The authors noted limitations including the self-reporting nature of the study, and that detailed information on the type of coffee – such as espresso or not – was unavailable.
“Only a randomized clinical trial can definitively demonstrate clear effects of coffee or caffeine consumption,” said Marcus. “But our study found no evidence that consuming caffeinated beverages increased the risk of arrhythmia. Coffee’s antioxidant and anti-inflammatory properties may play a role, and some properties of caffeine could be protective against some arrhythmias.”
Co-authors are Eun-jeong Kim, MD; Thomas J. Hoffmann, PhD; Gregory Nah, MA; Eric Vittinghoff, PhD; and Francesca Delling, MD, all of UCSF.
Disclosures can be found in the paper.
About this cardiovascular health news
Source: UCSF
Contact: Elizabeth Fernandez – UCSF
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Original Research: Closed access.
“Coffee Consumption and Incident Tachyarrhythmias: Reported Behavior, Mendelian Randomization, and Their Interactions” by Gregory Marcus et al. JAMA Internal Medicine
Abstract
Coffee Consumption and Incident Tachyarrhythmias: Reported Behavior, Mendelian Randomization, and Their Interactions
Importance
The notion that caffeine increases the risk of cardiac arrhythmias is common. However, evidence that the consumption of caffeinated products increases the risk of arrhythmias remains poorly substantiated.
Objective
To assess the association between consumption of common caffeinated products and the risk of arrhythmias.
Design, Setting, and Participants
This prospective cohort study analyzed longitudinal data from the UK Biobank between January 1, 2006, and December 31, 2018. After exclusion criteria were applied, 386 258 individuals were available for analyses.
Exposures
Daily coffee intake and genetic polymorphisms that affect caffeine metabolism.
Main Outcomes and Measures
Any cardiac arrhythmia, including atrial fibrillation or flutter, supraventricular tachycardia, ventricular tachycardia, premature atrial complexes, and premature ventricular complexes.
Results
A total of 386 258 individuals (mean [SD] age, 56 [8] years; 52.3% female) were assessed. During a mean (SD) follow-up of 4.5 (3.1) years, 16 979 participants developed an incident arrhythmia.
After adjustment for demographic characteristics, comorbid conditions, and lifestyle habits, each additional cup of habitual coffee consumed was associated with a 3% lower risk of incident arrhythmia (hazard ratio [HR], 0.97; 95% CI, 0.96-0.98; P < .001). In analyses of each arrhythmia alone, statistically significant associations exhibiting a similar magnitude were observed for atrial fibrillation and/or flutter (HR, 0.97; 95% CI, 0.96-0.98; P < .001) and supraventricular tachycardia (HR, 0.96; 95% CI, 0.94-0.99; P = .002).
Two distinct interaction analyses, one using a caffeine metabolism–related polygenic score of 7 genetic polymorphisms and another restricted to CYP1A2 rs762551 alone, did not reveal 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.
Conclusions and Relevance
In this prospective cohort study, greater amounts of habitual coffee consumption were inversely associated with a lower risk of arrhythmia, with no evidence that genetically mediated caffeine metabolism affected that association. Mendelian randomization failed to provide evidence that caffeine consumption was associated with arrhythmias.
