Editorial: The effects of coffee intake on the risk of cardiovascular disease

This editorial refers to ‘The impact of coffee subtypes on incident cardiovascular disease, arrhythmias, and mortality: long-term outcomes from the UK Biobank’, by D. Chieng et al., https://doi.org/10.1093/eurjpc/zwac189.

Coffee is one of the most consumed beverages globally and forms part of a daily routine for many to increase their alertness, energy, and ability to concentrate.¹ It is estimated that about 30–40% of the world population drink coffee, with figures over 60% in the USA, which is more than any other beverage including tap water.^2,3 For healthy adults, daily intake of 2–4 regular 125 mL cups of coffee (200–400 mg) is generally safe⁴ but several people exceed this amount without necessarily thinking about its health benefits or risks. The amount of coffee intake may differ because there is a wide variation on how people are sensitive to the effects of caffeine and how fast they metabolize it. Over time, concerns have been raised on the impact of coffee consumption on health outcomes with studies showing mixed results on the relationship of coffee intake and risk for incident cardiovascular disease (CVD) and other diseases like cancer.^5,6 More recently, epidemiological evidence points to dose-dependent health benefits of coffee intake on reducing incident CVD especially for healthy adults,^1,6,7 but negative outcomes for those with existing CVD.⁷ Other studies have shown increased risk of acute lymphocytic leukaemia and bladder cancer while others show inverse association with endometrial and liver cancers.⁵ This suggests the need for careful and prudent conclusions for the associations between coffee and disease incidence.

Coffee has one of the highest contents of caffeine¹ and also constitutes a class of complex carbonyl and amino compounds formed during the roasting of the beans.⁸ These compounds possess antioxidants (polyphenols),⁹ anti-inflammatory, and anti-hyperlipidaemia properties.⁸ The flavonoids, a type of polyphenols in coffee, initiate antihypertensive effects by increasing the bioavailability of nitric oxide, reducing oxidative stress of the endothelial cells or modulating vascular ion channel activity.¹⁰ Caffeine metabolism varies among individuals and whereas low–to-moderate doses may increase alertness and concentration, higher doses may be detrimental to health causing increased heart rate, insomnia, and anxiety.¹¹ The half-life of caffeine in adults is ∼2.5–5 h but low caffeine metabolism in pregnant women may increase caffeine half-life to up to 15 h.^1,4 Consequently, caffeine has been associated with spontaneous abortion and low birth weight and hence intake of decaffeinated instead of instant or ground coffee is advised in pregnancy, children, and those with impaired liver function tests.^1,4 Caffeine also affects the pharmacokinetic and pharmacodynamic levels of some medications. There is documented evidence of marked interaction between caffeine and quinolones, cardiovascular medications (such as antiarrhythmic drugs or calcium antagonists), antidepressants, antipsychotics, mood stabilizers, antianxiety, and sedative agents and anticonvulsant medications.⁴

The study by Chieng and colleagues¹² investigated the impact of consuming different types of coffee (caffeinated vs. decaffeinated) on the incident CVD, arrhythmia, and mortality. The main strength with this study is use of impressively large data set from the UK Biobank (n = 449, 563 participants, median age 58 years). The UK Biobank is a large biobank study which investigates genetic and environmental exposures to disease from half a million UK participants and therefore broadly applicable to a bigger population. In Chieng’s study, consumption of coffee was self-reported on the type of coffee, i.e. instant coffee, ground coffee, or decaffeinated coffee, categorized into six daily intake categories, consisting of 0, <1, 1, 2–3, 4–5, and >5 cups/day. The study analysed the relationship between coffee subtypes and incidence of arrythmias, CVD, and mortality over a period of 15 years January 2006–August 2021. Another strength of this study is the use of 100 510 participants who served as controls.

The authors¹² found that compared with nondrinkers, increasing levels of coffee consumption and incidence of any arrhythmia had a U-shaped relationship, with the lowest risk for arrhythmias among those who consumed 2–3 coffee cups/day. For atrial fibrillation, the peak risk reduction was seen in 4–5 cups/day and no significant reductions for consuming >5 cups/day. The study also found that habitual coffee intake of up to 5 cups/day was associated with significant reductions in the risk of incident CVD, with the lowest risk for those who consumed 2–3 cups/day. The greatest effect for reductions in all-cause mortality was found for those who consumed 2–3 cups/day. The authors noted that the relationship between instant coffee intake and the various CVD endpoints was a U shaped, which may due to interaction of both healthy and unhealthy effects of coffee consumption. These findings are in line with other studies which found nonlinear relationships and that coffee consumption is associated with reduced risk of CVD in participants from large epidemiological studies.^6,7 However, given the observational nature of these studies, similar to Chieng’s study, residual confounding variables cannot be entirely excluded.

For those who consumed decaffeinated coffee, the risk of CVD was optimal with an intake of 2–3 cups/day, with a U-shaped relationship between decaffeinated coffee intake and all-cause mortality.¹² Chieng and colleagues¹² noted neutral effect as regards the relationship between decaffeinated coffee and arrhythmias. These results should not be interpreted to mean that caffeinated coffee is better than decaffeinated coffee in reducing incident CVD or arrhythmias. Evidence shows that consumption of caffeinated and decaffeinated coffee are associated with reduction of CVD events but the differences in these types of coffee consumptions may be due frequency and amount of coffee consumption.¹³ For example, it is possible that differences observed Chieng’s study on the association between caffeinated vs. decaffeinated coffee and incident CVD was limited by much lower reported decaffeinated (15%) vs. caffeinated (62%) coffee consumption¹² and people may have switched between different types of coffee over time. It is also possible that coffee consumption may be a proxy for another behaviour such smoking, physical activity, or dietary factor that reduces or increases the risk of CVD, arrhythmia, or mortality, which may explain the U-shaped nature of the relationship.

In conclusion, the study by Chieng and colleagues clearly demonstrates some health benefits of coffee intake at 2–3 cups/day on reducing CVD events but caution should be taken not to engage in binge coffee intake to avoid intended effects. More targeted clinical studies on the mechanistic effects of specific components of coffee such as caffeine, phenols to provide more evidence on the healthy benefits of coffee intake and allowable limits of these substances in children, adults, and those with different health conditions. This will ensure safety for coffee consumption during activities of daily living and for persons that may be caffeine sensitive, pregnant, or taking medications that interact with caffeine or medical conditions that may be worsened by caffeine intake. In addition, clinicians should consider possible caffeine–drug interactions when prescribing medications to people with existing CVD or other health conditions. Further, to avoid the unintended consequences of consumption of coffee, patients with CVD or arrhythmias should consult their providers regarding coffee intake.

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Author notes