Excessive coffee consumption can lead to unpleasant sensations such as tachycardia and heart palpitations.
Our aim was to investigate if cardiovascular symptoms can lead to alterations in habitual patterns of coffee consumption.
We used information from up to 390,435 European ancestry participants in the UK Biobank, aged 39–73 y. Habitual coffee consumption was self-reported, and systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate were measured at baseline. Cardiovascular symptoms at baseline were based on hospital diagnoses, primary care records, and/or self-report. Mendelian randomization (MR) was used to examine genetic evidence for a causal association between SBP, DBP, and heart rate with habitual coffee consumption.
Participants with essential hypertension, angina, or heart arrhythmia were all more likely to drink less caffeinated coffee and to be non-habitual or decaffeinated coffee drinkers compared with those who did not report related symptoms (P ≤ 3.5 × 10−8 for all comparisons). Higher SBP and DBP were associated with lower caffeinated coffee consumption at baseline, with consistent genetic evidence to support a causal explanation across all methods [MR-Egger regression (MREggr) β: −0.21 cups/d (95% CI: −0.34, −0.07) per 10 mm Hg higher SBP and −0.33 (−0.61, −0.07) per 10 mm Hg higher DBP)]. In genetic analyses, higher resting heart rate was associated with a greater odds of being a decaffeinated coffee drinker (MREggr OR: 1.71; 95% CI: 1.31, 2.21) per 10 beats/min).
We provide causal genetic evidence for cardiovascular system–driven influences on habitual coffee intakes, suggesting that people tend to naturally regulate their coffee consumption based on blood pressure levels and heart rate. These findings suggest that observational studies of habitual coffee intakes are prone to influences by reverse causation, and caution is required when inferred health benefits result from comparisons with coffee abstainers or decaffeinated coffee drinkers.