Abstract
Background: Tea is frequently consumed worldwide, but the association of tea drinking with mortality risk remains inconclusive in populations where black tea is the main type consumed. Objective: To evaluate the associations of tea consumption with all-cause and cause-specific mortality and potential effect modification by genetic variation in caffeine metabolism. Design: Prospective cohort study. Setting: The UK Biobank. Participants: 498 043 men and women aged 40 to 69 years who completed the baseline touchscreen questionnaire from 2006 to 2010. Measurements: Self-reported tea intake and mortality from all causes and leading causes of death, including cancer, all cardiovascular disease (CVD), ischemic heart disease, stroke, and respiratory disease. Results: During a median follow-up of 11.2 years, higher tea intake was modestly associated with lower all-cause mortality risk among those who drank 2 or more cups per day. Relative to no tea drinking, the hazard ratios (95% CIs) for participants drinking 1 or fewer, 2 to 3, 4 to 5, 6 to 7, 8 to 9, and 10 or more cups per day were 0.95 (95% CI, 0.91 to 1.00), 0.87 (CI, 0.84 to 0.91), 0.88 (CI, 0.84 to 0.91), 0.88 (CI, 0.84 to 0.92), 0.91 (CI, 0.86 to 0.97), and 0.89 (CI, 0.84 to 0.95), respectively. Inverse associations were seen for mortality from all CVD, ischemic heart disease, and stroke. Findings were similar regardless of whether participants also drank coffee or not or of genetic score for caffeine metabolism. Limitation: Potentially important aspects of tea intake (for example, portion size and tea strength) were not assessed. Conclusion: Higher tea intake was associated with lower mortality risk among those drinking 2 or more cups per day, regardless of genetic variation in caffeine metabolism. These findings suggest that tea, even at higher levels of intake, can be part of a healthy diet.
Original language | English (US) |
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Pages (from-to) | 1201-1211 |
Number of pages | 11 |
Journal | Annals of internal medicine |
Volume | 175 |
Issue number | 9 |
DOIs | |
State | Published - Sep 1 2022 |
Funding
Acknowledgment: This study was conducted using the UK Biobank resource (applications 18623 and 21394). The UK Biobank was established by the Wellcome Trust, the Medical Research Council, the UK Department of Health, and the Scottish Government. The UK Biobank has also received funding from the Welsh Assembly Government, the British Heart Foundation, and Diabetes United Kingdom. This work used the computational resources of the NIH High-Performance Computing Biowulf cluster. Grant Support: By the NIH National Cancer Institute Intramural Research Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services.
ASJC Scopus subject areas
- Internal Medicine