Estimating dose-response relationships for vitamin D with coronary heart disease, stroke, and all-cause mortality: observational and Mendelian randomisation analyses
An erratum to this article was published (Lancet Diabetes Endocrinol, Apr 2025 ↗)
Authors' conclusion
Stratified Mendelian randomisation analyses suggest a lack of causal relationship for 25(OH)D concentrations with both cardiovascular and mortality outcomes for individuals at all levels of 25(OH)D. Our findings suggest that substantial reductions in mortality and cardiovascular morbidity due to long-term low-dose vitamin D supplementation are unlikely even if targeted at individuals with low vitamin D status.
Study context
- Population
- Middle-aged individuals of European ancestries in UK Biobank, EPIC-CVD and two Copenhagen population-based studies (MR); 33 prospective studies of individuals without known CHD or stroke at baseline (observational)MR
- Participants
- 386,406 individuals
- Exposure
- Genetically predicted 25D concentration and outcomes
- Outcome
- CHD (fatal ischaemic heart disease or non-fatal MI); stroke (any cerebrovascular disease); all-cause mortality
Methodological detailsdose-response, stratified Mendelian randomisation, population-based cohorts
- Dose-response
- Stratified Mendelian randomisation
- Population-based cohorts
Main finding
As reported in the abstract
CHD, OR per 10 nmol/L higher genetically predicted 25(OH)D
0.98
95% CI 0.95–1.01
Stroke, OR
1.01
0.97–1.05
All-cause mortality, OR
0.99
0.95–1.02
Observational data: associations, not effects.
Further findings
Observational associations
- Inverse associations of incident CHD, stroke and all-cause mortality with 25(OH)D at low 25(OH)D concentrations
Cause-specific mortality and stratified genetic analyses
- Null findings for cause-specific mortality and in stratified analyses for all outcomes at all observed 25(OH)D levels
Original publication
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