Imperial College London
Alternate

DrKostasTsilidis

Faculty of Medicine, School of Public Health

Reader in Cancer Epidemiology and Prevention
 
 
 
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Contact

 

+44 (0)20 7594 2623k.tsilidis

 
 
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Location

 

School of Public HealthWhite City Campus

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Summary

 

Publications

Citation

BibTex format

@article{Sofianopoulou:2021:10.1016/s2213-8587(21)00263-1,
author = {Sofianopoulou, E and Kaptoge, S and Afzal, S and Jiang, T and Gill, D and Willeit, J and Tsilidis, K and Heath, A and Danesh, J and Butterworth, A and Burgess, S},
doi = {10.1016/s2213-8587(21)00263-1},
journal = {The Lancet Diabetes & Endocrinology},
pages = {837--846},
title = {Estimating dose-response relationships for vitamin D with coronary heart disease, stroke, and all-cause mortality: observational and Mendelian randomisation analyses},
url = {http://dx.doi.org/10.1016/s2213-8587(21)00263-1},
volume = {9},
year = {2021}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - BackgroundRandomised trials of vitamin D supplementation for cardiovascular disease and all-cause mortality have generally reported null findings. However, generalisability of results to individuals with low vitamin D status is unclear. We aimed to characterise dose-response relationships between 25-hydroxyvitamin D (25[OH]D) concentrations and risk of coronary heart disease, stroke, and all-cause mortality in observational and Mendelian randomisation frameworks.MethodsObservational analyses were undertaken using data from 33 prospective studies comprising 500 962 individuals with no known history of coronary heart disease or stroke at baseline. Mendelian randomisation analyses were performed in four population-based cohort studies (UK Biobank, EPIC-CVD, and two Copenhagen population-based studies) comprising 386 406 middle-aged individuals of European ancestries, including 33 546 people who developed coronary heart disease, 18 166 people who had a stroke, and 27 885 people who died. Primary outcomes were coronary heart disease, defined as fatal ischaemic heart disease (International Classification of Diseases 10th revision code I20-I25) or non-fatal myocardial infarction (I21-I23); stroke, defined as any cerebrovascular disease (I60-I69); and all-cause mortality.FindingsObservational analyses suggested inverse associations between incident coronary heart disease, stroke, and all-cause mortality outcomes with 25(OH)D concentration at low 25(OH)D concentrations. In population-wide genetic analyses, there were no associations of genetically-predicted 25(OH)D with coronary heart disease, stroke, or all-cause mortality. However, for the participants with vitamin D deficiency (25[OH]D concentration <25 nmol/L), genetic analyses provided strong evidence for an inverse association with all-cause mortality (odds ratio [OR] per 10 nmol/L increase in genetically-predicted 25[OH]D concentration 0·69 [95% CI 0·59–0&middo
AU  - Sofianopoulou,E
AU  - Kaptoge,S
AU  - Afzal,S
AU  - Jiang,T
AU  - Gill,D
AU  - Willeit,J
AU  - Tsilidis,K
AU  - Heath,A
AU  - Danesh,J
AU  - Butterworth,A
AU  - Burgess,S
DO  - 10.1016/s2213-8587(21)00263-1
EP  - 846
PY  - 2021///
SN  - 2213-8587
SP  - 837
TI  - Estimating dose-response relationships for vitamin D with coronary heart disease, stroke, and all-cause mortality: observational and Mendelian randomisation analyses
T2  - The Lancet Diabetes & Endocrinology
UR  - http://dx.doi.org/10.1016/s2213-8587(21)00263-1
UR  - https://www.sciencedirect.com/science/article/pii/S2213858721002631?via%3Dihub
UR  - http://hdl.handle.net/10044/1/92392
VL  - 9
ER  -
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