Vitamin D Deficiency Increases Mortality Risk in the UK Biobank : A Nonlinear Mendelian Randomization Study
Sutherland JP, Zhou A, Hyppönen E
Annals of internal medicine · 98 citas
Cómo se estudió
- Diseño
- Estudio de cohortes (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Eventos clínicos como enfermedad o muerte
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- Medical Research Council
- Subvenciones
- Medical Research Council (MC_PC_17228)
Según 1 financiador declarado.
Publicación
- Publicado
- 2022-10-24 · Ann Intern Med · vol. 175 · número 11 · págs. 1552–1559
- Editorial
- American College of Physicians
- Citado
- 126 citas · más que el 100% de estudios similares · 16.6× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 39 trabajos
- Acceso
- De pago
- Áreas de investigación
- Vitamin D Research Studies · Genetic Associations and Epidemiology · Nutrition, Genetics, and Disease
- Palabras clave
- vitamin D deficiency, 25-hydroxyvitamin D, mortality, all-cause mortality, cardiovascular mortality, cancer mortality, respiratory mortality, causal inference, genetic variants, nonlinear dose-response relationship
- MeSH
- humans, neoplasms, cardiovascular diseases, vitamin d deficiency, vitamin d, risk factors, prospective studies, biological specimen banks, mendelian randomization analysis, united kingdom
3 autores
- Joshua P. Sutherland🇦🇺University of South Australia
- Ang Zhou🇦🇺University of South Australia; South Australian Health and Medical Research Institute
- Elina Hyppönen🇦🇺University of South Australia; South Australian Health and Medical Research Institute
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Low vitamin D status is associated with increased mortality, but randomized trials on severely deficient participants are lacking.
Objective
To assess genetic evidence for the causal role of low vitamin D status in mortality.
Design
Nonlinear Mendelian randomization analyses.
Setting
UK Biobank, a large-scale, prospective cohort from England, Scotland, and Wales with participants recruited between March 2006 and July 2010.
Participants
307 601 unrelated UK Biobank participants of White European ancestry (aged 37 to 73 years at recruitment) with available measurements of 25-hydroxyvitamin D (25-(OH)D) and genetic data.
Measurements
Genetically predicted 25-(OH)D was estimated using 35 confirmed variants of 25-(OH)D. All-cause and cause-specific mortality (cardiovascular disease [CVD], cancer, and respiratory) were recorded up to June 2020.
Results
There were 18 700 deaths during the 14 years of follow-up. The association of genetically predicted 25-(OH)D with all-cause mortality was L-shaped (P for nonlinearity P ≤ 0.033 for all outcomes). Odds of all-cause mortality in the genetic analysis were estimated to increase by 25% (odds ratio, 1.25 [95% CI, 1.16 to 1.35]) for participants with a measured 25-(OH)D concentration of 25 nmol/L compared with 50 nmol/L.
Limitations
Analyses were restricted to a White European population. A genetic approach is best suited to providing proof of principle on causality, whereas the strength of the association is approximate.
Conclusion
Our study supports a causal relationship between vitamin D deficiency and mortality. Additional research needs to identify strategies that meet the National Academy of Medicine's guideline of greater than 50 nmol/L and that reduce the premature risk for death associated with low vitamin D levels.
Primary funding source
National Health and Medical Research Council.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.
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