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Metaanálisis2014

Vitamin D and high blood pressure: causal association or epiphenomenon?

Kunutsor SK, Burgess S, Munroe PB, Khan H

European journal of epidemiology · 104 citas

Cómo se estudió

Diseño
Metaanálisis (indexado por PubMed)
Estudiado en
Personas
Resultado principal
Marcadores de salud y funcionamiento

Quién lo pagó

Financiación
Financiación independiente
Organización sin fines de lucro
Wellcome Trust
Gobierno
National Institute for Health and Care Research
Organización sin fines de lucro
British Heart Foundation
Gobierno
Medical Research Council
Gobierno
National Human Genome Research Institute
Gobierno
National Institute for Health Research (NIHR)
Subvenciones
National Institute for Health and Care Research (NF-SI-0512-10165); Medical Research Council (MR/L003120/1); Wellcome Trust (100114); British Heart Foundation (RG/08/014/24067)

Según 6 financiadores declarados.

Publicación

Publicado
2013-12-28 · Eur J Epidemiol · vol. 29 · número 1 · págs. 1–14
Editorial
Springer Science+Business Media
Citado
139 citas · más que el 98% de estudios similares · 9.1× el promedio de su campo
Impacto
Entre el 10 % más citado de su campo
Referencias
60 trabajos
Acceso
De pago
Áreas de investigación
Vitamin D Research Studies · Blood Pressure and Hypertension Studies · Parathyroid Disorders and Treatments
Palabras clave
vitamin D supplementation, hypertension, blood pressure, 25-hydroxyvitamin D, vitamin D deficiency, causal relationship, Mendelian randomization, CYP24A1, GC gene, DHCR7, CYP2R1, cardiometabolic disease, systolic blood pressure, diastolic blood pressure, randomized controlled trials, publication bias
MeSH
humans, hypertension, vitamin d, blood pressure, polymorphism, single nucleotide, dietary supplements, female, male, randomized controlled trials as topic, mendelian randomization analysis

4 autores

  • Setor Kwadzo Kunutsor🇬🇧 · autor de correspondenciaUniversity of Cambridge
  • Stephen Burgess🇬🇧University of Cambridge
  • Patricia B. Munroe🇬🇧Queen Mary University of London; William Harvey Research Institute
  • Hassan Khan🇬🇧 · autor de correspondenciaUniversity of Cambridge

Resumen

El texto original del estudio, en el idioma en que se publicó.

High plasma levels of vitamin D are associated with a reduced risk of high blood pressure, but whether this association is causal remains to be ascertained. We performed a meta-analysis of randomized clinical trials, to examine the effect of vitamin D supplementation on both systolic blood pressure (SBP) and diastolic blood pressure (DBP) and supplemented these results with a Mendelian randomization analysis to investigate the causal relationship between vitamin D status (25-hydroxyvitamin D [25(OH)D]) and BP. Pooled random effects meta-analysis of weighted mean differences across 16 trials of vitamin D supplementation showed a non-significant reduction in SBP (-0.94, 95% CI -2.98, 1.10 mmHg) and DBP (-0.52, 95% CI -1.18, 0.14 mmHg), with evidence of heterogeneity (I(2) = 67.9%, P < 0.001) and publication bias (P = 0.02) among trials of SBP. There was a significant reduction in DBP (-1.31, 95% CI -2.28, -0.34 mmHg, P = 0.01) in participants with pre-existing cardiometabolic disease. Variants at three published loci (GC, DHCR7, CYP2R1, and CYP24A1) for 25(OH)D, were not significantly associated with BP, but rs6013897 in CYP24A1 gene region had nominally significant associations with both SBP and DBP (P < 0.05). Evidence from the associations of the genetic variants with the risk of vitamin D deficiency (defined as a 25(OH)D level < 50 nmol/L) and BP showed that the causal effects of a doubling of genetically-elevated risk of vitamin D deficiency were 0.14 mmHg (95% CI -0.19, 0.47, P = 0.42), and 0.12 mmHg (95% CI -0.09, 0.33, P = 0.25) on SBP and DBP respectively. Additional evidence from genetic data are directionally consistent with clinical trial data, though underpowered to reliably demonstrate a strong causal effect of vitamin D status on BP. Further investigation may be warranted.

Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.

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