Non-linear Mendelian randomization analyses support a role for vitamin D deficiency in cardiovascular disease risk

孟德尔随机化 医学 维生素D与神经学 维生素D缺乏 置信区间 内科学 疾病 人口 心脏病学 入射(几何) 血压 内分泌学 遗传学 基因型 物理 环境卫生 遗传变异 基因 光学 生物
作者
Ang Zhou,Joseph B. Selvanayagam,Elina Hyppönen
出处
期刊:European Heart Journal [Oxford University Press]
卷期号:43 (18): 1731-1739 被引量:138
标识
DOI:10.1093/eurheartj/ehab809
摘要

Abstract Aims Low vitamin D status is associated with a higher risk for cardiovascular diseases (CVDs). Although most existing linear Mendelian randomization (MR) studies reported a null effect of vitamin D on CVD risk, a non-linear effect cannot be excluded. Our aim was to apply the non-linear MR design to investigate the association of serum 25-hydroxyvitamin D [25(OH)D] concentration with CVD risk. Methods and results The non-linear MR analysis was conducted in the UK Biobank with 44 519 CVD cases and 251 269 controls. Blood pressure (BP) and cardiac-imaging-derived phenotypes were included as secondary outcomes. Serum 25(OH)D concentration was instrumented using 35 confirmed genome-wide significant variants. We also estimated the potential reduction in CVD incidence attributable to correction of low vitamin D status. There was a L-shaped association between genetically predicted serum 25(OH)D and CVD risk (P non-linear = 0.007), where CVD risk initially decreased steeply with increasing concentrations and levelled off at around 50 nmol/L. A similar association was seen for systolic (P non-linear = 0.03) and diastolic (P non-linear = 0.07) BP. No evidence of association was seen for cardiac-imaging phenotypes (P = 0.05 for all). Correction of serum 25(OH)D level below 50 nmol/L was predicted to result in a 4.4% reduction in CVD incidence (95% confidence interval: 1.8– 7.3%). Conclusion Vitamin D deficiency can increase the risk of CVD. Burden of CVD could be reduced by population-wide correction of low vitamin D status.
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