1William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ UK.
2Centre for Genomic Health, Life Sciences, Queen Mary University of London, London, EC1M 6BQ UK.
Commun Biol. 2019 Mar 27;2:119. doi: 10.1038/s42003-019-0361-2. eCollection 2019.
There is evidence that lower height is associated with a higher risk of coronary artery disease (CAD) and increased risk of type 2 diabetes (T2D). It is not clear though whether these associations are causal, direct or mediated by other factors. Here we show that one standard deviation higher genetically determined height (~6.5 cm) is causally associated with a 16% decrease in CAD risk (OR = 0.84, 95% CI 0.80-0.87). This causal association remains after performing sensitivity analyses relaxing pleiotropy assumptions. The causal effect of height on CAD risk is reduced by 1-3% after adjustment for potential mediators (lipids, blood pressure, glycaemic traits, body mass index, socio-economic status). In contrast, our data suggest that lung function (measured by forced expiratory volume [FEV1] and forced vital capacity [FVC]) is a mediator of the effect of height on CAD. We observe no direct causal effect of height on the risk of T2D.
有证据表明，身高较低与冠心病（CAD）风险增加和 2 型糖尿病（T2D）风险增加有关。不过，这些关联是否具有因果关系、直接相关或由其他因素介导尚不清楚。在这里，我们表明，遗传决定的身高每增加一个标准差（约 6.5 厘米），与 CAD 风险降低 16%有关（OR=0.84，95%CI 0.80-0.87）。在放宽多效性假设进行敏感性分析后，这种因果关联仍然存在。在调整潜在中介因素（脂质、血压、血糖特征、体重指数、社会经济地位）后，身高对 CAD 风险的因果效应降低了 1-3%。相比之下，我们的数据表明，肺功能（通过用力呼气量[FEV1]和用力肺活量[FVC]测量）是身高对 CAD 影响的中介因素。我们没有观察到身高对 T2D 风险的直接因果效应。
