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- Title
Mendelian randomisation analyses find pulmonary factors mediate the effect of height on coronary artery disease.
- Authors
Marouli, Eirini; Del Greco, M. Fabiola; Astley, Christina M.; Yang, Jian; Ahmad, Shafqat; Berndt, Sonja I.; Caulfield, Mark J.; Evangelou, Evangelos; McKnight, Barbara; Medina-Gomez, Carolina; van Vliet-Ostaptchouk, Jana V.; Warren, Helen R.; Zhu, Zhihong; Hirschhorn, Joel N.; Loos, Ruth J. F.; Kutalik, Zoltan; Deloukas, Panos
- Abstract
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. Eirini Marouli et al. use Mendelian randomisation analyses to investigate the causal relationship between adult height, coronary artery disease (CAD) and type 2 diabetes (T2D) in the UK Biobank. They find that height has a causal effect on CAD, which is mediated by lung function, while there is no direct effect on the risk of T2D.
- Subjects
TYPE 2 diabetes; CORONARY arteries; BIOBANKS; GENETIC pleiotropy; BLOOD pressure
- Publication
Communications Biology, 2019, Vol 2, Issue 1, pN.PAG
- ISSN
2399-3642
- Publication type
Article
- DOI
10.1038/s42003-019-0361-2