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.

Additional Metadata
Persistent URL dx.doi.org/10.1038/s42003-019-0361-2, hdl.handle.net/1765/116164
Journal Communications Biology
Citation
Marouli, E, Del Greco, MF, Astley, C.M., Yang, J, Ahmad, S., Berndt, S.I, … Deloukas, P. (2019). Mendelian randomisation analyses find pulmonary factors mediate the effect of height on coronary artery disease. Communications Biology, 2. doi:10.1038/s42003-019-0361-2