Mendelian randomisation analyses find pulmonary factors mediate the effect of height on coronary artery disease.
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2019
- doi: 10.1038/s42003-019-0361-2
- issn: 2399-3642
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info:eu-repo/semantics/altIdentifier/doi/10.1038/s42003-019-0361-2
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info:eu-repo/semantics/altIdentifier/pmid/30937401
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info:eu-repo/semantics/altIdentifier/eissn/2399-3642
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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_B241E0087C220
info:eu-repo/semantics/openAccess , CC BY 4.0 , https://creativecommons.org/licenses/by/4.0/
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E. Marouli et al., « Mendelian randomisation analyses find pulmonary factors mediate the effect of height on coronary artery disease. », Serveur académique Lausannois, ID : 10.1038/s42003-019-0361-2
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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.