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Mendelian randomisation analyses find pulmonary factors mediate the effect of height on coronary artery disease
Queen Mary Univ London, Barts & London Sch Med & Dent, William Harvey Res Inst, London EC1M 6BQ, England;Queen Mary Univ London, Ctr Genom Hlth, Life Sci, London EC1M 6BQ, England.
Univ Lubeck, Inst Biomed, Eurac Res, Affiliated Inst, I-39100 Bolzano, Italy.
Boston Childrens Hosp, Boston, MA 02115 USA;Broad Inst MIT & Harvard, Cambridge, MA 02142 USA.
Univ Queensland, Inst Mol Biosci, Brisbane, Qld 4072, Australia;Univ Queensland, Queensland Brain Inst, Brisbane, Qld 4072, Australia.ORCID iD: 0000-0003-2001-2474
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2019 (English)In: COMMUNICATIONS BIOLOGY, ISSN 2399-3642, Vol. 2, article id 119Article in journal (Refereed) Published
Abstract [en]

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 (similar to 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.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP , 2019. Vol. 2, article id 119
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Medical Genetics
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URN: urn:nbn:se:uu:diva-382527DOI: 10.1038/s42003-019-0361-2ISI: 000463365700001PubMedID: 30937401OAI: oai:DiVA.org:uu-382527DiVA, id: diva2:1307384
Available from: 2019-04-26 Created: 2019-04-26 Last updated: 2019-04-26Bibliographically approved

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