Mendelian randomisation analyses find pulmonary factors mediate the effect of height on coronary artery disease.

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License: CC BY 4.0
Serval ID
serval:BIB_B241E0087C22
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Mendelian randomisation analyses find pulmonary factors mediate the effect of height on coronary artery disease.
Journal
Communications biology
Author(s)
Marouli E., Del Greco M.F., Astley C.M., Yang J., Ahmad S., Berndt S.I., Caulfield M.J., Evangelou E., McKnight B., Medina-Gomez C., van Vliet-Ostaptchouk J.V., Warren H.R., Zhu Z., Hirschhorn J.N., Loos RJF, Kutalik Z., Deloukas P.
ISSN
2399-3642 (Electronic)
ISSN-L
2399-3642
Publication state
Published
Issued date
2019
Peer-reviewed
Oui
Volume
2
Pages
119
Language
english
Notes
Publication types: Journal Article
Publication Status: epublish
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.
Pubmed
Web of science
Open Access
Yes
Create date
15/04/2019 8:37
Last modification date
20/08/2019 15:20
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