Mendelian randomisation analyses find pulmonary factors mediate the effect of height on coronary artery disease View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2019-03-27

AUTHORS

Eirini Marouli, M. Fabiola Del Greco, Christina M. Astley, Jian Yang, Shafqat Ahmad, Sonja I. Berndt, Mark J. Caulfield, Evangelos Evangelou, Barbara McKnight, Carolina Medina-Gomez, Jana V. van Vliet-Ostaptchouk, Helen R. Warren, Zhihong Zhu, Joel N. Hirschhorn, Ruth J. F. Loos, Zoltan Kutalik, Panos Deloukas

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. More... »

PAGES

119

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s42003-019-0361-2

    DOI

    http://dx.doi.org/10.1038/s42003-019-0361-2

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1113004301

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30937401


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