Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

Type 2 diabetes (T2D) is an important heritable risk factor for coronary artery disease (CAD), the risk of both diseases being increased by metabolic syndrome (MS). With the availability of large-scale genome-wide association data, we aimed to elucidate the genetic burden of CAD risk in T2D predisposed individuals within the context of MS and their shared genetic architecture. Mendelian randomization (MR) analyses supported a causal relationship between T2D and CAD [odds ratio (OR) = 1.13 per log-odds unit 95% confidence interval (CI): 1.10-1.16; p = 1.59 × 10-17 ]. Simultaneously adjusting MR analyses for the effects of the T2D instrument including blood pressure, dyslipidaemia, and obesity attenuated the association between T2D and CAD (OR = 1.07, 95% CI: 1.04-1.11). Bayesian locus-overlap analysis identified 44 regions with the same causal variant underlying T2D and CAD genetic signals (FDR 0.7; five (MHC, LPL, ABO, RAI1 and MC4R) of these regions contain genome-wide significant (p 

Original publication

DOI

10.1002/gepi.22434

Type

Journal article

Journal

Genet Epidemiol

Publication Date

21/10/2021

Keywords

Mendelian randomization, genetics, metabolic syndrome