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Endocrine Abstracts (2015) 38 P182 | DOI: 10.1530/endoabs.38.P182

SFEBES2015 Poster Presentations Obesity, diabetes, metabolism and cardiovascular (108 abstracts)

Testing causality in the association of plasma cortisol with risk of coronary heart disease: a Mendelian randomisation study

Andrew Crawford 1, , Nicholas Timpson 2 , George Davey Smith 2 & Brian Walker 1,


1University/BHF Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK; 2MRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK


Background: Elevated morning plasma cortisol is associated with multiple cardiovascular risk factors in metabolic syndrome. Epidemiological studies have also reported a positive association between plasma cortisol and coronary heart disease (CHD), although not all estimates are statistically significant (OR 1.10 (95% CI 0.97 to 1.25)) (Davey Smith et al. Circulation 2005). Importantly, observational studies are unable to infer causality and results may be confounded.

Methods: A two-sample Mendelian randomisation approach was used to estimate the causal effect of plasma cortisol on risk of CHD. A genetic instrument for plasma cortisol comprised three SNPs which were associated with plasma cortisol in the recent Cortisol Network (CORNET) genome wide association meta-analysis (n=12,597) (Bolton et al. PLoS Genetics 2014). We investigated the association between this genetic instrument for plasma cortisol and risk of CHD in up to 22,223 cases/64,762 controls from the publicly available CARDIOGRAM consortium.

Results: Each standard deviation rise in genetically predicted plasma cortisol was associated with an odds ratio of 1.27 (95% CI: 1.01 to 1.60) for CHD.

Conclusions: These results are compatible with a causal effect for the observational association between plasma cortisol and CHD. The inconsistent results from observational studies may be explained by: the inverse association between cortisol and obesity, which confounded the positive association of cortisol with other cardiovascular risk factors; and the use of single ‘snapshot’ plasma cortisol measurement rather than cumulative measure of cortisol exposure provided by genetic prediction. A bidirectional Mendelian randomisation analysis between plasma cortisol and BMI may yield greater clarity. Measurements of cortisol may add value to predictions of CHD risk.

Volume 38

Society for Endocrinology BES 2015

Edinburgh, UK
02 Nov 2015 - 04 Nov 2015

Society for Endocrinology 

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