Hostname: page-component-7479d7b7d-68ccn Total loading time: 0 Render date: 2024-07-11T20:22:58.615Z Has data issue: false hasContentIssue false

The Heritability of CHD Mortality in Danish Twins After Controlling for Smoking and BMI

Published online by Cambridge University Press:  21 February 2012

Andreas Wienke*
Affiliation:
Institute of Medical Epidemiology, Biostatistics and Informatics, Martin-Luther-University Halle-Wittenberg, Halle, Germany. andreas.wienke@medizin.uni-halle.de
Anne M. Herskind
Affiliation:
Odense University Hospital, Odense, Denmark.
Kaare Christensen
Affiliation:
Danish Center for Demographic Research, and the Danish Twin Registry, University of Southern Denmark, Odense, Denmark.
Axel Skytthe
Affiliation:
Danish Center for Demographic Research, and the Danish Twin Registry, University of Southern Denmark, Odense, Denmark.
Anatoli I. Yashin
Affiliation:
Center for Demographic Studies, Duke University, Durham, United States of America.
*
*Address for correspondence: Andreas Wienke, Martin-Luther-University Halle-Wittenberg, Medical Faculty, Institute of Medical Epidemiology, Biostatistics and Informatics, Magdeburger Strasse 27, 06097 Halle, Germany.

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Cause-specific mortality data on Danish monozygotic and dizygotic twins are used to analyze heritability estimates of susceptibility to coronary heart disease (CHD) after controlling for smoking and Body Mass Index (BMI). The sample includes 1209 like-sexed twin pairs born between 1890 and 1920, where both individuals were still alive in 1966. The participants completed a questionnaire in 1966 which included questions on smoking, height and weight. The analysis was conducted with both sexes pooled due to the relatively small number of twin pairs. Follow-up was conducted from January 1, 1966 to December 31, 1993. The correlated gammafrailty model with observed covariates was used for the genetic analysis of frailty to account for censoring and truncation in the lifetime data. During the follow-up, 1437 deaths occurred, including 435 deaths due to CHD. Proportions of variance of frailty attributable to genetic and environmental factors were analyzed using the structural equation model approach. Different standard biometric models are fitted to the data to evaluate the magnitude and nature of genetic and environmental factors on mortality. Using the best-fitting model without covariates, heritability of frailty to CHD was found to be 0.45 (0.11). This result changes only slightly to 0.55 (0.13) in a DE model after controlling for smoking and BMI. This analysis underlines the existence of a substantial genetic influence on individual frailty associated with mortality caused by CHD.

Type
Articles
Copyright
Copyright © Cambridge University Press 2005