Wienke Andreas, Herskind Anne M, Christensen Kaare, Skytthe Axel, Yashin Anatoli I
Institute of Medical Epidemiology, Biostatistics and Informatics, Martin-Luther-University Halle-Wittenberg, Halle, Germany.
Twin Res Hum Genet. 2005 Feb;8(1):53-9. doi: 10.1375/1832427053435328.
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.
丹麦单卵双胞胎和双卵双胞胎的死因特异性死亡率数据被用于分析在控制吸烟和体重指数(BMI)后冠心病(CHD)易感性的遗传度估计。样本包括1890年至1920年出生的1209对同性双胞胎,其中两人在1966年时仍然在世。参与者于1966年完成了一份问卷,其中包括关于吸烟、身高和体重的问题。由于双胞胎对数量相对较少,分析是将两性合并进行的。随访时间为1966年1月1日至1993年12月31日。使用具有观察协变量的相关伽马脆弱模型对脆弱性进行遗传分析,以考虑寿命数据中的删失和截断。在随访期间,共发生1437例死亡,其中435例死于冠心病。使用结构方程模型方法分析了脆弱性方差中可归因于遗传和环境因素的比例。对数据拟合不同的标准生物统计学模型,以评估遗传和环境因素对死亡率的影响程度和性质。使用无协变量的最佳拟合模型,发现冠心病脆弱性的遗传度为0.45(0.11)。在控制吸烟和BMI后,在一个DE模型中,这一结果仅略有变化,变为0.55(0.13)。该分析强调了存在对与冠心病导致的死亡相关的个体脆弱性有重大遗传影响。