Heritability of longitudinal changes in coronary-heart-disease risk factors in women twins

被引:41
作者
Friedlander, Y
Austin, MA
Newman, B
Edwards, K
MayerDavis, EJ
King, MC
机构
[1] HADASSAH UNIV HOSP,DEPT SOCIAL MED,SCH PUBL HLTH,IL-91120 JERUSALEM,ISRAEL
[2] UNIV WASHINGTON,SCH PUBL HLTH & COMMUNITY MED,DEPT EPIDEMIOL,SEATTLE,WA 98195
[3] UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195
[4] UNIV WASHINGTON,DEPT GENET,SEATTLE,WA 98195
[5] UNIV N CAROLINA,SCH PUBL HLTH,DEPT EPIDEMIOL,CHAPEL HILL,NC
[6] WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PUBL HLTH SCI,WINSTON SALEM,NC 27103
关键词
D O I
10.1086/515462
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Numerous studies have demonstrated genetic influences on levels of coronary heart disease (CHD) risk factors, but there also may be genetic effects on the intraindividual variation in these risk factors over time. Changes in risk factors are likely to reflect genetic- environmental interactions and may have important implications for understanding CHD risk. The present study examines the heritability of changes in CHD risk factors, using data from the two examinations by the Kaiser Permanente Women Twins Study, performed a decade apart. The sample consisted of 348 pairs of women twins who participated in both examinations, including 203 MZ pairs and 145 DZ pairs. Average ages at the two examinations were 41 and 51 years, respectively. By means of three different statistical analytic approaches, moderate heritability estimates were demonstrated for changes in LDL cholesterol (h(2) = .25 - .36) and in HDL cholesterol (h(2) = .23 - .58), some of which were statistically significant. Although small to moderate heritability estimates were found for systolic blood pressure (.18 - .37; P < .05 for some estimates), no genetic influence on changes in diastolic blood pressure was detected. Based on longitudinal twin data in women, this study demonstrates a genetic influence on changes in both lipoprotein risk factors and systolic blood pressure over a decade. In addition to environmental factors, which clearly are operating, the effect of various ''variability genes'' may be acting independently of the genetic influences on the absolute levels of these risk factors. Both mapping the gene(s) underlying intraindividual variations in these CHD risk factors and understanding their function(s) could lead to targeted intervention strategies to reduce CHD risk among genetically susceptible individuals.
引用
收藏
页码:1502 / 1512
页数:11
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