Heritability of LDL peak particle diameter in the Quebec Family Study
Article first published online: 18 NOV 2003
© 2003 Wiley-Liss, Inc.
Volume 25, Issue 4, pages 375–381, December 2003
How to Cite
Bossé, Y., Vohl, M.-C., Després, J.-P., Lamarche, B., Rice, T., Rao, D.C., Bouchard, C. and Pérusse, L. (2003), Heritability of LDL peak particle diameter in the Quebec Family Study. Genet. Epidemiol., 25: 375–381. doi: 10.1002/gepi.10272
- Issue published online: 18 NOV 2003
- Article first published online: 18 NOV 2003
- Manuscript Accepted: 9 JUN 2003
- Manuscript Received: 17 APR 2003
- Canadian Institutes of Health Research. Grant Numbers: MT-13960, MOP-14014, GR-15187
- LDL size
LDL size has been associated with the risk of coronary heart disease. The objective of the present study was to verify whether familial factors influence LDL peak particle diameter (LDL-PPD), a quantitative trait reflecting the size of the major LDL subclass. LDL-PPD was measured by 2–16% polyacrylamide gradient gel electrophoresis in 681 members of 236 nuclear families participating in the Quebec Family Study. LDL-PPD was adjusted for age (LDL-PPD1), age and body mass index (LDL-PPD2), or age, body mass index, and plasma triglyceride levels (LDL-PPD3) separately in men and women. The residual scores were used to test for familial aggregation, using an ANOVA and to compute maximum likelihood estimates of familial correlations. The ANOVA test revealed that family lines accounted for 47.4%, 46.7%, and 48.9% of the variance in the LDL-PPD1, LDL-PPD2, and LDL-PPD3 phenotypes, respectively. The pattern of familial correlations revealed no significant spouse correlations but significant parent-offspring and sibling correlations for the three LDL-PPD phenotypes, with maximal heritability estimates of 59%, 58%, and 52% for LDL-PPD1, LDL-PPD2, and LDL-PPD3, respectively. These results suggest that LDL-PPD strongly aggregates in families, and that the familial resemblance appears to be primarily attributable to genetic factors. Genes responsible for this genetic contribution remain to be identified. Genet Epidemiol 25:375–381, 2003. © 2003 Wiley-Liss, Inc.