a1 Genetic Epidemiology Unit, Queensland Institute of Medical Research, Australia; School of Medicine, The University of Queensland, Australia. firstname.lastname@example.org
a2 Genetic Epidemiology Unit, Queensland Institute of Medical Research, Australia.
a3 Genetic Epidemiology Unit, Queensland Institute of Medical Research, Australia.
Plasma lipids such as high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol and triglyceride levels contribute to variation in the risk of cardiovascular disease. The early stages of atherosclerosis in childhood have also been associated with changes in triglycerides, LDL and HDL. Heritability estimates for lipids and lipoproteins for adolescents are in the range .71 to .82, but little is known about changes of genetic and environmental influences over time in adolescence. We have investigated the contribution of genetic and environmental influences to variation in lipids in adolescent twins and their nontwin siblings using longitudinal twin and family data. Plasma HDL and LDL cholesterol, total cholesterol and triglycerides data from 965 twin pairs at 12, 14 and 16 years of age and their siblings have been analyzed. Longitudinal genetic models that included effects of age, sex and their interaction were fitted to assess whether the same or different genes influence each trait at different ages. Results suggested that more than one genetic factor influences HDL, LDL, total cholesterol and triglycerides over time at ages 12, 14 and 16 years. There was no evidence of shared environmental effects except for HDL and little evidence of long-term nonshared environmental effects was found. Our study suggested that there are developmental changes in the genes affecting plasma lipid concentrations across adolescence.
(Received October 12 2006)
(Accepted November 29 2006)
c1 Address for correspondence: Rita P. S. Middelberg, Genetic Epidemiology Unit, Queensland Institute of Medical Research, PO Royal Brisbane Hospital, QLD 4029, Australia.