We conducted a cross-sectional analysis of the genetic and environmental contributions to the variance of lipoprotein cholesterol and its subfractions in children during early adolescence. Univariate path analysis was used to determine the relative contributions of genes, individual environment, and family environment to these measures in 233 11-year-old Caucasian twin pairs. For high density lipoprotein, high density lipoprotein 2 , low density lipoprotein, very low density lipoprotein, and triglycerides, a model that incorporated genes and individual environmental variation but not common environment was sufficient to explain the variation. Different magnitudes of genetic effects were seen for total cholesterol in boys and girls. High density lipoprotein 3 showed different magnitudes by sex for genetic and individual environmental effect. Intermediate density lipoprotein was the only cholesterol subfraction in which shared, or common, environment was found to make a statistically significant contribution to the variation. (Arteriosclerosis and Thrombosis 1991;ll:844-850) H eart disease tends to cluster in families.
1Certain rare genetic disorders such as familial hypercholesterolemia that are poorly responsive to dietary and other environmental changes are responsible for only a small fraction of the prevalence of coronary heart disease. The genetic contribution versus the environmental effects of other lipid and lipoprotein abnormalities to the familial aggregation of cardiovascular disease is less well known, yet broad public health recommendations have been made both for children and adults of both sexes to reduce their cholesterol intake. Plasma concentrations of low density lipoprotein (LDL) cholesterol have been shown to be directly related to the risk of cardiovascular disease in adults.2 High density lipoprotein (HDL) cholesterol has shown an inverse relation. A key question concerns the extent to which environmental differences account for variation in lipoprotein cholesterol concentrations in children Received June 22, 1990; revision accepted February 8, 1991. because the efficacy of alternative intervention strategies could depend on the issue. To explore, in early-pubertal children, the genetic and environmental contributions to variation in cholesterol and its major subfractions, HDL (including HDL 2 and HDL 3 ), intermediate density lipoprotein (IDL), LDL, and very low density lipoprotein (VLDL) cholesterol and triglycerides, we measured these variables in 233 11-year-old Caucasian twin pairs and obtained point estimates of the additive genetic, shared environmental, unique environmental, and sex-specific genetic effects on these traits.
MethodsFrom school rosters we ascertained 233 Caucasian twin pairs living in Virginia who represent an unbiased volunteer sample of the central Virginia twin population. The twins were examined at times as near to their 11th birthdays as possible. Informed consent for the institutionally approved protocol was obtained from the twins and their parents. Zygosity...