SHARED AND UNIQUE GENETIC-EFFECTS AMONG 7 HDL PHENOTYPES

The purpose of this study was to investigate the genetic control of va rious HDL measures and to determine the proportion of genetic variance explained by shared genes (ie, pleiotropy) and the proportion unique to each trait. The data used were drawn from large, randomly ascertain ed pedigrees of Mexican Americans participating in the San Antonio Fam ily Heart Study. Data were available for 655 individuals (258 men and 397 women) in 26 families. We performed a multivariate quantitative ge netic analysis to simultaneously estimate both the additive genetic an d random environmental correlations among seven HDL phenotypes. These seven HDL phenotypes can be divided into two categories: measures of c oncentration and estimates of particle size. Concentration was measure d for apo A-I, apo A-II, esterified cholesterol, and unesterified chol esterol, and particle size was estimated for apo A-I, apo A-II, and es terified cholesterol. The heritabilities (h(2)) for each of the seven traits were significantly greater than zero (P<.05) and ranged from 0. 2 to 0.6. When considered in a pairwise fashion, all combinations of t hese traits showed marked genetic correlations (rho(G)=0.33 to 0.87) a nd all were significantly greater than zero (P<.05), indicative of ple iotropic effects. However, we found substantial unique genetic varianc e for each of these traits even after accounting for the effects share d in common with all the remaining measures. We conclude that the gene tic variation in these HDL phenotypes is a result of the action of com mon as well as unique genes.