Genetic Heritability and Common Environmental
Components of Resting and Stressed Blood Pressures,
Lipids, and Body Mass Index in Utah Pedigrees and Twins
Hunt SC, Hasstedt SJ, Kuida H, Stults BM, Hopkins PN, Williams RR
U. of Utah School of Medicine, Salt Lake City 84108.
American Journal of Epidemiology, 129(3):625-638 (1989)
Abstract
The relative contributions of genes and shared environment to cardiovascular risk factors
were studied in twins and pedigrees in 1983-1985. Sitting, standing, isometric hand grip,
bicycling, and mentally stressed (serial subtraction) blood pressures were obtained from 146
male monozygous twins, 162 male dizygous twins, and 1,102 healthy adults in 67 Utah
pedigrees. Fasting total plasma cholesterol, triglycerides, high density lipoprotein
cholesterol (HDL), and body mass index were also measured. Heritability was estimated
before and after adjusting for 12 environmental variables (measures of socioeconomic
status; personality types; exercise levels; use of tobacco, alcohol, coffee, etc.) by using
age-adjusted twin intraclass correlations. These heritabilities were compared with those
obtained from a variance components analysis of the pedigree data separating genetic and
common household effects. Sitting and standing blood pressure heritability estimates were
much higher from twin than from pedigree data (39-63% in twins vs. 16-22% in
pedigrees), as were those for cholesterol and triglycerides (65 and 75% from twins vs. 42
and 37% from pedigrees) and body mass index (51 vs. 21%). Estimates were similar for
heritability of HDL cholesterol (51 vs. 45%). Most of the stressed blood pressure
heritabilities were similar to sitting blood pressure estimates. No common household effect
(except for adjusted HDL cholesterol (24%), p less than 0.01) was statistically significant
for the lipids, blood pressures, or body mass index. Environmental variables correlated
much better in monozygous twins and spouses than in dizygous twins, brothers, or sisters.
Spouse correlations for lipids, blood pressures, and body mass index were low, with a
maximum of 0.12 (p less than 0.05) for HDL cholesterol. We conclude that genes
contribute much more than shared environment to the well-recognized familial correlation
of blood pressures, lipids, and body mass index.
Variance component linkage analysis