Genetic and environmental contributions to cardiovascular risk factors in Mexican Americans. The San Antonio Family Heart Study.
BACKGROUND
The familial aggregation of coronary heart disease can be in large part accounted for by a clustering of cardiovascular disease risk factors. To elucidate the determinants of cardiovascular disease, many epidemiological studies have focused on the behavioral and lifestyle determinants of these risk factors, whereas others have examined whether specific candidate genes influence quantitative variation in these phenotypes.


RESULTS
Among Mexican Americans from San Antonio (Tex), we quantified the relative contributions of both genetic and environmental influences to a large panel of cardiovascular risk factors, including serum levels of lipids, lipoproteins, glucose, hormones, adiposity, and blood pressure. Members of 42 extended families were studied, including 1236 first-, second-, and third-degree relatives of randomly ascertained probands and their spouses. In addition to the phenotypic assessments, information was obtained regarding usual dietary and physical activity patterns, medication use, smoking habits, alcohol consumption, and other lifestyle behaviors and medical factors. Maximum likelihood methods were used to partition the variance of each phenotype into components attributable to the measured covariates, additive genetic effects (heritability), household effects, and an unmeasured environmental residual. For the lipid and lipoprotein phenotypes, age, gender, and other environmental covariates accounted in general for < 15% of the total phenotypic variance, whereas genes accounted for 30% to 45% of the phenotypic variation. Similarly, genes accounted for 15% to 30% of the phenotypic variation in measures of glucose, hormones, adiposity, and blood pressure.


CONCLUSIONS
These results highlight the importance of considering genetic factors in studies of risk factors for cardiovascular disease.
Mitchell
B D
BD
Department of Genetics, Southwest Foundation for Biomedical Research, San Antonio, Tex 78245-0549, USA. bmitchel@darwin.sfbr.org
Kammerer
C M
CM
Blangero
J
J
Mahaney
M C
MC
Rainwater
D L
DL
Dyke
B
B
Hixson
J E
JE
Henkel
R D
RD
Sharp
R M
RM
Comuzzie
A G
AG
VandeBerg
J L
JL
Stern
M P
MP
MacCluer
J W
JW
D000328:Adult; D000367:Age Factors; D000368:Aged; D000886:Anthropometry; D001054:Apolipoproteins A / Q000097:blood; D001786:Blood Glucose; D001794:Blood Pressure; D002318:Cardiovascular Diseases / Q000150:complications / Q000453:epidemiology* / Q000235:genetics*; D008076:Cholesterol, HDL / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000453:epidemiology; D005192:Family Health; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D008297:Male; D017058:Mexican Americans; D008875:Middle Aged; D010375:Pedigree; D010641:Phenotype; D015995:Prevalence; D012307:Risk Factors; D012737:Sex Factors; D012738:Sex Hormone-Binding Globulin / Q000378:metabolism; D013781:Texas / Q000453:epidemiology
D001054:Apolipoproteins A; D001786:Blood Glucose; D008076:Cholesterol, HDL; D007328:Insulin; D012738:Sex Hormone-Binding Globulin; D019314:Dehydroepiandrosterone Sulfate