TY - JOUR
T1 - The cincinnati myocardial infarction and hormone family study
T2 - Family resemblance for dehydroepiandrosterone sulfate in control and myocardial infarction families
AU - Rice, Treva
AU - Sprecher, Dennis L.
AU - Borecki, Ingrid B.
AU - Mitchell, Laura E.
AU - Laskarzewski, Peter M.
AU - Rao, D. C.
N1 - Funding Information:
From the Division of Biostatistics and the Departments of Genetics and Psychiatry, Washington CJniversityS chool of Medicine, St Louis. MO; and the Lipid Research Division, Department of internal Medicine, Universiry of Cincinnati, Cincinnati, OH. Submitted August 3, 1992; accepted November 23. 1992. Supported by grants from the National Institutes of Health (GM 28719 and HD 18281) and the National Institutes of Mental Health (MH31302). Address reprint requests to Treva Rice, PhD, Washington Unrversi~ School of Medicine, Division of Biostatistics, Box 8067, 660 S Euclid Ave. St Louis, MO 63110. Copyright 0 1993 by W.B. Saunders Compaq 00260495193/4210-0009$03.OOiO
PY - 1993/10
Y1 - 1993/10
N2 - Dehydroepiandrosterone sulfate (DHEAS) was examined in random (control) and nonrandom (case) families participating in the Cincinnati Myocardial Infarction and Hormone (CIMIH) family study. The case families were ascertained through white men who survived a myocardial infarction (MI) before the age of 56, whereas control families were recruited through advertisements and through an adolescent boy maturation study. Both familial correlations and genetic effects of DHEAS were investigated. First, maximum likilihood estimates of the sex-specific familial correlations (corrected for nonrandom ascertainment) suggested that there was significant heterogeneity between the two sampling types. This heterogeneity was isolated to the male sibling correlation, which was higher in the case than control families. Post hoc analyses suggested that the sibling group heterogeneity may be in part a function of age, since the control sample offspring were on average much younger than those in case families. No sex differences other than those for the siblings were noted in the familial correlations. Second, heritability was investigated in control families using a simple path model (TAU) that allowed for sex differences. The only significant model parameter was the sex-specific familiality (combined polygenic and familial environmental effects), which was larger in females (74%) than in males (29%). In general, these analyses suggested that (1) DHEAS may play only a limited role in the increased risk for premature MI, and (2) the degree of heritable (familial) variation may be dependent on sex.
AB - Dehydroepiandrosterone sulfate (DHEAS) was examined in random (control) and nonrandom (case) families participating in the Cincinnati Myocardial Infarction and Hormone (CIMIH) family study. The case families were ascertained through white men who survived a myocardial infarction (MI) before the age of 56, whereas control families were recruited through advertisements and through an adolescent boy maturation study. Both familial correlations and genetic effects of DHEAS were investigated. First, maximum likilihood estimates of the sex-specific familial correlations (corrected for nonrandom ascertainment) suggested that there was significant heterogeneity between the two sampling types. This heterogeneity was isolated to the male sibling correlation, which was higher in the case than control families. Post hoc analyses suggested that the sibling group heterogeneity may be in part a function of age, since the control sample offspring were on average much younger than those in case families. No sex differences other than those for the siblings were noted in the familial correlations. Second, heritability was investigated in control families using a simple path model (TAU) that allowed for sex differences. The only significant model parameter was the sex-specific familiality (combined polygenic and familial environmental effects), which was larger in females (74%) than in males (29%). In general, these analyses suggested that (1) DHEAS may play only a limited role in the increased risk for premature MI, and (2) the degree of heritable (familial) variation may be dependent on sex.
UR - http://www.scopus.com/inward/record.url?scp=0027524735&partnerID=8YFLogxK
U2 - 10.1016/0026-0495(93)90126-9
DO - 10.1016/0026-0495(93)90126-9
M3 - Article
C2 - 8412740
AN - SCOPUS:0027524735
SN - 0026-0495
VL - 42
SP - 1284
EP - 1290
JO - Metabolism
JF - Metabolism
IS - 10
ER -