Cardiovascular risk factors in a french canadian population: Resolution of genetic and familial environmental effects on blood pressure using twins, adoptees, and extensive information on environmental correlates
dc.contributor.author | Rice, Treva | en_US |
dc.contributor.author | Vogler, George P. | en_US |
dc.contributor.author | Pérusse, Louis | en_US |
dc.contributor.author | Bouchard, Claude | en_US |
dc.contributor.author | Rao, D. C. | en_US |
dc.contributor.author | Williams, Roger R. | en_US |
dc.date.accessioned | 2013-12-04T18:58:16Z | |
dc.date.available | 2013-12-04T18:58:16Z | |
dc.date.issued | 1989 | en_US |
dc.identifier.citation | Rice, Treva; Vogler, George P.; Pérusse, Louis ; Bouchard, Claude; Rao, D. C.; Williams, Roger R. (1989). "Cardiovascular risk factors in a french canadian population: Resolution of genetic and familial environmental effects on blood pressure using twins, adoptees, and extensive information on environmental correlates." Genetic Epidemiology 6(5): 571-588. <http://hdl.handle.net/2027.42/101882> | en_US |
dc.identifier.issn | 0741-0395 | en_US |
dc.identifier.issn | 1098-2272 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/101882 | |
dc.description.abstract | Genetic and environmental influences on systolic (SBP), diastolic (DBP), and mean arterial (MBP) blood pressure were examined using an expanded version of a path model in which parents and their singleton, twin, and adopted offspring were incorporated, and which also included an environmental index as an estimate of the underlying familial environmental component. Estimates of genetic heritability are lower in parents (10–15%) than in offspring (40–50%). Cultural heritability was significant for SBP (0.31) and MBP (0.40), and an intergenerational effect was found for DBP, with higher estimates in parents (0.42) than in offspring (0.21). Marital resemblance was significant, and no support was found for differential maternal and paternal cultural transmission. Two novel results arising from this study are 1) gender‐specific sibling effects, with greater female than male resemblance for SBP and MBP and the opposite pattern for DBP, and 2) the suggestion of extra twin resemblance arising on account of additional shared environments and resulting in greater like‐sex than opposite‐sex twin resemblance. The major conclusions drawn from this study are that 1) parameter estimates are stable with or without the use of extensive environmental indices, and 2) the addition of twins and adoptees did not significantly impact the results, with the exception of a possible influence of the adoptees in estimates of cultural heritability for DBP. Combining both these features (i.e., extended relatives and environmental indices) enables testing for additional sources of familial aggregation, which is not possible using the traditional nuclear family approach and results in a more accurate assessment of the relative roles of heredity and environment on blood pressure than has been previously possible. | en_US |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Gender Differences | en_US |
dc.subject.other | Heritability | en_US |
dc.subject.other | Nuclear Families | en_US |
dc.title | Cardiovascular risk factors in a french canadian population: Resolution of genetic and familial environmental effects on blood pressure using twins, adoptees, and extensive information on environmental correlates | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbsecondlevel | Genetics | en_US |
dc.subject.hlbsecondlevel | Biological Chemistry | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationother | Departments of Psychiatry and Genetics, Washington University School of Medicine, St. Louis | en_US |
dc.contributor.affiliationother | Physical Activity Sciences Laboratory, Laval University, Ste‐Foy, Québec, Canada | en_US |
dc.contributor.affiliationother | Division of Biostatistics, Washington University School of Medicine, St. Louis | en_US |
dc.identifier.pmid | 2591728 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/101882/1/1370060503_ftp.pdf | |
dc.identifier.doi | 10.1002/gepi.1370060503 | en_US |
dc.identifier.source | Genetic Epidemiology | en_US |
dc.identifier.citedreference | Feinleib M, Garrison RJ ( 1979 ): The contribution of family studies to the partitioning of population variation of blood pressure. In Sing CF, Skolnick M (eds):“ Genetic Analysis of Common Diseases: Applications to Predictive Factors in Coronary Disease.” New York: Alan R. Liss, Inc.,pp 653 – 673. | en_US |
dc.identifier.citedreference | Annest JD, Sing CF, Biron P, Mongeau JG ( 1979 ): Familial aggregation of blood pressure and weight in adoptive families. II. Estimation of the relative contributions of genetic and common environmental factors to blood pressure correlations between family members. Am J Epidemiol 110: 492 – 503. | en_US |
dc.identifier.citedreference | Burns TL, Lauer RM ( 1986 ): Blood pressure in children. In Pierpont MEM, Moller JH (eds):“ The Genetics of Cardiovascular Disease.” Boston: Martinus Nijhoff,pp 305 – 317. | en_US |
dc.identifier.citedreference | Després JP, Tremblay A, Thériault G, Pérusse, L, Leblanc C, Bouchard C ( 1988 ): Relationships between body fatness, adipose tissue distribution and blood pressure in men and women. J Clin Epidemiol 41: 889 – 897. | en_US |
dc.identifier.citedreference | Rao DC, Laskarzewski PM, Morrison JA, Khoury P, Kelly K, Wette R, Russell J, Glueck CJ ( 1982 ): The Cincinnati Lipid Research Clinic Family Study: Cultural and biological determinants of lipids and lipoprotein concentrations. Am J Hum Genet 34: 888 – 903. | en_US |
dc.identifier.citedreference | Williams RR, Dadone MM, Hunt SC, Jorde LB, Hopkins PN, Smith JB, Ash KO, Kuida H ( 1984 ): The genetic epidemiology of hypertension: A review of past studies and current results for 948 persons in 48 Utah pedigrees. In Rao DC, Elston RC, Kuller LH, Feinleib M, Carter C, Havlik R (eds):“ Genetic Epidemiology of Coronary Heart Disease: Past, Present, and Future.” New York: Alan R. Liss, Inc.,pp 419 – 442. | en_US |
dc.identifier.citedreference | Rao DC, Morton NE, Yee S ( 1974 ): Analysis of family resemblance. II. A linear model for familial correlation. Am J Hum Genet 26: 331 – 359. | en_US |
dc.identifier.citedreference | Rao DC, McGue M, Wette R, Glueck CJ ( 1984 ): Path analysis in genetic epidemiology. In Chakravarti A (ed):“ Human Population Genetics: The Pittsburgh Symposium.” Stroudsburg, PA: Van Nostrand Reinhold,pp 35 – 81. | en_US |
dc.identifier.citedreference | Pérusse L, Rice T, Bouchard C, Vogler GP, Rao DC ( 1989 ):Cardiovascular risk factors in a French Canadian population: Resolution of genetic and familial environmental effects on blood pressure using extensive information on environmental correlates. Am J Hum Genet (in press). | en_US |
dc.identifier.citedreference | Morton NE, Gulbrandsen CL, Rao DC, Rhoads GG, Kagan A ( 1980 ): Determinants of blood pressure in Japanese‐American families. Hum Genet 53: 261 – 266. | en_US |
dc.identifier.citedreference | Li CC ( 1975 ):“ Path analysis: A primer.” Pacific Grove: Boxwood. | en_US |
dc.identifier.citedreference | Krieger H, Morton NE, Rao DC, Azevedo E ( 1980 ): Familial determinants of blood pressure in Northeastern Brazil. Hum Genet 53: 415 – 418. | en_US |
dc.identifier.citedreference | Havlik RJ, Garrison RJ, Katz SH, Ellison RC, Feinleib M, Myrianthopoulos NC ( 1979 ): Detection of genetic variance in blood pressure of seven‐year‐old twins. Am J Epidemiol 109: 512 – 516. | en_US |
dc.identifier.citedreference | Akaike H ( 1974 ): A new look at the statistical model identification. IEEE Trans Automat Control AC. 19: 716 – 723. | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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