This Article Full Text Full Text (PDF) All Versions of this Article: 40/1/7    most recent 01.HYP.0000022693.11752.E9v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cui, J. Articles by Harrap, S. B. Search for Related Content PubMed PubMed Citation Articles by Cui, J. Articles by Harrap, S. B. Related Collections Genetics of cardiovascular disease

(Hypertension. 2002;40:7.)
© 2002 American Heart Association, Inc.

Scientific Contributions

Genes and Family Environment Explain Correlations Between Blood Pressure and Body Mass Index

From the Centre for Genetic Epidemiology (J.C., J.L.H.) and Department of Physiology (S.B.H.), The University of Melbourne, Parkville, Australia.

Correspondence to Prof Stephen B. Harrap, Department of Physiology, The University of Melbourne, Grattan Street, Parkville, Victoria 3010, Australia. E-mail s.harrap{at}unimelb.edu.au

The correlations between systolic blood pressure (SBP) and diastolic blood pressure (DBP), and between SBP and body mass index (BMI), might result from genetic or environmental factors that determine variation in 2 or more phenotypes and are shared by family members. In 767 adult nuclear families (n=2912 individuals, including 66 pairs of monozygotic twins and 84 pairs of dizygotic twins), we used a multivariate normal model and the software FISHER to estimate genetic and environmental components of variation and covariation. Mean phenotypes were adjusted for age, gender, and generation, and for antihypertensive treatment. Genetic and shared family environmental factors accounted for 46% and 31% of total variance in SBP, respectively. Adjustment of SBP for DBP reduced considerably both the additive genetic (86.7 to 21.0) and shared environmental (59.7 to 21.0) components of variance. Smaller reductions in genetic (86.7 to 84.9) and shared environmental (59.7 to 51.1) components were observed after adjustment of SBP for BMI. For SBP and DBP, the correlation between the effects of genes was 1.00 and between shared environmental effects was 0.52. For SBP and BMI the correlations were 0.30 for genetic and 0.22 for shared environmental effects. Our findings suggest that the same genes and many of the same family environmental factors determine variation in both SBP and DBP. In contrast, SBP and BMI share genetic and family environmental determinants to a lesser degree. These observations are relevant to multifactorial cardiovascular risk reduction based on genetic and family environmental approaches.

Key Words: systole • diastole • body mass index • genetics • risk factors • twins

This article has been cited by other articles:

				N. T. Tuan, L. S. Adair, K. He, and B. M. Popkin Optimal Cutoff Values for Overweight: Using Body Mass Index to Predict Incidence of Hypertension in 18- to 65-Year-Old Chinese Adults J. Nutr., July 1, 2008; 138(7): 1377 - 1382. [Abstract] [Full Text] [PDF]

				K. Skov, H. Eiskjaer, H. E. Hansen, J. K. Madsen, S. Kvist, and M. J. Mulvany Treatment of Young Subjects at High Familial Risk of Future Hypertension With an Angiotensin-Receptor Blocker Hypertension, July 1, 2007; 50(1): 89 - 95. [Abstract] [Full Text] [PDF]

				D. A. Lawlor, A. Hubinette, P. Tynelius, D. A. Leon, G. D. Smith, and F. Rasmussen Associations of Gestational Age and Intrauterine Growth With Systolic Blood Pressure in a Family-Based Study of 386 485 Men in 331 089 Families Circulation, February 6, 2007; 115(5): 562 - 568. [Abstract] [Full Text] [PDF]

				B. K. Rana, P. A. Insel, S. H. Payne, K. Abel, E. Beutler, M. G. Ziegler, N. J. Schork, and D. T. O'Connor Population-Based Sample Reveals Gene-Gender Interactions in Blood Pressure in White Americans Hypertension, January 1, 2007; 49(1): 96 - 106. [Abstract] [Full Text] [PDF]

				K. Skov, J. K. Madsen, H. E. Hansen, L. Zagato, E. Frandsen, G. Bianchi, and M. J. Mulvany Renal Haemodynamics are not Related to Genotypes in Offspring of Parents with Essential Hypertension Journal of Renin-Angiotensin-Aldosterone System, March 1, 2006; 7(1): 47 - 55. [Abstract] [PDF]

				K. Masuo, T. Katsuya, Y. Fu, H. Rakugi, T. Ogihara, and M. L. Tuck {beta}2- and {beta}3-Adrenergic Receptor Polymorphisms Are Related to the Onset of Weight Gain and Blood Pressure Elevation Over 5 Years Circulation, June 28, 2005; 111(25): 3429 - 3434. [Abstract] [Full Text] [PDF]

				J. Merlo, K. Asplund, J. Lynch, L. Rastam, and A. Dobson Population Effects on Individual Systolic Blood Pressure: A Multilevel Analysis of the World Health Organization MONICA Project Am. J. Epidemiol., June 15, 2004; 159(12): 1168 - 1179. [Abstract] [Full Text] [PDF]

				F. C. Luft Geneticism of Essential Hypertension Hypertension, June 1, 2004; 43(6): 1155 - 1159. [Full Text] [PDF]

				L. J. Palmer Loosening the Cuff: Important New Advances in Modeling Antihypertensive Treatment Effects in Genetic Studies of Hypertension Hypertension, February 1, 2003; 41(2): 197 - 198. [Full Text] [PDF]

				J. S. Cui, J. L. Hopper, and S. B. Harrap Antihypertensive Treatments Obscure Familial Contributions to Blood Pressure Variation Hypertension, February 1, 2003; 41(2): 207 - 210. [Abstract] [Full Text] [PDF]