Journal article
Childhood adiposity, adult adiposity, and the ACE gene insertion/deletion polymorphism: Evidence of gene-environment interaction effects on adult blood pressure and hypertension status in adulthood
C Sun, AL Ponsonby, JB Carlin, M Bui, CG Magnussen, TL Burns, T Lehtimaki, NH Wardrop, M Juonala, JSA Viikari, AJ Venn, OT Raitakari, T Dwyer
Journal of Hypertension | LIPPINCOTT WILLIAMS & WILKINS | Published : 2018
Abstract
Background: Genetic variants may modify the associations of adiposity measures with blood pressure (BP) and hypertension. The insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene is an attractive candidate. Aims: To examine interaction effects between I/D polymorphism and adiposity measures (BMI, waist circumference, waist-to-hip ratio, and skinfold thickness) during childhood and adulthood in relation to adult BP and hypertension. Methods: Data were available for 4835 participants from three prospective cohort studies. Multivariable linear regression models for adult SBP and DBP, and multivariable logistic regression models for hypertension were fit that inc..
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Awarded by National Institutes of Health
Funding Acknowledgements
We thank the contributions of the Childhood Determinants of Adult Health Study, the Cardiovascular Risk in Young Finns Study, and the Muscatine Study's staff and volunteers, and the study participants who made these studies possible. We also thank Andrea Polanowski and Alison West for their contributions to the design, performance and quality control analyses for the ACE gene genotyping for the Childhood Determinants of Adult Health Study. The Childhood Determinants of Adult Health Study was funded by grants from the Australian National Health and Medical Research Council (NHMRC), the Australian National Heart Foundation, the Tasmanian Community Fund, and Veolia Environmental Services. Sponsorship support was also provided by Sanitarium Health Food Company, ASICS Oceania, and Target Australia. The Cardiovascular Risk in Young Finns Study has been financially supported by the Academy of Finland: grants 286284 (T.L.), 134309, 126925, 121584, 124282, 129378, 117787, and 41071; the Social Insurance Institution of Finland; Kuopio, Tampere and Turku University Hospital Medical Funds (grant X51001 for T.L.); Juho Vainio Foundation; Paavo Nurmi Foundation; Finnish Foundation of Cardiovascular Research; Finnish Cultural Foundation; Tampere Tuberculosis Foundation (T.L.); Emil Aaltonen Foundation (T.L.); and Yrjo Jahnsson Foundation (T.L.). The Muscatine Study was supported by grants from the National Heart, Lung, and Blood Institute (HL-14230, HL-54730 and HL-61357), and the General Clinical Research Centers Program (RR-00059) of the NIH, and by a grant from the American Heart Association award number #0265155Y. C.S. is supported by the NHMRC Early Career Public Health Fellowship (1013538). C.G.M. is supported by a National Heart Foundation of Australia Future Leader Fellowship (100849). A.-L.P. and A.J.V. are supported by the NHMRC Senior Research Fellowship.