Published online before print April 23, 2007, doi: 10.1161/HYPERTENSIONAHA.106.085597
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(Hypertension. 2007;49:1415.)
© 2007 American Heart Association, Inc.
Original Articles |
Childhood Growth and Hypertension in Later Life
From the National Public Health Institute (J.G.E., T.J.F., E.K.), Department of Health Promotion and Chronic Disease Prevention, Diabetes Unit, Helsinki, Finland; the Department of Public Health (J.G.E.), University of Helsinki, Helsinki, Finland; MRC Epidemiology Resource Centre (C.O.), University of Southampton, Southampton General Hospital, Southampton, United Kingdom; and the Heart Research Center (D.J.P.B.), Oregon Health and Sciences University, Portland, Ore.
Correspondence to David J.P. Barker, Developmental Origins of Health and Disease (MP 887), University of Southampton, Princess Anne Hospital, Southampton SO16 5YA, United Kingdom. E-mail djpb{at}mrc.soton.ac.uk
Few studies have examined the effects of both prenatal and postnatal growth on hypertension. We report on hypertension in 2003 people aged 62 years who were randomly selected from the Helsinki birth cohort and examined in a clinic. Their heights and weights had been recorded serially up to age 11 years. A total of 644 had already been diagnosed with hypertension. Compared with normotensive people, they were obese and insulin resistant. At birth they were thin and short, and they gained weight slowly up to age 2 years; thereafter they grew rapidly so that at age 11 years their body size was around the average. The odds ratio associated with each kilogram of birthweight was 0.42 (95% CI: 0.32 to 0.56); with each 10 kg of current weight it was 1.85 (95% CI: 1.66 to 2.05). The blood pressures of another 802 people were classified as hypertensive under current definitions. They were overweight and had an atherogenic lipid profile. At birth they were short, and after birth they grew slowly so that at age 11 years they were short and thin. The odds ratio associated with each kilogram of weight at age 2 years was 0.75 (95% CI: 0.68 to 0.84); with each 10 kg of current weight it was 1.42 (95% CI: 1.28 to 1.57). We conclude that 2 different paths of childhood growth precede the development of hypertension. We suggest that they lead to hypertension through different biological mechanisms and may respond differently to medication.
Key Words: hypertension • kidney • fetal programming • early growth • renin angiotensin system
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