(Hypertension. 2000;36:790.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
Fetal and Childhood Growth and Hypertension in Adult Life
From the National Public Health Institute, Department of Epidemiology and Health Promotion, Diabetes and Genetic Epidemiology Unit, Helsinki, Finland (J.E., T.F., J.T.), and Medical Research Council Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, United Kingdom (C.O., D.B.).
Correspondence to Professor David Barker, University of Southampton, Southampton General Hospital, Southampton S016 6YD, UK. E-mail david.barker{at}mrc.soton.ac.uk
Abstract—The association between low birth weight and raised blood pressure has been extensively replicated. Little is known about the way childhood growth modifies the effects of low birth weight. We report on the fetal and childhood growth of 1958 men and women who received treatment for hypertension and belong to a cohort of 7086 people born in Helsinki, Finland, during 1924–1933. As expected, the men and women who developed hypertension had low birth weight (P=0.002). They were also shorter in body length at birth (P=0.02). After birth they experienced accelerated growth, so that by 7 years their heights and weights were approximately average. In a simultaneous regression, both birth length and tall height had statistically significant although opposing effects on hypertension (P=0.003 for birth length and 0.009 for height at 7 years). Accelerated postnatal growth was associated with better childhood living conditions. Children who later developed both hypertension and type 2 diabetes, rather than hypertension alone, had small placental size as well as small body size at birth, and their accelerated postnatal growth continued beyond 7 years. We suggest that hypertension may originate through retarded growth in utero followed by accelerated postnatal growth as a result of good living conditions. Retarded fetal growth leads to permanently reduced cell numbers in the kidney and other tissues, and subsequent accelerated growth may lead to excessive metabolic demand on this limited cell mass.
Key Words: hypertension • fetal growth • childhood growth • placenta
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