Published Online
on July 9, 2007

A more recent version of this article appeared on September 1, 2007

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Submitted on March 27, 2007
Revised on April 16, 2007

Maternal and Social Origins of Hypertension

David J.P. Barker^*; Clive Osmond; Tom J. Forsen; Eero Kajantie; and Johan G. Eriksson

From the Heart Research Center (D.J.P.B.), Oregon Health and Science University, Portland; the MRC Epidemiology Resource Centre (C.O.), University of Southampton, Southampton General Hospital, Southampton, United Kingdom; and the National Public Health Institute (T.J.F., E.K., J.G.E.), Department of Epidemiology and Health Promotion, and the Department of Public Health (J.G.E.), University of Helsinki, Helsinki, Finland.

^* To whom correspondence should be addressed. E-mail: djpb{at}mrc.soton.ac.uk.

Abstract--We previously reported that in 2003 people from the Helsinki birth cohort whose blood pressures were measured, 2 different paths of growth preceded the development of hypertension. People already diagnosed with hypertension were small at birth but of average body size at age 11 years. People newly diagnosed with hypertension grew slowly in utero and through childhood. We have now examined how the mother’s body size, placental size, and living conditions after birth, 3 influences that affect growth, affect hypertension. Diagnosed hypertension was associated with low placental weight and poor living conditions after birth. The odds ratios were 1.6 (95% CI, 1.1 to 2.3) in people with placental weights <550 g, compared with those with weights >750 g, and 2.2 (95% CI, 1.5 to 3.3) in people whose fathers were laborers compared with those in upper middle-class families. Newly diagnosed hypertension was associated with a small anteroposterior diameter of the mother’s bony pelvis, a known consequence of rickets or lesser degrees of malnutrition in infancy. The odds ratio was 2.2 (95% CI, 1.4 to 3.5) in people whose mothers’ pelvic external conjugate diameters were <18 cm when compared with people whose mothers’ diameters were 19 cm. We conclude that one path of growth that leads to hypertension is initiated by fetal undernutrition, which may make a baby vulnerable to postnatal stress, whereas the other originates in a functional incapacity in the mother’s metabolism, possibly protein metabolism, which she acquired through undernutrition during her infancy.

Key words: hypertension • fetal programming • early growth • placenta • protein metabolism

Related Article:

Divergent Origins of Slow Fetal Growth: Relevance to Adult Cardiovascular Disease

Barbara T. Alexander
Hypertension 2007 50: 465-466. [Extract] [Full Text] [PDF]

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