Fetal Growth and Hypertension

The evidence for the association of adverse adult outcomes with lower birth weights is strongest for blood pressure and impaired glucose tolerance. In a 1988 study of a hospital-based Swedish population, Gennser et al. reported a higher risk of increased diastolic blood pressure in early adult life among men who were growth-retarded at birth than among those whose birth weights were appropriate for gestational age.173

Barker et al. published in 1989 an inverse relation independent of gestational age between systolic blood pressure and birth weight among a British sample of 9921 10-year-olds and 3259 adults aged 36 years.174 They also showed that 10-year-olds living in areas with high cardiovascular mortality in England and Wales were shorter and had higher resting pulse rates than those living in other areas. Their mothers were also shorter and had higher diastolic blood pressures. The authors suggested that besides intrauterine environment, persisting geographical differences in childhood environment may contribute to the observed risk from hypertension. Another report from Barker's team in 1992 showed a strong trend of higher blood pressure in adult life with lower birth weight, lower ponderal index, and greater placental weight.175

Law et al. reported in 1993 that people of all ages beyond infancy who had lower birth weights also had higher systolic blood pressures. The systolic blood pressure was not related to growth during infancy independently of birth weight. The relation between systolic pressure and birth weight became larger with increasing age. Thus, after allowing for current body mass, systolic pressure at ages 64

through 71 years decreased by 5.2 mmHg for every kilogram increase in birth weight. They concluded that essential hypertension was initiated in fetal life, and elevated blood pressure was amplified from infancy to old age.176

Martyn et al., in a study of 337 adults reported in 1995, documented raised blood pressure in adult life in association with impaired fetal growth and showed that it was associated with decreased compliance in the conduit arteries of the trunk and legs.163 Leon et al. suggested in 1996 that adult blood pressure is more markedly affected by obesity in individuals with intrauterine growth retardation than in those without growth retardation.177

A systematic review by Law et al. of all studies available in 1996 revealed that cross-sectional studies of prepubertal children and adults showed a negative relationship between blood pressure and birth weight that was independent of size at the time of the study.178 The magnitude of the change in blood pressure tended to increase with age during childhood and adult life. However, the relationship in adolescents was inconsistent.

A subsequent study of Leningrad siege victims published in 1997 by Stanner et al. also showed that blood pressure was positively related to obesity.155 However, the relationship between body mass index (BMI) and blood pressure (systolic and diastolic) was significantly stronger in the intrauterine group than in the infant group. This suggests that siege exposure and adult obesity may act synergistically to increase susceptibility to hypertension.

The latest publication of Barker's team179 notes that children with low birth weights and thinness at birth followed by rapid compensatory growth (high BMIs at age 12), living in poor social conditions during childhood (low social class, few rooms in homes, poor educational achievements) had added risks of developing hypertension. However, the team's finding that living conditions in adult life did not present this influence is not well explained. One suggested explanation is that the influence of small birth weight on adult hypertension is related to the reduced number of nephrons in the kidneys of these children secondary to intrauterine malnutrition.180 This reduction led to hyperperfusion of existing nephrons and early nephrosclero-sis.181 Rapid growth in childhood may exacerbate this process by increasing hyper-perfusion and may explain the lack of influence of factors in adult life.

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