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  • Title: Maternal nutritional status in pregnancy and blood pressure in childhood.
    Author: Godfrey KM, Forrester T, Barker DJ, Jackson AA, Landman JP, Hall JS, Cox V, Osmond C.
    Journal: Br J Obstet Gynaecol; 1994 May; 101(5):398-403. PubMed ID: 8018610.
    Abstract:
    OBJECTIVE: To examine the relation between indices of maternal nutrition during pregnancy, including haemoglobin concentration, skinfold thickness and body weight, and the child's blood pressure at 10 to 12 years of age. DESIGN: Follow up study of children whose mothers had haemoglobin estimations, weights and skinfold thicknesses recorded during pregnancy. SETTING: Kingston, Jamaica. SUBJECTS: Seventy-seven children whose mothers took part in a prospective study of nutrition during pregnancy in relation to fetal growth. MAIN OUTCOME MEASURE: Blood pressure at 10 to 12 years of age. RESULTS: The child's mean systolic pressure adjusted for current weight rose by 2.6 mmHg (95% CI 0.5-4.6, P = 0.01) for each 1 g/dl fall in the mother's lowest haemoglobin during pregnancy. Mothers with a lower haemoglobin had thinner skinfold thicknesses, especially over the triceps (P = 0.005). In multiple regression analyses, taking account of the child's sex and current weight, there was a strong association between thin maternal triceps skinfold thickness at 15 weeks of gestation and raised blood pressure in the offspring. Taking account of the mother's triceps skinfold thickness abolished the relation between lower haemoglobin and raised blood pressure in the child. Lower weight gain between 15 and 35 weeks of gestation was independently associated with raised children's blood pressure. Systolic pressure rose by 10.7 mmHg (95% CI 5.7 to 15.6, P = 0.0001) for each log mm decrease in the mother's triceps skinfold thickness, and by 0.6 mmHg (95% CI 0.1 to 1.0, P = 0.02) for each 1 kg decrease in the mother's weight gain during pregnancy. CONCLUSIONS: These results parallel animal experiments suggesting that impaired maternal nutrition may underlie the programming of adult hypertension during fetal life. In the early 1990s, researchers followed up on 77 children, 10.4-12.2 years old, who had attended the outpatient clinic at the University Hospital of the West Indies in Kingston, Jamaica, as infants during 1979-1981 to determine whether maternal nutrition during pregnancy sets the stage for adult hypertension. The mothers had received prenatal care early in the pregnancy. The overall mean systolic pressure was 94.8 mmHg. For each log mm decrease in the mother's triceps skinfold thickness at 15 weeks gestation, the child's systolic pressure increased by 10.7 mmHg (p = 0.0001). For each 1 kg reduction in maternal weight gain between 15 and 35 weeks gestation, child's systolic pressure increased by 0.6 mmHg (p = 0.02). Mothers with a lower hemoglobin level had thinner skinfold thicknesses, particularly of the triceps (p = 0.005). The child's systolic blood pressure increased by 2.6 mmHg for each 1 g/dl decline in the mother's hemoglobin (p = 0.01), but this effect was not consistent or strong. Nevertheless, it adds more credence to the theory that poor maternal nutrition status is linked to the programming of hypertension in fetuses. These findings correspond to findings of experiments with rats. Further research is needed to confirm these findings. These findings illustrate the need to expand our knowledge about how maternal nutrition affects the fetus and how the fetus responds to poor maternal nutrition.
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