Early growth, infant feeding and childhood cardiovascular risk factors

The aim of this study was to investigate the hypothesised positive association of preexisting and pregnancy-induced hypertension with the offspring’s weight and height gain in the first 14 months of life. We studied 3994 pregnant women and their offspring in a prospective community-based cohort study, starting between 2003 and 2004 (Amsterdam Born Children and their Development, ABCD study). Questionnaires obtaining information about hypertension during pregnancy were completed, and this was complemented with additional information from the obstetric caregiver. Anthropometry of the offspring was followed during the first 14 months of life. Main outcome measures were presence or absence of growth acceleration in weight or height (normal: ΔSDS ≤0.67 vs. growth acceleration: ΔSDS >0.67). The relation between hypertension during pregnancy and offspring’s weight and height gain was assessed by logistic regression analyses. We found that pre-existing hypertension was related to growth acceleration in weight and height. After correction for birth weight and pregnancy duration, the effect remained significant for growth acceleration in weight (OR 1.89; 95% CI 1.21–2.97; P<0.01). Pregnancy-induced hypertension showed similar results, although correction for birth weight and pregnancy duration rendered the associations non-significant. In conclusion, infants of women with pre-existing hypertension during pregnancy more frequently have growth acceleration in weight and height, and yet the mechanisms acting on postnatal growth appear to be different. INTRODUCTION The ‘Developmental Origins of Health and Disease’ hypothesis postulates that several chronic diseases in adulthood originate from adaptation to the (compromised) nutritional environment during early (antenatal or postnatal) life. (75) These adaptations, which appear to be mediated by certain epigenetic processes, may result in vascular, metabolic or endocrine changes in the structure and function of the body in adult life. (9) An array of epidemiological studies in several countries have provided evidence supporting this hypothesis. They have documented that subjects with fetal growth retardation due to intrauterine malnutrition have a higher risk of developing hypertension, obesity, diabetes and coronary heart disease in later life. (43,76-82) In addition to fetal growth retardation, prematurity has been identified as an independent risk factor for high blood pressure and cardiovascular risk in later life. (24) Moreover, evolving evidence suggests an independent role of rapid infant growth (also referred to as ‘catch-up growth’) on cardiovascular disease in later life (the accelerated growth hypothesis). Rapid growth in early postnatal life may be driven particularly by an aim to compensate for intrauterine growth retardation or prematurity, which consequently may increase the adverse effect on cardiovascular disease risk in later life. (25,76,78,80,83,84) Although rapid postnatal growth also occurs in normal birth weight infants, it may still be the consequence of a fetal response to a compromised intrauterine environment. (9) One adverse antenatal factor that is potentially associated with fetal adaptation (reprogramming) is maternal hypertension. As maternal hypertension is one of the factors associated with placental dysfunction(12), resulting in restricted maternoplacental delivery of nutrients and oxygen to the fetus, the offspring of mothers with hypertension are expected to have a higher risk of retarded fetal growth and preterm birth. This may however be restricted to those with severe hypertension. (13-18) It is unknown whether maternal hypertension is related to postnatal growth acceleration in the offspring, independent from birth weight and pregnancy duration. The aim of this study was to determine the putative independent role of maternal hypertension (pre-existing and pregnancy-induced hypertension) on the offspring’s growth. We hypothesised that maternal pre-existing hypertension and pregnancyinduced hypertension are independent determinants of the offspring’s growth acceleration, in addition to birth weight, pregnancy duration and potential confounding variables. When confirmed, these hypotheses provide novel insights into the role of the potential determinants of cardiovascular diseases in later life.