Maternal Hypertensive Disorders of Pregnancy and Offspring Phenotypic and Somatotropic Development: A Critical Narrative Review

Abstract

Maternal hypertensive disorders of pregnancy (HDP)—encompassing chronic hypertension, gestational hypertension, preeclampsia, and superimposed preeclampsia—complicate a substantial proportion of pregnancies worldwide and are increasingly recognised as determinants of offspring health that extend well beyond the perinatal period. This critical narrative review synthesises the available evidence on how intrauterine exposure to HDP shapes offspring phenotypic and somatotropic development, from fetal growth restriction through infancy, childhood, and adolescence. The review draws on epidemiological cohort studies, systematic reviews and meta-analyses, and mechanistic investigations addressing placental dysfunction, the growth hormone–insulin-like growth factor axis, postnatal catch-up growth, cardiometabolic phenotype, and pubertal timing. The evidence indicates that offspring exposed to HDP, and particularly to preeclampsia, are frequently born smaller for gestational age and subsequently undergo accelerated postnatal weight gain, a pattern consistent with disrupted somatotropic signalling and associated with modestly but consistently elevated blood pressure, adiposity, and diabetes risk later in life. However, the magnitude, timing, and sex-specificity of these associations vary considerably across studies, and much of the observed association may be confounded by shared maternal-offspring genetic and lifestyle factors, gestational age at birth, and birth-weight-related mediation rather than a direct intrauterine programming effect. Methodological heterogeneity—in HDP subtype definition, outcome ascertainment, follow-up duration, and confounder adjustment—substantially limits comparability across the literature. This review identifies persistent uncertainty regarding the independent contribution of HDP subtype, severity, and timing of onset to somatic growth trajectories, the paucity of longitudinal data linking cord-blood biomarkers of the growth hormone–insulin-like growth factor axis to later-life anthropometric outcomes, and the underrepresentation of low- and middle-income populations in the evidence base. Future research priorities include sibling-comparison and Mendelian randomisation designs capable of distinguishing intrauterine programming from confounding, standardised longitudinal anthropometric and endocrine phenotyping from birth through puberty, and mechanistic studies bridging placental pathology with postnatal somatotropic regulation. Clarifying these relationships carries direct implications for growth surveillance and cardiometabolic risk stratification in children born after hypertensive pregnancies.