Consistent with the paradigm shifting observations of David Barker and colleagues that revealed a powerful relationship between decreased weight through 2 years of age and adult disease, intrauterine growth restriction (IUGR) and preterm birth are independent risk factors for the development of subsequent hypertension. Animal models have been indispensable in defining the mechanisms responsible for these associations and the potential targets for therapeutic intervention. Among the modifiable risk factors, micronutrient deficiency, physical immobility, exaggerated stress hormone exposure and deficient trophic hormone production are leading candidates for targeted therapies. With the strong inverse relationship seen between gestational age at delivery and the risk of hypertension in adulthood trumping all other major cardiovascular risk factors, improvements in neonatal care are required. Unfortunately, therapeutic breakthroughs have not kept pace with rapidly improving perinatal survival, and groundbreaking bench-to-bedside studies are urgently needed to mitigate and ultimately prevent the tsunami of prematurity-related adult cardiovascular disease that may be on the horizon. This review highlights our current understanding of the developmental origins of hypertension and draws attention to the importance of increasing the availability of lactation consultants, nutritionists, pharmacists and physical therapists as critical allies in the battle that IUGR or premature infants are waging not just for survival but also for their future cardiometabolic health.

Perinatal leptin deficiency and reduced intake of mother’s milk may contribute to the development of childhood obesity. Preterm infants have reduced leptin production, and they are at heightened risk of neonatal leptin deficiency. Because fresh human milk contains significantly more leptin than donor milk, we used a cross-over design to determine if blood leptin levels in maternal milk-fed preterm infants fall during conversion to donor human milk. Infants born between 22 0/7 and 31 6/7 weeks gestation on exclusive maternal milk feedings were enrolled into a 21-day cross-over trial. On days 1–7 and 15–21, infants were fed maternal milk, and on days 8–14, infants were fed donor milk. On day 1, study infants had a mean postmenstrual age of 33 weeks. Plasma leptin correlated with milk leptin, and leptin levels in maternal milk far exceed the leptin levels of donor milk. Plasma leptin did not increase during donor milk administration, but it did following resumption of maternal milk (p < 0.05). In this crossover trial, preterm infant blood leptin levels correlated with milk leptin content. This suggests that preterm infants can enterally absorb leptin from human milk, and leptin-rich breast milk may be a targeted therapy for the prevention of obesity.

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We report a rare co-occurrence of intestinal malrotation and Hirschsprung's disease (HSCR) in a male neonate with a large 38.8 Mb interstitial deletion of chromosome 13 extending from q21.31 to q33.1 including the EDNRB gene, who presented with craniofacial dysmorphic features and central nervous system malformations. The loss of EDNRB gene in addition to bilateral hearing loss and HSCR suggested an additional diagnosis of Waardenburg–Shah's syndrome. This case highlights the fact that prior knowledge of this rare association in infants with 13q deletion syndrome would enable early diagnosis and prompt interventions to prevent gastrointestinal complications.