Monitoring the growth of neonates in the Neonatal Intensive Care Unit (NICU) using growth charts constitutes an essential part of preterm infant care. Preterm infants are at increased risk for extrauterine growth restriction (EUGR) due to increased energy needs and clinical complications. This retrospective study compares the prevalence of small for gestational age (SGA) at birth and EUGR at discharge in extremely and very preterm neonates hospitalized in the NICU of a tertiary hospital in Greece, using different growth curves, and it examines the associated nutritional and clinical factors. Fenton2013 and INTERGROWTH-21st growth curves were used to calculate z-scores of birth weight (BW) and weight, length, and head circumference at discharge. The study includes 462 newborns with a mean BW of 1341.5 g and mean GA of 29.6 weeks. At birth, 6.3% of neonates were classified as SGA based on Fenton2013 curves compared to 9.3% with INTERGROWTH-21st growth curves. At discharge, 45.9% of neonates were characterized as having EUGR based on the Fenton2013 weight curves and 29.2% were characterized based οn INTERGROWTH-21st curves. Nutritional factors such as the day of initiation, attainment of full enteral feeding, and the duration of parenteral nutrition were associated with EUGR by both curves. The prevalence of SGA and EUGR neonates differs between the two growth references. This shows that further evaluation of these charts is needed to determine the most appropriate way to monitor infant growth.

Background/Objectives: Postnatal growth faltering (PGF) significantly affects premature neonates, leading to compromised neurodevelopment and an increased risk of long-term health complications. Methods: This retrospective study at a level III NICU of a tertiary hospital analyzed 650 preterm neonates born before 33 weeks. Postnatal growth was evaluated using the Fenton2013 and INTERGROWTH-21st growth charts, with changes in weight z-scores from birth to discharge classified as normal growth (ΔZ ≥ −1), non-severe PGF (−2 ≤ ΔZ < −1), and severe PGF (ΔZ < −2). Results: Mean gestational and postmenstrual age at discharge was 30 weeks (SD 1.9) and 37.1 weeks (SD 2.7), respectively. Fenton2013 growth curves revealed a higher prevalence of non-severe and severe PGF (43% and 14.6%) compared to INTERGROWTH-21st (24.5% and 10.3%). A more rapid establishment of full enteral feeds was strongly associated with reduced severe PGF prevalence in both growth charts (p < 0.001), as was shorter hospitalization. Late-onset sepsis was associated with an increased risk of severe PGF, while being small for gestational age (SGA) was protective against severe PGF across both growth charts (p < 0.001). A trend of decreasing PGF prevalence was noted over the study years, most probably attributed to the implementation of updated nutritional guidelines. Interestingly, when machine learning classification models were evaluated in our Greek cohort, a notable decline in predictive accuracy depending on the growth standard applied was observed. Conclusions: Our study highlights the need for standardizing PGF definition in an attempt to enhance nutritional management and further investigate the long-term impacts of nutritional interventions on growth, neurodevelopment, and overall health outcomes.

Non-communicable diseases remain the dominant cause of adult morbidity and mortality, yet cardiometabolic, vascular and renal risk may originate before birth. This structured narrative review critically evaluates human evidence linking pregnancy-related exposures, placental pathophysiology and later offspring health within a maternal–placental–fetal–life-course framework. Evidence published from 2020 to 2026 was emphasised, while seminal earlier cohorts were retained when they provided uniquely long follow-up or direct placental measurements. The most consistent associations concern maternal obesity, gestational diabetes, excessive gestational weight gain and hypertensive disorders, which are linked with higher offspring blood pressure, greater adiposity and adverse glucose–insulin profiles. Human placental studies implicate vascular malperfusion, altered nutrient transport, inflammatory and oxidative signalling, endocrine function and epigenetic regulation. Few studies, however, have measured the prenatal exposure, a specific placental phenotype and a long-term offspring outcome within the same longitudinal design; most proposed placental pathways are supported by convergent evidence or biological plausibility rather than demonstrated mediation. Preterm birth and fetal growth restriction are clinically observable, etiologically heterogeneous sentinel phenotypes, not obligatory mediators. Placental and offspring epigenetic signatures, telomere biology and mitochondrial function represent distinct domains of biological embedding; their causal and prognostic significance remains uncertain. Longitudinal studies integrating maternal exposures, placental histopathology and molecular phenotypes, fetal organ development, childhood cardiometabolic trajectories and adult clinical outcomes are needed to determine whether, and under what circumstances, the placenta plays an intermediary role rather than merely serving as a marker of an adverse pregnancy environment.