Background: International guidelines suggest that growth of preterm infants should match intrauterine rates. However, the trajectory for extrauterine growth may deviate from the birth percentile due to an irreversible, physiological loss of extracellular fluid during postnatal adaptation to extrauterine conditions. To which "new" physiological growth trajectory preterm infants should adjust to after completed postnatal adaptation is unknown. This study analyzes the postnatal growth trajectories of healthy preterm infants using prospective criteria defining minimal support, as a model for physiological adaptation. Methods: International, multi-center, longitudinal, observational study at five neonatal intensive care units (NICUs). Daily weights until day of life (DoL) 21 of infants with undisturbed postnatal adaptation were analyzed (gestational ages: (i) 25-29 wk, (ii) 30-34 wk). results: 981 out of 3,703 admitted infants included. Maximum weight loss was 11% (i) and 7% (ii) by DoL 5, birth weight regained by DoL 15 (i) and 13 (ii). Infants transitioned to growth trajectories parallel to Fenton chart percentiles, 0.8 z-scores below their birth percentiles. The new trajectory after completed postnatal adaptation could be predicted for DoL 21 with R 2 = 0.96. conclusion: This study provides a robust estimate for physiological growth trajectories of infants after undisturbed postnatal adaptation. In the future, the concept of a target postnatal trajectory during NICU care may be useful. i mproved survival rates of very-low-birth-weight (<1,500 g birth weight) infants have shifted the focus of neonatal care onto improving postnatal growth and nutrition, aiming to achieve growth rates that optimize later health outcomes (1). Pediatric societies in North America and Europe have recommended that postnatal growth of preterm infants match the in utero growth rates of fetuses that remain in utero until full-term (2-4). These recommendations gain importance in light of the Developmental Origins of Health and Disease (DOHaD) hypothesis (5). The DOHaD concept suggests that suboptimal growth of a fetus or a newborn infant can impact the early onset of adult metabolic and cardiovascular diseases. In utero, the growth rate of an individual fetus is determined by its genetic potential and modified by "environmental" factors such as maternal nutrition, body composition, pathologies, or altitude above sea level. After birth, growth patterns of preterm infants are under external control by neonatal staff who modify the infants' nutrient intake. Figure 1 shows three hypothetical postnatal trajectories for a given preterm infant (27 wk of gestation, birth weight 1,000 g). It is of interest to note that these trajectories have similar slopes and hence not dramatically different growth rates. However, postnatal adjustment to different percentiles during the phase of stable growth will lead to different body compositions-potentially affecting later health outcomes.The current evidence for optimal postnatal growth trajectories is scarce....

Studies have implicated signaling through glycogen synthase kinase (GSK) 3α/β in the activation of pro-atherogenic pathways and the accelerated development of atherosclerosis. By using a mouse model, we examined the role of GSK3α in the development and progression of accelerated atherosclerosis. We crossed Gsk3a/GSK3α-knockout mice with low-density lipoprotein receptor (Ldlr) knockout mice. Five-week-old Ldlr(-/-);Gsk3a(+/+), Ldlr(-/-);Gsk3a(+/-), and Ldlr(-/-);Gsk3a(-/-) mice were fed a chow diet or a high-fat diet for 10 weeks and then sacrificed. GSK3α deficiency had no detectible effect on any measured parameters in chow-fed mice. High-fat-diet fed Ldlr(-/-) mice that were deficient for GSK3α had significantly less hepatic lipid accumulation and smaller atherosclerotic lesions (60% smaller in Ldlr(-/-);Gsk3a(+/-) mice, 80% smaller in Ldlr(-/-);Gsk3a(-/-) mice; P < 0.05), compared with Ldlr(-/-);Gsk3a(+/+) controls. GSK3α deficiency was associated with a significant increase in plasma IL-10 concentration and IL-10 expression in isolated macrophages. A twofold to threefold enhancement in endoplasmic reticulum stress-induced IL-10 expression was observed in Thp-1-derived macrophages that were pretreated with the GSK3α/β inhibitor CT99021. Together, these results suggest that GSK3α plays a pro-atherogenic role, possibly by mediating the effects of endoplasmic reticulum stress in the activation of pro-atherogenic pathways.

Using BMI-SDS to determine nutritional status in a sick population is not considered an appropriate clinical tool for identifying individual underweight or overweight children or adolescents. However, BMI-SDS may be appropriate for longitudinal measurements or for screening purposes in large field studies. When accurate nutritional status classification of a sick patient is needed for clinical purposes, nutritional status will be assessed more accurately using methods that accurately measure %BF, such as DXA.

Percentile charts should be examined for the described systematic error and, if necessary, corrected.