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Mothers’ own milk is the best source of nutrition for nearly all infants. Beyond somatic growth, breast milk as a biologic fluid has a variety of other benefits, including modulation of postnatal intestinal function, immune ontogeny, and brain development. Although breastfeeding is highly recommended, breastfeeding may not always be possible, suitable or solely adequate. Infant formula is an industrially produced substitute for infant consumption. Infant formula attempts to mimic the nutritional composition of breast milk as closely as possible, and is based on cow’s milk or soymilk. A number of alternatives to cow’s milk-based formula also exist. In this article, we review the nutritional information of breast milk and infant formulas for better understanding of the importance of breastfeeding and the uses of infant formula from birth to 12 months of age when a substitute form of nutrition is required.

The findings in the HLBW INT group provide support for preschool education to make long-term changes in a diverse group of children who are at developmental risk. The lack of observable benefit in the LLBW group raises questions about the biological and educational factors that foster or inhibit sustained effects of early educational intervention.

Objective To measure the changes in whole blood fatty acid levels in premature infants and evaluate their association with neonatal morbidities. Study design Retrospective cohort study of 88 infants born at < 30 weeks of gestation. Serial fatty acid profiles during the first postnatal month and infant outcomes, including chronic lung disease (CLD), retinopathy of prematurity (ROP), and late-onset sepsis, were analyzed. Regression modeling was applied to determine the association between fatty acid levels and neonatal morbidities. Results DHA and AA levels declined rapidly in the first postnatal week with a concomitant increase in linoleic acid (LA) levels. Decreased DHA levels were associated with an increased risk of CLD (OR 2.5; 95% CI 1.3 – 5.0). Decreased AA levels were associated with an increased risk of late-onset sepsis (hazard ratio 1.4; 95% CI 1.1 – 1.7). The balance between fatty acids was also a predictor of CLD and late-onset sepsis. An increased LA:DHA ratio was associated with an increased risk of CLD (OR 8.6; 95% CI 1.4 – 53.1) and late-onset sepsis (hazard ratio 4.6; 95% CI 1.5 – 14.1). Conclusion Altered postnatal fatty acid levels in premature infants are associated with an increased risk of CLD and late-onset sepsis.

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Objective To evaluate neurodevelopment following necrotizing enterocolitis (NEC) and late bacteremia, alone and together. Study design Sample included 1155 infants born at 23-27 weeks’ gestation. NEC was classified by the Modified Bell’s staging criteria and grouped as medical NEC or surgical NEC. Late bacteremia was defined as a positive blood culture after the first postnatal week. Neurodevelopment was assessed at 24 months corrected age. Multivariable models estimated the risk of developmental dysfunction and microcephaly associated with medical or surgical NEC with and without late bacteremia. Results Children who had surgical NEC unaccompanied by late bacteremia were at increased risk of Psychomotor Developmental Indices <70 [OR=2.7 (1.2, 6.4)], and children who had both surgical NEC and late bacteremia were at increased risk of diparetic cerebral palsy [OR=8.4 (1.9, 39)] and microcephaly [OR=9.3 (2.2, 40)]. In contrast, children who had medical NEC with or without late bacteremia were not at increased risk of any developmental dysfunction. Conclusion The risk of neurodevelopmental dysfunction and microcephaly is increased in children who had surgical NEC, especially if they also had late bacteremia. These observations support the hypothesis that bowel injury might initiate systemic inflammation potentially affecting the developing brain.

BackgroundExocrine pancreatic insufficiency (EPI) is characterized by a deficiency of exocrine pancreatic enzymes, resulting in malabsorption. Numerous conditions account for the etiology of EPI, with the most common being diseases of the pancreatic parenchyma including chronic pancreatitis, cystic fibrosis, and a history of extensive necrotizing acute pancreatitis. Treatment for EPI includes dietary management, lifestyle changes (i.e., decrease in alcohol consumption and smoking cessation), and pancreatic enzyme replacement therapy.DiscussionMany diagnostic tests are available to diagnose EPI, however, the criteria of choice remain unclear and the causes for a false-positive test are not yet understood. Despite multiple studies on the treatment of EPI using exogenous pancreatic enzymes, there remains confusion amongst medical practitioners with regard to the best approach to diagnose EPI, as well as dosing and administration of pancreatic enzymes.SummaryAppropriate use of diagnostics and treatment approaches using pancreatic enzymes in EPI is essential for patients. This opinion piece aims to address the existing myths, remove the current confusion, and function as a practical guide to the diagnosis and treatment of EPI.