title: Preterm nutrition and the brain.
abstract: The brain is the most highly metabolic organ in the preterm neonate and consumes the greatest amount of nutrient resources for its function and growth. As preterm infants survive at greater rates, neurodevelopment has become the primary morbidity outcome of interest. While many factors influence neurodevelopmental outcomes in preterm infants, nutrition is of particular importance because the healthcare team has a great deal of control over its provision. Studies over the past 30 years have emphasized the negative neurodevelopmental consequences of poor nutrition and growth in the preterm infant. While all nutrients are important for brain development, certain ones including glucose, protein, fats (including long-chain polyunsaturated fatty acids), iron, zinc, copper, iodine, folate and choline have particularly large roles in the preterm infant. They affect major brain processes such as neurogenesis, neuronal differentiation, myelination and synaptogenesis, all of which are proceeding at a rapid pace between 22 and 42 weeks' post-conception. At the macronutrient level, weight gain, linear growth (independent of weight gain) and head circumference growth are markers of nutritional status. Each has been associated with long-term neurodevelopment. The relationship of micronutrients to neurodevelopment in preterm infants is understudied in spite of the large effect these nutrients have in other young populations. Nutrients do not function alone to stimulate brain development, but rather in concert with growth factors, which in turn are dependent on adequate nutrient status (e.g. protein, zinc) as well as on physiologic status. Non-nutritional factors such as infection, corticosteroids, and inflammation alter how nutrients are accreted and distributed, and also suppress growth factor synthesis. Thus, nutritional strategies to optimize brain growth and development include assessment of status at birth, aggressive provision of nutrients that are critical in this time period, control of non-nutritional factors that impede brain growth and repletion of nutrient deficits.
authors.affiliation: Division of Neonatology, University of Minnesota Amplatz Children's Hospital, University of Minnesota School of Medicine, Minneapolis, Minn., USA.
authors.forename: Sara E
authors.initials: SE
authors.lastname: Ramel
authors.forename: Michael K
authors.initials: MK
authors.lastname: Georgieff
mesh_terms: D001921:Brain / Q000254:growth & development*; D002657:Child Development / Q000502:physiology; D002149:Energy Intake; D006801:Humans; D007223:Infant; D007227:Infant Nutritional Physiological Phenomena; D007234:Infant, Premature / Q000254:growth & development*; D018977:Micronutrients / Q000008:administration & dosage; D009751:Nutritional Requirements; D009752:Nutritional Status; D018529:Nutritional Support / Q000379:methods; D011181:Postnatal Care; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D015430:Weight Gain
chemical_list: D018977:Micronutrients; C546842:MTOR protein, human; D058570:TOR Serine-Threonine Kinases