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Reviews

Evidence-based feeding strategies before and after the development of necrotizing enterocolitis

, &
Pages 875-884 | Published online: 05 Jun 2014
 

Abstract

Necrotizing enterocolitis (NEC) is a devastating disease of premature infants and is associated with significant morbidity and mortality. While the pathogenesis of NEC remains incompletely understood, it is well established that the risk of disease is increased by the administration of infant formula and decreased by the administration of breast milk. This review will focus on the mechanisms by which breast milk may serve to protect against NEC, and will review the evidence regarding various feeding strategies that may be utilized before and after an episode of NEC.

Financial & competing interests disclosure

CP Sodhi and DJ Hackam are supported by R01GM078238 and R01DK083752 from the National Institutes of Health. DJ Hackam is also supported by a research grant from Abbott Nutrition. MG is supported by 5K12HD052892-05 from the National Institutes of Health, The Children's Hospital of Pittsburgh of the UPMC Health System and The Gerber Foundation. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Key issues

  • Necrotizing enterocolitis (NEC) is a devastating disease of premature infants, and feeding practices have been suggested to be a modifiable risk factor.

  • Breast milk is the most effective protective agent for NEC.

  • Various components of breast milk are thought to mediate protection against NEC and include nitrate/nitrite, lactoferrin, human milk oligosaccharides and growth factors.

  • Further investigation is needed to address the safest way to feed a premature infant after an episode of NEC to prevent recurrence.

  • Toll-like receptor 4 signaling is important in the pathogenesis of NEC, and further identification of toll-like receptor 4 inhibitors should be investigated for their role in the prevention of NEC.

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