The dynamic effects of breastfeeding on intestinal development and host defense

Abstract

In this review, evidence is provided to support the hypothesis that human milk provides a link between the mother and her newborn infant in the extrauterine environment in a manner similar to the placental link between mother and fetus in utero. In addition, breastfeeding helps prevent age-related diseases affecting the gastrointestinal tract during the newborn period. To provide evidence to support this hypothesis, anecdotal clinical studies are sited to suggest that human milk contains factors that may be missing in inherited diseases of inborn errors in metabolism and provide passive protective factors that lessen the expression of neonatal allergic and infectious diseases. In some instances, by providing the missing factor in an inherited disease, the newborn may be protected from serious damage to its developing brain. A second line of evidence to support this hypothesis is the observation that the composition of human milk varies with the infant's needs. To illustrate this principal, the composition of milk from mothers delivering prematurely and milk of mothers of full-term infants were compared, and the differences in trophic and protective factors in colostrum versus mature milk from mothers delivering full-term are cited. Finally, using observations from the laboratory that define the immaturities in neonatal and premature human intestinal defenses as the neonate's host defense deficiency, the specific effect that anti-inflammatory and maturational factors in human milk has on these immaturities is discussed. The active stimulus of maternal milk on the rapid development of host defenses is underscored. These cited examples of human milk effects in the newborn help support the stated hypothesis. Additional studies of human immature gut function along with translational and clinical studies are necessary to provide further objective evidence in support of breastfeeding for all neonates, particularly premature neonates.