The critical diseases of prematurity are due to an imbalance of antioxidant defense and exposure to free radicals brought about by hypoxia /reperfusion injury (Saugstad, 1998 and Sullivan, 1998).
HM of the PT infant would compensate for this underdevelopment, as it does for the compensation of essential nutrients (Lonnerdal, 1995). Formulas for PT infants are heavily fortified with vitamins E, A, and C (the small –molecule antioxidants), which are found in higher concentration in formulas than in HM (Abbott, 1999). This implies that the protective effect of milk is due to factors other than these antioxidants and may involve milk enzymes, but upon pasteurization of the HM and inactivation of these enzymes, its antioxidant properties were not compromised upon oxidative stress, suggesting that HM exhibits alternate, and equally effective, means of dealing with excess oxidative stress and does not depend solely upon the known antioxidant enzymes (L’Abbe, 2000). A large body of evidence clearly supports that breastfeeding enhances host defense mechanisms. In addition; breastfed infants have been shown to have a lower prevalence of various infections compared to exclusively formula fed infants (James et al., 2002). Finally, breastfed infants have been observed to excrete greater amounts of IgA and lactoferrin in their faces and urine (Goldblum, 1989). Such results suggest that human milk may improve infants’ host defenses through local actions in the gastrointestinal and urinary tracts (Schanler, 2001). Premature (PT) infant’s mother’s milk may provide antioxidant advantages compared with milk from mothers of full-term (FT) infants, and human milk may provide antioxidant properties not seen in infant formulas. |
