How breast milk wards off severe intestinal disease in premature babies

A new study conducted on mice has revealed how breast milk protects premature babies from severe intestinal disease.

A team of scientists led by Johns Hopkins pediatric surgeon-in-chief David Hackam, M.D., Ph.D., showed breast milk works to ward off the development of necrotizing enterocolitis (NEC), a devastating intestinal disorder that affects 12 percent of premature babies and claims the lives of one in four of those who have it.

The research revealed that a substance found in animal and human breast milk called epidermal growth factor, or EGF, blocks the activation of a protein responsible for unlocking the damaging immune cascade that culminates in NEC, a disease marked by the swift and irreversible death of intestinal tissue that remains one of the most-challenging-to-treat conditions.

New therapies are acutely needed for NEC, the research team says, because current treatment is limited to surgical removal of the dying, or necrotizing, portions of a baby's intestine. The approach halts further necrosis and can save a baby's life, but it often leaves infants with insufficient intestine and puts them at risk for long-term complications, such as short bowel syndrome, which requires feeding support for life due to the intestines' decreased ability to absorb enough nutrients. Pinpointing EGF as a key factor in NEC should offer new therapeutic targets that obviate or reduce the need for drastic surgery, the researchers say.

Study author Misty Good, M.D., at the University of Pittsburgh Medical Center Taken said that together the findings show that EGF was a key factor present in breast milk that prevents the onset of NEC in two ways: EGF prevents intestinal cells from dying while at the same time restoring the cell growth that promotes gut healing. Importantly, their experiments stressed on the importance of providing breast milk to premature babies to prevent this deadly disease.

The study is published in the journal Mucosal Immunology.