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Breast Milk Protects Again

Prevents sepsis in low birth weight infants, study says

TUESDAY, May 4, 2004 (HealthDayNews) -- Human milk helps ward off sepsis infection in extremely low birth weight babies, says a Cincinnati Children's Hospital Medical Center study.

Sepsis is a major cause of death, illness and long-term disability in extremely low birth weight infants. As many as 30 percent of babies with sepsis develop an overwhelming infection and as many as 20 percent die.

Researchers analyzed data on 1,270 infants at 15 medical centers. The 39 percent of those infants who had sepsis received significantly less human milk than infants who didn't have sepsis, the study found.

The extremely low birth weight infants who developed sepsis received human milk as 29 percent of their total nutritional intake, while infants who weren't infected received milk as 33 percent of their total intake.

"Despite all the technological advancements of recent years, outcomes for extremely low birth weight infants haven't improved all that much. But human milk makes a difference, and there's no reason to believe the benefits wouldn't extend to higher birth weight infants," researcher Jareen Meinzen-Derr, from the hospital's Center for Epidemiology and Biostatistics, said in a prepared statement.

The study was presented this week at the Pediatric Academic Societies' annual meeting in San Francisco.

Extremely low birth weight infants weight 1 pound to just less than 2.2 pounds. They're too tiny to be nursed by their mothers and must be fed through a mouth tube.

"We encourage mothers to pump and collect their own breast milk and bring it to the hospital to be fed to their baby. It's not an easy thing to ask of mothers, and I think caregivers can probably do a better job of supporting them in this endeavor," study co-author Dr. Edward Donovan, neonatologist at Cincinnati Children's, said in a prepared statement.

More information

The Nemours Foundation has more about sepsis.

SOURCE: Pediatric Academic Societies, news release, May 1, 2004
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