Formula, Not Breast Milk, Toxic to In-Vitro Cells
Free fatty acids created in the digestion of infant formula cause cell death that may contribute to necrotizing enterocolitis, a severe intestinal condition often fatal occuring most commonly in premature infants
The study was done by University of California, San Diego bioengineers. Their report, which was based on in vitro tests comparing the digestion of fresh human breast milk and nine different infant formulas, was published online in the journal Pediatric Research.
Scientists have long known that premature infants fed formula are more likely to develop necrotizing enterocolitis than those fed breast milk. The condition is the leading cause of death from gastrointestinal diseases in premature infants, but the underlying mechanism has not been understood.
Alexander Penn, a research scientist working in the Microcirculation Laboratory of bioengineering Professor Geert Schmid-Schönbein from the UC San Diego Jacobs School of Engineering, believes they have come closer to an answer.
Research had previously determined that
partially digested food in an adult intestine
is capable of killing cells, due to free fatty acids
which have a "detergent" like effect
damaging to cell membranes.
The intestines of healthy adults and older
children have a mature mucosal barrier that
may prevent damage due to having free fatty acids.
However, the intestine is leakier at birth,
particularly for preterm infants,
which could be why they are more
susceptible to necrotizing enterocolitis.
Therefore, researchers wanted to know what happens to breast milk as compared to infant formula when exposed to digestive enzymes. They "digested," in vitro, infant formulas marketed for full term and preterm infants as well as fresh human breast milk using pancreatic enzymes or fluid from an intestine. They then tested the formula and milk for levels of free fatty acids. They also tested whether these fatty acids killed off three types of cells involved in necrotizing enterocolitis: epithelial cells that line the intestine, endothelial cells that line blood vessels, and neutrophils, a type of white blood cell that is a kind of "first responder" to inflammation caused by trauma in the body.
Overwhelmingly, the digestion of formula led to cellular death, or cytotoxicity in less than 5 minutes in some cases while breast milk did not. For example, digestion of formula caused death in 47 percent to 99 percent of neutrophils while only 6 percent of them died as a result of milk digestion. The study found that breast milk appears to have a built-in mechanism to prevent cytotoxicity. The research team believes most food, like formula, releases high levels of free fatty acids during digestion, but that breast milk is digested in a slower, more controlled, process.
Currently, many neonatal intensive care
units are formula-free environments,
but breastfeeding a premature infant can be
challenging, if not physically impossible,
and supplies of donor breast milk are limited.
To meet the demand if breast milk is unavailable, researchers feel less cytotoxic milk replacements will need to be designed that pose less risk for cell damage and for necrotizing enterocolitis.This will benefit not only premature infants, but also full-term infants at higher risk for problems associated with gastrointestinal disorders and leaky intestines, such as babies with autism spectrum disorder.
Dr. Sharon Taylor, professor of pediatric medicine at UC San Diego School of Medicine and a pediatric gastroenterologist at Rady Children's Hospital, San Diego, believes the study offers more support to an already ongoing push by hospital neonatal intensive care units, to encourage breastfeeding even in the more challenging circumstances of a NICU. For patients too premature or frail to nurse, Dr. Taylor hopes hospital staff will provide consultation and resources for a mother to pump breast milk that can be fed to her baby through a tube.
The researchers conclude that breast milk has a significant ability to reduce cytotoxicity that formula does not have. A next step is to replicate these results with animal studies and to determine if intervention can prevent free fatty acids from causing intestinal damage or death from necrotizing enterocolitis.
The research was carried out in collaboration with Dr. Taylor, Karen Dobkins of the Department of Psychology, and Angelina Altshuler and James Small of the Department of Bioengineering at UC San Diego and was funded by the National Institutes of Health (NS071580 and GM85072).
Original article: http://www.cell.com/developmental-cell/abstract/S1534-5807(12)00478-9