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People often use the expression, "Breast is best", when describing the benefits of breast-feeding infants. However, the benefits of breast milk do not seem to just stop at nutrition for baby. A recent study performed by researchers at the University of Buffalo has found that a protein complex in human breast milk may have the ability to reverse antibiotic resistance in bacteria. The findings are promising, especially in a time when hospitals are struggling to combat drug-resistant superbugs like MRSA and drug resistance is on the rise.

Researchers administered the protein complex, called HAMLET, to Streptococcus pneumoniae, which had grown resistant to penicillin, and Staphylococcus aureus, which was resistant against methicillin. As a result, the drug-resistant bacteria reverted to its previous abilities, succumbing to drugs that they had previously been able to beat.

"Unlike synthetic drugs, HAMLET is a naturally occurring human milk protein-lipid complex, and so is not associated with the types of toxic side effects that we so frequently see with the high-powered antibiotics needed to kill drug-resistant organisms," Laura R. Marks, from the university's Department of Microbiology and Immunology, said in a statement.

HAMLET stands for human alpha-lactalbumin made lethal to tumor cells. Discovered in Sweden, the protein has been shown to be lethal against tumor cells as well as against bacteria. It works by setting off a chemical reaction that causes the bacteria to self-destruct.

The protein would have much use for treatment purposes. "The pharmaceutical industry is currently reluctant to develop antibiotics because they are only used for a short time and they will be used infrequently initially and only when nothing else works," Hazeline Hakansson stated. "HAMLET, on the other hand, is more of an adjuvant and can be used widely in combination with common antibiotics; it already has a huge potential market that is only going to increase the next couple of years as antibiotic resistance increases."

The study was published in the journal PLoS One.