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For decades, livestock producers have used low doses of antibiotics to expedite animal growth. The practice, dubbed sub-therapeutic antibiotic therapy (STAT), lowers feed costs while increasing meat production, and nearly 80 percent of the antibiotics used in the United States are for this purpose.
Because STAT can encourage the growth of antibiotic-resistant “superbugs,” it’s banned in many countries, but remains common in the U.S., despite recent public pleas to stop it by two former FDA commissioners. Although STAT has been in use since the 1950s, how it works has long been a mystery. But evidence is mounting that it might be due to antibiotics killing microorganisms that populate animals’ guts.
If so, antibiotics could do the same thing to humans. In support of this idea, a paper published last month in
Nature identifies a correlation between diversity of gut microflora and human obesity. A nine-year study, led by S. Dusko Ehrlich of France’s National Institute for Agricultural Research, compared microbiotas-the 100-trillion-member microbial ecosystems that populate the body-of slim and obese people. The team found obese people have lower microbial diversity in their bellies. This is consistent with earlier research in mice, as well as a paper published last year in
Journal of Obesity that found a strong correlation between young children’s exposure to antibiotics and later obesity.
Perhaps more significantly, the team behind the
Nature study found a correlation between low microbial diversity and heart disease, diabetes and cancer, regardless of weight. “Even lean people who are poor in bacterial species have a higher risk of developing these pathologies,” Ehrlich told NPR.
Our understanding of human microbiota is in its infancy, but the possible implications of such research are profound. Could our frequent use of antibiotics, both to treat human sickness and to encourage animal growth, be having unintended consequences on our health?