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A press conference highlighted exciting new studies on the human microbiome-including one suggesting that antibiotic use may be behind the obesity epidemic.
BOSTON, MA—A press conference at the annual meeting of the Infectious Diseases Society of America (IDSA) highlighted several exciting new studies on the role of the human microbiome—the wide assortment of microorganisms that live on and inside us even when we are perfectly healthy and can play an important role in helping us stay healthy.
The conference’s moderator, David Relman, MD, vice president of IDSA and professor of medicine, microbiology, and immunology at Stanford University, explained in his introductory remarks that doctors have demonized microbes in the past and failed to recognize their positive contributions.
“We as physicians have probably focused too heavily on microbes as just agents of disease and we have unfortunately promoted this idea to the public, who all now believe that perhaps the only good microbe is a dead one,” he said. “This idea is wrong. We are them; they are us. They play essential roles in immune system development, nutrition, in protection against pathogens, in detoxification of environmental chemicals, and the list goes on and on.”
Indeed, the conference’s first presenter, Martin Blaser, MD, chairman of the department of medicine at New York University School of Medicine, outlined a study suggesting that disruption of the natural human microbiome may be responsible for the current obesity epidemic.
Are Antibiotics Making Us Fat?
The typical explanation for increasing obesity around the world—increased caloric intake and reduced exercise—are insufficient to explain the magnitude of the problem and its early onset in individuals, argued Blaser. Perhaps the real culprit is antibiotic use in early childhood.
Farmers have long known that early exposure to antibiotics leads to increased weight gain in farm animals, so Blaser and his team set out to test whether antibiotics might help explain the obesity epidemic in humans.
To test this hypothesis, mice were given antibiotics in a manner designed to mimic the exposure of children to the drugs. Mice in an experimental group received three short courses of antibiotics (either tylosin, amoxicillin, or alternating tylosin and amoxicillin) within the first 40 days of life, while control mice received no antibiotics.
The mice were weighed throughout the experiment and analyzed using Dual-Energy X-ray absorptiometry to detect changes in mass distribution and bone composition. Changes in gut microbiome were monitored as well. The results showed that the mice exposed to antibiotics grew 6.9% faster than the control mice and had significantly higher average total mass, lean mass, bone mineral content, and bone area. Their microbiome was also significantly altered, though it normalized by day 135 of life.
Relman cautioned that, so far, only an association between antibiotic use and increased growth rate had been established and that results from a mouse model might not carry over to humans. Asked by a questioner how the effects of the antibiotics could be separated from the effects of the altered microbiome, Blaser said that we have 60 years of evidence from farms that antibiotics have growth-promoting qualities.
A second questioner asked how one could go about demonstrating a causal relationship between antibiotic use and obesity in children, given limitations on human experiments. Blaser replied that epidemiological studies are planned to look for a relationship between the number of courses, type, and timing of antibiotics consumed by children and their body characteristics.
A final questioner asked whether we may ultimately be faced with balancing the benefits of antibiotics in fighting disease with the possible deleterious effects being uncovered by this research. Blaser agreed that we may end up recognizing that there is a hidden long-term cost to antibiotics to be taken into account along with their short-term benefits. Possible solutions could include strengthening existing advice against using antibiotics in marginal situations, encouraging development of much narrower-spectrum antibiotics, and possibly taking probiotics along with antibiotics to minimize perturbation of the microbiome.
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