Most of the cells in our bodies don’t belong to use; instead, they represent the host of micorganisms in our digestive tracts and play a critical role in extracting the nutrients from the foods we eat.
Yet until recently, scientists have paid little attention to the role these critters may play in our health, other than to ensure we get the nourishment we need to keep our own cells alive and well.
But as regular readers know, studies are revealing that they may play roles in the onset of a wide range of illnesses, ranging from multiple sclerosis and rheumatoid arthritis [our own affliction] to anorexia, chronic fatigue syndrome, and Alzheimer’s disease.
We also know that antibiotics, the drugs we’ve invented to treat once-fatal bacterial infections, can have a lethal impact on those same internally resident creatures, as we’ve sometimes experienced in the diarrhea often accompanying a heavy dose of antibiotics.
By killing off much of our internal alien population, could we actually be contributing to the rise of other dangerous conditions?
Specially, in this case, diabetes?
The answer may well be yes.
From the New York University Langone Medical Center:
In doses equivalent to those used regularly in human children, antibiotics changed the mix of gut microbes in young mice to dramatically increase their risk for type 1 diabetes. That is the finding of a study led by researchers from NYU Langone Medical Center with support from the Juvenile Diabetes Research Foundation (JDRF), and published August 22 in Nature Microbiology [$32 to download].
The study results center on the microbiome, the bacterial species in our guts that co-evolved with humans to play roles in digestion, metabolism, and immunity. As children’s exposure to microbe-killing antibiotics has increased in recent decades, the incidence of autoimmune diseases like type 1 diabetes has more than doubled. The average American child currently receives 10 courses of antibiotics by age 10.
Specifically, the new study found that short pulses of antibiotics cause mice that are susceptible to type 1 diabetes to develop the disease more quickly and more often than mice not treated with antibiotics.
“Our study begins to clarify the mechanisms by which antibiotic-driven changes in gut microbiomes may increase risk for type 1 diabetes,” says Martin Blaser, MD, the Muriel G. and George W. Singer Professor of Translational Medicine at NYU School of Medicine, and the study’s senior author. “This work uses NOD mice, the best model of type 1 diabetes to date, and doses of antibiotics like those received by most children to treat common infections.”
“This latest study result is compelling, linking the effects of use of antibiotics in mice to type 1 diabetes,” says Jessica Dunne, director of discovery research at JDRF. “This is the first study of its kind suggesting that antibiotic use can alter the microbiota and have lasting effects on immunological and metabolic development, resulting in autoimmunity. We’re eager to see how these findings may impact the discovery of type 1 diabetes preventive treatments in the future and continued research in the area of vaccines.”
More after the jump. . .