Moises Velasquez-Manoff in The New York Times:
IN the last half-century, the prevalence of autoimmune disease — disorders in which the immune system attacks healthy tissue in the body — has increased sharply in the developed world. An estimated one in 13 Americans has one of these often debilitating, generally lifelong conditions. Many, like Type 1 diabetes and celiac disease, are linked with specific gene variants of the immune system, suggesting a strong genetic component. But their prevalence has increased much faster — in two or three generations — than it’s likely the human gene pool has changed. Many researchers are interested in how the human microbiome — the community of microbes that live mostly in the gut and are thought to calibrate our immune systems — may have contributed to the rise of these disorders. Perhaps society-wide shifts in these microbial communities, driven by changes in what we eat and in the quantity and type of microbes we’re exposed to in our daily lives, have increased our vulnerability. To test this possibility, some years ago, a team of scientists began following 33 newborns who were genetically at risk of developing Type 1 diabetes, a condition in which the immune system destroys the insulin-producing cells of the pancreas.
The children were mostly Finnish. Finland has the highest prevalence — nearly one in 200 under the age of 15 — of Type 1 diabetes in the world. (At about one in 300, the United States isn’t far behind.) After three years, four of the children developed the condition. The scientists had periodically sampled the children’s microbes, and when they looked back at this record, they discovered that the microbiome of children who developed the disease changed in predictable ways nearly a year before the disease appeared. Diversity declined and inflammatory microbes bloomed. It was as if a gradually maturing ecosystem had been struck by a blight and overgrown by weeds. The study, published last year, was small. But for Ramnik Xavier, a molecular biologist at the Broad Institute in Cambridge, Mass., and a senior author on the study, the findings suggested for the first time that intervention might be possible. Maybe clinicians could catch and correct the microbial derangement in time to slow — or even prevent — the emergence of the disorder.
More here.
