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Crohn's, Colitis May Have Genetic Underpinnings, Study Finds

FRIDAY, Dec. 19, 2014 (HealthDay News) -- The intestinal bacteria that cause inflammatory bowel disease, which includes Crohn's disease and ulcerative colitis, may be inherited, researchers report.

The findings, published recently in the journal Genome Medicine, could help in efforts to prevent the disease and treat the 1.6 million Americans with Crohn's or colitis, the study authors added.

"The intestinal bacteria, or 'gut microbiome,' you develop at a very young age can have a big impact on your health for the rest of your life," lead author Dan Knights, an assistant professor in the department of computer science and engineering and the Biotechnology Institute at the University of Minnesota, said in a journal news release.

"We have found groups of genes that may play a role in shaping the development of imbalanced gut microbes," he explained.

The study of 474 adults with inflammatory bowel disease who live in the United States, Canada and the Netherlands found a link between the participants' DNA and their gut bacteria DNA. The Crohn's and colitis patients also had less variety of gut bacteria and more opportunistic bacteria than the general population.

The findings are an important step in creating new drugs for the treatment of Crohn's and colitis, the researchers said.

The investigators also found that antibiotics can worsen the imbalances in intestinal bacteria associated with inflammatory bowel disease.

"In many cases, we're still learning how these bacteria influence our risk of disease, but understanding the human genetics component is a necessary step in unraveling the mystery," Knights said.

Previous research has identified associations between gut bacteria and increased risks for health problems such as diabetes, autism, heart disease and some types of cancer, the researchers said.

More information

The U.S. Centers for Disease Control and Prevention has more about inflammatory bowel disease.

SOURCE: Genome Medicine, news release, Dec. 16, 2014


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