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Ulcerative Colitis and CD Risk Linked to City Life


Is the increased risk of IBD due to pollution, a too-clean home, or antibiotics? Or none of the above?

For several decades, epidemiologists have been seeking clues to the cause of inflammatory bowel disorders (IBDs), which is a challenge because they are complex and heterogeneous. Now the influence of environmental factors related to modern society has received another boost.

A new study published in BMC Gastroenterology supports the widely held belief that IBDs are associated with industrialization. The study found a positive association between urban environment and both ulcerative colitis (UC) and Crohn disease (CD). The association was stronger in CD.

In a systematic literature search that began with nearly 7000 citations, a team from the University of Calgary in Alberta selected 40 studies, including 25 case-control and cohort studies that investigated the relationship between urban environment and UC and 30 that investigated this relationship with CD. They calculated a pooled incidence rate ratio for urban to rural environment of 1.17 for UC and 1.42 for CD.

The Canadian researchers cite several theories, including the “Hygiene Hypothesis,” to explain the increased incidence of IBD in urban societies. (The Hygiene Hypothesis suggests that a clean environment, with a lack of early exposure to childhood infections, increases the risk of autoimmune disorders, including IBD.) Other environmental risk factors for IBD that are more predominant in urban societies include smoking, lack of exposure to parasitic worms, and antibiotic use. They note that some studies have associated air pollution in urban areas or urban occupations such as driving and manufacturing as risk factors for IBD.

Researchers Charles Bernstein of the University of Manitoba and Fergus Shanahan of the National University of Ireland, who were not involved with the meta-analysis, instead propose some as-yet poorly understood influence of microbes that changes the risk for IBDs. “The increased frequency of IBD, which has been consistently observed as society becomes developed or modernized, may be linked with changes in gastrointestinal microbiota which, in turn, may affect the development of the immune system and influence the risk of inflammatory diseases,” they write in  Current Opinion in Gastroenterology. They note a “disturbing increase” in comorbidity with Clostridium difficile–associated disease, which they believe has “important implications in an era of increased use of immunomodulatory drugs.”

Let’s not forget the lesson learned from the link between Helicobacter pylori and peptic ulcer disease. The solutions to some chronic disorders may not be found by studying the human host alone, Bernstein and Shanahan suggest in another article, this one in the journal Gut. They pose 2 questions: “Could IBDs (or a subset thereof) be due to an infectious agent, waiting to be identified? Or is the relationship between host susceptibility and the microbial environment a more subtle one?”

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