Numerous genetic risk markers have been identified for CD and UC.
Some of these genetic markers are strongly associated with development of IBD, including CARD15, which has more than 60 variations, of which three play a role in 27% of patients with CD.
(Along with HLA-DQA1 variants, which are associated with UC.)1 However, it is important to note that while these genetic risk factors are permissive (they have the potential for IBD development), neither of them are causative (the presence of even the strongest genetic risk factor does not mean that the disease will inevitably develop).
Alterations of the intestinal barrier defense mechanism most commonly occur due to a broad spectrum of enteric infections, with Salmonella and Campylobacter being the most frequent triggers.2
The current theory of IBD development gives the main role to the intestinal microbiota, which is necessary for intestinal homeostasis and function, and colonization with specific microbes might be detrimental, leading to disease. For instance, the presence of Mycobacterium avium and adherent-invasive Escherichia coli is increased in CD patients and the presence of Clostridium difficile is increased in both CD and UC.3
Various medications have been associated with the risk of IBD development: antibiotics, oral contraceptives, nonsteroidal anti-inflammatory drugs, and hormone replacement therapy.4
There are several additional environmental risk factors that are thought to contribute to the development of IBD; however, the data is not conclusive. For example, tobacco use is generally considered to be protective in UC, but may increase the risk of CD.5 In addition, the “protective” symptom of tobacco use was most reported among current smokers, but discontinuation of tobacco was associated with an increased risk of UC.
There have been numerous studies into dietary influence on IBD development, but they did not identify any strong and statistically significant dietary risk factors. However, high fiber diets rich in fruits and vegetables have been reported to provide protection against IBD development.6