Environmental triggers of IBD
Inflammatory Bowel Disease encompasses both Crohn's disease (CD) and Ulcerative Colitis (UC), both of which are autoimmune conditions. These conditions are believed to be influenced by various environmental triggers. It is estimated that autoimminity is 30% genetics and 70% environmental. Even with a genetic predisposition, this does not guarantee development, a trigger in the environment still has to create autoreactive B and T cells in the immune system.
In a comprehensive population-based cohort study involving over 6 million individuals aged 10 and above, a notable link was established between antibiotic usage and an increased risk of developing IBD. This association held across all age groups, with the highest risk observed in individuals aged 40-60 years. The peak risk period occurred 1-2 years after antibiotic use, particularly when these antibiotics were prescribed to combat gastrointestinal tract pathogens (3).
Additionally, environmental factors, such as heavy metals and other contaminants found in drinking water, have been identified as potential contributors to IBD risk. A prospective cohort study conducted in southeast China, which followed 25,490 participants for 5.24 years, studied the presence of contaminants in drinking water, including manganese, mercury, selenium, SO4, chlorine, and NO3N in relation to IBD. Their findings indicated that for each 1 standard deviation increase in the concentration of these contaminants, the risk of developing IBD increased (5).
Another significant environmental factor impacting IBD is smoking, particularly in individuals with CD. Smokers with CD tend to experience more severe symptoms and undergo surgery at a higher rate than non-smokers, with surgery rates as high as 60.3% compared to 38.3% for non-smokers (1). Cotinine, a metabolite of nicotine, has emerged as a valuable biomarker for quantifying smoking habits, outperforming self-reported data. Widbom's research in 2020 found that healthy individuals with the highest cotinine levels were most likely to develop IBD within five years, but this correlation was observed solely among cigarette smokers, not those using smokeless tobacco. This suggests that factors other than nicotine in cigarettes may contribute to this increased risk. Notably, e-cigarette use appears to have no significant association with an increased risk of IBD, according to a case-control study (2). (though I do not support their use :) )
References:
1. Chen, B.-C., Weng, M.-T., Chang, C.-H., Huang, L.-Y., & Wei, S.-C. (2022). Effect of smoking on the development and outcomes of inflammatory bowel disease in Taiwan: a hospital-based cohort study. Scientific Reports, 12(1).
2. Sheehan, G. T., Twardus, S. W., Cagan, A., & Ananthakrishnan, A. N. (2023). E-cigarette Use and Disease Outcomes in Inflammatory Bowel Diseases: A Case-Control Study. Digestive Diseases and Sciences, 68(1), 208–213.
3. Shimodaira, Y., Watanabe, K., & Iijima, K. (2022). The risk of antibiotics and enterocolitis for the development of inflammatory bowel disease: a Japanese administrative database analysis. Scientific Reports, 12(1).
4. Widbom, L., Schneede, J., Midttun, O., Ueland, P. M., Karling, P., Hultdin, J., & Bonovas, S. (2020). Elevated plasma cotinine is associated with an increased risk of developing IBD, especially among users of combusted tobacco. PLoS ONE, 15(7), e0235536.
5. Zhou, S., Chai, P., Dong, X., Liang, Z., Yang, Z., Li, J., Teng, G., Sun, S., Xu, M., Zheng, Z.-J., Wang, J., Zhang, Z., & Chen, K. (2023). Drinking water quality and inflammatory bowel disease: a prospective cohort study. Environmental Science and Pollution Research, 1–13.
