The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Disorders of a modern lifestyle: reconciling the epidemiology of inflammatory bowel diseases
Abstract
Few would contest that advances in uncovering genetic risk factors for Crohn’s disease and ulcerative colitis over the past decade have changed the way we think about inflammatory bowel diseases (IBDs). Perhaps the most important message has been that much of the genetically determined risk lies in how the host interprets its microbial environment.1–3 However, the primacy of environmental factors was already evident from several sources; notably, studies of genetically identical twins showing a relatively low concordance rate for both Crohn’s disease (<50%) and ulcerative colitis (<10%), and the increased frequency of both disorders in many countries during a period too short to involve significant changes in the population gene pool.4 What are the environmental or lifestyle risk factors for IBD? How do they collude with genetic susceptibility? The lesson of Helicobacter pylori and peptic ulcer disease was that the solution to some chronic disorders cannot be found by studying the human host alone. Rather, the answer may lie at the interface with the microbial environment. A more sobering lesson was the failure of conventional epidemiological studies to recognise that peptic ulcer disease is caused by a transmissible agent. How did disparate epidemiological observations miss this association and fail to guide medical scientists toward this conclusion? 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? While the complexity and heterogeneity of these diseases surely accounts for some of this dilemma, it seems reasonable to ask whether several decades of epidemiological studies have directed or distracted researchers seeking clues to the cause of IBD. Some of the false leads and false promises of epidemiology have been highlighted elsewhere, with the most vigorous attacks in the …
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Cites
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Cited by
Molodecky, N. A., Soon, I. S., Rabi, D. M., Ghali, W. A., Ferris, M., Chernoff, G., Benchimol, E. I., Panaccione, R., Ghosh, S., Barkema, H. W., et al. (2012) · Gastroenterology · doi:10.1053/j.gastro.2011.10.001 · Cited by 4,833
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Immunopathogenesis of IBD: current state of the art
de Souza, H. S. P., & Fiocchi, C. (2016) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2015.186 · Cited by 1,551
Manichanh, C., Borruel, N., Casellas, F., & Guarner, F. (2012) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2012.152 · Cited by 1,160
Ng, S. C., Tang, W., Ching, J. Y., Wong, M., Chow, C. M., Hui, A. J., Wong, T. C., Leung, V. K., Tsang, S. W., Yu, H. H., et al. (2013) · Gastroenterology · doi:10.1053/j.gastro.2013.04.007 · Cited by 830
Ng, S. C., Kaplan, G. G., Tang, W., Banerjee, R., Adigopula, B., Underwood, F. E., Tanyingoh, D., Wei, S.-C., Lin, W.-C., Lin, H.-H., et al. (2019) · American Journal of Gastroenterology · doi:10.1038/s41395-018-0233-2 · Cited by 261
Benchimol, E. I., Mack, D. R., Guttmann, A., Nguyen, G. C., To, T., Mojaverian, N., Quach, P., & Manuel, D. G. (2015) · American Journal of Gastroenterology · doi:10.1038/ajg.2015.52 · Cited by 258
Raison, C. L., Lowry, C. A., & Rook, G. A. W. (2010) · Archives of General Psychiatry · doi:10.1001/archgenpsychiatry.2010.161 · Cited by 169
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Inflammatory bowel disease epidemiology in São Paulo State, Brazil
Galhardi Gasparini, R., Sassaki, L. Y., & Saad-Hossne, R. (2018) · Clinical and Experimental Gastroenterology · doi:10.2147/ceg.s176583 · Cited by 50
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Metadata
- Authors
- Bernstein, C. N., & Shanahan, F.
- Venue
- Gut
- Publisher
- BMJ
- Published
- 2008-05-30
- Volume
- 57
- Issue
- 9
- Pages
- 1185-1191
- ISSN
- 0017-5749 (ISSN-L)
- 1468-3288
- OpenAlex
- W2103669303
- Cited by
- 290
- References
- 5
- FWCI
- 11.07
- Type
- journal article
- Language
- en
- Open access
- closed
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