Irritable bowel syndrome causes
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]
Overview
There is no definite cause for irritable bowel syndrome (IBS). However, an interplay of several factors contribute to the development of IBS such as emotional disturbances, stress, adverse early life events, history of inflammatory bowel disease, and acute gastrointestinal infections. Less common causes of IBS include genetics and hormonal changes.
Causes
Irritable bowel syndrome (IBS) results from a complex interaction among multiple factors. These may include psychological, epidemiological, genetic, and infectious factors. To review these factors in detail, click here.
Genetic causes
Genetic causes IBS is associated with high twin concordance, familial aggregation, Single nucleotide polymorphisms and TNF polymorphisms in genes.[1][2]
- IBS has high twin concordance and familial aggregation:[3][4][5][6][7][8]
- IBS has higher concordance in monozygotic as compared to dizygotic twins.[3][4][5][9]
- The risk of developing IBS in individuals with a biologic relative with IBS is twice compared to subjects with no family history. [10]
- Single nucleotide polymorphisms (SNPs) in genes:
- IBS has SNPs in genes playing an important role in host-microbiota interaction (TLR9, IL-6 and CDH1), immune activation and epithelial barriers.
- SNPs cause inflammation and increased permeability of the gastrointestinal tract, leading to abdominal discomfort and increased motility.[11][12]
- Mutation of type V (alpha subunit) of SCN5A encoded voltage gated sodium channel causes IBS.[13][14]
- Genome wide DNA methylation profiling is impaired in IBS and this involves genes linked to neuropeptide hormone function and oxidative stress.[15]
- IBS causes mutation in the neuropeptide S receptor gene (NPSR1) involved in nociception, inflammation and anxiety with abdominal pain.[16]
- Genes involved in the regulation of hepatic bile acid synthesis (such as a functional Klothoβ gene) are mutated in IBS.[17][18]
- TNF polymorphisms:
- SNPs in tumour necrosis factor alpha (TNFα) and genes encoding for superfamily member 15 (TNFSF15) have been proved to be associated with IBS.[12][19][20]
- TNF polymorphisms are also associated with post infectious IBS such as rs4263839 in TNFSF15 and IBS, particularly IBS associated with constipation.[20][19]
References
- ↑ Makker J, Chilimuri S, Bella JN (2015). "Genetic epidemiology of irritable bowel syndrome". World J. Gastroenterol. 21 (40): 11353–61. doi:10.3748/wjg.v21.i40.11353. PMC 4616211. PMID 26525775.
- ↑ Tanaka Y, Kanazawa M, Fukudo S, Drossman DA (2011). "Biopsychosocial model of irritable bowel syndrome". J Neurogastroenterol Motil. 17 (2): 131–9. doi:10.5056/jnm.2011.17.2.131. PMC 3093004. PMID 21602989.
- ↑ 3.0 3.1 Levy RL, Jones KR, Whitehead WE, Feld SI, Talley NJ, Corey LA (2001). "Irritable bowel syndrome in twins: heredity and social learning both contribute to etiology". Gastroenterology. 121 (4): 799–804. PMID 11606493.
- ↑ 4.0 4.1 Morris-Yates A, Talley NJ, Boyce PM, Nandurkar S, Andrews G (1998). "Evidence of a genetic contribution to functional bowel disorder". Am. J. Gastroenterol. 93 (8): 1311–7. doi:10.1111/j.1572-0241.1998.440_j.x. PMID 9707057.
- ↑ 5.0 5.1 Lembo A, Zaman M, Jones M, Talley NJ (2007). "Influence of genetics on irritable bowel syndrome, gastro-oesophageal reflux and dyspepsia: a twin study". Aliment. Pharmacol. Ther. 25 (11): 1343–50. doi:10.1111/j.1365-2036.2007.03326.x. PMID 17509102.
- ↑ Saito YA, Petersen GM, Locke GR, Talley NJ (2005). "The genetics of irritable bowel syndrome". Clin. Gastroenterol. Hepatol. 3 (11): 1057–65. PMID 16271334.
- ↑ Wouters MM, Lambrechts D, Knapp M, Cleynen I, Whorwell P, Agréus L, Dlugosz A, Schmidt PT, Halfvarson J, Simrén M, Ohlsson B, Karling P, Van Wanrooy S, Mondelaers S, Vermeire S, Lindberg G, Spiller R, Dukes G, D'Amato M, Boeckxstaens G (2014). "Genetic variants in CDC42 and NXPH1 as susceptibility factors for constipation and diarrhoea predominant irritable bowel syndrome". Gut. 63 (7): 1103–11. doi:10.1136/gutjnl-2013-304570. PMID 24041540.
- ↑ Saito YA, Petersen GM, Larson JJ, Atkinson EJ, Fridley BL, de Andrade M, Locke GR, Zimmerman JM, Almazar-Elder AE, Talley NJ (2010). "Familial aggregation of irritable bowel syndrome: a family case-control study". Am. J. Gastroenterol. 105 (4): 833–41. doi:10.1038/ajg.2010.116. PMC 2875200. PMID 20234344.
- ↑ Bengtson MB, Rønning T, Vatn MH, Harris JR (2006). "Irritable bowel syndrome in twins: genes and environment". Gut. 55 (12): 1754–9. doi:10.1136/gut.2006.097287. PMC 1856463. PMID 17008364.
- ↑ Locke GR, Zinsmeister AR, Talley NJ, Fett SL, Melton LJ (2000). "Familial association in adults with functional gastrointestinal disorders". Mayo Clin. Proc. 75 (9): 907–12. doi:10.4065/75.9.907. PMID 10994826.
- ↑ Villani AC, Lemire M, Thabane M, Belisle A, Geneau G, Garg AX, Clark WF, Moayyedi P, Collins SM, Franchimont D, Marshall JK (2010). "Genetic risk factors for post-infectious irritable bowel syndrome following a waterborne outbreak of gastroenteritis". Gastroenterology. 138 (4): 1502–13. doi:10.1053/j.gastro.2009.12.049. PMID 20044998.
- ↑ 12.0 12.1 Gonsalkorale WM, Perrey C, Pravica V, Whorwell PJ, Hutchinson IV (2003). "Interleukin 10 genotypes in irritable bowel syndrome: evidence for an inflammatory component?". Gut. 52 (1): 91–3. PMC 1773523. PMID 12477767.
- ↑ Locke GR, Ackerman MJ, Zinsmeister AR, Thapa P, Farrugia G (2006). "Gastrointestinal symptoms in families of patients with an SCN5A-encoded cardiac channelopathy: evidence of an intestinal channelopathy". Am. J. Gastroenterol. 101 (6): 1299–304. doi:10.1111/j.1572-0241.2006.00507.x. PMID 16771953.
- ↑ Saito YA, Strege PR, Tester DJ, Locke GR, Talley NJ, Bernard CE, Rae JL, Makielski JC, Ackerman MJ, Farrugia G (2009). "Sodium channel mutation in irritable bowel syndrome: evidence for an ion channelopathy". Am. J. Physiol. Gastrointest. Liver Physiol. 296 (2): G211–8. doi:10.1152/ajpgi.90571.2008. PMC 2643921. PMID 19056759.
- ↑ Mahurkar S, Polytarchou C, Iliopoulos D, Pothoulakis C, Mayer EA, Chang L (2016). "Genome-wide DNA methylation profiling of peripheral blood mononuclear cells in irritable bowel syndrome". Neurogastroenterol. Motil. 28 (3): 410–22. doi:10.1111/nmo.12741. PMC 4760882. PMID 26670691.
- ↑ Camilleri M, Carlson P, Zinsmeister AR, McKinzie S, Busciglio I, Burton D, Zucchelli M, D'Amato M (2010). "Neuropeptide S receptor induces neuropeptide expression and associates with intermediate phenotypes of functional gastrointestinal disorders". Gastroenterology. 138 (1): 98–107.e4. doi:10.1053/j.gastro.2009.08.051. PMC 2813358. PMID 19732772.
- ↑ Wong BS, Camilleri M, Carlson P, McKinzie S, Busciglio I, Bondar O, Dyer RB, Lamsam J, Zinsmeister AR (2012). "Increased bile acid biosynthesis is associated with irritable bowel syndrome with diarrhea". Clin. Gastroenterol. Hepatol. 10 (9): 1009–15.e3. doi:10.1016/j.cgh.2012.05.006. PMC 3565429. PMID 22610000.
- ↑ Wong BS, Camilleri M, Carlson PJ, Guicciardi ME, Burton D, McKinzie S, Rao AS, Zinsmeister AR, Gores GJ (2011). "A Klothoβ variant mediates protein stability and associates with colon transit in irritable bowel syndrome with diarrhea". Gastroenterology. 140 (7): 1934–42. doi:10.1053/j.gastro.2011.02.063. PMC 3109206. PMID 21396369.
- ↑ 19.0 19.1 Swan C, Duroudier NP, Campbell E, Zaitoun A, Hastings M, Dukes GE, Cox J, Kelly FM, Wilde J, Lennon MG, Neal KR, Whorwell PJ, Hall IP, Spiller RC (2013). "Identifying and testing candidate genetic polymorphisms in the irritable bowel syndrome (IBS): association with TNFSF15 and TNFα". Gut. 62 (7): 985–94. doi:10.1136/gutjnl-2011-301213. PMID 22684480.
- ↑ 20.0 20.1 Zucchelli M, Camilleri M, Andreasson AN, Bresso F, Dlugosz A, Halfvarson J, Törkvist L, Schmidt PT, Karling P, Ohlsson B, Duerr RH, Simren M, Lindberg G, Agreus L, Carlson P, Zinsmeister AR, D'Amato M (2011). "Association of TNFSF15 polymorphism with irritable bowel syndrome". Gut. 60 (12): 1671–1677. doi:10.1136/gut.2011.241877. PMC 3922294. PMID 21636646.