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{{Irritable bowel syndrome }}
{{Irritable bowel syndrome }}


{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} {{Cherry}}
==Overview==
==Overview==


The most common cause of IBS is emotional disturbances, stress, adverse early life events, history of [[Inflammatory bowel disease]], acute gastrointestinal infections. Less common causes of IBS include genetics and hormonal changes.
There is no definite cause for [[irritable bowel syndrome]] ([[Irritable bowel syndrome|IBS]]). However, an interplay of several factors contribute to the development of [[Irritable bowel syndrome|IBS]] such as [[Emotion|emotional]] disturbances, [[Stress (medicine)|stress]], adverse early life events, history of [[inflammatory bowel disease]], and acute [[Gastrointestinal tract|gastrointestinal]] [[Infection|infections]]. Less common causes of IBS include [[genetics]] and [[Hormone|hormonal]] changes.


==Causes==
==Causes==
===Common Causes===
[[Irritable bowel syndrome]] ([[Irritable bowel syndrome|IBS]]) results from a complex interaction among multiple factors. These may include [[Psychological Science (journal)|psychological]], [[Epidemiology|epidemiological]], [[Genetics|genetic]], and [[Infection|infectious]] factors. To review these factors in detail, '''[[Irritable bowel syndrome risk factors|click here]].'''
IBS may be caused by:
===Genetic causes===
* Emotional disturbance or stress
[[Genetic]] causes [[Irritable bowel syndrome|IBS]] is associated with high [[twin]] [[Concordance (genetics)|concordance]], [[Family|familial]] [[aggregation]], [[Single nucleotide polymorphism|Single nucleotide polymorphisms]] and [[Tumor necrosis factors|TNF]] [[polymorphisms]] in [[Gene|genes]].<ref name="pmid26525775">{{cite journal |vauthors=Makker J, Chilimuri S, Bella JN |title=Genetic epidemiology of irritable bowel syndrome |journal=World J. Gastroenterol. |volume=21 |issue=40 |pages=11353–61 |year=2015 |pmid=26525775 |pmc=4616211 |doi=10.3748/wjg.v21.i40.11353 |url=}}</ref><ref name="pmid21602989">{{cite journal |vauthors=Tanaka Y, Kanazawa M, Fukudo S, Drossman DA |title=Biopsychosocial model of irritable bowel syndrome |journal=J Neurogastroenterol Motil |volume=17 |issue=2 |pages=131–9 |year=2011 |pmid=21602989 |pmc=3093004 |doi=10.5056/jnm.2011.17.2.131 |url=}}</ref>
* Adverse early life events
*IBS has high '''[[twin]] [[Concordance (genetics)|concordance]] and [[Family|familial]] [[aggregation]]''':<ref name="pmid11606493">{{cite journal |vauthors=Levy RL, Jones KR, Whitehead WE, Feld SI, Talley NJ, Corey LA |title=Irritable bowel syndrome in twins: heredity and social learning both contribute to etiology |journal=Gastroenterology |volume=121 |issue=4 |pages=799–804 |year=2001 |pmid=11606493 |doi= |url=}}</ref><ref name="pmid9707057">{{cite journal |vauthors=Morris-Yates A, Talley NJ, Boyce PM, Nandurkar S, Andrews G |title=Evidence of a genetic contribution to functional bowel disorder |journal=Am. J. Gastroenterol. |volume=93 |issue=8 |pages=1311–7 |year=1998 |pmid=9707057 |doi=10.1111/j.1572-0241.1998.440_j.x |url=}}</ref><ref name="pmid17509102">{{cite journal |vauthors=Lembo A, Zaman M, Jones M, Talley NJ |title=Influence of genetics on irritable bowel syndrome, gastro-oesophageal reflux and dyspepsia: a twin study |journal=Aliment. Pharmacol. Ther. |volume=25 |issue=11 |pages=1343–50 |year=2007 |pmid=17509102 |doi=10.1111/j.1365-2036.2007.03326.x |url=}}</ref><ref name="pmid16271334">{{cite journal |vauthors=Saito YA, Petersen GM, Locke GR, Talley NJ |title=The genetics of irritable bowel syndrome |journal=Clin. Gastroenterol. Hepatol. |volume=3 |issue=11 |pages=1057–65 |year=2005 |pmid=16271334 |doi= |url=}}</ref><ref name="pmid24041540">{{cite journal |vauthors=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 |title=Genetic variants in CDC42 and NXPH1 as susceptibility factors for constipation and diarrhoea predominant irritable bowel syndrome |journal=Gut |volume=63 |issue=7 |pages=1103–11 |year=2014 |pmid=24041540 |doi=10.1136/gutjnl-2013-304570 |url=}}</ref><ref name="pmid20234344">{{cite journal |vauthors=Saito YA, Petersen GM, Larson JJ, Atkinson EJ, Fridley BL, de Andrade M, Locke GR, Zimmerman JM, Almazar-Elder AE, Talley NJ |title=Familial aggregation of irritable bowel syndrome: a family case-control study |journal=Am. J. Gastroenterol. |volume=105 |issue=4 |pages=833–41 |year=2010 |pmid=20234344 |pmc=2875200 |doi=10.1038/ajg.2010.116 |url=}}</ref>
* Anxiety, [[depression]]
**IBS has higher [[Concordance (genetics)|concordance]] in [[Monozygotic twins|monozygotic]] as compared to [[dizygotic twins]].<ref name="pmid11606493" /><ref name="pmid9707057" /><ref name="pmid17509102" /><ref name="pmid17008364">{{cite journal |vauthors=Bengtson MB, Rønning T, Vatn MH, Harris JR |title=Irritable bowel syndrome in twins: genes and environment |journal=Gut |volume=55 |issue=12 |pages=1754–9 |year=2006 |pmid=17008364 |pmc=1856463 |doi=10.1136/gut.2006.097287 |url=}}</ref>
* History of acute GI infections e.g. [[Salmonella]] infection, [[Giardiasis]]
**The risk of developing IBS in individuals with a biologic relative with [[Irritable bowel syndrome|IBS]] is twice compared to subjects with no [[family history]]. <ref name="pmid10994826">{{cite journal |vauthors=Locke GR, Zinsmeister AR, Talley NJ, Fett SL, Melton LJ |title=Familial association in adults with functional gastrointestinal disorders |journal=Mayo Clin. Proc. |volume=75 |issue=9 |pages=907–12 |year=2000 |pmid=10994826 |doi=10.4065/75.9.907 |url=}}</ref>
* Antibiotic use causing alteration of gut microflora
*'''[[Single nucleotide polymorphism|Single nucleotide polymorphisms (SNPs)]] in [[genes]]:'''
* History of gastrointestinal disorders like [[Inflammatory bowel disease|IBD]]
**IBS has [[Single nucleotide polymorphism|SNPs]] in [[genes]] playing an important role in host-[[Microbiome|microbiota]] interaction ([[Toll-like receptor|TLR9]], [[Interleukin 6|IL-6]] and [[CDH11|CDH1]]), [[Immunity (medical)|immune]] activation and [[Epithelium|epithelial]] barriers.
* Immune causes: history of [[Inflammatory bowel disease|IBD]], [[Celiac disease]], [[microscopic colitis]]
**[[Single nucleotide polymorphism|SNPs]] cause [[inflammation]] and increased [[permeability]] of the [[gastrointestinal tract]], leading to [[Abdominal pain|abdominal discomfort]] and increased [[motility]].<ref name="pmid20044998">{{cite journal |vauthors=Villani AC, Lemire M, Thabane M, Belisle A, Geneau G, Garg AX, Clark WF, Moayyedi P, Collins SM, Franchimont D, Marshall JK |title=Genetic risk factors for post-infectious irritable bowel syndrome following a waterborne outbreak of gastroenteritis |journal=Gastroenterology |volume=138 |issue=4 |pages=1502–13 |year=2010 |pmid=20044998 |doi=10.1053/j.gastro.2009.12.049 |url=}}</ref><ref name="pmid12477767">{{cite journal |vauthors=Gonsalkorale WM, Perrey C, Pravica V, Whorwell PJ, Hutchinson IV |title=Interleukin 10 genotypes in irritable bowel syndrome: evidence for an inflammatory component? |journal=Gut |volume=52 |issue=1 |pages=91–3 |year=2003 |pmid=12477767 |pmc=1773523 |doi= |url=}}</ref>
 
**[[Mutation]] of type V (alpha [[Protein subunit|subunit]]) of [[SCN5A]] encoded [[Voltage-gated ion channel|voltage gated]] [[sodium channel]] causes [[Irritable bowel syndrome|IBS]].<ref name="pmid16771953">{{cite journal |vauthors=Locke GR, Ackerman MJ, Zinsmeister AR, Thapa P, Farrugia G |title=Gastrointestinal symptoms in families of patients with an SCN5A-encoded cardiac channelopathy: evidence of an intestinal channelopathy |journal=Am. J. Gastroenterol. |volume=101 |issue=6 |pages=1299–304 |year=2006 |pmid=16771953 |doi=10.1111/j.1572-0241.2006.00507.x |url=}}</ref><ref name="pmid19056759">{{cite journal |vauthors=Saito YA, Strege PR, Tester DJ, Locke GR, Talley NJ, Bernard CE, Rae JL, Makielski JC, Ackerman MJ, Farrugia G |title=Sodium channel mutation in irritable bowel syndrome: evidence for an ion channelopathy |journal=Am. J. Physiol. Gastrointest. Liver Physiol. |volume=296 |issue=2 |pages=G211–8 |year=2009 |pmid=19056759 |pmc=2643921 |doi=10.1152/ajpgi.90571.2008 |url=}}</ref>
===Less Common Causes===
**[[Genome]] wide [[DNA methylation]] profiling is impaired in [[Irritable bowel syndrome|IBS]] and this involves [[genes]] linked to [[neuropeptide]] [[hormone]] function and [[Oxidative stress|oxidative]] stress.<ref name="pmid26670691">{{cite journal |vauthors=Mahurkar S, Polytarchou C, Iliopoulos D, Pothoulakis C, Mayer EA, Chang L |title=Genome-wide DNA methylation profiling of peripheral blood mononuclear cells in irritable bowel syndrome |journal=Neurogastroenterol. Motil. |volume=28 |issue=3 |pages=410–22 |year=2016 |pmid=26670691 |pmc=4760882 |doi=10.1111/nmo.12741 |url=}}</ref>
Less common causes of [[disease name]] include:
**IBS causes [[mutation]] in the [[neuropeptide]] S [[Receptor (biochemistry)|receptor]] [[gene]] (NPSR1) involved in [[Pain and nociception|nociception]], [[inflammation]] and [[anxiety]] with [[abdominal pain]].<ref name="pmid19732772">{{cite journal |vauthors=Camilleri M, Carlson P, Zinsmeister AR, McKinzie S, Busciglio I, Burton D, Zucchelli M, D'Amato M |title=Neuropeptide S receptor induces neuropeptide expression and associates with intermediate phenotypes of functional gastrointestinal disorders |journal=Gastroenterology |volume=138 |issue=1 |pages=98–107.e4 |year=2010 |pmid=19732772 |pmc=2813358 |doi=10.1053/j.gastro.2009.08.051 |url=}}</ref> 
*Genetics
**[[Gene|Genes]] involved in the regulation of [[Liver|hepatic]] [[bile acid]] [[Chemical synthesis|synthesis]] (such as a functional Klothoβ [[gene]]) are mutated in [[Irritable bowel syndrome|IBS]].<ref name="pmid22610000">{{cite journal |vauthors=Wong BS, Camilleri M, Carlson P, McKinzie S, Busciglio I, Bondar O, Dyer RB, Lamsam J, Zinsmeister AR |title=Increased bile acid biosynthesis is associated with irritable bowel syndrome with diarrhea |journal=Clin. Gastroenterol. Hepatol. |volume=10 |issue=9 |pages=1009–15.e3 |year=2012 |pmid=22610000 |pmc=3565429 |doi=10.1016/j.cgh.2012.05.006 |url=}}</ref><ref name="pmid21396369">{{cite journal |vauthors=Wong BS, Camilleri M, Carlson PJ, Guicciardi ME, Burton D, McKinzie S, Rao AS, Zinsmeister AR, Gores GJ |title=A Klothoβ variant mediates protein stability and associates with colon transit in irritable bowel syndrome with diarrhea |journal=Gastroenterology |volume=140 |issue=7 |pages=1934–42 |year=2011 |pmid=21396369 |pmc=3109206 |doi=10.1053/j.gastro.2011.02.063 |url=}}</ref>
*Hormonal changes
*'''TNF polymorphisms:'''
 
**[[Single nucleotide polymorphism|SNPs]] in [[Tumour necrosis factor|tumour necrosis factor alpha]] ([[Tumor necrosis factor-alpha|TNFα)]] and [[genes]] encoding for superfamily member 15 ([[TNFSF15]]) have been proved to be associated with [[Irritable bowel syndrome|IBS]].<ref name="pmid12477767" /><ref name="pmid22684480">{{cite journal |vauthors=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 |title=Identifying and testing candidate genetic polymorphisms in the irritable bowel syndrome (IBS): association with TNFSF15 and TNFα |journal=Gut |volume=62 |issue=7 |pages=985–94 |year=2013 |pmid=22684480 |doi=10.1136/gutjnl-2011-301213 |url=}}</ref><ref name="pmid21636646">{{cite journal |vauthors=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 |title=Association of TNFSF15 polymorphism with irritable bowel syndrome |journal=Gut |volume=60 |issue=12 |pages=1671–1677 |year=2011 |pmid=21636646 |pmc=3922294 |doi=10.1136/gut.2011.241877 |url=}}</ref>
===Genetic Causes===
**[[Tumor necrosis factors|TNF]] [[polymorphisms]] are also associated with post [[Infection|infectious]] [[Irritable bowel syndrome|IBS]] such as rs4263839 in [[TNFSF15]] and [[Irritable bowel syndrome|IBS]], particularly IBS associated with [[constipation]].<ref name="pmid21636646" /><ref name="pmid22684480" />
*IBS is caused by a mutation of type V (alpha subunit) of ''SCN5A''-encoded voltage gated sodium channel gene. Other genes such as [[Tumour necrosis factor|tumor necrosis factor]] alpha (TNFα) and genes coding for superfamily member 15 (''TNFSF15'') are also involved.
*SNPs (Single Nucleotide Polymorphisms) in genes play an important role in host-microbiota interaction (TLR9, IL-6 and CDH1), immune activation and epithelial barriers.
*Genes involved in the regulation of [[Liver|hepatic]] [[bile acid]] synthesis such as a functional Klothoβ gene variant are mutated in IBS patients.
*Genome wide DNA methylation profiling is different in IBS patients, especially involving genes linked to [[neuropeptide]] hormone function and oxidative stress.


==References==
==References==
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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]

References

  1. ↑ 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.
  2. ↑ 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. ↑ 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. ↑ 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. ↑ 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.
  6. ↑ Saito YA, Petersen GM, Locke GR, Talley NJ (2005). "The genetics of irritable bowel syndrome". Clin. Gastroenterol. Hepatol. 3 (11): 1057–65. PMID 16271334.
  7. ↑ 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.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ 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. ↑ 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.
  13. ↑ 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.
  14. ↑ 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.
  15. ↑ 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.
  16. ↑ 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.
  17. ↑ 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.
  18. ↑ 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. ↑ 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. ↑ 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.

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