What causes IBS?
Even though its exact cause is unknown, the following factors are known to influence the development of IBS:
- Diarrhea and infections (post-infectious IBS)
- Changes in the intestinal flora (microbiome)
- Bacterial overgrowth
- Inflammation in the intestine
- Damaged intestinal barrier
- Increased permeability of the mucous membrane
- Disruption of the autonomic nervous system and the gut-brain axis
- Disordered bowel muscle activity (motility)
- Intestinal hypersensitivity (visceral hypersensitivity)
- Genetic predisposition
- Stress and anxiety
- Poor nutrition
- Food intolerance
- Carbohydrate malabsorption
- Medications (e.g. antibiotics)
- Low birthweight
- Environmental factors (e.g. air pollution, radiation exposure)
Infections which can cause IBS (post-infectious IBS)
Over the life course, almost everyone gets a gastrointestinal infection (gastroenteritis), such as salmonella or campylobacter, which causes diarrhea. After gastroenteritis, the risk of developing IBS is seven times as high.
After infection, up to 30% of people experience long-term gastrointestinal issues—mainly diarrhea—which qualify as post-infectious IBS. Even after the infection has healed, micro-inflammations remain in the intestinal wall.
In response to infection, the microbiome changes for a long period of time. This disturbed microbiome could influence intestinal hypersensitivity, inflammation in the intestinal wall, and other symptoms.
Damaged intestinal barrier
A mucous membrane covers the intestinal wall and separates the body from the contents of the intestine. This creates a barrier to foreign and harmful substances that is similar to the body's outer skin. In order to maintain this barrier, the microbiome is very important.
When IBS develops, the intestinal wall becomes more permeable—often called leaky gut syndrome—and the intestinal barrier is damaged. As a result, foreign substances and bacteria can more easily penetrate the intestinal wall, which causes inflammation and an immune response. This could worsen the symptom of pain sensitivity, for instance.
These changes can result from:
- Food allergies or hypersensitivities (e.g. gluten, FODMAPs)
- Stress and anxiety
- Disturbed bile metabolism
- Bile acid, fat, or carbohydrate malabsorption
- Disorders of the hormone and immune system
- Disturbances to the intestinal flora (dysbiosis)
Because many of these factors influence one another, it is difficult sometimes to differentiate between cause and effect.
Mental health and IBS
The psyche, microbiome, and intestine communicate via nerves and hormones along what is called the gut-brain axis. Among those with IBS, there is a documented change in the concentration of the hormone serotonin, which plays an important role in depression. For those with diarrhea as their main symptom (IBS-D), serotonin levels frequently rise; for those who mainly experience constipation (IBS-C), serotonin tends to decrease.
In the long term, post-infectious IBS can lead to mental illness, even if the initial cause of post-infectious IBS is purely physical. At the same time, this psychological aspect can promote the maintenance of subjective symptoms, even if no physical cause of IBS is found (somatization). The risk of somatization depends on the severity of the infection and on the individual's background. For example, a history of an anxiety disorder, depression, or significant stress increases the risk.
Visceral hypersensitivity and IBS
Visceral hypersensitivity** **occurs when there is a reduction in pain threshold, and the intestine becomes generally hypersensitive to pain. Stimuli that go unnoticed or are not painful for healthy people are rated as painful for those with IBS.
Higher intestinal pressure or irritants can cause abdominal pain and the feeling of fullness much faster. Currently, it is still unknown how this hypersensitivity in IBS occurs.
In post-infectious IBS, nerve endings in the intestine are irritated by inflammation. After the infection subsides, the nerves reactivate and transmit feelings of pain, but they remain hypersensitive and never return to their original resting state.
Intestinal motility and IBS
Intestinal motility is the transportation of food through the intestine via muscle activity. A complex interaction occurs between the nervous system of the intestine, the brain, and the intestinal muscles in order to create healthy motility. The food pulp is moved through the intestine with targeted tension and relaxation of different sections, similar to squeezing a tube of toothpaste.
For those with IBS, the transport of food through the intestine is disrupted. For those with IBS-D, the transport is faster; for those IBS-C, it is slower. This is due to increased or decreased motility, respectively.
It is still unclear whether motility disorders are a cause or a consequence of IBS. Further research is needed.
Is IBS inherited?
As a result of both genetic and environmental factors, IBS is more common in some families, and it is suspected that IBS may be inherited. The identification of a genetic component is difficult and usually possible through conducting twin studies. Because twins are almost genetically identical, these studies examine how certain diseases like IBS develop in twins who grow up in different families and environments.
The risk of developing IBS is slightly higher among twins, even if they grow up in different households. Because twins have different social, psychological, and environmental influences when living with different families, this demonstrates that IBS has a genetic component.
Studies show that developing IBS could alter genes that are important for intestinal motility or the tolerance of certain foods. Although no single gene has been identified, it is believed that various genes contribute to the development of IBS and are influenced by environmental factors, such as exposure to long-term air pollution and radiation.
_Read more CARA CARE articles about IBS here. _
Andresen V, Layer P, Hohendorf H, Sumenko A, Schemann M, Keller J. Gesteigerte Kontraktilität des Rektums in Antwort auf Ballondistension beim Reizdarmsyndrom: Signifikante Assoziation mit viszeraler Hypersensitivität. Z Gastroenterologie. 2010;48(08):269 doi: 10.1055/s-0030-1263709
Barbara, G., Grover, M., Bercik, P., Corsetti, M., Ghoshal, U. C., Ohman, L., & Rajilić-Stojanović, M. (2019). Rome Foundation Working Team Report on Post-Infection Irritable Bowel Syndrome. Gastroenterology, 156(1), 46-58.e7. https://doi.org/10.1053/j.gastro.2018.07.011
Bengtson MB, Rønning T, Vatn MH, Harris JR. Irritable bowel syndrome in twins: genes and environment. Gut. 2006;55(12):1754–1759. doi:10.1136/gut.2006.097287
Camilleri M, Lasch K, Zhou W. Irritable bowel syndrome: methods, mechanisms, and pathophysiology. The confluence of increased permeability, inflammation, and pain in irritable bowel syndrome. Am J Physiol Gastrointest Liver Physiol. 2012;303(7):G775–G785. doi:10.1152/ajpgi.00155.2012
Frieling T, Schemann M. Reizdarmsyndrom–Epidemiologie und Pathophysiologie. coloproctology. 2014;36(3):181-189. doi: 10.1007/s00053-014-0435-z.
Halvorson HA, Schlett CD, Riddle MS. Postinfectious irritable bowel syndrome--a meta-analysis. Am J Gastroenterol. 2006;101(8):1894–1942. doi:10.1111/j.1572-0241.2006.00654.x
IACOB, T., ŢĂŢULESCU, D. F., & DUMITRAŞCU, D. L. (2017). Therapy of the postinfectious irritable bowel syndrome: An update. Clujul Medical, 90(2), 133–138. https://doi.org/10.15386/cjmed-752
Macsharry, J., O’Mahony, L., Fanning, A., Bairead, E., Sherlock, G., Tiesman, J., Fulmer, A., Kiely, B., Dinan, T. G., Shanahan, F., & Quigley, E. M. M. (2008). Mucosal cytokine imbalance in irritable bowel syndrome. Scandinavian Journal of Gastroenterology, 43(12), 1467–1476. https://doi.org/10.1080/00365520802276127
Marynowski, M., Likońska, A., Zatorski, H., & Fichna, J. (2015). Role of environmental pollution in irritable bowel syndrome. World Journal of Gastroenterology : WJG, 21(40), 11371–11378. https://doi.org/10.3748/wjg.v21.i40.11371
Mavrangelos, C., Campaniello, M. A., Andrews, J. M., Bampton, P. A., & Hughes, P. A. (2018). Longitudinal analysis indicates symptom severity influences immune profile in irritable bowel syndrome. Gut, 67(2), 398–399. https://doi.org/10.1136/gutjnl-2017-314308
Mohammed I, Cherkas LF, Riley SA, Spector TD, Trudgill NJ. Genetic influences in irritable bowel syndrome: a twin study. Am J Gastroenterol. 2005;100(6):1340–1344. doi:10.1111/j.1572-0241.2005.41700.x
Nam, S. Y., Kim, B. C., Ryu, K. H., & Park, B. J. (2010). Prevalence and Risk Factors of Irritable Bowel Syndrome in Healthy Screenee Undergoing Colonoscopy and Laboratory Tests. Journal of Neurogastroenterology and Motility, 16(1), 47–51. https://doi.org/10.5056/jnm.2010.16.1.47
Ohman L, Simrén M. Pathogenesis of IBS: role of inflammation, immunity and neuroimmune interactions. Nat Rev Gastroenterol Hepatol. 2010;7(3):163–173. doi:10.1038/nrgastro.2010.4
Tan, T.-K., Saps, M., Lin, C.-L., & Wei, C.-C. (2019). Is Long-term Ambient Air Pollutant Exposure a Risk Factor for Irritable Bowel Syndrome in Children? A 12-year Longitudinal Cohort Study. Journal of Neurogastroenterology and Motility, 25(2), 241–249. https://doi.org/10.5056/jnm18135
von Wulffen M, Lohse A, Broicher W, et al. Post-infektiöses Reizdarmsyndrom (RDS) nach schwerer EHEC-(O104: H4)-Enterokolitis: Kohortenstudie mit prospektiver Nachverfolgung zu Häufigkeit und Risikofaktoren. Z Gastroenterologie. 2013;51(08):V09. doi: 10.1055/s-0033-1352621