The cause(s) of IBS are not clear. Stress, altered gut bacteria, genetics, and food sensitivities may all be involved. One theory proposes that altered serotonin metabolism within the gastrointestinal (GI) tract and/or abnormalities in pain perception pathways causes hypersensitivity to abdominal pain, while other hypotheses have pointed to stress-induced inflammation, gastroenteritis, and a history of traumatic events as factors that contribute to the development of IBS.
Disrupted brain-gut communication
Some evidence suggests that altered communication between the brain and gut may contribute to pain hypersensitivity and/or motility disturbances in IBS. The mechanisms behind these phenomena are unclear.
Stress and anxiety appear to contribute, at least in part, to gut hypersensitivity via modulation of neural pain-processing hormones.
Small intestinal bacterial overgrowth (SIBO).
Small intestinal bacterial overgrowth is a condition characterized by overgrowth of microbes in the small intestine. As a result, fermentation of food begins before it has been thoroughly digested and absorbed, which can lead to gas formation. SIBO is more common in people with motility disturbances, low stomach acid production, and bowel obstruction. The prevalence of small intestinal bacterial overgrowth in IBS varies across studies, but estimates range from about 20-84%.
Medications that may contribute to IBS development
Certain medications may contribute to the development of IBS. Proton pump inhibitors (eg, omeprazole) which are used to treat heartburn, can alter intestinal barrier function, affect intestinal microflora, and are known to have a positive association with IBS. Similarly, many common analgesics, such as non-steroidal anti-inflammatory drugs (NSAIDs), are known to damage the intestinal epithelium, an important barrier against harmful substances. Although broad-spectrum antibiotics are designed to target systemic infections, antibiotics are known to alter the colonic flora. Indeed, a study showed that the use of broad-spectrum antibiotics, particularly macrolides, was associated with IBS development.
Food sensitivities may have a role in IBS. Please see "how to prevent" section lower down.
Gluten is a protein component of some grains, especially wheat. Sensitivity to gluten is common and is associated with a spectrum of symptoms ranging in severity from minor skin conditions to severe gastrointestinal compromise. Some evidence suggests gluten sensitivity potentially contributes to IBS symptoms. Although evidence is not yet strong enough to support a recommendation that all IBS patients avoid gluten, findings from at least one study indicate that using a blood test to detect immunoglobulin G (IgG) antibodies against components of wheat may help identify patients with diarrhea-predominant IBS who are likely to respond positively to a gluten-free diet.
Some cases of IBS arise following a gastrointestinal infection, usually with a bacterial or parasitic pathogen. This is called post-infectious IBS and occurs in up to about 30% of individuals who contract an acute gastrointestinal infection.
Some evidence suggests a potential role for sex hormone imbalance(s) in IBS. For example, women often experience worsening of IBS symptoms near menstruation, which coincides with natural changes in sex hormone levels. One study found that women with IBS have generally lower estradiol levels than their healthy counterparts. However, postmenopausal women have fewer symptoms compared to women who are still menstruating.