Causes and Risk Factors
The cause(s) of IBS are not clear (Torpy 2011). Stress, altered gut bacteria, genetics, and food sensitivities may all be involved (Spiller 2012). One theory proposes that altered serotonin metabolism within the gastrointestinal (GI) tract and/or abnormalities in pain perception pathways causes hypersensitivity to abdominal pain (Kanazawa 2011; Spiller 2007; Mayer 2008), 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 (Spiller 2012; Lee 2012).
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 (Fichna 2012; Stasi 2012; Mach 2004; Orr 1997). The mechanisms behind these phenomena are unclear, but some studies have identified altered autonomic and central nervous function in individuals with IBS (Orr 1997; Azpiroz 2002; Jarrett 2003). Another study employed magnetic resonance imaging to examine the brains of people with IBS and identified some structural changes that may contribute to enteric hypersensitivity (Davis 2008). Stress and anxiety appear to contribute, at least in part, to gut hypersensitivity via modulation of neural pain-processing pathways by glucocorticoid hormones, which are also called “stress hormones” (Greenwood-Van Meerveld 2001). Another aspect of this impaired brain-gut communication may stem from altered levels of chemical messengers called neurotransmitters. Levels and activity of the neurotransmitter serotonin in particular appear to be somewhat abnormal in people with IBS (Dunlop 2005; Atkinson 2006).
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 (Yamini 2010; Pyleris 2012). SIBO is more common in people with motility disturbances, low stomach acid production, and bowel obstruction (Yamini 2010). The prevalence of small intestinal bacterial overgrowth in IBS varies across studies, but estimates range from about 20-84% (Reddymasu 2010; Yakoob 2011; Sachdeva 2011).
Medications that may contribute to IBS development
Certain medications may contribute to the development of IBS (Keszthelyi 2012). Proton pump inhibitors (eg, omeprazole [Prilosec®]), which are used to treat heartburn, can alter intestinal barrier function, affect intestinal microflora, and are known to have a positive association with IBS (Keszthelyi 2012). 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. This tissue damage may compromise intestinal permeability (Kerckhoffs 2010). Although broad-spectrum antibiotics are designed to target systemic infections, antibiotics are known to alter the colonic flora (Villarreal 2012). Indeed, a study showed that the use of broad-spectrum antibiotics, particularly macrolides (eg, erythromycin) or tetracyclines (eg, tetracycline, doxycycline), was associated with IBS development (Villarreal 2012).
Food sensitivities may have a role in IBS. Please see the Dietary Considerations section of this protocol for an exploration of this topic.
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 in the case of celiac disease (Pietzak 2012; Di Sabatino 2012; Lundin 2012; Usai 2007). Some evidence suggests gluten sensitivity potentially contributes to IBS symptoms (Verdu 2009; Pietzak 2012). 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 (Wahnschaffe 2007).
Some cases of IBS arise following a gastrointestinal infection, usually with a bacterial or parasitic pathogen (Qin 2011). This is called post-infectious IBS, or PI-IBS, and occurs in up to about 30% of individuals who contract an acute gastrointestinal infection (Ghoshal 2011; Thabane 2009). Symptoms of PI-IBS typically resemble IBS-D (Ghoshal 2011). Irritable bowel symptoms are thought to arise following enteric infection due to inflammatory damage to the gut epithelium, which increases intestinal permeability; alterations in intestinal flora may also contribute (Serghini 2012; Pallotti 2011; Thabane 2009). Some estimates suggest as many as one-third of all IBS cases may arise post-infection (Schwille-Kiuntke 2011).
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 (Heitkemper 2009; Jane 2011). One study found that women with IBS have generally lower estradiol levels than their healthy counterparts (Cui 2006). However, postmenopausal women have fewer symptoms compared to women who are still menstruating (NDDIC 2012).