What causes IBS-C
Executive summary
Irritable bowel syndrome with constipation (IBS‑C) has no single proven cause; instead clinicians and researchers describe a multifactorial disorder driven by altered gut motility, visceral hypersensitivity, disordered gut–brain communication, microbiome changes and environmental triggers such as infection or diet [1] [2] [3]. Current guidelines treat IBS‑C as a “disorder of gut‑brain interaction” where multiple, interacting mechanisms—rather than one defective organ—produce the characteristic pain, bloating and constipation [4] [5].
1. A motility problem that slows stool transit, but not the whole story
Many experts point to slow or uncoordinated muscle contractions in the colon as a core contributor to constipation-dominant symptoms: slowed transit and excessive fluid absorption make stool hard and difficult to pass, which is often reported in IBS‑C [1] [6]. Yet motility alone does not explain the severe pain and bloating that distinguish IBS‑C from ordinary chronic constipation, so clinicians consider motility a necessary but insufficient piece of the puzzle [7] [8].
2. Nerves that overreact: visceral hypersensitivity and the gut–brain axis
Heightened sensitivity of intestinal nerves and faulty signaling between gut and brain are repeatedly cited: normal bowel sensations become painful and bowel reflexes can change when the “two‑way street” between the gut and central nervous system malfunctions [2] [4]. This altered pain processing helps explain why abdominal pain often improves after defecation in IBS and why psychological factors—stress, anxiety or prior psychiatric illness—frequently coexist with symptom flares [9] [5].
3. Microbiome shifts, methane and postinfectious triggers
Research links changes in gut microbes (dysbiosis), small intestinal bacterial overgrowth (SIBO) and methane-producing organisms with constipation severity: higher breath methane correlates with worse constipation, and modifying methanogenesis can improve symptoms, suggesting a microbial role in slowing transit [3]. Additionally, a subset of IBS cases begins after a gastrointestinal infection—postinfectious IBS—implicating immune and microbial sequelae as causal contributors in some patients [10] [9].
4. Diet, food intolerances and inconsistent evidence
Dietary factors—FODMAPs, individual food intolerances and low fiber—are associated with symptom flares in many people with IBS‑C, but objective proof that specific foods cause the condition is variable and patient‑specific [3] [6]. A low‑FODMAP diet can reduce gas and distension for some, yet such restrictive diets may lower fiber and paradoxically worsen constipation in others, underscoring the heterogeneity of triggers [3] [11].
5. Overlap with other conditions and diagnostic limits
IBS‑C lacks a definitive lab test; diagnosis relies on symptom criteria (Rome definitions) and excluding “alarm” features that suggest alternative diseases [5] [7]. This diagnostic ambiguity fuels overlap with chronic idiopathic constipation and other disorders—meaning similar bowel patterns can have different underlying mechanisms and require different treatments [7] [12].
6. Why uncertainty persists and what that means for patients
The prevailing medical view is candid: the precise cause of IBS‑C remains unknown and is almost certainly heterogeneous—different patients may have different dominant drivers such as motility defects, microbiome changes, nerve sensitivity, postinfectious immune changes or psychosocial factors [1] [3] [10]. That uncertainty shapes practice: clinicians target multiple pathways (diet, microbiome, motility agents, neuromodulators and psychological therapies) rather than chasing a single cure, and researchers continue to probe which mechanisms dominate in which patients [13] [8].