What Causes IBS? The 9 Evidence-Based Drivers of Irritable Bowel Syndrome

IBS is caused by a combination of gut-brain axis dysregulation, visceral hypersensitivity (gut nerves firing pain signals at normal stimuli), altered motility, and often a triggering event , most commonly a gastrointestinal infection (post-infectious IBS), a period of significant stress, or early-life adversity. Microbiome imbalance, genetic predisposition, FODMAP malabsorption, and hormonal cycling modulate how severely the syndrome presents. No single cause. Multiple converging pathways.

Most people arriving at the question "what causes IBS" are looking for a single answer. A food, a bacteria, a gene, a stressor. That explains their symptoms and points to one fix. IBS is not that kind of condition. Research published over the last three decades, consolidated under the Rome Foundation framework led by Douglas Drossman and colleagues, consistently describes IBS as a disorder of gut-brain interaction (the current preferred terminology, updated in Rome IV). The condition arises from dysregulated signalling between the central nervous system, the enteric nervous system, and the gut itself, with contributions from multiple biological, psychological, and environmental factors.

This is why single-lever treatments tend to produce partial relief at best. Eliminating FODMAPs helps many people, but around 25-30% of patients do not respond. Antispasmodics calm motility, but symptoms return on discontinuation. Antidepressants at low doses can reduce visceral pain, but they do not address motility or diet. Each intervention targets one or two of the drivers. The drivers that are not addressed keep the syndrome alive.

IBS is a syndrome, not a disease. Syndromes are defined by pattern (in this case, the Rome IV symptom criteria) rather than by a single mechanism. Two people with the same IBS diagnosis can have quite different combinations of underlying drivers. One predominantly post-infectious with strong visceral hypersensitivity, another predominantly stress-driven with FODMAP sensitivity layered on top. Both meet the diagnostic criteria. Both are correctly diagnosed. Both will respond best to different treatment emphases.

The nine sections below walk through each of the evidence-based drivers. Reading them with the mindset of "which of these are likely in me?" tends to be more useful than hunting for a single cause.

A note on terminology: older clinical writing treated "IBS" and "spastic colon" and "nervous stomach" as rough synonyms, and the disorder was sometimes dismissed as "functional" in the pejorative sense. Contemporary research has comprehensively retired that framing. IBS has measurable, reproducible biological abnormalities. Reduced rectal distension thresholds, altered central pain processing on fMRI, shifted microbiome profiles, detectable low-grade immune activation in post-infectious cases, altered enteric serotonin signalling, and modified vagal tone. The mechanism is real. The evidence base is robust. The treatment implication is that effective care typically works at multiple levels simultaneously rather than chasing a single lever.

Each of the drivers below contributes independently, but they almost always interact. The diagram below shows the nine converging pathways around the central IBS phenotype. Most adults with IBS have two to four active drivers at any given time.

The gut-brain axis is the bidirectional communication network between the central nervous system and the enteric nervous system (the roughly 500 million neurons embedded in the gut wall, sometimes called the "second brain"). This axis runs primarily through the vagus nerve, with additional signalling through spinal pathways, the HPA (hypothalamic-pituitary-adrenal) axis, gut hormones, and immune messengers. In healthy function, the brain and gut exchange constant information about digestion, fullness, threat, and homeostatic balance without the person being consciously aware of most of it.

In IBS, this signalling becomes dysregulated. Clinical research led by Mayer and colleagues at UCLA has published extensively on the gut-brain axis across two decades. fMRI studies consistently find altered activation in pain-processing regions (anterior cingulate cortex, insula, amygdala) when IBS patients experience rectal distension compared to healthy controls. The same physical stimulus is interpreted and experienced differently by the dysregulated brain.

Vagal tone. A measure of parasympathetic nervous system activity. Is typically reduced in IBS patients. This matters because the vagus nerve is the main "brake" on stress physiology. Low vagal tone means the nervous system is biased toward sympathetic (fight-or-flight) dominance, which in turn alters gut motility, reduces digestive secretions, and heightens pain perception. Interventions that improve vagal tone (slow breathing, meditation, clinical hypnosis) tend to produce corresponding improvements in gut symptoms.

Interoception. The nervous system's perception of the internal state of the body. Is also often altered in IBS. Normal gut sensations (peristalsis, gas movement, stretching after a meal) that healthy people barely notice become conscious, uncomfortable, or painful in IBS. This is the clinical substrate of visceral hypersensitivity, which is itself the next driver covered below.

A related and frequently overlooked part of the gut-brain axis is the HPA axis feedback loop. The hypothalamus releases corticotropin-releasing factor (CRF) in response to stress; CRF then drives cortisol release and directly modulates gut motility and visceral sensitivity. In IBS, research repeatedly reports elevated or dysregulated HPA axis signalling, including exaggerated cortisol responses to stressors and altered CRF receptor sensitivity in the gut itself. This is part of why life stress can produce gut symptoms within hours.

The gut-brain axis is the central organising concept for why IBS exists as a category. Rome IV specifically reframed the entire class of conditions as "disorders of gut-brain interaction" to put this mechanism at the centre of how clinicians think about diagnosis and treatment. Read more in the gut-brain connection pillar.

Visceral hypersensitivity is the single most consistently measured finding in IBS research. It is the phenomenon where the nerves innervating the gut fire pain signals at stimuli that, in a healthy gut, would not register as painful at all. Rectal distension testing. Inflating a small balloon in the rectum at controlled volumes. Has been used in dozens of studies to quantify this. IBS patients consistently report pain at lower distension volumes than healthy controls. The sensation threshold is measurably lower.

Two mechanisms are thought to drive this. The first is peripheral sensitisation: the sensory neurons in the gut wall become more reactive, often following inflammation (as in post-infectious IBS) or chronic stress exposure. They fire at a lower threshold and send stronger signals up the spinal cord for a given stimulus. The second is central sensitisation: the spinal cord and brain regions that process those signals amplify them, so even a normal-strength signal arriving centrally is interpreted as painful.

This is why people with IBS often describe sensations as out of proportion to what their partner, parent, or co-worker would feel after the same meal. The gut itself may be producing broadly similar mechanical activity; the nervous system processing that activity is fundamentally different.

Visceral hypersensitivity is also the driver that gut-directed hypnotherapy most directly targets. Clinical research. Including Whorwell's original 1984 Lancet study and the 40+ years of subsequent work. Has shown that hypnotherapy measurably reduces rectal distension pain thresholds (meaning patients tolerate larger volumes before registering pain) after completing the protocol. The intervention appears to work primarily by retraining the central sensitisation component: changing how the brain interprets gut signals, rather than changing the gut itself.

Research shows that visceral hypersensitivity often persists even when the original trigger (an infection, a period of intense stress, a course of antibiotics) is long resolved. This is why "the food poisoning was years ago, why am I still like this?" is such a common IBS story. The trigger started the sensitisation; the sensitisation is now self-sustaining.

A practical consequence of centrally-maintained visceral hypersensitivity is that treatments directed purely at the gut. Dietary restriction, probiotics, antispasmodics. Often produce incomplete or temporary relief. The peripheral gut environment is only half the picture. For clients with strong visceral hypersensitivity features (disproportionate pain, hypervigilance to gut sensations, persistent symptoms despite normal workup), interventions that retrain central processing tend to be the missing piece.

Gut motility. The coordinated contractions that move food and waste through the GI tract. Is consistently altered in IBS, and the pattern of alteration is what defines the three main subtypes under Rome IV.

Motility is controlled by the enteric nervous system, modulated by the autonomic nervous system (vagal and sympathetic input), and influenced by gut hormones, serotonin signalling (most of the body's serotonin lives in the gut), and the local microbial environment. In IBS, research has documented abnormal patterns of small and large bowel contractions, altered response to meals (exaggerated or blunted gastrocolic reflex), and differences in rectal sensitivity that interact with motility to produce the clinical picture.

Importantly, motility is one of the drivers that gut-directed hypnotherapy does not directly retrain. What hypnotherapy does change is the nervous system context around motility. Vagal tone, stress response, visceral perception. For some clients this is enough to normalise the motility pattern indirectly. For others, motility remains altered even when symptoms improve, because the pain and urgency that defined the experience have reduced. Understanding this distinction helps set realistic expectations.

Motility-targeted interventions (osmotic laxatives, antispasmodics, prokinetics, linaclotide, peppermint oil) work on this driver directly and can combine well with gut-directed hypnotherapy for patients whose motility is a significant component.

One of the best-characterised IBS subtypes is post-infectious IBS, which develops in the weeks and months following an episode of acute gastroenteritis. Systematic reviews. Including foundational work by Halvorson et al. and Spiller and colleagues. Report that roughly 6% to 17% of people who experience a bacterial or viral gut infection go on to meet IBS criteria within 12 months. The risk is elevated by a factor of 4 to 6 relative to people who have not had such an infection.

Risk factors for developing PI-IBS after a gut infection include:

• Severity and duration of the original infection (longer and worse infections carry higher risk)
• Female sex
• Younger age at the time of infection
• Pre-existing anxiety or depression
• Significant life stress around the time of infection
• Use of antibiotics during or after the infection
• Specific pathogens. Campylobacter, Salmonella, Shigella, norovirus, Giardia are all documented triggers

The mechanism appears to involve persistent low-grade inflammation in the gut wall after the acute infection resolves, lasting changes to the enteric nervous system (serotonin-containing enterochromaffin cell density is often increased), altered intestinal permeability, and microbiome disruption that fails to fully recover. The result is a gut that looks structurally normal on endoscopy but behaves like one with chronic low-level immune activation.

Since 2020, research has increasingly documented post-COVID functional GI presentations. COVID-19 has clear gastrointestinal involvement. The virus binds to ACE2 receptors in the gut, and a subset of patients experience GI symptoms as a primary or secondary manifestation. Follow-up studies have reported elevated rates of new-onset IBS, functional dyspepsia, and other gut-brain disorders in COVID survivors, consistent with the broader post-infectious IBS pattern.

The natural history of PI-IBS is somewhat more favourable than IBS arising from other pathways. Longitudinal research suggests that up to 50% of PI-IBS cases resolve over 5-10 years, though often with persistent vulnerability. For the substantial fraction that does not spontaneously resolve, gut-directed hypnotherapy is particularly well-suited because the central mechanism , sensitisation of the gut-brain axis following an inflammatory insult. Is exactly what the protocol is designed to retrain.

A practical marker for suspecting PI-IBS: the person can usually name a specific event. A travel-related stomach bug, a bout of food poisoning, a stomach flu, a documented Campylobacter or Giardia infection, a COVID infection with GI involvement. After which their gut was never the same. Pre-event, they ate normally and had a predictable GI pattern. Post-event, the pattern changed and did not recover.

The relationship between stress and IBS is frequently misunderstood as "IBS is just stress." Research does not support that framing. What research does support is that stress. Particularly sustained stress and early-life adversity , is a powerful modulator of the gut-brain axis and a consistent contributor to the development and maintenance of IBS symptoms.

The HPA axis (hypothalamic-pituitary-adrenal) is the body's primary stress response system, releasing cortisol and other stress mediators. Chronic activation of the HPA axis has been shown to increase gut permeability, alter motility, modulate the microbiome, and sensitise visceral pain pathways. All of these are the same physiological changes observed in IBS. In effect, sustained stress physiology creates conditions that look like IBS at the tissue level.

Early-life adversity. Adverse childhood experiences (ACEs), early trauma, chronic stress in childhood. Appears to be a particularly strong background risk factor. Epidemiological studies have consistently found that IBS patients report higher rates of childhood adversity than matched controls. The mechanism is thought to be developmental: the HPA axis and the stress-response architecture of the nervous system calibrate during childhood, and early adversity sets a more reactive default state that persists into adulthood. This makes the nervous system more prone to sensitisation later, when triggers (infection, acute stress, dietary changes) appear.

This is also why treatments that address nervous-system regulation. Gut-directed hypnotherapy, CBT for IBS, mindfulness-based interventions, somatic approaches , tend to show strong effect sizes in IBS research. They are not treating "psychological" symptoms in the colloquial sense. They are retraining the stress-response architecture that is driving gut physiology.

The distinction that matters clinically: acute stress at the time of onset (usually something major. Bereavement, divorce, job loss, relocation, severe illness, an accident) often acts as the triggering event, while sustained background stress and early-life adversity act as the soil that made the trigger take root. Two people can experience the same acute stressor; the one with a more sensitised stress-response architecture is the one more likely to leave that period with IBS. This is not a moral failing or a reflection of weak psychological resilience. It is a neurobiological setting that was calibrated by factors largely outside the person's control.

For a deeper look at the specific overlap between IBS and anxiety, see IBS and anxiety.

The gut microbiome. The roughly 10-100 trillion bacteria, archaea, fungi, and viruses living in the human GI tract. Is an area of rapidly expanding IBS research. Clinical reviews consistently report differences between the microbiomes of IBS patients and healthy controls, though the specific pattern varies across studies and subtypes. Commonly reported findings include:

• Reduced overall microbial diversity (lower alpha diversity)
• Altered ratios of major phyla, particularly Firmicutes to Bacteroidetes
• Lower abundance of beneficial butyrate-producing species
• Higher abundance of pro-inflammatory or pathobiont species
• Increased risk of small intestinal bacterial overgrowth (SIBO), documented in a subset of IBS patients

Whether microbiome changes are a cause or a consequence of IBS is still being worked out. Research supports both directions: dysbiosis can drive inflammation, alter motility via microbial metabolites, and influence visceral sensitivity. At the same time, altered gut motility, altered secretions, and dietary changes in IBS patients can themselves shape the microbial environment, creating a feedback loop.

Interventions targeting the microbiome. Specific probiotics (Bifidobacterium infantis 35624 has the best evidence base), rifaximin (a gut-targeted antibiotic approved for IBS-D in some jurisdictions), dietary changes including FODMAP restriction, and fermentable fibre supplementation. All have evidence for helping subsets of IBS patients. No single microbiome intervention works for everyone, consistent with the multi-factorial framing.

Gut-directed hypnotherapy does not directly change microbiome composition. Some research has reported secondary microbiome shifts after hypnotherapy protocols, likely reflecting downstream effects of improved motility, reduced stress physiology, and normalised eating patterns rather than a direct microbial mechanism. For clients whose IBS is substantially microbiome-driven (suspected SIBO, clear antibiotic-triggered onset, strong response to specific probiotics), combining hypnotherapy with microbiome-targeted care tends to produce the best outcomes.

Clinically, a useful marker for suspecting a significant microbiome contribution is onset shortly after a course of broad-spectrum antibiotics, a documented gut infection that shifted the microbial environment, or after bariatric surgery or other structural changes that alter microbial ecology. Breath testing for SIBO (lactulose or glucose hydrogen breath tests) can be useful in the subset of IBS patients whose presentation suggests small intestinal overgrowth. Particularly bloating that peaks post-meal, diarrhea, and poor response to low-FODMAP alone.

IBS runs in families at rates higher than shared environment alone would explain. Twin studies have found higher concordance in monozygotic (identical) twins than dizygotic (fraternal) twins, consistent with a meaningful genetic component. Epidemiological work by Longstreth and others has consistently placed the global prevalence of IBS at roughly 10-15% of the adult population, with a clear familial clustering pattern.

However, no single-gene cause has been identified, and IBS does not follow a Mendelian inheritance pattern. Genome-wide association studies (GWAS) have identified susceptibility loci. Regions of the genome where variation is associated with elevated IBS risk. But each individual variant contributes only a small increment of risk. The identified loci cluster in biologically plausible pathways: genes involved in gut-brain signalling, serotonin metabolism, immune function, intestinal barrier integrity, and stress-response regulation.

The emerging picture is that genetics sets a background vulnerability. A tendency for the gut-brain axis to respond more strongly, for visceral nerves to sensitise more readily, for the stress response to calibrate more reactively. Whether that vulnerability translates into clinical IBS depends on environmental triggers (infection, stress, dietary exposures, life circumstances). Two siblings with similar genetic risk can end up with very different gut health depending on what they encounter across their life course.

Practically, this means family history is a useful data point for assessing likelihood and for calibrating expectations about long-term management. A person with strong family history and multiple affected relatives may find that symptoms flare more readily under stress or dietary indiscretion, even after a successful treatment course. It does not mean IBS is hereditary in the deterministic sense people usually mean by that word.

Food is one of the most consistent symptom triggers in IBS and also one of the most frequently misunderstood. The central clarification: food sensitivities in IBS are generally not food allergies. True food allergy is an IgE-mediated immune response to a protein (peanut, shellfish, etc.), is usually rapid and sometimes dangerous, and is uncommon in IBS. What most IBS patients experience is non-allergic food sensitivity, most often mediated by FODMAPs.

FODMAPs stands for Fermentable Oligosaccharides, Disaccharides, Monosaccharides And Polyols. A group of short-chain carbohydrates that are poorly absorbed in the small intestine. In a healthy gut, these pass to the large intestine where bacteria ferment them, producing gas and short-chain fatty acids without causing significant symptoms. In an IBS gut, the same process produces bloating, pain, and altered motility because of the existing visceral hypersensitivity and altered handling of osmotic load.

The Monash University low-FODMAP protocol. A structured elimination-reintroduction diet. Has strong evidence for reducing IBS symptoms. Peters 2016 (PMID 27397586) is a particularly instructive trial here: the researchers directly compared gut-directed hypnotherapy to the low-FODMAP diet in a randomised design and found them equivalent on GI symptoms, with hypnotherapy superior on psychological outcomes. The two work through different pathways , diet reduces the fermentable substrate reaching the sensitive gut; hypnotherapy reduces the sensitivity itself. Many clients benefit from combining them.

Beyond FODMAPs, some IBS patients report sensitivity to specific foods that do not fit the FODMAP pattern. Caffeine, alcohol, spicy food, high-fat meals, artificial sweeteners, or specific individual foods. These reflect a mix of mechanisms including direct motility effects, gut-brain signalling, and sometimes true non-celiac gluten sensitivity or histamine intolerance. Personalised symptom diaries are more useful than generic lists.

For the relationship between dietary and nervous-system approaches, see low-FODMAP vs hypnotherapy.

The consistent finding that women are roughly twice as likely as men to be diagnosed with IBS is not a coincidence of reporting or help-seeking behaviour. There is a measurable biological signal driven substantially by sex hormones, particularly estrogen and progesterone.

Estrogen and progesterone both modulate gut motility, visceral pain thresholds, and aspects of the gut-brain axis. Estrogen tends to heighten visceral sensitivity; progesterone tends to slow motility. The cyclical interaction of these hormones across the menstrual cycle is why many women report predictable symptom flares around menstruation. Often the days immediately before and during the period, when hormone levels shift sharply. This pattern is well-documented in research and is one of the practical markers clinicians use to assess hormonal contribution.

Perimenopause is another recognised high-risk window. The hormonal variability of perimenopause. Estrogen and progesterone levels fluctuating more widely and unpredictably than during the regular menstrual cycle. Appears to destabilise the gut-brain axis in many women. New-onset IBS or significant worsening of existing IBS during perimenopause is a common clinical presentation. Post-menopause, once hormone levels stabilise at their new lower baseline, symptoms sometimes ease again, though not reliably.

Pregnancy is more variable. Some women with IBS report improvement during pregnancy (possibly from the sustained high progesterone and the anti-inflammatory shift of pregnancy physiology), while others report worsening. Postpartum is often a high-risk period for symptom return or worsening, coinciding with hormonal recalibration, sleep deprivation, and stress.

Men are not exempt from hormonal contributions. Testosterone also modulates gut motility and visceral sensitivity. But the effect size is smaller and the cycling is absent, which likely accounts for a meaningful portion of the male-female prevalence gap. Awareness of the hormonal component is particularly important for women evaluating treatment response, because symptom variation across the cycle can mask or exaggerate perceived treatment benefits if not accounted for.

Given all nine drivers, how is IBS actually diagnosed in my hypnotherapy practice? Since the 2016 publication of Rome IV (Drossman and colleagues), IBS is diagnosed by symptom pattern rather than by imaging or laboratory findings. The Rome IV criteria require recurrent abdominal pain, on average at least 1 day per week in the previous 3 months, associated with 2 or more of: pain related to defecation, change in stool frequency, or change in stool form. Symptoms must have started at least 6 months before diagnosis.

Subtypes. IBS-D, IBS-C, IBS-M, and IBS-U (unclassified). Are assigned based on the predominant stool form on symptomatic days, using the Bristol Stool Scale.

Importantly, Rome IV reframed the entire family of functional GI disorders as "disorders of gut-brain interaction" (DGBI). This was a deliberate shift away from the older "functional" language, which sometimes carried a dismissive connotation ("it's functional" treated as "it's not real"). DGBI explicitly names the gut-brain axis as the organising mechanism.

Before a Rome IV diagnosis of IBS is accepted, clinicians rule out alarm features that could indicate other conditions: unexplained weight loss, blood in stool, fever, nocturnal symptoms waking the patient from sleep, onset over age 50 without prior GI history, family history of colorectal cancer or inflammatory bowel disease, and specific lab abnormalities. Celiac disease, IBD, microscopic colitis, SIBO, and bile acid malabsorption are the most common conditions that can mimic IBS.

A practical implication of Rome IV for patients: a diagnosis of IBS is a positive diagnosis made on symptom pattern, not a diagnosis of exclusion arrived at by process of elimination after every test comes back normal. If alarm features are absent and the Rome IV symptom pattern is present, IBS can be confidently diagnosed without exhaustive testing. Clinicians increasingly treat a Rome IV-confirmed IBS diagnosis as a definitive starting point for targeted treatment rather than a temporary label to be revised once something else gets found.

With nine drivers on the table, a reasonable question is: which of them does gut-directed hypnotherapy actually address? The honest clinical answer is that it directly targets the two most central drivers. Gut-brain axis dysregulation and visceral hypersensitivity. And indirectly modulates several others through improved vagal tone and normalised stress physiology.

What the research supports:

• Directly retrains: gut-brain signalling, central sensitisation of visceral pain, vagal tone, stress-response reactivity.
• Indirectly improves: motility (via autonomic normalisation), microbiome (via downstream effects on stress and eating patterns), food tolerance (via reduced visceral sensitivity).
• Does not directly change: genetic predisposition, microbiome composition in a targeted way, structural motility abnormalities, hormonal cycling, or underlying FODMAP malabsorption.

This is why the evidence base shows robust effect sizes. Miller 2015 (PMID 25736234) reported 76% response in 1,000 IBS patients on the Manchester Protocol, with benefits persisting at 5-year follow-up. But also why hypnotherapy is not a universal answer. For clients whose IBS is dominated by motility abnormalities, suspected SIBO, hormonal cycling, or specific food sensitivity, combining hypnotherapy with treatments targeting the other drivers tends to produce the best outcomes.

Peters 2016 (PMID 27397586) found that gut-directed hypnotherapy was equivalent to the low-FODMAP diet on GI symptom reduction and superior on psychological outcomes, reinforcing that the two work on different drivers. The Manchester Protocol (which this clinic follows) is the structural basis for most modern clinician-delivered programs, and the protocol itself is consistent with the mechanistic picture above.

One additional mechanism worth noting: clinical research has shown that gut-directed hypnotherapy appears to reduce the cognitive and attentional component of visceral pain as well as the sensory component. Patients often report that, after a full protocol, the gut sensations that remain feel less threatening and less cognitively intrusive, even when they are not entirely absent. This aligns with the broader research picture that central processing of visceral signals. Not just the signals themselves. Is a key part of the IBS experience, and that retraining that processing is what meaningful treatment often involves.

The nine drivers above rarely appear in isolation. A typical adult presenting with IBS will have two to four of them actively contributing. Common combinations include:

• Post-infectious origin + persistent visceral hypersensitivity + stress amplification (common IBS-D pattern)
• Chronic stress + altered motility + FODMAP sensitivity (common mixed-type pattern)
• Early-life adversity + gut-brain dysregulation + hormonal cycling (common presentation in women, often with perimenopause flares)
• Genetic predisposition + microbiome disruption after antibiotic course + stress at onset (common IBS-C pattern)

Clinically, working out which drivers are most active for a given person is what makes treatment more effective than one-size-fits-all protocols. A careful intake . Timeline of onset, relationship to infections, stress history, family history, dietary patterns, hormonal patterns, sleep and autonomic signs. Usually makes the dominant drivers visible within one or two sessions.

This is also why the "what caused my IBS?" question is worth asking, but the more useful version is "which of the nine drivers are most active for me right now, and what targets each of them?"

One final framing that the research consistently supports: IBS is a condition of altered system regulation rather than permanent system damage. This matters because it means meaningful improvement is possible for most people, even decades into the condition. The Miller 2015 audit documented sustained benefit at 5-year follow-up in the majority of gut-directed hypnotherapy responders, including patients who had lived with refractory IBS for 10, 15, or 20 years before treatment. Longstreth and other epidemiologists have documented that a meaningful fraction of people diagnosed with IBS experience natural remission over time. Put together, the picture is not one of a fixed, degenerative disease. It is one of a dysregulated system that can be retrained, with the success rate depending heavily on whether the right combination of drivers is being addressed.

Related reading: Hypnotherapy for IBS · The gut-brain connection · Visceral hypersensitivity · IBS and anxiety · Low-FODMAP vs hypnotherapy