The Power of the Mind‑Gut Axis: Psychological Factors in Gastrointestinal Disorders
Introduction
The mind‑gut axis refers to the bidirectional communication network that links the central nervous system (CNS) and the gastrointestinal (GI) tract. This network involves neural (vagus and autonomic nerves), endocrine (hypothalamic–pituitary–adrenal, or HPA, axis), immune and metabolic pathways [1]. Growing evidence indicates that the gut microbiota plays a crucial role in this communication, modulating both physical and mental health [2]. The significance of this axis is underscored by the high burden of functional and inflammatory GI disorders: irritable bowel syndrome (IBS) affects around 4–10 % of the global population, with a two‑fold predominance in women [3], and inflammatory bowel disease (IBD) is a chronic immune‑mediated disorder causing significant morbidity. Importantly, IBS and IBD are strongly associated with psychological comorbidities. Meta‑analyses report that approximately 39 % of individuals with IBS suffer from anxiety and 29 % from depression [4], and one‑third of IBD patients experience anxiety while nearly one‑quarter have depression [5]. Furthermore, around 25 % of IBD patients exhibit moderate to severe post‑traumatic stress disorder (PTSD) [6]. This article argues that psychological factors—including stress, mood disorders, trauma and early life adversity—modulate gut physiology and symptom perception in GI disorders. Integrating psychotherapeutic approaches with standard medical care can therefore enhance patient outcomes.
Background and Literature Review
Key Definitions
Mind–gut axis – The overarching term describing bidirectional communication between the brain and the GI tract via neural, endocrine, immune and metabolic pathways [7].
Gut–brain–microbiota axis – A specific aspect of the mind‑gut axis emphasising the role of the gut microbiota and its metabolites in neural, immune and hormonal signaling [8].
HPA axis – A major neuroendocrine system activated by stress; corticotropin‑releasing factor (CRF) released from the hypothalamus stimulates adrenocorticotropic hormone (ACTH) secretion from the pituitary, leading to cortisol release from the adrenal cortex [1].
Historical Development of the Mind–Gut Concept
Links between emotions and digestive function were recognised as early as Hippocrates and Galen. Nineteenth‑century physicians introduced the notion of “nervous dyspepsia”, implicating the nervous system in digestive complaints. Formal psychogastroenterology emerged in the mid‑1980s when British clinicians trialled gut‑directed hypnotherapy for refractory IBS. Cognitive behavioural therapy (CBT) was adapted for IBS in the 1990s, and subsequent decades have seen rapid growth in brain–gut behavioural therapies (BGBTs) and neuroimaging studies demonstrating altered brain activity in IBS [1]. Advances in microbiome science and psychoneuroimmunology now allow integration of microbial, immune and neuroendocrine mechanisms.
Epidemiology of Gastrointestinal Disorders and Mental‑Health Comorbidities
IBS is one of the most common disorders of gut–brain interaction. Using Rome IV diagnostic criteria, prevalence is estimated at 4 % globally; earlier Rome III criteria yield figures closer to 10 %, with women being twice as likely to be affected [3]. Meta‑analyses show that 39 % of IBS patients experience anxiety symptoms and 29 % depressive symptoms [4], and up to 50–90 % have some psychiatric comorbidity [9]. IBD (comprising Crohn’s disease and ulcerative colitis) is less common (about 0.3–0.5 % prevalence in Western populations) but has marked psychological burden; around one‑third of patients report anxiety and nearly one‑quarter report depression [5]. Mental health conditions correlate with disease activity and quality of life, and PTSD related to medical trauma is present in approximately 25 % of IBD patients [6]. Across GI disorders more broadly, around 60 % of patients have psychiatric disorders, predominantly anxiety and depression [10].
Theoretical Frameworks
Several models explain how psychological factors influence GI physiology:
HPA axis dysregulation – Stress activates hypothalamic CRF, stimulating ACTH and cortisol release. Sustained cortisol alters intestinal permeability, motility and immune responses [11]. CRH administration has been shown to increase gut motility, whereas CRH antagonists reduce this effect [1].
Autonomic nervous system and vagal pathways – Stress enhances sympathetic activity and suppresses parasympathetic (vagal) tone, leading to dysbiosis, increased gut permeability and low‑grade inflammation [12]. Vagus‑nerve stimulation activates the “cholinergic anti‑inflammatory reflex”, dampening inflammation and improving mood and GI symptoms [13].
Microbiota–gut–brain axis – Gut microbes produce neuroactive compounds (e.g., serotonin, gamma‑aminobutyric acid) and modulate cytokine production. Dysbiosis may trigger immune activation and alter neural signaling [8]. Psychobiotic probiotics can restore microbial balance and influence neural and hormonal pathways [2].
Neuroimmune interactions – Psychological stress induces mast‑cell degranulation and cytokine release, resulting in neuroinflammation. Animal studies show antidepressants can reduce colitis and neuroinflammation [14].
Pathophysiological Mechanisms
Chronic stress elevates CRF, ACTH and cortisol, increasing gut permeability and motility, disrupting the mucosal barrier and promoting bacterial translocation [11]. Sympathetic dominance and vagal inhibition lead to dysbiosis and inflammation [12]. Dysbiosis alters microbial metabolites and immune responses, which in turn influence neurotransmission and mood. In IBD, neuroinflammation and impaired hippocampal neurogenesis occur. Epigenomic modifications triggered by early life stress can persistently alter HPA regulation and gene expression (e.g., methylation of the glucocorticoid receptor gene NR3C1) [15]. Early life stress is associated with lasting changes in gut motility, barrier function and microbiota composition [15], making individuals more susceptible to GI disorders. Antidepressants have been shown in animal models to reduce colitis and inflammatory markers [14].
Current Research Gaps
Research is limited by heterogeneous diagnostic criteria, small sample sizes and variation in intervention modalities. Many studies are conducted in Western populations, leaving cultural and socioeconomic diversity underexplored. Long‑term follow‑up data on psychological interventions are scarce. Additionally, gastroenterologists frequently neglect mental health assessment [16], resulting in underdiagnosis of psychological comorbidities.
Methodology and Analytical Approach
This narrative review synthesises evidence from peer‑reviewed literature published up to July 2025. Searches were conducted in PubMed/MEDLINE, Web of Science, Scopus and Google Scholar using keywords such as irritable bowel syndrome, inflammatory bowel disease, gut‑brain axis, stress, anxiety, depression, epigenetic, psychobiotic, cognitive behavioural therapy, and hypnotherapy. Inclusion criteria encompassed randomised controlled trials, observational studies, systematic reviews and narrative reviews relating to psychological factors and GI disorders. Non‑English language studies, paediatric‑only studies, case reports and conference abstracts were excluded. Data were extracted on study design, sample size, interventions, outcomes and effect sizes. Methodological quality was assessed using the Cochrane risk‑of‑bias tool for RCTs and the Newcastle–Ottawa scale for observational studies. Where heterogeneity precluded meta‑analysis, findings were summarised qualitatively. The article employs an integrative analytical framework to connect psychological constructs with physiological mechanisms and clinical outcomes.
Psychological Factors in Gastrointestinal Disorders
Stress
Stress is a ubiquitous psychological factor implicated in the onset and exacerbation of GI disorders. Acute stressors (e.g., public speaking, medical procedures) transiently activate the HPA axis; chronic stress leads to sustained elevations of CRF, ACTH ,and cortisol [11]. These hormones increase gut permeability and motility, disrupt tight junction proteins and facilitate bacterial translocation, contributing to visceral hypersensitivity and inflammation. CRH administration in experimental models increases gut motility, while CRH antagonists mitigate this response [1]. Observational studies show that stress exacerbates IBS symptoms and can precipitate flares in IBD. Stress also promotes unhealthy eating patterns and alters microbiota composition [17]. Interventions that reduce stress—such as CBT, mindfulness and exercise—improve GI symptoms and quality of life.
Anxiety and Depression
Anxiety and depression are highly prevalent among individuals with IBS and IBD. Meta‑analyses indicate that 39 % of IBS patients have anxiety symptoms and 29 % have depressive symptoms [4]. In IBD, approximately one‑third of patients experience anxiety and one‑quarter have depression [5]. Longitudinal studies reveal a bidirectional relationship: pre‑existing anxiety or depression increases the risk of developing IBS [4], while chronic GI symptoms contribute to the onset or worsening of mood disorders. Neuroimaging shows altered activity in limbic regions (amygdala, anterior cingulate cortex and insula) and dysregulated connectivity between cortical and visceral processing areas in IBS [1]. Dysregulation of the HPA axis, increased pro‑inflammatory cytokines and gut dysbiosis are shared mechanisms underlying both mood disorders and GI dysfunction. Antidepressant therapy can alleviate depressive symptoms and may reduce intestinal inflammation [14].
Post‑Traumatic Stress Disorder and Hypervigilance
PTSD is common among patients with severe GI disorders; about 25 % of IBD patients exhibit PTSD related to disease flares, surgeries or medical trauma [6]. Individuals with PTSD often display hypervigilance to visceral sensations and heightened interoceptive awareness, amplifying pain perception and contributing to central sensitisation. Similar patterns of trauma and hypervigilance are observed in a subset of IBS patients. Trauma‑informed care and therapies addressing fear and avoidance (e.g., exposure therapy, ACT) may benefit these patients.
Early Life Stress and Adverse Childhood Experiences
Adverse childhood experiences (ACEs) such as abuse, neglect and maternal stress have lasting effects on the brain‑gut axis. Trauma early in life can disrupt HPA axis regulation and lead to epigenetic modifications (e.g., methylation of NR3C1) that influence stress responsivity [15]. Early life stress is associated with changes in gut motility, barrier function and microbiota composition [15]. Animal models show that neonatal maternal separation induces visceral hypersensitivity and alters Toll‑like receptor 4 and neurokinin 1 receptor signalling [18]. Cohort studies link early adverse exposures (e.g., maternal high‑fat diet, caesarean delivery, antibiotic use, low birth weight) to increased risk of IBS later in life [19]. These findings underscore the importance of early life interventions and highlight potential epigenetic targets for therapy.
Stigma, Body Image and Quality of Life
Patients with IBS and IBD often face stigma due to unpredictable bowel symptoms, dietary restrictions and social embarrassment. A 2024 cross‑sectional study reported that individuals with IBS exhibited greater psychological distress, lower body appreciation and higher self‑criticism compared with controls [20]. Stigma arises from the unpredictability of symptoms and a perceived lack of empathy from peers and clinicians, leading to fear, shame and embarrassment [21]. Negative body image and self‑criticism mediate the relationship between IBS and depression/anxiety [20]. Addressing stigma and body image concerns through psychoeducation and support groups can improve adherence and quality of life.
Socioeconomic and Cultural Factors
Prevalence and perception of GI disorders vary across cultures and socioeconomic strata. A 2022–2023 U.S. community health survey found that IBS prevalence was highest among non‑Hispanic whites (10 %), lower among Hispanics (5 %), non‑Hispanic Black individuals (4 %) and other racial groups (3 %). Female sex was associated with higher odds of IBS, while non‑white race was associated with lower odds [22]. These disparities may reflect differences in symptom reporting, healthcare access, cultural stigma and diagnostic patterns. Women and individuals with limited social support report greater psychological burden [23], underscoring the need for culturally sensitive interventions and improved access to mental health care.
Summary of Psychological Factors
Stress, anxiety, depression, PTSD, early adversity, stigma and socioeconomic factors interact synergistically to influence GI symptom perception, coping strategies and disease progression. These factors modulate the HPA axis, autonomic nervous system and microbiota, reinforcing the need for integrated care. Psychological distress may exacerbate intestinal inflammation and visceral hypersensitivity, while chronic GI symptoms may precipitate or worsen mood disorders. Recognising these interactions is essential for tailoring interventions.
Therapeutic Interventions and Their Efficacy
Brain–Gut Behavioural Therapies (BGBTs)
BGBTs encompass CBT, gut‑directed hypnotherapy, mindfulness‑based stress reduction and acceptance and commitment therapy (ACT). These therapies aim to modify maladaptive thoughts, reduce catastrophising, enhance coping skills and regulate physiological stress responses. Randomised controlled trials demonstrate that BGBTs provide clinically meaningful improvements in IBS symptoms. A systematic review of eight RCTs (n = 464) reported that gut‑directed hypnotherapy achieved symptom relief with a relative risk (RR) of 1.69 and a number needed to treat of five [24]. A meta‑analysis of six RCTs (n = 639) found that the risk of remaining symptomatic after hypnotherapy was 0.73 compared with education/support and 0.67 compared with waiting lists [24]. Long‑term follow‑up studies show that 71 % of patients respond to hypnotherapy initially and 81 % maintain improvement [25]. Self‑guided and minimal‑contact CBT are as effective as standard CBT, making them suitable for telehealth delivery. ACT trials in IBS and IBD populations show improvements in psychological flexibility and anxiety, though effects on depression are modest [26].
Mechanistically, BGBTs normalise activity in brain regions involved in pain modulation (e.g., anterior cingulate cortex) and may modulate gut microbiota and inflammatory markers. They are generally safe, with minimal adverse effects.
Hypnotherapy and Guided Imagery
Gut‑directed hypnotherapy is recommended as a second‑line treatment for IBS when first‑line diet and pharmacological therapies fail. Controlled trials and meta‑analyses demonstrate superior symptom improvement compared with education/support, with sustained benefits up to a year [24]. Large clinical series report response rates exceeding 75 %, even in patients refractory to medical therapy [25]. Group hypnotherapy and nurse‑delivered formats are as efficacious as individual therapy [27]. Digital audio programs and tele‑hypnotherapy expand access but may face adherence challenges. Hypnotherapy is associated with improved psychological wellbeing and extraintestinal symptoms.
Psychopharmacology and Psychobiotics
Antidepressants and Anxiolytics
Tricyclic antidepressants (e.g., amitriptyline), selective serotonin reuptake inhibitors (SSRIs) and serotonin–noradrenaline reuptake inhibitors (SNRIs) are commonly used off‑label for IBS and IBD. They modulate central pain processing, enhance descending inhibition, regulate bowel motility and exert anti‑inflammatory effects. A 2024 systematic review and meta‑analysis of RCTs concluded that antidepressants provide overall benefit for depressive symptoms and quality of life in IBD compared with placebo, with SNRIs (e.g., duloxetine, venlafaxine) showing particular improvement in anxiety [28]. However, evidence is limited by small sample sizes and heterogeneity, and large placebo‑controlled trials are needed. Animal studies demonstrate that antidepressants reduce colitis and neuroinflammation [14]. Clinicians should weigh benefits against potential adverse effects (e.g., anticholinergic effects of tricyclics) and consider comorbid mood disorders when prescribing.
Psychobiotics and Prebiotics
Psychobiotics are probiotic strains that influence mental health by modulating the microbiota–gut–brain axis. They restore microbial balance, enhance barrier integrity, reduce pro‑inflammatory cytokines and produce neuroactive compounds (such as gamma‑aminobutyric acid and serotonin) [2]. The World Gastroenterology Organisation suggests that appropriate probiotic therapy can alleviate IBS symptoms, mainly by reducing bloating and improving bowel rhythm [29]. Evidence supports specific strains: Lactiplantibacillus plantarum 299v improves IBS symptoms and reduces anxiety and depressive states [29]; Bifidobacterium infantis 35624, Lactobacillus rhamnosus NCIMB 30 174 and Saccharomyces boulardii CNCM I‑745 have documented benefits [29]. Psychobiotics that may reduce stress‑induced GI complaints include Lactobacillus helveticus R0052 and Bifidobacterium longum R0175 [29]. Prebiotics (non‑digestible fibres that promote beneficial bacteria) and synbiotics (probiotic + prebiotic combinations) are being studied but evidence is preliminary. Fecal microbiota transplantation (FMT) has shown mixed results in IBS and is not recommended outside clinical trials.
Integrative and Personalised Medicine
Optimal management of GI disorders requires a biopsychosocial approach integrating diet, physical activity, stress management and psychological therapy. Dietary interventions include the low‑FODMAP diet, which reduces fermentable oligosaccharides, disaccharides, monosaccharides and polyols and is effective in reducing IBS symptoms [30]. Exercise and sleep hygiene improve overall wellbeing. Mindfulness‑based stress reduction and yoga have shown benefits in small trials. Personalised medicine approaches that combine genetic, microbiota and psychological profiles aim to tailor interventions. For example, identifying dysbiotic patterns may inform choice of psychobiotics or diet modifications. Wearable devices and mobile apps can monitor symptoms and stress responses, enabling just‑in‑time interventions.
Implementation Challenges and Access
Barriers to integrating psychological therapies into GI care include limited availability of trained psychogastroenterologists, time constraints in busy clinics, cost and insurance coverage and cultural stigma surrounding mental health. Clinicians may lack training and confidence to address psychological issues [16]. Telehealth and digital platforms for CBT, hypnotherapy and ACT can overcome geographical barriers. Group-based interventions and nurse‑delivered programs reduce costs and improve scalability [27]. Integration of mental health professionals into GI clinics and collaborative care models are essential.
Case Studies and Clinical Vignettes
Case 1 – A 35‑year‑old woman with diarrhoea‑predominant IBS experienced severe anxiety and fear of leaving the house. She underwent CBT focusing on cognitive restructuring, relaxation training and exposure to feared situations. After twelve sessions, her IBS Severity Scoring System (IBS‑SSS) score decreased by 70 points and anxiety symptoms improved. She also commenced a low‑FODMAP diet and resumed physical activity.
Case 2 – A 40‑year‑old man with ulcerative colitis and PTSD following emergency colectomy reported nightmares and hypervigilance. ACT emphasising values-driven action and acceptance of symptoms, combined with trauma‑informed psychotherapy, reduced his avoidance behaviours and improved his quality of life. He started duloxetine, which alleviated depressive symptoms and reduced intestinal inflammation.
These cases illustrate the need for psychological assessment and individualised therapy in GI care.
Ethical and Cultural Considerations
Delivering psychological interventions requires informed consent, respect for patient autonomy and confidentiality. Clinicians should avoid pathologising normal emotional responses and recognise cultural differences in symptom expression and help‑seeking behaviour. Some cultures may attribute GI symptoms to spiritual or environmental factors; culturally sensitive psychoeducation is vital. Telehealth interventions must ensure data security and privacy. Practitioners should be aware of potential biases when interpreting symptom reports across cultures and socioeconomic backgrounds.
Critical Analysis and Discussion
The evidence base for BGBTs and psychobiotics has grown substantially, with multiple RCTs showing moderate effect sizes and long‑term benefits [31] [2]. Psychobiotics offer a promising adjunct to dietary therapy but require further high‑quality trials. Antidepressants can improve mood and quality of life in IBD [28]; however, small sample sizes and heterogeneity limit generalisability. Placebo effects are substantial in IBS trials, emphasising the need for rigorous blinding. Many studies exclude patients with severe psychiatric illness or comorbid functional pain syndromes, limiting external validity. Research is predominantly Western; cross-cultural investigations are needed. Longitudinal data on the durability of psychological treatments and their impact on disease progression are scarce. Importantly, the mind‑gut axis model discourages dichotomising “psychological” versus “organic” causes, advocating a biopsychosocial perspective.
Implications for Clinical Practice
Routine mental health screening – GI clinics should incorporate validated tools (e.g., Hospital Anxiety and Depression Scale, PTSD Checklist) to identify anxiety, depression and PTSD. Early identification facilitates timely referral and intervention.
Interdisciplinary collaboration – Gastroenterologists should work closely with psychologists, dietitians and primary‑care providers. Patients with moderate to severe psychological symptoms should be referred to mental health professionals.
Tailored treatment plans – Interventions should consider individual psychological profiles, gender, cultural background and socioeconomic context. Women and individuals with limited social support may require additional resources [23].
Education and destigmatisation – Educating patients about the mind‑gut axis helps legitimise psychological interventions and reduces stigma. Support groups and patient education materials should emphasise the normalcy of stress responses and the potential for symptom improvement with therapy.
Use of digital tools – Telehealth delivery of CBT, hypnotherapy and ACT can expand access, particularly in rural areas. Mobile apps for symptom tracking and stress management may enhance adherence.
Monitoring and follow‑up – Clinicians should monitor treatment response and adjust therapy accordingly. Shared decision‑making fosters adherence and empowers patients.
Future Directions and Research Gaps
Large, high‑quality RCTs – Trials with robust blinding and adequate power are needed to evaluate BGBTs, psychobiotics and antidepressants in IBS and IBD. Subgroup analyses should explore differential responses based on microbiota profiles, genetic polymorphisms and psychological phenotypes.
Mechanistic studies – Integrative omics (metabolomics, microbiomics, epigenomics) should elucidate how psychological interventions modulate the gut microbiota, immune responses and neural circuits. Studies should examine how epigenetic modifications from early life stress influence treatment responsiveness.
Digital therapeutics – Development and evaluation of digital platforms delivering personalised CBT, ACT and hypnotherapy are needed, including wearable devices that provide real‑time stress feedback.
Early intervention and resilience – Prospective cohorts should examine how interventions targeting early life stress or enhancing resilience (e.g., parent–infant bonding programs, social support) affect GI disease risk.
Cross‑cultural research – Future studies should include diverse populations to ensure generalisability. Socioeconomic determinants of access to psychogastroenterology services must be addressed.
Neuromodulation and epigenetics – Emerging therapies such as vagus nerve stimulation, sacral nerve stimulation and transcranial magnetic stimulation have potential to modulate the mind‑gut axis. Understanding how these interventions interact with epigenomic processes may open new therapeutic avenues [15] [32].
Conclusion
The mind‑gut axis highlights the intricate interplay between psychological processes and gastrointestinal physiology. Stress, mood disorders, trauma and early life adversity influence gut motility, permeability, immune responses and the microbiota. Psychological comorbidities are highly prevalent in IBS and IBD, and they significantly impact quality of life and disease outcomes [4] [5]. Integrating psychological assessment and brain–gut therapies into standard GI care can improve symptom control, reduce healthcare utilisation and enhance patient wellbeing. BGBTs, hypnotherapy, psychobiotics and antidepressants offer evidence‑based options; however, individualised care and long‑term follow‑up are essential. A biopsychosocial model that acknowledges cultural and socioeconomic factors should guide clinical practice. Future research should focus on high‑quality trials, mechanistic insights, digital therapeutics and strategies to address early life stress. By recognising the power of the mind‑gut axis, medical practitioners can deliver holistic care that addresses both the psychological and physiological dimensions of GI disorders.
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