Copyright: ©Author(s) 2026.
Artif Intell Gastroenterol. Nov 8, 2026; 7(3): 127488
Published online Nov 8, 2026. doi: 10.35712/aig.127488
Published online Nov 8, 2026. doi: 10.35712/aig.127488
Table 1 Summary of representative artificial intelligence studies in irritable bowel syndrome, with evidence grade
| Ref. | AI method and task | Population and sample size | Primary outcome definition | Validation approach | Reported performance and uncertainty | Events or responders reported | Evidence grade | Key limitation |
| Maslekar et al[19], 2010 | Artificial neural network; predict organic pathology to prioritise colonoscopy | 300 unselected colorectal-clinic attendees; no IBS cohort | Positive finding at lower gastrointestinal endoscopy (polyp, cancer, diverticular disease or colitis) | Internal validation plus external set of 50 patients | 95% training; 90% internal validation (95%CI: 84-96) vs 75% clinical assessment; 89% external | Not reported | Indirect | Non-IBS population; predates modern validation standards |
| Tap et al[21], 2017 | Supervised discriminant analysis; microbiota signature of symptom severity | IBS patients and controls; faecal and mucosal microbiota | IBS symptom severity category (severe vs mild-to-moderate) | Internal only | 90-OTU signature tracking severity, independent of bowel-habit subtype; no discrimination metric reported | Not reported | Direct | Association only; not a diagnostic model |
| Vervier et al[28], 2022 | Unsupervised metagenomic stratification; subtypes and low-FODMAP response | IBS patients; shotgun metagenomics | Metagenomic subtype assignment (IBSP/IBSH) and symptom response to low-FODMAP diet | Internal only | Greater FODMAP response in IBSP (P = 0.02); no AUC or confidence interval reported | Not reported | Direct | Small cohort; requires external validation |
| Mars et al[10], 2020 | Longitudinal multi-omics integration; subset-specific mechanisms | IBS-C, IBS-D and controls; serial multi-omics | Not applicable; mechanistic analysis with no prediction target | Not applicable | Purine metabolism identified as a host-microbial pathway; no predictive metric | Not applicable | Direct | Mechanistic; no predictive classifier derived |
| Kraszewski et al[17], 2021 | Random forest; classify IBD from routine laboratory markers | 702 records (Crohn’s, ulcerative colitis, non-inflammatory controls); no IBS patients | Crohn’s disease or ulcerative colitis vs non-inflammatory control status | Internal discovery cohort only | Mean average precision 97% (Crohn’s), 91% (ulcerative colitis); no confidence intervals reported | 702 records from 372 patients (192 Crohn’s disease, 180 ulcerative colitis) | Indirect | No IBS group; not a test of IBS discrimination |
| Bennet et al[41], 2018 | Multivariate model; predict low-FODMAP responsiveness | 61 IBS patients analysed; faecal bacterial profiles | Responder defined as a reduction in IBS-SSS of at least 50 points | None | Responders discriminated from non-responders; no sensitivity, specificity or AUC reported | 61 of 67 randomised patients analysed; responder counts not reported by arm | Direct | No discrimination metrics; no external validation |
| Chumpitazi et al[42], 2015 | Association analysis; baseline taxa and low-FODMAP response | 33 children with IBS; 48-hour crossover diet periods | Responder defined as at least 50% reduction in abdominal pain frequency | None | Responders enriched at baseline for saccharolytic taxa; no discrimination metric reported | 33 children; 48-hour diet periods with 5-day washout | Direct (paediatric) | No predictive model; direction of effect discordant with Bennet et al[41] |
| Su et al[30], 2026 | Deep learning; donor-recipient microbiome matching for FMT | 515 FMTs, 30 cohorts, 12 indications including IBS | Clinical response following faecal microbiota transplantation | Retrospective simulation across cohorts | AUC 0.88; 78.7% outcome accuracy; simulated response 49%→71%; no confidence intervals reported | 515 FMTs across 30 cohorts and 12 indications | Indirect | Not IBS-specific; retrospective and simulated, not prospective |
| Dowrick et al[14], 2024 | Unsupervised machine learning; subtyping disorders of gut-brain interaction | Population symptom data | Not applicable; evaluates stability of unsupervised subtypes | Not applicable | Demonstrates instability of data-driven subtyping | Not applicable | Direct (DGBI) | Cautionary; subgroups sensitive to methodological choice |
| Bhagavathula et al[18], 2025 | Systematic review; diagnostic accuracy of AI in IBS | 6 studies; 1366 participants | Diagnostic accuracy of AI models against the reference IBS diagnosis | Not applicable (systematic review) | Accuracy 54%-98%; AUC 0.61-0.99 across studies; meta-analysis not feasible | 6 studies; 1366 participants | Direct (review) | Few studies; variable biomarkers and validation |
Table 2 Artificial intelligence methods and their current status in irritable bowel syndrome
| Method family | Core principle | Typical application | Current status in IBS |
| Supervised learning (random forest, support vector machine, gradient boosting) | Learns a mapping from labelled examples to a defined outcome | Diagnostic classification; treatment-response prediction | The most common approach; small single-centre cohorts, little external validation |
| Unsupervised learning (clustering, latent class and mixture models) | Identifies structure without predefined labels | Subtype and endotype discovery | Applied to microbiota and symptom subgrouping; subgroup stability sensitive to method |
| Deep learning - convolutional neural networks | Hierarchical feature learning from images | Endoscopic image analysis; optical histology prediction | Established in luminal endoscopy; minimal role in functional disease |
| Deep learning - recurrent networks and transformers | Models sequential or multi-modal data | Longitudinal risk prediction from clinical records | Demonstrated in general clinical records; no published IBS application |
| Natural language processing and large language models | Extracts structured information from free text | Symptom and outcome extraction from notes and narratives | Demonstrated in inflammatory bowel disease; not yet reported in IBS |
| Reinforcement learning | Optimises sequential decisions from outcome feedback | Adaptive treatment protocols | Conceptual only in IBS; demonstrated in critical care |
Table 3 Key challenges to clinical translation of artificial intelligence in irritable bowel syndrome and corresponding mitigation strategies
| Challenge | Why it matters for IBS | Mitigation strategies |
| Data standardization | Heterogeneous diagnostic criteria, symptom instruments, and sequencing protocols limit generalizability | Rome Foundation frameworks; harmonized data-collection standards; shared microbiome pipelines |
| Model interpretability | “Black-box” predictions are hard for clinicians to trust or act on | Explainable AI (SHAP values, attention visualization); prefer interpretable models for high-stakes decisions |
| External validation | Most models are single-center; performance may not transfer across settings | Independent multi-region cohorts; temporal validation; TRIPOD+AI-compliant reporting |
| Privacy, consent & bias | Sensitive microbiome and psychological data; non-representative data can entrench disparities | GDPR/HIPAA-aligned governance; federated learning; fairness audits on representative datasets |
| Cost-effectiveness | Development and maintenance are costly; value must be demonstrated | Health-economic modeling; evidence of reduced diagnostic delay and unnecessary colonoscopy |
| Regulatory landscape | Adaptive and continuously learning tools face evolving oversight | FDA software-as-a-medical-device pathways; predetermined change-control plans; harmonized standards |
| Patient acceptance and trust | Concerns about bias, transparency, and loss of human connection shape adoption | Transparency, clinician-in-the-loop design, patient education; dedicated acceptance studies |
Table 4 Proposed minimum design and reporting standards for future artificial intelligence studies in irritable bowel syndrome
| Domain | Minimum standard proposed | Why it matters in IBS |
| Intended use | State the clinical question, target population, care setting and the decision the model informs; specify whether it is diagnostic, prognostic or predictive of treatment response | Most IBS models report discrimination without stating the decision they are intended to support |
| Reference standard | Define how labels were assigned (Rome IV criteria with documented exclusion of organic disease), who applied them and whether assessment was blinded | IBS has no biomarker, so label uncertainty is inherited directly by any supervised model |
| Data elements | Pre-specify candidate features and their provenance; report missing data and how it was handled; for microbiome data report extraction, sequencing and bioinformatic pipeline | Technical factors are a dominant source of microbiome variance and differ between centres |
| External validation | Evaluate in at least one cohort independent of the development cohort in geography and recruitment pathway | Reported IBS models are overwhelmingly validated internally only |
| Temporal validation | Test stability over time and across changes in diagnostic criteria, symptom instruments and sequencing protocols | The shift from Rome III to Rome IV alters both prevalence and case mix |
| Calibration | Report calibration slope and intercept, or a calibration plot, alongside discrimination | Calibration determines whether a predicted probability of treatment response can be acted upon; it is almost never reported |
| Fairness | Report performance across sex, age, ethnicity and socioeconomic strata, and state explicitly any outcome proxy used in place of the outcome of interest | The evidence base is geographically narrow and IBS cohorts are predominantly female |
| Prospective impact | Before adoption, evaluate the effect on clinical decisions, resource use and patient outcomes in a prospective comparative design | No prospective impact study has been undertaken in IBS |
| Reporting standards | Report to TRIPOD+AI[58]; appraise risk of bias with PROBAST+AI[59]; follow DECIDE-AI[60] for early clinical evaluation | Aligns IBS work with current reporting norms for AI prediction models |
- Citation: Issa IA, Issa T. Role of artificial intelligence in irritable bowel syndrome: A narrative review. Artif Intell Gastroenterol 2026; 7(3): 127488
- URL: https://www.wjgnet.com/2644-3236/full/v7/i3/127488.htm
- DOI: https://dx.doi.org/10.35712/aig.127488