Bidirectional Associations Between Anxiety and Gastrointestinal Disorders: A Retrospective Cohort Study Using the TriNetX Database
Zachary Li, Leah Morgan, Taylor M Gong, Manasa Mula, Eduardo Espiridion
TL;DR
This study finds that anxiety and irritable bowel syndrome are strongly linked in both directions, but the same isn't true for anxiety and inflammatory bowel disease.
Contribution
Quantifies bidirectional associations between anxiety and GI disorders using a large real-world dataset.
Findings
Anxiety increases IBS risk by 2.7-fold and IBD risk by 1.6-fold.
IBS increases anxiety risk by 2.2-fold, but IBD does not significantly increase anxiety risk.
Strong gut-brain axis and neuroimmune interactions are implicated in anxiety and IBS.
Abstract
Introduction: Irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) are common gastrointestinal (GI) disorders often linked with anxiety and depression. IBS is defined by recurrent abdominal pain and altered bowel habits without a detectable organic disease, whereas IBD involves chronic, relapsing intestinal inflammation. Bidirectional communication through the gut-brain axis, gut dysbiosis, neuroimmune interactions, and shared genetic susceptibility may underlie these associations. This study aims to quantify and compare the bidirectional associations between anxiety and IBS or IBD using a large, real-world multicenter dataset. Methods: A retrospective cohort study was conducted using TriNetX, a global network of de-identified electronic health records from over 100 healthcare organizations. Adults diagnosed with anxiety disorders, IBS, and IBD between January 1, 2021,…
Genes, proteins, chemicals, diseases, species, mutations and cell lines named across the full text — each resolved to its canonical identifier and authoritative record.
| Category | Codes Used | Rationale |
| Anxiety disorders | ICD-10: F41.9 | Cohort inclusion for bidirectional analysis |
| Irritable Bowel Syndrome | ICD-10: K58 | Cohort inclusion for bidirectional analysis |
| Inflammatory Bowel Disease | ICD-10: K50–K51 | Cohort inclusion for bidirectional analysis |
| Psychiatric Exclusions | ICD-10: F31, F20–F29 | Exclusion criteria: confounders affecting anxiety/GI outcomes |
| GI Condition Exclusions | ICD-10: K90.0, C19 | Exclusion criteria: prevent confounding with major GI disease |
| Infectious GI disease | ICD-10: A00–A09 | Exclusion criteria: prevent post-infectious IBS/anxiety bias |
| Medication Exclusions | Antidepressants (NLM:VA:CN600) Benzodiazepines/sedatives (NLM:VA:CN302) Antipsychotics (ATC:N05A) Opioids (NLM:VA:CN101) | Exclusion criteria: avoid pharmacologic confounding |
| Prior diagnosis of outcome | Outcome-specific ICD-10 codes | Exclusion criteria: Ensure temporal clarity |
| Characteristic | Analysis 1: Anxiety → IBS + IBD Cohorts | Analysis 2: IBS → Anxiety Cohorts | Analysis 3: IBD → Anxiety Cohorts |
| Sample Size (Matched) | 601,315 | 127,205 | 89,509 |
| Age, mean ± SD | 42.7 ± 18.2 | 49.2 ± 18.3 | 47.9 ± 18.1 |
| Sex | |||
| Female | 398,287 (66.2%) | 87,261 (68.6%) | 43,828 (49.0%) |
| Male | 202,659 (33.7%) | 39,889 (31.4%) | 45,624 (51.0%) |
| Race | |||
| White | 385,873 (64.2%) | 75,190 (59.1%) | 52,260 (58.8%) |
| Black or African American | 68,713 (11.4%) | 8,387 (6.6%) | 6,500 (7.3%) |
| Asian | 20,325 (3.4%) | 5,003 (3.9%) | 2,994 (3.3%) |
| Other race | 25,956 (4.3%) | 6,625 (5.2%) | 2,932 (3.3%) |
| Unknown race | 95,631 (15.9%) | 31,405 (24.7%) | 23,598 (26.4) |
| Ethnicity | |||
| Hispanic or Latino | 48,437 (8.1%) | 4,978 (3.9%) | 3,050 (3.4%) |
| Not Hispanic or Latino | 385,522 (64.1%) | 66,081 (51.9%) | 48,456 (54.1%) |
| Unknown ethnicity | 167,356 (27.8%) | 56,155 (44.1%) | 38,003 (42.5%) |
| Comparison | Exposure Pre-Match | Control Pre-Match | Final Matched Exposure | Final Matched Control |
| Analysis 1: Anxiety → IBS + IBD | 601,342 (7.38%) | 7,544,665 (92.62%) | 601,315 (50%) | 601,315 (50%) |
| Analysis 2: IBS → Anxiety | 127,205 (1.61%) | 7,759,661 (98.39%) | 127,205 (50%) | 127,205 (50%) |
| Analysis 3: IBD → Anxiety | 89,509 (1.15%) | 7,693,156 (98.85%) | 89,509 (50%) | 89,509 (50%) |
| Comparison | Exposure Events | Control Events | Exposure Risk (%) | Control Risk (%) | Risk Difference (95% CI) | Risk Ratio (95% CI) | P-value |
| Anxiety → IBS | 6,724 | 2,457 | 1.10% | 0.40% | 0.007 (0.007–0.007) | 2.737 (2.613–2.866) | <0.001 |
| Anxiety → IBD | 1,412 | 908 | 0.20% | 0.20% | 0.001 (0.001–0.001) | 1.555 (1.431–1.690) | <0.001 |
| IBS → Anxiety | 8,334 | 3,770 | 6.60% | 3.00% | 0.036 (0.034–0.038) | 2.211 (2.129–2.295) | <0.001 |
| IBD → Anxiety | 2,354 | 2,383 | 2.60% | 2.70% | -0.000 (-0.002–0.001) | 0.988 (0.934–1.045) | 0.669 |
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Taxonomy
TopicsGastrointestinal motility and disorders · Inflammatory Bowel Disease · Gut microbiota and health
Introduction
Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal (GI) disorders, affecting an estimated 5-10% of the global population, with higher prevalence among women and notable regional variation [1,2]. IBS is characterized by recurrent abdominal pain associated with altered bowel habits in the absence of a detectable organic disease [1]. Common symptoms include abdominal pain, bloating, diarrhea, constipation, or mixed bowel patterns, in addition to extraintestinal symptoms such as headaches and fatigue. The pathophysiology of IBS is multifactorial, involving dysregulation of the gut-brain axis (GBA), visceral hypersensitivity, dysmotility, immune activation, changes in the gut microbiota, and psychosocial factors [2,3]. Current management focuses on lifestyle and dietary modifications along with pharmacologic therapy tailored to the IBS subtype.
Inflammatory bowel disease (IBD), encompassing Crohn’s disease and ulcerative colitis, is characterized by chronic, relapsing inflammation of the GI tract. Although its exact cause remains unclear, IBD is thought to result from an inappropriate immune response to intestinal microbiota in genetically susceptible individuals, influenced by environmental factors such as smoking [4,5]. Both subtypes are associated with significant morbidity, including reduced quality of life and increased colorectal cancer risk. Current management of IBD centers around aminosalicylates, corticosteroids, and immunomodulators such as tumor necrosis factor inhibitors [6].
The GBA is a bidirectional communication network linking the central nervous system (CNS) and the GI tract through neural, immune, and hormonal pathways [7,8]. Disruptions in the GBA have been associated with GI and psychiatric conditions, including IBS, IBD, and anxiety disorders [1,4]. IBS is thought to reflect functional dysregulation within the GBA, whereas IBD involves immune-mediated inflammatory disturbances that may also interact with brain signaling [9]. Anxiety and depression may not only arise as secondary consequences but also act as risk factors for the subsequent development of GI disease [5,7]. Longitudinal studies show that anxiety or heightened stress can precede GI symptoms, increasing the risk of IBS and IBD [5,10]. Conversely, GI symptoms and chronic intestinal inflammation can precede anxiety, highlighting bidirectional gut-brain interactions in psychiatric and GI disease [1,11].
This framework underscores the importance of studying gut-brain interactions across both functional and inflammatory contexts, with the potential to inform novel treatments for GI and psychiatric disorders. Despite growing recognition of these links, large-scale, real-world data describing the strength and direction of these associations remain limited. The TriNetX Global Collaborative Network provides an opportunity to examine these relationships across diverse health systems. This study aims to quantify and compare the bidirectional association between anxiety and both IBS and IBD using multicenter electronic health record data.
Materials and methods
This retrospective cohort study used TriNetX, a multi-national federated research network that aggregates de-identified electronic health records from over 100 healthcare organizations, the majority of which are based in the United States. The data used in this study were collected between January 1, 2021, and January 1, 2024, using the TriNetX Global Collaborative Network, which provides access to electronic medical records (diagnoses, laboratory values, procedures, genomic information, medications) from approximately 162 healthcare organizations. Institutional Review Board (IRB) approval was not required for this study. The index event was defined as the first recorded occurrence of the relevant diagnostic code, and patients whose index event occurred more than 20 years before analysis were excluded. Diagnoses were identified using International Classification of Diseases, Tenth Revision (ICD-10) codes, a classification system maintained by the World Health Organization for disease classification. Medication exposures were identified with National Library of Medicine (NLM) codes, Anatomical Therapeutic Chemical Classification System (ATC) codes, and Veterans Affairs (VA) classifications.
Five cohorts were created to examine the associations between anxiety disorders and GI conditions, specifically IBS and IBD. Three separate temporal analyses were created in order to analyze the risk. For analyses evaluating the risk of IBS or IBD following anxiety, adults aged 18 years or older with a diagnosis of an anxiety disorder were identified, along with a control cohort consisting of adults with encounters for routine health examinations and no diagnosis of anxiety. Individuals with a prior diagnosis of IBS or IBD were excluded.
For reciprocal analyses evaluating the risk of anxiety following GI disease, separate cohorts of adults with IBS or IBD and no prior history of anxiety or the alternate GI condition were identified. A corresponding control cohort included adults with routine health examinations and no history of anxiety, IBS, or IBD.
Across all cohorts, uniform exclusion criteria were applied to reduce confounding with pharmacologic, psychiatric, and GI factors. Patients were excluded if they had prior use of antidepressants, benzodiazepine derivatives, or other sedative-hypnotics, antipsychotics, and/or opioids, as these medications may independently influence mood and GI function [12,13]. Additional exclusions included a history of bipolar disorder, schizophrenia, schizotypal disorder, delusional disorder, other non-mood psychotic disorders, celiac disease, malignant neoplasm of the rectosigmoid junction, and intestinal infectious disease within the preceding six months, given the potential of these conditions to affect both GI and psychiatric outcomes [14,15]. For analyses involving IBS and IBD as exposures, patients with a prior diagnosis of IBS were excluded from the IBD cohort, and vice versa, to preserve diagnostic clarity. Lastly, individuals with pre-existing diagnoses of the outcome of interest were excluded to ensure temporal clarity. A complete list of diagnostic codes and exclusion criteria used for cohort construction is provided in Table 1.
Propensity score matching was performed using a nearest-neighbor algorithm with a caliper of 0.1 to balance each exposure cohort with its respective control on age, sex, race, ethnicity, smoking status, and history of depressive episode. After matching, each analysis yielded two balanced cohorts for outcome assessment. For analyses in which anxiety was the exposure, the primary outcomes were new diagnoses of IBS or IBD. For analyses in which IBS or IBD served as the exposure, the primary outcome was a new diagnosis of an anxiety disorder. Outcomes were assessed over a five-year follow-up period beginning one day after the index event. Risk analyses were conducted using the TriNetX Analytics platform and are reported as risk ratios (RRs), risk differences (RDs), and odds ratios (ORs) with corresponding 95% confidence intervals (CIs).
Results
This study evaluated the associations between anxiety and gastrointestinal conditions using separate longitudinal analyses with propensity-matched cohorts derived from the TriNetX Global Collaborative Network.
Prior to matching, the anxiety cohort consisted of N = 636,712 patients with no history of IBS or IBD, and the control cohort consisted of N = 7,890,540 individuals with no diagnoses of anxiety, IBS, or IBD. For the reciprocal analyses, the IBS cohort included N = 141,752 individuals with no prior IBD or anxiety, the IBD cohort included N = 97,228 individuals with no prior IBS or anxiety, and the corresponding control group included N = 8,042,284 individuals without anxiety or gastrointestinal disease. Following matching, each analysis yielded balanced cohorts of equal size: 601,315 patients in the anxiety versus control analysis, 127,205 in the IBS versus control analysis, and 89,509 patients in the IBD versus control analysis. Baseline demographic and clinical characteristics of the propensity-matched cohorts are summarized in Table 2. Cohort sizes before and after propensity score matching for each analytic comparison are shown in Table 3.
Among patients with anxiety and matched controls, 6,724 individuals (1.1%) in the anxiety cohort developed IBS compared with 2,457 individuals (0.4%) in the control cohort. The RD was 0.007 (95% CI: 0.007, 0.007, p < 0.001), corresponding to a RR of 2.737 (95% CI: 2.613, 2.866) and an OR of 2.756 (95% CI: 2.631, 2.887). For IBD, 1,412 patients (0.2%) in the anxiety cohort developed the condition compared with 908 patients (0.2%) in the control cohort. The RD was 0.001 (95% CI: 0.001, 0.001, p < 0.001), with a RR of 1.555 (95% CI: 1.431, 1.690) and an OR of 1.556 (95% CI: 1.432, 1.692).
In the reciprocal analysis of IBS and anxiety, 8,334 patients (6.6%) in the IBS cohort developed anxiety compared with 3,770 patients (3.0%) in the control group. The RD was 0.036 (95% CI: 0.034, 0.038, p < 0.001), with a RR of 2.211 (95% CI: 2.129, 2.295) and an OR of 2.295 (95% CI: 2.207, 2.387). For the IBD analysis, 2,354 patients (2.6%) in the IBD cohort developed anxiety compared with 2,383 patients (2.7%) in the control cohort. The RD was -0.000 (95% CI: -0.002, 0.001, p = 0.669), with a RR of 0.988 (95% CI: 0.934, 1.045) and an OR of 0.988 (95% CI: 0.932, 1.046). Risk estimates for all primary analyses, including RDs and RRs, are summarized in Table 4.
Discussion
This large, multi-institutional cohort study found strong bidirectional associations between anxiety and IBS in separate temporal analyses, and weaker, inconsistent associations between anxiety and IBD. After propensity score matching across demographic and clinical variables, patients with a diagnosis of anxiety demonstrated a significantly higher incidence of both subsequent IBS and IBD diagnoses compared to controls over a five-year follow-up period. In the reciprocal analysis, patients with IBS had a significantly higher incidence of a subsequent diagnosis of anxiety, whereas patients with IBD showed no significant difference in anxiety incidence.
The consistent relationship between anxiety and IBS observed in this study is consistent with prior research. Meta-analyses have previously shown that IBS is associated with increased anxiety compared to healthy controls, and that anxiety and heightened stress sensitivity are significant risk factors for the development and exacerbation of IBS, reinforcing that both these disorders are sensitive to disruptions within the GBA [1,16]. To explain these associations, prior research has identified neurobiological and psychosocial pathways that link emotional regulation with GI function.
The enteric nervous system (ENS) comprises interconnected neural networks that are responsible for regulating gut motility, secretion, and sensation. The ENS interacts closely with the gut microbiome and communicates with the CNS through vagal and sympathetic pathways. Dysregulation of these circuits through psychosocial or gut-derived stress has been implicated in both IBS and anxiety [1]. For example, studies demonstrate that stress, microbial dysbiosis, and alterations in neurotransmitter signaling can influence both gut function and emotional processing [17,18].
Genetic studies further support shared biological pathways. Genes such as CADM2 and NCAM1 are implicated in synaptic organization and ENS development and thus associated with anxiety, depression, and IBS [19,20]. Neuroimaging research also shows that IBS patients exhibit differences such as decreased volume in brain regions related to emotional regulation and interoception, including the prefrontal cortex, anterior insula, and hippocampus [21]. Collectively, these data reinforce the concept of IBS as a disorder deeply rooted in gut-brain-microbiome interactions.
However, the associations between anxiety and IBD are weaker and asymmetric, with higher rates of anxiety and depression observed particularly during disease flares [7]. This relationship appears less connected to disease onset, which is a key distinction when compared with IBS. Mechanistically, IBD-related inflammation may influence mood through cytokine-mediated neuroimmune signaling, vagal and nociceptive pathways, microbial metabolites, and increased blood-brain barrier permeability [8,11]. Microglial activation and inflammatory changes in brain regions implicated in anxiety, such as the anterior cingulate cortex, have also been described. However, these mechanisms likely operate selectively depending on disease severity, intestinal location, and individual inflammatory profiles [8].
Notably, several studies suggest that psychological distress may precede or promote IBD onset more strongly than IBD promotes future anxiety, which aligns with our study results [5]. Chronic stress may potentiate mucosal inflammation through hypothalamic-pituitary-adrenal axis dysregulation, neuroimmune activation, and enteric glial responses [22]. Variability across studies assessing the influence of IBD on the development of anxiety may reflect heterogeneity in disease activity, treatment intensity, and timing of psychiatric assessment. Although our study did not identify a significant association between IBD and subsequent anxiety, these findings are consistent with prior work demonstrating that psychological symptoms nonetheless influence IBD activity [7,18].
Comparison across disorders indicates that the associations in both temporal directions between anxiety and IBS are substantially stronger than those between anxiety and IBD. Several mechanisms may contribute to this distinction. IBS involves heightened sensitivity within the GBA, strong psychosocial modulation, and substantial genetic and neurobiological overlap with anxiety disorders. In contrast, IBD is driven primarily by immune-mediated pathology, with psychological factors exerting more influence on disease course than on disease initiation. These mechanistic differences are further reflected in the way patients perceive their illness, with prior research showing that IBS patients often have more negative illness perceptions and greater concern about their condition compared with patients with IBD. This may, in turn, heighten anxiety responses and contribute to symptom amplification [23]. Together, these differences underscore the importance of tailoring psychological assessment and intervention strategies to the underlying pathophysiology of each condition.
Understanding the relationship between GI disorders and common neuropsychiatric comorbidities highlights the importance of bidirectional screening, both for neuropsychiatric disorders in patients receiving care for GI conditions and for the development of GI disorders in patients with neuropsychiatric conditions. Furthermore, recognizing the mechanisms linking neuropsychiatric disorders, such as anxiety, with GI disorders supports treatments that address both domains. These considerations underscore the need for integrated, multidisciplinary care that targets both GI and psychiatric symptoms.
Although our analysis did not evaluate therapeutic outcomes, the observed associations have implications for integrated clinical management. For example, prior research has shown that gut-brain neuromodulators such as TCAs, SSRIs, and SNRIs have efficacy in reducing global and abdominal IBS symptoms and improving anxiety [24]. Similar agents may improve IBD outcomes by reducing inflammation, modulating pain pathways, and altering the gut microbiota [25,26]. Recognizing anxiety as both a risk factor for and consequence of GI symptoms supports early identification and multidisciplinary care. Anxiety can worsen GI symptoms once established, reinforcing a feedback loop that may exacerbate disease burden. Collaboration between gastroenterologists, psychiatrists, and behavioral health specialists may therefore help break this cycle, particularly in individuals with subclinical anxiety preceding GI symptom onset.
This study has several limitations related to its retrospective design and use of electronic health record data. First, due to the observational and retrospective nature of this study, we are not able to draw any causal relationships despite the associations between anxiety and GI disorders identified in this study. Secondly, the identification of IBS, IBD, and anxiety relied on ICD-10 diagnostic codes. Misclassification is possible given that the coding and diagnostic accuracy may differ across health care organizations and providers associated with the TriNetX platform. In addition, reliance on these codes may underestimate the true prevalence of anxiety and GI disease, as many patients with subclinical symptoms or those treated outside formal psychiatric settings may not receive coded diagnoses. The use of diagnostic codes also limits the ability to assess disease severity, preventing distinctions between mild and severe disease. Moreover, medication exposure may be under-captured if prescriptions were written outside participating health systems.
Third, although propensity score matching was used to reduce confounding, residual confounding from unmeasured variables remains possible. TriNetX lacks consistent data on factors such as socioeconomic status, dietary habits, stress levels, and medication adherence, all of which may influence both anxiety and GI outcomes. Although we excluded patients with documented exposure to antidepressants, benzodiazepines, antipsychotics, and opioids, residual confounding from unmeasured or other medication exposure such as corticosteroids, may have influenced both GI and psychiatric outcomes. In addition, it was not possible to determine whether anxiety symptoms occurred in relation to GI disease flares or changes in disease activity; only the presence of a diagnosis could be recorded. Furthermore, the number, timing, and duration of GI or psychiatric symptom episodes could not be assessed. Finally, the extensive exclusion criteria required to minimize pharmacologic, psychiatric, and GI confounding may limit generalizability. Patients with complex psychiatric histories, recent GI infections, or exposure to psychotropic or opioid medications were excluded, and these populations may experience different patterns of gut-brain interactions than those represented in this analysis. Nonetheless, our study supports important clinical relationships between anxiety, IBS, and IBD.
Future research should aim to overcome the limitations associated with this retrospective study to better uncover the mechanisms underlying the association demonstrated in this study and the broader gut-brain relationship. Prospective, longitudinal cohorts using standardized diagnostic criteria for anxiety, IBS, and IBD are needed to establish temporal relationships between these conditions. In addition, interventional randomized controlled trials could be beneficial in identifying multimodal treatment strategies to address these disease processes. For example, whether treating anxiety through modalities like CBT or pharmacological approaches could reduce IBS or IBD risk or symptom severity, and conversely, whether optimizing GI disease control improves psychiatric outcomes. Lastly, future studies could combine health record data with analysis of microbiome sequencing and neuroendocrine markers to identify key biological intermediates that link anxiety and GI disease. More broadly, these intermediates could be compared with those in other GI disorders with psychiatric comorbidities to better elucidate the complex gut-brain axis. Future large-scale cohort studies should aim to clarify the magnitude of psychiatric-to-GI disease risk as well as the converse relationship, and further explore any differences found in the magnitude of these associations.
Conclusions
In this large, multi-institutional retrospective cohort study, anxiety and IBS demonstrated strong bidirectional associations based on two separate analyses, while the relationship between anxiety and IBD was weaker and asymmetric. These findings highlight important differences in how functional and inflammatory GI disorders interact with psychological symptoms and the GBA. Although mechanistic pathways likely differ across conditions, the consistent association between anxiety and GI outcomes underscores the clinical importance of recognizing and addressing psychological symptoms in GI care, as well as remaining vigilant for GI symptoms in patients presenting with psychiatric disorders to improve overall outcomes.
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