Neuroimmune Crossroads: Pathophysiological Links Between Bipolar Disorder and Inflammatory Bowel Disease.
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| Title: | Neuroimmune Crossroads: Pathophysiological Links Between Bipolar Disorder and Inflammatory Bowel Disease. |
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| Authors: | Marano, Giuseppe1,2 giuseppemaranogm@gmail.com, Bardi, Francesca1,2, De Chiara, Emanuela1,2, Lisci, Francesco Maria1,2, Brisi, Caterina1,2, Caroppo, Emanuele3, Sani, Gabriele1,2, Gasbarrini, Antonio4, Pola, Roberto5, Gaetani, Eleonora6,7, Mazza, Marianna1,2 |
| Source: | Actas Espanolas de Psiquiatria. 2025, Vol. 53 Issue 6, p1432-1447. 16p. |
| Subjects: | BIPOLAR disorder, INFLAMMATORY bowel diseases, GENETIC pleiotropy, INFLAMMATION, CYTOKINES, NEUROIMMUNOLOGY, COMORBIDITY, GUT microbiota |
| Abstract: | Background: Bipolar disorder (BD) and inflammatory bowel disease (IBD) frequently co-occur, posing unique treatment challenges and implicating shared inflammatory mechanisms. Although each condition has been extensively studied in isolation, the clinical and pathophysiological interplay between BD and IBD remains poorly characterized. Methods: We conducted a narrative review of peerreviewed literature from January 2000 through May 2025, retrieved from PubMed, Web of Science, and PsycINFO. Search terms included "bipolar disorder", "inflammatory bowel disease", "comorbidity", and related inflammatory markers. Titles/abstracts were screened by two reviewers, and eligible studies reporting clinical, epidemiological, or mechanistic data on BD–IBD overlap were included. Results: Prevalence estimates suggest that BD affects approximately 3–7% of IBD patients, compared with 1–2% in the general population. Comorbid BD–IBD is associated with increased hospitalization rates, more severe gastrointestinal and psychiatric symptoms, and reduced quality of life. Treatment interactions are complex: mood stabilizers and antipsychotics may exacerbate gastrointestinal inflammation, while corticosteroids and biologics can destabilize mood. Mechanistic studies highlight dysregulated cytokine profiles (e.g., elevated Interleukin-6, Tumor Necrosis Factor-alpha I), gut-microbiome alterations, and genetic pleiotropy as convergent pathways. Conclusions: The intersection of BD and IBD underscores a bidirectional gut–brain neuroimmune axis, with systemic inflammation as a central mediator. Recognizing and managing this comorbidity requires integrated multidisciplinary care. Future research should focus on longitudinal studies and targeted anti-inflammatory interventions to improve outcomes in this high-risk population. [ABSTRACT FROM AUTHOR] |
| Copyright of Actas Espanolas de Psiquiatria is the property of Maria Lopez-Ibor and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | MedicLatina |
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