ReviewActas espanolas de psiquiatria2025
Neuroimmune Crossroads: Pathophysiological Links Between Bipolar Disorder and Inflammatory Bowel Disease.
Review in Actas espanolas de psiquiatria, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
11 authors.
Funding
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Abstract
backgroundBipolar 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.
methodsWe conducted a narrative review of peer-reviewed 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.
resultsPrevalence 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.
conclusionsThe 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.
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