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Bidirectional brain–gut axis effects influence mood and prognosis in IBD: a systematic review and meta-analysis
  1. Keeley M Fairbrass1,2,
  2. Jessica Lovatt1,
  3. Brigida Barberio3,
  4. Yuhong Yuan4,
  5. David J Gracie1,2,
  6. Alexander C Ford1,2
  1. 1Leeds Gastroenterology Institute, St James's University Hospital, Leeds, UK
  2. 2Leeds Institute of Medical Research at St. James’s, University of Leeds, Leeds, UK
  3. 3Department of Surgery, Oncology and Gastroenterology, University of Padua, Padova, Italy
  4. 4Division of Gastroenterology, Department of Medicine, McMaster University, Hamilton, Ontario, Canada
  1. Correspondence to Professor Alexander C Ford, Leeds Gastroenterology Institute, St James's University Hospital, Leeds, UK; alexf12399{at}yahoo.com

Abstract

Objective The role of the brain–gut axis is of increasing interest in IBD, as the link between common mental disorders and GI inflammation may be bidirectional. We performed a systematic review examining these issues.

Design We searched EMBASE Classic and EMBASE, Medline, and APA PsychInfo (to 11 July 2021) for longitudinal follow-up studies examining effect of symptoms of anxiety or depression on subsequent adverse outcomes in IBD, or effect of active IBD on subsequent development of symptoms of anxiety or depression. We pooled relative risks (RRs) and HRs with 95% CIs for adverse outcomes (flare, escalation of therapy, hospitalisation, emergency department attendance, surgery or a composite of any of these) according to presence of symptoms of anxiety or depression at baseline, or RRs and HRs with 95% CIs for new onset of symptoms of anxiety or depression according to presence of active IBD at baseline.

Results We included 12 separate studies, recruiting 9192 patients. All 12 studies examined brain-to-gut effects. Anxiety at baseline was associated with significantly higher risks of escalation of therapy (RR=1.68; 95% CI 1.18 to 2.40), hospitalisation (RR=1.72; 95% CI 1.01 to 2.95), emergency department attendance (RR=1.30; 95% CI 1.21 to 1.39), or a composite of any adverse outcome. Depression at baseline was associated with higher risks of flare (RR=1.60; 95% CI 1.21 to 2.12), escalation of therapy (RR=1.41; 95% CI 1.08 to 1.84), hospitalisation (RR=1.35; 95% CI 1.17 to 1.57), emergency department attendance (RR=1.38; 95% CI 1.22 to 1.56), surgery (RR=1.63; 95% CI 1.19 to 2.22) or a composite of any of these. Three studies examined gut-to-brain effects. Active disease at baseline was associated with future development of anxiety or depression (RR=2.24; 95% CI 1.25 to 4.01 and RR=1.49; 95% CI 1.11 to 1.98, respectively).

Conclusion Bidirectional effects of the brain–gut axis are present in IBD and may influence both the natural history of the disease and psychological health.

  • inflammatory bowel disease
  • psychology
  • crohn's disease
  • ulcerative colitis
  • brain/gut interaction

Data availability statement

Data are available upon reasonable request.

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Data availability statement

Data are available upon reasonable request.

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Footnotes

  • DJG and ACF are joint last authors.

  • Twitter @bribarberio, @alex_ford12399

  • Contributors Study concept and design: ACF, DJG and KMF conceived and drafted the study. KMF and ACF analysed and interpreted the data. KMF, DJG and ACF drafted the manuscript. All authors have approved the final draft of the manuscript. ACF is guarantor. He accepts full responsibility for the work and the conduct of the study, had access to the data and the decision to publish. The corresponding author attests that all listed authors meet authorship criteria and that no others meeting the criteria have been omitted.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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