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Gut 61:1284-1290 doi:10.1136/gutjnl-2011-300474
  • Neurogasteroenterology
  • Original article

The brain–gut pathway in functional gastrointestinal disorders is bidirectional: a 12-year prospective population-based study

  1. N J Talley1
  1. 1Faculty of Health, University of Newcastle, Callaghan, New South Wales, Australia
  2. 2Department of Psychology, Macquarie University, North Ryde, New South Wales, Australia
  3. 3Department of Gastroenterology & Hepatology, Nepean Hospital, Penrith, New South Wales, Australia
  1. Correspondence to Professor Nicholas Talley,Faculty of Health, University of Newcastle, Callaghan, New South Wales, 2308, Australia; nicholas.talley{at}newcastle.edu.au
  1. Contributors NAK—study concept and design, acquisition of data, interpretation of data, drafting of manuscript. MJ—analysis and interpretation of data, drafting of manuscript. JK—administration, study supervision, critical revision of manuscript. MW—administration, study supervision, critical revision of manuscript. JZ—acquisition of data, critical revision of manuscript. NJT—study design and concept, obtained funding, interpretation of data, critical revision of manuscript.

  • Revised 2 December 2011
  • Accepted 6 December 2011
  • Published Online First 10 January 2012

Abstract

Objective Psychological factors are known to be associated with functional gastrointestinal disorders (FGIDs) including irritable bowel syndrome (IBS) and functional dyspepsia (FD). No prospective studies have evaluated whether it is the brain (eg, via anxiety) that drives gut symptoms, or whether gut dysfunction precipitates the central nervous system features such as anxiety. In a 12-year longitudinal, prospective, population-based study, we aimed to determine the directionality of the brain–gut mechanism in FGIDs.

Design Participants (n=1775) were a random population sample from Australia who responded to a survey on FGIDs in 1997 and agreed to be contacted for future research; 1002 completed the 12-year follow-up survey (response rate =60%), with 217, 82 and 45 people meeting Rome II for new onset FGIDs, IBS and FD, respectively. Anxiety and depression were measured using the Delusions Symptom States Inventory at baseline and follow-up.

Results Among people free of a FGID at baseline, higher levels of anxiety (OR 1.11; 95% CI 1.03 to 1.19, p=0.006) but not depression at baseline was a significant independent predictor of developing new onset FGIDs 12 years later. Among people who did not have elevated levels of anxiety and depression at baseline, those with a FGID at baseline had significantly higher levels of anxiety and depression at follow-up (mean difference coefficient 0.76, p<0.001 and 0.30, p=0.01 for anxiety and depression, respectively). In IBS higher levels of anxiety and depression at baseline were predictive of IBS at follow-up, while only depression was predictive of FD at follow-up.

Conclusions The central nervous system and gut interact bidirectionally in FGIDs.

Footnotes

  • Competing interests None.

  • Ethics approval Ethics approval was provided by Sydney West Area Health Service Human Research Ethics Committee.

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