There might be independent gut-to-brain and brain-to-gut pathways in patients with irritable bowel syndrome (IBS), researchers from Australia report.
"This is an exciting time as the causes of IBS and other functional gastrointestinal disorders (FGIDs) are slowly being unraveled," DrNicholas J. Talley from the University of Newcastle, New South Wales, told Reuters Health.
"The recognition that while nerve signaling is bidirectional, either the gut or the brain can initiate and drive IBS and other FGIDs is another important step forward in helping to solve the mystery of why and how these syndromes occur," he said.
Despite some experimental evidence, the whole idea of a distinct gut-to-brain pathway underlying FGIDs remains controversial.
Dr Talley's team used a validated survey containing questions on Rome III IBS and functional dyspepsia (FD) and the Hospital Anxiety and Depression Scale to test their hypothesis that there is a specific gut-to-brain syndrome where gastrointestinal symptoms precede the onset of psychological distress in some patients with an FGID.
At baseline, 16.5% of the 1,900 individuals had IBS, 14.2% had FD, 11.8% had postprandial distress syndrome, and 6.1% had epigastric pain syndrome, the researchers report in Alimentary Pharmacology & Therapeutics, online July 22.
During the course of the one-year study, 6.4% developed new onset IBS and 7.2% developed FD, whereas nearly half of those individuals with IBS and FD at baseline lost their symptoms.
Individuals who had higher levels of anxiety and depression at baseline were significantly more likely to develop IBS and FD during the year of follow-up, and individuals with documented IBS and FD at baseline were more likely to report anxiety and depression during the year of follow-up.
Overall, among the 90 individuals in whom the order of incidence could be determined, one-third had a mood disorder preceding FGID and two-thirds had FGID preceding their mood disorder.
"We speculated that there are two distinct types of functional gastrointestinal disease that others have not recognized," Dr Talley said. "For example, IBS in a subgroup may first begin with gut symptoms (pain, diarrhea, constipation, bloating, etc.) in those free of psychological distress and only later does new-onset anxiety or depression develop, implicating gut disease as the primary driver of the entire symptom complex (a gut-to-brain disease)."
"On the other hand," he said, "we speculated there is another quite different subgroup where disease begins with anxiety or depression and only later do new onset gut symptoms develop, and this is likely primarily a central nervous system cause (probably through the stress system), or a brain-to-gut disease."
"This is exactly what we found, with gut disease occurring first followed by new onset psychological distress in about two-thirds of people from the community over a one-year follow-up," he said.
"Our novel observations may have profound treatment implications, because if anxiety begins first targeting this brain problem may provide the most benefit, but if gut symptoms begin first directing therapy to the gut may be the more effective approach, a hypothesis now worth testing in clinical trials," Dr Talley concluded. "Mixing up the different gut-brain and brain-gut groups may have caused confusion in the interpretation of all the treatment studies to date."
Dr Paul Enck from the University of Tübingen in Germany, who has published extensively on IBS and its treatment, told Reuters Health by email, "In any given patient showing up in a practice or hospital with both psychiatric and intestinal symptoms suggestive of IBS, the sequence of the two remains to be elucidated and cannot be taken for granted: psychiatric symptoms may be comorbid conditions to GI dysfunctions, and intestinal symptoms may be comorbid conditions to psychiatric abnormalities."
"Thinking about this, I still wonder why the authors believe the two 'pathways' are independent, as long as we do not know (and do not learn from this study) the kinetics between the two: GI symptoms may develop at a different speed after psychiatric symptom occurrence, than psychiatric symptoms after a GI incidence, e.g. following a gastrointestinal infection (called: post-infectious IBS)," Dr Enck said. "If so, the two would not be 'independent' at all."
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