24 Jul Gut and Brain Communicate To Drive Irritable Bowel Syndrome
MedicalResearch.com Interview with:
Laureate Professor Nicholas J. Talley, MBBS (Hons.)(NSW), MD (NSW), PhD (Syd), MMedSci (Clin Epi)(Newc.), FRACP, FAFPHM, FAHMS, FRCP (Lond. & Edin.), FACP, FACG, AGAF, FAMS, FRCPI (Hon), GAICD
Pro Vice-Chancellor, Global Research,
University of Newcastle, Australia
Professor of Medicine, Faculty of Health and Medicine, University of Newcastle, Australia
President, Royal Australasian College of Physicians
Chair, Committee of Presidents of Medical Colleges
Hon. Treasurer, Australian Academy of Health and Medical Sciences
Editor-in-Chief, Medical Journal of Australia
Senior Staff Specialist, John Hunter Hospital, Newcastle, Australia
Professor of Medicine and Professor of Epidemiology, Joint Supplemental Consultant Gastroenterology and Health Sciences Research, Mayo Clinic, Rochester, MN, USA
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: Functional gastrointestinal diseases (FGIDs) like the irritable bowl syndrome (IBS) are very common, cause major distress including pain and psychological dysfunction, impact on quality of life and drive high health care costs. We speculated that there are two distinct types of functional gastrointestinal disease that others have not recognized.
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, 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.
MedicalResearch.com: What should readers take away from your report?
Response: This is an exciting time as the causes of IBS and other FGIDs is slowly being unravelled. 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.
MedicalResearch.com: What recommendations do you have for future research as a result of this study?
Response: We are starting to understand drivers of gut-brain disease. We have previously shown in the irritable bowel syndrome (IBS) with diarrhea that there is an increase in circulating TNF alpha and other cytokines and TNF alpha correlates with anxiety; blocking cytokines may be a therapeutic approach to relieve both psychological and gut symptoms. Another approach is to change the gut bacteria with therapy because they may induce gut symptoms when disturbed.
MedicalResearch.com: Is there anything else you would like to add?
Response: 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. Mixing up the different gut-brain and brain-gut groups may have caused confusion in the interpretation of all the treatment studies to date.
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Koloski, N. A., Jones, M. and Talley, N. J. (2016), Evidence that independent gut-to-brain and brain-to-gut pathways operate in the irritable bowel syndrome and functional dyspepsia: a 1-year population-based prospective study. Alimentary Pharmacology & Therapeutics. doi: 10.1111/apt.13738
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