Irritable bowel syndrome (IBS)

Irritable bowel syndrome (IBS) is a gastrointestinal disorder characterized by chronic abdominal pain and altered bowel habits. It is the most commonly diagnosed gastrointestinal condition: the prevalence of IBS in North America is estimated to be approximately 10 to 15 percent Until the advent of culture-independent studies, physicians supposed IBS was a psychosomatic (functional) disorder as there was limited indication of an organic cause, with physicians complaining that patients were unmotivated to seek out cognitive behavioral therapy.1)

However, the notion that IBS is a psychological disorder has come under serious challenge.2) Recent research demonstrates that IBS is characterized by significant alterations in the gut microbiotaThe bacterial community which causes chronic diseases - one which almost certainly includes multiple species and bacterial forms..3)

The Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. treats IBS by reactivating the innate immune responseThe body's first line of defense against intracellular and other pathogens. According to the Marshall Pathogenesis the innate immune system becomes disabled as patients develop chronic disease.. In the course of treatment, patients' disease symptoms may become worse due to a process called immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed..


As a matter of course, symptoms of IBS will fluctuate while a patient is on the Marshall Protocol (MP). In addition to the strategies outline in the Managing immunopathology article, the following may also be helpful:

  • constipation – MP patients with constipation should have the symptom treated for immediate relief and then measures should be adopted to prevent constipation.
  • diarrhea – Patients with diarrhea may wish to increase fluid intake and/or take anti-diarrheal medication. 4)
  • loss of appetite – If nausea is preventing a patient from eating, it's very important to palliate the nausea. Over the counter medications such as Gravol (dramamine) may be helpful. If not, patients should ask their doctor for a prescription antiemetic, such as hydroxyzine.
IBS is characterized by microbial dysbiosis. Electron micrograph of the cytoplasm of an enteroendocrine cell from a patient with IBS showing a structure resembling an intermediate body of Chlamydia (arrow) with characteristic condensed nucleoids. Dark homogenous structures are granules. M = Mitochondria, N = Nucleus, Bar = 0.5 μm. (Source: Dlugosz et al., 2010)

Evidence of infectious cause

Recent studies provide increasing support for the concept that disturbances in gut flora occur in patients with irritable bowel syndrome and that such abnormalities may contribute to irritable bowel syndrome-type symptoms.

Riordan et al.5)

Onset following gastrointestinal infection

Epidemiologic studies have shown that gastrointestinal infection is the strongest environmental risk factor for the development of IBS.6) 7) Although most patients with gastroenteritis become asymptomatic, a small but significant proportion of subjects (7%–31%) develop postinfectious IBS, dyspepsia, or both. A recent systematic review and meta-analysis identified that the incidence for IBS development after infectious gastroenteritis was 10%.8)

Abnormal composition

Small intestinal bacterial overgrowth (SIBO) has been documented in a proportion of patients with IBS (10%–84%). For example, in 2012, Greek researchers enrolled patients needing upper gastrointestinal (GI) tract endoscopy. Among 320 subjects SIBO was diagnosed in 62 (19.4%) with 42 of those having IBS (67.7%). Of all IBS sufferers, SIBO was found in 37.5%. Escherichia coli, Enterococcus spp. and Klebsiella pneumoniae were the most common isolates within patients with SIBO. Several researchers have shown that eradicating SIBO results in symptomatic improvement.9) 10)

Higher temporal instability

Accumulating evidence shows that patients with IBS have a higher temporal instability of the bacterial populations and that the microbiota composition is different compared with healthy controls.11) 12)


Free versus total serum 25-hydroxyvitamin D in a murine modelA model of disease which uses rats or mice to mimic human conditions. of colitis. 13)

Further research

Findings suggest that neither olmesartanMedication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. Also known by the trade name Benicar. nor other ARBs were associated with diarrhea among patients undergoing endoscopy. The spruelike enteropathy recently associated with olmesartan is likely a rare adverse effect and milder presentations are unlikely. 14)

In a methotrexate-induced model of intestinal mucositis, olmesartan reduced inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. and induced enteropathy characterized by severe diarrhea, weight loss, and reduced sucrose activity. 15)

Mast cell activation syndromes 16)

Gastrointestinal (GI) symptoms are commonly reported in patients with mast cell disease. 17)

Mast cells are located in close proximity to the vasculature, and vasoactive mediators released upon their activation can promote endothelial activation leading to blood brain barrier (BBB) dysfunction. 18)

Mast cell activation plays an important role in stress-mediated disease pathogenesis. 19)

Patient interviews

Melinda Stiles

Lyme disease, irritable bowel syndrome/ulcerative colitis, radiculitis

Read the interview

Chris Eastlund

diabetes, sarcoidosis, irritable bowel syndrome

Read the interview

Interviews of patients with other diseases are also available.

Notes and comments


Motivation for psychotherapy in patients with functional gastrointestinal disorders.
Martens U, Enck P, Matheis A, Herzog W, Klosterhalfen S, Rühl A, Zipfel S, Sammet I
Psychosomatics51p225-9(2010 May-Jun)
Irritable bowel syndrome.
Talley NJ
Intern Med J36p724-8(2006 Nov)
Bacterial overgrowth as a cause of irritable bowel syndrome.
Riordan SM, Kim R
Curr Opin Gastroenterol22p669-73(2006 Nov)
Risk of irritable bowel syndrome after an episode of bacterial gastroenteritis in general practice: influence of comorbidities.
Ruigómez A, García Rodríguez LA, Panés J
Clin Gastroenterol Hepatol5p465-9(2007 Apr)
Systematic review and meta-analysis: The incidence and prognosis of post-infectious irritable bowel syndrome.
Thabane M, Kottachchi DT, Marshall JK
Aliment Pharmacol Ther26p535-44(2007 Aug 15)
Composition and temporal stability of gastrointestinal microbiota in irritable bowel syndrome--a longitudinal study in IBS and control subjects.
Mättö J, Maunuksela L, Kajander K, Palva A, Korpela R, Kassinen A, Saarela M
FEMS Immunol Med Microbiol43p213-22(2005 Feb 1)
A molecular analysis of fecal and mucosal bacterial communities in irritable bowel syndrome.
Codling C, O'Mahony L, Shanahan F, Quigley EM, Marchesi JR
Dig Dis Sci55p392-7(2010 Feb)
Free versus total serum 25-hydroxyvitamin D in a murine model of colitis.
Larner DP, Jenkinson C, Chun RF, Westgate CSJ, Adams JS, Hewison M
J Steroid Biochem Mol Biolp(2019 Jan 30)
Olmesartan, other antihypertensives, and chronic diarrhea among patients undergoing endoscopic procedures: a case-control study.
Greywoode R, Braunstein ED, Arguelles-Grande C, Green PH, Lebwohl B
Mayo Clin Proc89p1239-43(2014 Sep)
In a methotrexate-induced model of intestinal mucositis, olmesartan reduced inflammation and induced enteropathy characterized by severe diarrhea, weight loss, and reduced sucrose activity.
de Araújo AA, Borba PB, de Souza FH, Nogueira AC, Saldanha TS, Araújo TE, da Silva AI, de Araújo Júnior RF
Biol Pharm Bull38p746-52(2015)
Mast cell activation syndromes.
Akin C
J Allergy Clin Immunol140p349-355(2017 Aug)
Gastrointestinal Involvement in Mast Cell Activation Disorders.
Hsieh FH
Immunol Allergy Clin North Am38p429-441(2018 Aug)
Mast Cells Induce Blood Brain Barrier Damage in SCD by Causing Endoplasmic Reticulum Stress in the Endothelium.
Tran H, Mittal A, Sagi V, Luk K, Nguyen A, Gupta M, Nguyen J, Lamarre Y, Lei J, Guedes A, Gupta K
Front Cell Neurosci13p56(2019)
Mast Cells in Stress, Pain, Blood-Brain Barrier, Neuroinflammation and Alzheimer's Disease.
Kempuraj D, Mentor S, Thangavel R, Ahmed ME, Selvakumar GP, Raikwar SP, Dubova I, Zaheer S, Iyer SS, Zaheer A
Front Cell Neurosci13p54(2019)
home/diseases/ibs.txt · Last modified: 07.04.2022 (external edit)
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