IBS Research and Cell-Mediated Immune Response
Gastroenterology. 2007 Mar; 132(3):913-20.
Immune activation in patients with irritable bowel syndrome
Researchers test the hypothesis that irritable bowel syndrome is characterized by a cellular immune response with the production of pro-inflammatory cytokines and also explore psychiatric symptoms associated with IBS. IBS-D patients who had greater than 3 bowel movements per day with watery stools, pain and cramping showed significantly higher cytokine levels in all categories, with accompanying anxiety.
Cytokine activation is indicative of an immune response: It’s not all in your head
Gut 1996 Jul; 39(1) 130-5
Double blind, placebo controlled food reactions do not correlate to IgE allergy in the diagnosis of staple food related gastrointestinal symptoms
In this study, they took patients who exhibited gastrointestinal symptoms in response to foods and did blinded challenge of these patients along with skin prick testing and RAST testing, classic measures of IgE sensitivities and for the control and atopic group there was no evidence that IgE or classic allergies were involved, suggesting other immune mechanisms were at play.
The immune reaction is not your classic IgE or allergic reaction
Am J Gastroenterology 2005 Jul;100(7):1558-9
IgG-mediated food intolerance in irritable bowel syndrome: a real phenomenon or an epiphenomenon?
Shows mediocre results emerging from disease management that relies on the old method of IgG testing to detect sensitivities but hints that foods do play a role) Right idea. Wrong testing.
Dis Manag Advis.2004 Jan; 10(1):6-10, 1
Alternative approach to IBS and migraine is winning over providers.
A description of the LEAP Program’s successes in pinpointing triggers for IBS, migraine and even the more delayed and enigmatic fibromyalgia
Am J Gastroenterology 2000 Jan;95(1):157-65
Risk factors for irritable bowel syndrome: role of analgesics and food sensitivities. Locke GR 3rd, Zinsmeister AR, Talley NJ, Fett SL, Melton LJ
Migraine Research- Is Food Making You Sick? Why?
The frequency of migraine has been studied in adult patients with suspected adverse reaction to foods.
Migraine was present in 41 out of 300 patients (13.6%). 38 of these 41 subjects have been treated with elimination diet; 25 (65.7%) obtained a significant improvement of migraine and subsequently, performed challenge test. 24 patients were affected by food intolerance and only one by food allergy. The remaining 13 non-responder subjects suffering from migraine have been subsequently submitted to pharmacological treatment.
Recenti Prog Med 1989 Feb;80(2):53-5
2/3 migraine patients responded to an elimination diet, 96% had “food intolerance” not food allergy —- non-IgE in other words
A remarkable thing is that this “food intolerance” activates the immune system. In this study, migraine patients receiving a food challenge were found to have an increase in T cells showing lymphocyte activation.
T cells Expressing IL-2 Receptor in Migraine (Food Induced).
Martelletti P. Centro Cefalee, Universita La Sapienza, Roma, Italia.
We studied a group of migraine patients for circulating immune complexes, lymphocyte subpopulations, IgG4 and anti-IgG antibodies, before, after 4 hours and after 72 hours a specific challenge test.
We found an increased incidence of circulating immune complexes. Total T cells showed a marked increase after challenge test. The most important finding was the presence of T-activated cells. Also K and NK cells showed an early increase after the challenge.
In commenting on the outcomes of this investigation, it must be stressed that the evidence of an early lymphocyte activation after the challenge test indicates an involvement of interleukin-2 related receptor in food-induced migraine.
The results have reinforced the idea of immune mechanism involvement in food-induced migraine, but it seems to be a different mechanism from that previously hypothesized, with the involvement of the “complex cytokines” network.
Acta Neurol (Napoli) 1991 Oct;13(5):448-56
So, it is not merely a vague intolerance but an immune activation involving proliferation of T-Cells)
In this study, there is the search to find whether the cause of the “food intolerance” is IgG activation …………….
Evidence For an Immune-Mediated Mechanism in Food-Induced Migraine from a Study on Activated T-cells, IgG4 subclass, anti-IgG Antibodies and Circulating Immune Complexes.
Martelletti P, Sutherland J, Anastasi E, Di Mario U, Giacovazzo M.
Various immunological studies have revealed controversial outcomes on pathogenic mechanisms of food-induced migraine. In order to better define the immune status of this disease we studied 21 patients (cow milk provoked migraines) for circulating immune complexes (CIC). Six out of them were also studied for lymphocyte subpopulations, IgG4 and anti-IgG antibodies, before oral challenge (TO), 4 hours after oral challenge (T4), and 72 hours after oral challenge (T72) with 250 ml of cow milk. The ClqSp assay was used to determine CIC. Lymphocyte subpopulations were defined by the following monoclonal antibodies (Mab): OKT3, OKT4, OKT8, 4F2, H366, TAC, 5E9, L.243 and DA6.231. IgG4 subclass was assessed by using a mouse specific Mab. Anti-IgG antibodies were determined by using HPLC.
No significant variation was observed in the study of the expression of DR antigens (L.243 and DA6.231) at the three times. IgG4 and anti-IgG antibodies values showed no variation in their time-course.
However, the results showed an increased incidence (3x) of CIC (28.6%) when compared to the control group (10%). Total T-cells (OKT3+) showed a marked increase at T4 (p less than 0.01) and a subsequent decrease at T72 (p less than 0.02). Interestingly, T-activated cells (4F2+ and TAC+) showed a parallel trend at T4 (respectively p less than 0.02 and less than 0.01) and a subsequent decrease at T72 only for the Tac+ cells (p less than 0.05). Also K and NK cells (H366+) showed an early increase at T4 (p less than 0.05).
All of which suggest an aberrant cell-mediated immune response to the food antigen challenge.
but most likely a cell mediated, delayed-type hypersensitivity reaction or Type 4 reaction is concluded to be the cause.
Inability of Proton Pump Inhibitors to Control Acid Reflux
Evidence that antacids do NOT always control reflux, a common symptom of food sensitivities
2010 Digestive Disease Week, held in New Orleans, USA
Donald O. Castell, MD, Director, Esophageal Disorders Program, Medical University of South Carolina, Charleston, USA, was invited to deliver a State of the Art Lecture on improving treatment outcomes in GERD patients. He provided insight about why current therapies do not always achieve durable symptom relief. In particular, he suggested that the long-term focus on acid control has been a successful strategy for healing of lesions caused by GERD but it may not be always be sufficient for control of symptoms and that, after the initial great response of 90% initial remission, only 36% maintain remission on proton pump inhibitor therapy.
DALLAS – Nov. 19, 2009 – Contrary to current thinking, a condition called gastroesophageal reflux disease (GERD) might not develop as a direct result of acidic digestive juices burning the esophagus, UT
Southwestern Medical Center researchers have found in an animal study. UT Southwestern researchers report that rather, gastroesophageal reflux spurs the esophageal cells to release chemicals called cytokines, which attract inflammatory cells to the esophagus. It is those inflammatory cells, drawn to the esophagus by cytokines, that cause the esophageal damage that is characteristic of GERD. The condition is manifested by symptoms such as heartburn and chest pain.