# IgG Food Allergies/Anyone have experience?



## ms.m (Jan 23, 2008)

Has anyone had IgG allergy testing done? If so, have you had any success on eliminating those foods that you tested positive for? I had it done and supposedly have a food allergy to quite a lot of things and my diet is really limited. Now I feel quite a bit better for the last month and a half than I have in a long time but I think it's other supplements I'm on, not the elimination diet. Because I was on the elimination diet for almost two months and didn't feel better at all. Then I started taking digestive enzymes & these fiber supplements and feel quite a big better (although there's a ways to go). So I'm not really sure if the diet has made a difference or not.I've recently read up on the IgG allergy testing and I'm now really skeptical about it. The incredibly restricted diet is terrible but I'm more than willing to stick it out if it's legitimate. I just wanted to know if anyone has had experience with these tests and the elimination diets you're placed on after you find what your allergies are. Thanks!


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## Noah (Sep 24, 2007)

I have done Genovas allergy test and was mild IgG for everything apart from 2 things I think. My guess is that my small intestine is irritated and this may be the reason, but I haven't a clue. I haven't paid much attention to the result, since I don't seem the allergic type ... and would only really believe it if I did the test twice and got the same results.


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## eric (Jul 8, 1999)

FYI"The Australasian Society of Clinical Immunology and Allergy has issued this paper on Allergy testing and treatments."Unorthodox Techniques for the Diagnosis and Treatment of Allergy, Asthma and Immune Disorders "Inappropriate use of Conventional TestingAdverse consequences may also arise if conventional laboratory tests are used in inappropriate clinical situations, or where results are presented in a manner amenable to misinterpretation. Food specific IgG, IgG4Use: Diagnosis of food sensitivity / allergy. Method: Antibodies to food are measured using standard laboratory techniques. Evidence: Level II Comment: IgG antibodies to food are commonly detectable in healthy adult patients and children, independent of the presence of absence of food-related symptoms. There is no credible evidence that measuring IgG antibodies is useful for diagnosing food allergy or intolerance, nor that IgG antibodies cause symptoms. In fact, IgG antibodies reflect exposure to allergen but not the presence of disease. The exception is that gliadin IgG antibodies are sometimes useful in monitoring adherence to a gluten-free diet patients with histologically confirmed coeliac disease. Otherwise, inappropriate use of food allergy testing (or misinterpretation of results) in patients with inhalant allergy, for example, may lead to inappropriate and unnecessary dietary restrictions, with particular nutritional implications in children. Despite studies showing the uselessness of this technique, it continues to be promoted in the community, even for diagnosing disorders for which no evidence of immune system involvement exists. "http://www.allergy.org.au/pospapers/unorthodox.htmI am not sure if you are lookingat this as the cause of IBS, but foods don't cause IBS. They can act as triggers for a lot of reasons, including the "act of eating itself."


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## ms.m (Jan 23, 2008)

Thanks for the info. I've been reading similar things. I was never told nor never believed it caused my IBS, just that it may aggravate my symptoms. Just wondering if anyone had personal experiences with it working or not working in regards to helping their IBS symptoms. Thanks for the article, I've read a lot of studies recently about it on the internet and hadn't come across that.


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## eric (Jul 8, 1999)

Ms.M, there is a cell involved in IBS called a mast cell, have you ever heard of mast cells. They are most commonly know for allergies, but have roles in at least some IBSers. The researchers for IBS have a lot of evidence for the d and c and d/c in IBS and the role of serotonin in the gut released from another cell called enterochromaffin (EC) cells. EC cells and mast cells can basically cause all of the symptoms of IBS, although its all not completely understood yet.altered serotonin signaling and ibs compilation http://www.ibsgroup.org/forums/index.php?showtopic=80198


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## TexasMom (May 27, 2006)

I work with food sensitivity testing that has worked extremely well - it's called mediator release testing. IBS is mainly caused by type IV delayed hypersensitivities. This is a cell-mediated reaction. IgG testing is a small part of the picture and is antibody mediated. Mediator release testing captures both type III (antibody mediated) and type IV. We put the patients on a diet eating only their non-reactive foods for 1 month. I usually see an 80% improvement in symptoms within 1 week. There are many docs all over the country that offer this type of testing. Here is one: http://ezinearticles.com/?MRT-Testing-Is-H...s&id=757842Also, there is a lot of research on inflammatory mediators triggered by food antigens causing IBS. Here is some: "Use of the LEAP-Mediator Release Test to Identify Non-IgE Mediated Immunologic Food Reactions That Trigger Diarrhea Predominant IBS Symptoms Results in Marked Improvement of Symptoms Through Use of an Elimination Diet"American College of Gastroenterology Annual Scientific Meeting Meeting, November, 2004; Williams, Fred H., M.D., Department of Gastroenterology, St. John's Mercy Medical Center, St. Louis, Missouri ----------------Alternative Approach to IBS and Migraine is Winning Over Providers. Disease Management Advisor. 2004 Jan;10(1):6-10, 1 ------------------Segmental Intestinal Perfusion. A New technique For Human Studies" Lakartidningen, 1994, May 11;91(19):1941-6. Knutson L, Hallgren R, Ahrenstedt O, Bengtsson U, et al.; Kirurgiska Kliniken, Akademiska Sjukhuset, Uppsala, SwedenDuring these investigations the authors reported "&#8230;Luminal provocation with different food antigens in cases of Celiac Disease and Food Intolerance not only activated cells in the intestinal mucosa but also increased the leakage of plasma and lymph. " ---------------------Immune Activation in Patients with Irritable Bowel Syndrome. Liebgrets T, Adams B, et alDepartment of Gastroenterology and Hepatology, University of Adelaide, Royal Adelaide Hospital, South Australia; Nerve-Gut Research Laboratory, Hanson Institute, Adelaide, SA, Australia.Gastroenterology. 2007 Mar;132(3):913-20. Epub 2007 Jan 26 ------------------------Post-infectious irritable bowel syndrome.Spiller R, Campbell E.Wolfson Digestive Diseases Centre, University Hospital, Nottingham, UK. Curr Opin Gastroenterol. 2006 Jan;22(1):13-7.the authors state "&#8230;increased inflammatory cytokines in both mucosa and blood have been demonstrated in Irritable Bowel Syndrome&#8230;" ------------------------These inflammatory cytokines can me detected using Signet Diagnostic's mediator release testing, developed by immunologist Dr. Mark Pasula, PhD........ (note: I do not work for Signet, but I do use their test, which works so well for IBS-D or IBS cyclic, that I've toyed with the idea of offering a money-back guarantee!) Susan


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## eric (Jul 8, 1999)

Susan, your posting inaccurate information."IBS is mainly caused by type IV delayed hypersensitivities."This is False! IBS is not caused by foods or food allergies."Also, there is a lot of research on inflammatory mediators triggered by food antigens causing IBS. "I don't think you fully understand the whole picture with inflammation and IBS. There is also more to IBS then inflammation for one. They can also already partly explain the reasons for d and c and d/c. This is not a food reaction.We had Mike No lomotil on here explaining all there is about leap and also psting bad IBS information.There is also a big difference between food allergy and food intolerences as you must know one is a immune system reation, food allergies and food intolerences are not immune system reaction.The connection between IBS and food allergies is through the mast cell. But mast cells are also not the only issues in IBS or the only way to trigger them. There is strong evidence the release of serotonin from EC cells in the enteric nervous system, causes the d and c and d/c. Your not up to date on IBSSome of the quotes your quoting there are not even what what your actually presenting as a problem and some have nothing to do with IBS.I will post some information here.This first one is from the Chairman of the Rome committe to legtimize and diagnose IBS.Dr. Drossman is a Co-director of the Center and Professor of Medicine and Psychiatry at UNC-CH. He established a program of research in functional gastrointestinal disorders at UNC more than 15 years ago and has published more than 250 books, articles, and abstracts relating to epidemiology, psychosocial and quality of life assessment, design of treatment trials, and outcomes research in gastrointestinal disorders.Dr Drossman's comments on foods for IBS Health.Shawn,To say that people with IBS may get symptoms from food intolerances is an acceptable possibility, since the gut will over react to stressors of all types including food (high fat or large volumes of food in particular). Futhermore, there can be specific intolerances. So if you have a lactose intolerance for example, it can exacerbate, or even mimic IBS. Other examples of food substances causing diarrhea would be high consumers of caffeine or alcohol which can stimulate intestinal secretion or with the latter, pull water into the bowel (osmotic diarrhea). The same would be true for overdoing certain poorly absorbed sugars that can cause an osmotic type of diarrhea Sorbitol, found in sugarless gum and sugar substituted foods can also produce such an osmotic diarrhea. Even more naturally, people who consume a large amount of fruits, juices or other processed foods enriched with fructose, can get diarrhea because it is not as easily absorbed by the bowel and goes to the colon where it pulls in water. So if you have IBS, all of these food items would make it worse. *However, it is important to separate factors that worsen IBS (e.g., foods as above, stress, hormonal changes, etc.) from the cause or pathophysiology of IBS. Just like stress doesn't cause IBS, (though it can make it worse), foods must be understood as aggravating rather than etiological in nature. *The cause of IBS is yet to be determined. However, modern research understands IBS as a disorder of increased reactivity of the bowel, visceral hypersensitivity and dysfunction of the brain-gut axis. There are subgroups being defined as well, including post-infectious IBS which can lead to IBS symptoms. Other work using brain imaging shows that the pain regulation center of the brain (cingulate cortex) can be impaired, as well as good evidence for there being abnormalities in motility which can at least in part explain the diarrhea and constipation. So finding a specific "cause" of IBS has grown out of general interest in place of understanding physiological subgroups that may become amenable to more specific treatments. Hope that helps.Doug DrossmanMisconceptions Linger Around Irritable Bowel SyndromeIBS DietDiet, food and eating can affect symptoms in IBS. Many people with irritable bowel syndrome (IBS) notice that their symptoms appear to get worse following a meal. They may wonder if they have a dietary allergy or intolerance. More confusing, they may notice that a food seems to upset them on one day but not another. Among the most common questions IBS patients have is what food to avoid. This can drive a person to go looking for a diet or a test that might help sort all this out. A bewildering amount of often conflicting advice is available, especially on the Internet. Much of it is associated with a considerable cost."http://www.aboutibs.org/site/about-ibs/management/ibs-dietWhat Patients Know About Irritable Bowel Syndrome (IBS) and What They Would Like to Know"The most prevalent IBS misconceptions included (% of subjects agreeing with the statement): IBS is caused by lack of digestive enzymes (52%), is a form of colitis (42.8%), will worsen with age (47.9%), and can develop into colitis (43%) or malnutrition (37.7%) or cancer (21.4%). IBS patients were interested in learning about (% of subjects choosing an item): (1) foods to avoid (63.3%), (2) causes of IBS (62%), (3) coping strategies (59.4%), (4) medications (55.2%), (5) will they have to live with IBS for life (51.6%), and (6) research studies (48.6%). Patients using the Web were better informed about IBS.*Conclusion: (1) Many patients hold misconceptions about IBS being caused by dietary habits, developing into cancer, colitis, causing malnutrition, or worsening with age; (2) patients most often seek information about dietary changes; and (3) educational needs may be different for persons using the internet for medical information."*http://www.ibsgroup.org/php/articles.phtml...&toid=90774Does allergy play a role in irritable bowel syndrome (IBS) and in constipation? http://www.aboutibs.org/site/news-events/n...ws#allergy-kidsThere is a lot more on all this.This is newhttp://www.ibsgroup.org/forums/index.php?showtopic=93270If you have actual food allergies or food intolerences and IBS they can aggravate each other, but if you elininate the food allergies you still have the underlying IBS.


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## eric (Jul 8, 1999)

This is brand new state of the art IBS information.2007 IFFGD Symposium Summary Report, Very much worth reading/state of the art researchhttp://www.ibsgroup.org/forums/index.php?showtopic=92806PS so far most of the inflammation seen in IBSers comes from Post Infectious IBS studies. There are structural cell changes in the colon, including an increase in EC cells and mast cells.also if bloating or distension is an issue.Review Article: Abdominal Bloating and Distension in Functional Gastrointestinal Disorders -- Epidemiology and Exploration of Possible Mechanisms Medscapehttp://www.ibsgroup.org/forums/index.php?showtopic=93456In D IBS patients they can also detect and increase in serotonin release after eating a meal. Increasingly our understanding of IBS is that it is a heterogeneous disorder - that is, multiple factors contribute to the well defined symptoms of the disorder. One of these suspected underlying dysfunctions involves serotonin, which is a neurotransmitter or messenger to nerves. Most serotonin in the body is in cells that line the gut where it senses what is going on and through receptors signals nerves that stimulate a response. The serotonin must then be reabsorbed (a process called re-uptake) into cells. This process appears to be disrupted in people with IBS.Serotonin and SERTHow does serotonin affect gut function? An interview with Gary M. Mawe, PhD, Professor of Anatomy and Neurobiology, University of Vermont, Burlington, VT. Dr. Mawe is a basic scientist.http://www.aboutibs.org/site/learning-cent...orner/serotoninVideo Corner: Inflammation In some people with IBS a subtle inflammation persists for some time after recovery from an initial infection and obvious inflammation. This can cause increased sensation in the intestines and changes in gut motility consistent with symptoms of IBS.InflammationDoes inflammation have a role in generating IBS symptoms? An interview with Gary M. Mawe, PhD, Professor of Anatomy and Neurobiology, University of Vermont, Burlington, VT. Dr. Mawe is a basic scientist.http://www.aboutibs.org/site/learning-cent...er/inflammationVideo Corner: Causes and TreatmentsA functional GI disorder such as irritable bowel syndrome (IBS) has very specific symptoms. Over the past 5-10 years we've developed an understanding that many different components contribute to these symptoms. Brain-gut interactions, changes in serotonin signaling, motility, inflammation, gut sensitivity, genetic predispositions, and bacterial flora all can contribute to varying degrees in an individual having this condition. Not only will this help with developing more effective treatments, but better understanding of the factors that underlie symptoms in each individual will enable more reliable treatments that will work earlier on rather than trying hit or miss one after another.Functional GI disorders, such as IBS, present challenges to both the patient and the doctor or other healthcare provider. For the patient, education about their disorder is important to improving management of their condition. For the doctor, understanding the many facets involved with the condition and addressing those that are most evident in each individual is important. Patients and many physicians alike will benefit from the recent and continuing advances, which not only further our understanding but also confirm the validity of the functional GI disorders.http://www.aboutibs.org/site/learning-cent...o-corner/causes


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## TexasMom (May 27, 2006)

Eric, I am not an immunologist, and I agree that foods are not the original cause of IBS and I'm sorry if I implied that. It is the loss of oral tolerance to foods/chemicals that triggers the immune response that provoke the release of pro-inflammatory and pro-algesic mediators. This has been shown time and again through in vivo and in vitro challenges, such as the jejunal isolation challenges, done in Sweden, where the jejunum was isolated, food antigens were injected, and the release of mediators was measured. Healthy controls did not have a significant response, but non-healthy controls did. http://www.docguide.com/news/content.nsf/n...5256C8300631F11Full Thickness Biopsy of the Jejunum Reveals Inflammation and Enteric Neuropathy in Irritable Bowel Syndrome Gastroenterology 2002 Dec;123(6):1972-9 Tornblom H, Lindberg G, Nyberg B, Veress B. Karolinska Institutet Department of Medicine, Huddinge University Hospital, Stockholm, Sweden -----------------Relation between food provocation and systemic immune activation in patients with food intolerance. The Lancet, Volume 356, Issue 9227, Pages 400-401M. Jacobsen, P. Aukrust, E. Kittang, F. Müller, T. Ueland, J. Bratlie, V. Bjerkeli, M. Vatn -----------------Characterisation of immune mediator release during the immediate response to segmental mucosal challenge in the jejunum of patients with food allergy J Santosa, C Bayarria, E Saperasa, C Nogueirasb, M Antolína, M Mourellea, A Cadahiab, J-R Malageladaaa Digestive System Research Unit, Hospital General Vall d'Hebron, Autonomous University of Barcelona, Spain, b Allergy Department, Hospital General Vall d'Hebron, Autonomous University of Barcelona, SpainCorrespondence to: Dr J Santos, McMaster University, Intestinal Disease Research Programme, 1200 Main Street West, Room 3NZ5, Hamilton, Ontario L8N 3Z5, Canada. Accepted for publication 27 April 1999BACKGROUNDFood allergy is a common complaint among patients with a broad spectrum of abdominal and extra-abdominal symptoms that must be distinguished from other more common non-immunological food intolerances.AIMSTo investigate whether human intestinal hypersensitivity reactions are associated with detectable release of inflammatory mediators from activated cells, which may serve as a biological marker of true allergic reactions.PATIENTS/METHODSIn eight patients with food allergy and seven healthy volunteers, a closed-segment perfusion technique was used to investigate the effects of jejunal food challenge on luminal release of tryptase, histamine, prostaglandin D2, eosinophil cationic protein, peroxidase activity, and water flux.RESULTSIntraluminal administration of food antigens induced a rapid increase in intestinal release of tryptase, histamine, prostaglandin D2, and peroxidase activity (p<0.05 v basal period) but not eosinophil cationic protein. The increased release of these mediators was associated with a notable water secretory response.CONCLUSIONSThese results suggest that human intestinal hypersensitivity reactions are characterised by prompt activation of mast cells and other immune cells, with notable and immediate secretion of water and inflammatory mediators into the intestinal lumen. Analysis of the profile of markers released into the jejunum after food provocation may be useful for the objective diagnosis of food allergy. -----------------------Even with Crohn's disease: Aliment Pharmacol Ther. 2002 Nov;16(11):1903- 15. Gut mucosal response to food antigens in Crohn's disease.a.. Van Den Bogaerde J,b.. Cahill J,c.. Emmanuel AV,d.. Vaizey CJ,e.. Talbot IC,f.. Knight SC,g.. Kamm MA.St Mark's Hospital, Harrow, Middlesex, UK.BACKGROUND: Food antigens may contribute to gut inflammation in Crohn's disease.AIM: To assess in vivo sensitization to food antigens, ascertain whether sensitivity is gut specific, assess food sensitization in vitro, and correlate in vivo changes with histological and blood changes.METHODS: Skin testing and rectal exposure to six food antigens (cereal, cabbage, citrus, milk, yeast and peanut) and control saline were assessed double-blind by immediate and 3.5-h laser Doppler blood flowmetry, and rectal biopsies were taken. Peripheral blood lymphocyte proliferation was measured in response to the same antigens.RESULTS: Ten patients with Crohn's disease and 10 healthy controls were studied. Blood flow increased in 24 of 60 antigen sites in Crohn's disease patients and six of 60 antigen sites in controls (P < 0.0001) after 3.5 h. The Crohn's disease group demonstrated higher rectal blood flow than controls in response to all food antigens, and this was significantly different for the responses to yeast (P = 0.036) and citrus fruits (P = 0.038). Lymphocyte proliferation occurred in 32 of 60 tests in Crohn's disease patients and eight of 60 tests in controls (P < 0.0001). There were no skin responses. Submucosal oedema corresponded to increased mucosal flow.CONCLUSIONS: Crohn's disease patients demonstrate in vivo and in vitro sensitization to food antigens, which is gut specific. Mucosal flowmetry allows the identification of sensitization to gut antigens. ------------------There is much much more if you search. Foods do trigger an immune response in many immune compromised individuals with IBS and other inflammatory conditions. Again, I am not an immunologist, but I can say that out of 400 patients that I've tested, 397 have dramatically improved (80% improvement on average). Whether that technically "cured" their IBS or not...... I don't know....... but they don't have any more diarrhea, cramping, bloating, headaches, etc. And, I follow the patients for 3 months and the symptoms do not return (unless they go back to old habits, which they don't want to do, so it's not an issue). Susan


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## eric (Jul 8, 1999)

Your posting some older work and they are much farther ahead now and some of what your posting again has nothing to do with IBS.We also have no way to know what people coming to see you were diagnosed with the rome critira, because I am sure some people with food issues come to see you.your also talking about neurogenic inflammation in IBS, WITHOUT EVEN REALIZING IT."Eric, I am not an immunologist, and I agree that foods are not the original cause of IBS and I'm sorry if I implied that. It is the loss of oral tolerance to foods/chemicals that triggers the immune response that provoke the release of pro-inflammatory and pro-algesic mediators. "This may sound good but there is no evdidence for this in IBS research other then some foods can trigger the mast cells, but you are not posting about that with the "Full Thickness Biopsy of the Jejunum Reveals Inflammation and Enteric Neuropathy in Irritable Bowel Syndrome Gastroenterology study."You would also need to follow the patients for a year, because there is a very high placebo responce rate in IBS. This is recognized with all researcher studying IBS and clinical trials. We also hear this kind of thing alot on the bb here in the past from food testing people, but there never any clinical trials ort actual research howing anything like the results mentioned here.IBS is already a brain gut axis disorder. It is a functional disorder "how the body works" and they have found *STRUCTURAL CELL *abnormalities in IBS.Allergies: Dubious Diagnosis and Treatment "The LEAP Program, in which the Mediator Release Test (MRT) is used to identify "delayed food allergies" and treatment involves dietary manipulation and possibly supplements and/or herbs. "http://www.quackwatch.org/01QuackeryRelate...lergytests.htmlNeuromuscular Dysfunction and IBS: Clinical Implications"Several investigators have demonstrated increased levels of inflammatory cells and mediators in a subset of IBS patients,[4,5] but these data have been inconsistent"http://www.medscape.com/viewarticle/548600These *are* experts in immunology, food allergy and IBS and they don't agree with what your saying here.FYI"You have two brains: one in your head and another in your gut. Dr. Jackie D. Wood is a renowned physiologist at The Ohio State University. He calls the second brain, "the-little-brain-in-the-gut." This enteric nervous system is part of the autonomic nervous system and contains over one hundred million neurons, which is as many as are in the spinal cord. This complex network of nerves lines the walls of the digestive tract form the esophagus all the way down to the colon. This little brain in the gut is connected to the big brain by the vagus nerves, bundles of nerve fibers running from the GI tract to the head. All neurotransmitters, such as serotonin that are found in the brain are also present in the gut.*Dr Wood has discovered that this little-brain-in-the-gut has programs that are designed for our protection and which are very much like computer programs. They respond to perceived threats in the same way that the limbic system or the emotional brain does. So the threat of a gastrointestinal infection can activate the program that increases gut contractions in order to get rid of the infection. The symptoms are abdominal cramping and diarrhea. Dr. Wood has determined that a type of cell found in the body and the gut, called the mast cell, is a key to understanding the connection of the big brain in the head with the little-brain-in-the-gut. Mast cells are involved in defense of the body. In response to certain threats or triggers, such as pollen or infection, mast cells release chemicals, such as histamine, that help to fight off the invader. Histamine is one of the chemicals that causes the symptoms of an allergy or a cold. When an infection of the gut occurs, such as food poisoning or gastroenteritis, the mast cells of the gut release histamine. The little-brain-in-the-gut interprets the mast cell signal of histamine release as a threat and calls up a protective program designed to remove the threat â€" at the expense of symptoms: abdominal pain and diarrhea. The brain to mast cell connection has a direct clinical relevance for irritable bowel syndrome and other functional gastrointestinal syndromes. It implies a mechanism for linking allostasis and the good stress response to irritable states (e.g., abdominal pain and diarrhea) of the gut. Mast cells can be activated to release histamine in response to perceived psychological stress, whether the stressor or trigger is consciously perceived or not. So the end result is the same as if an infection activated the program in the-little-brain-in-the-gut: abdominal pain and diarrhea."*http://www.parkviewpub.com/nuggets/n5.html Dr Wood's comments for me"Dr. Jack Wood, a renowned physiologist at The Ohio State University calls the ENS the little-brain-in-the-gut. "Dear Shawn:Sorry for the delayed reply to your question. I generally agree with Dr. Drosssman's response. *A subgroup of individuals when they become sensitized to specific molecules in certain foods respond to ingestion of the molecules with symptoms of cramping abdominal pain, fecal urgency and explosive watery diarrhea. These are also the primary symptoms of diarrhea-predominant IBS. Enteric mast cells, by mechanisms we don't understand, become sensitized to the food molecule and respond to its presence by releasing a signal to the brain-in-the-gut (ENS) which is interpreted as a threat. The ENS responds by running a program which organizes secretion and motility into a behavior pattern of the bowel, which rapidly clears the threat from the lumen. Because to be effective secretion occurs in large volumes and the contractions that accomplish rapid propulsion are strong, running of the program has the side effects of diarrhea and cramping pain. Big brain input to mast cells during stress activates the mast cells to evoke the symptoms resulting from exposure of the mast cells to sensitizing food antigens. Aside from food allergens and mast cells, certain chemicals such as those in hot peppers, stimulate sensory nerves in the ENS and we are beginning to understand how this can also lead to food-related symptoms that might mimic or exacerbate IBS.*Hope this helps,Jackie (Jack) D. Wood " Mast cell and cellularity of the colonic mucosa correlated with fatigue and depression in the irritable bowel syndrome."CONCLUSIONS: Elevated MCs counts are a key feature of the low grade inflammatory infiltrate in the caecal mucosa of IBS. Fatigue and depression are associated with mucosal cell counts, in particular MCs suggesting that psychological factors are associated to the low-grade inflammatory infiltrate in IBS."http://www.ibsgroup.org/forums/index.php?showtopic=93117Dietary interventions for recurrent abdominal pain (RAP) and irritable bowel syndrome (IBS) in childhood."AUTHORS' CONCLUSIONS: There is a lack of high quality evidence on the effectiveness of dietary interventions. This review provides no evidence that fibre supplements, lactose free diets or lactobacillus supplementation are effective in the management of children with RAP."http://www.ibsgroup.org/forums/index.php?showtopic=93790I know you could not have gone through all the information above yet, but they are not showing what your saying about foods and IBS. There have been people here before you posting almost exactly the same info you are now years ago? They are five to six years however more advanced then they were then on IBS research. There are also some major issues with Leap testing itself as well as the below."The Australasian Society of Clinical Immunology and Allergy has issued this paper on Allergy testing and treatments."Unorthodox Techniques for the Diagnosis and Treatment of Allergy, Asthma and Immune Disorders "Inappropriate use of Conventional Testing"Comment: *Inappropriate used may be divided into three areas. (1) Inappropriate patient selection. As with any diagnostic test, use in patients where there is no evidence that food allergy plays a role in pathogenesis increases the likelihood of irrelevant false positive results. Use of food allergy testing in patients with inhalant allergy, for example, may lead to inappropriate and unnecessary dietary restrictions, with particular nutritional implications in children. (2) Misinterpretation of results. Low levels of food-reactive IgE are found in some healthy individuals without clinical reactivity. Challenge studies have shown a correlation between allergen-specific IgE and then likelihood of reactivity to some (such as cows milk, egg and peanut) but not all foods. In the absence of a history of clinical reactivity, low levels of allergen-specific IgE are usually of little diagnostic significance. (3) Inappropriate data presentation. Presentation of data as "raw counts" has no scientific or clinical rationale, has not been shown to correlate with clinical reactivity and renders results more liable to misinterpretation. "*http://www.allergy.org.au/pospapers/unorthodox.htmThe mast cells are also not the only problem, just a part of the problem. There is a lot already know about them and a lot more being done on them now, they are connected to the brain's immune responce and gut immune responce and also to the bodies stress system to protect the entire organism from ANY threats. Mast cells can be degranulated by foods, stress, hot and cold, and certain medications among many other reasons.


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## TexasMom (May 27, 2006)

Eric, I think I could go round and round with you and I won't..... some of the research was older , some wasn't..... and it showed that food antigens provoked an immune response.......... as far as placebo effect......... 99% of the time? 80% improvement? Wow, that's quite a placebo effect........... I follow the patients for 3 months.......... placebo effect for that long? In all cases? I have actually called my severe cases after 9 months or so just to see how they were doing and they were doing very well......... many gastroenterologists have been doing this for many years, and if their patients came back after a time and were back at square one, they wouldn't keep doing it........ not putting their professional reputations on the line. As far as Mr. Quackwatch, he's got troubles of his own..... being sued and losing...... also, making accusations without being willing to look at the research when being given the opportunity. That guy is a piece of work. Finally, even if it is a placebo effect...... heck if I was having daily migraines for years, I would welcome a placebo effect that left me migraine free ........ or if I was having daily diarrhea and cramping for 1 1/2 years (these are actual patients), then if I could be diarrhea free after two days of eliminating reactive foods, then I would welcome a placebo effect! Susan


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## eric (Jul 8, 1999)

I know all about all of the research you posted. I don't think you really know about IBS. It is a distint entity and is not caused by foods.The placebo responce in IBS is from thrity to 80% and can last a year. I will find the research for you. Also I have nothing agasint placebo, but your not offering a placebo.Your also just giving anecdotal evidence and no science on any of this, because the things you posted you don't fully understand. Your also as I mentioned posting the exact thing Mike No Lomo did who was a leap guy 5 years ago. As I have said the condition is much more understood now. It is not food caused allergies. IT is much much more complex then simple food allergies. There is no evidence of IgE mediated food responces in IBS, unless the person already had a food allergy. IgG there is no eveidence that causes any symptoms regarless of IBS.You you know what post infectious IBS is?They already also have a lot of real eveidence the d and c and D/c is caused as I posted above by serotonin dsyregulation. The pain in IBS is also not caused by foods, but by the underlying disorder, foods can be triggers, but so can stress, hormones, the weather and many other reason.Only 2 or so percent of the entire population in the US has REAL food allergies, many of them have no digetive problems like both my nephews and 20% of the US population has IBS, a higher percentage of women.There is a big problem with those numbers.I am going to post some other important issues about all this and actual IBS such as the gastro colonic responce and d IBSers, which can go off immediately after eating regarless of what foods they ate.Or this that shows drinking cold water can set it off.J Gastroenterol Hepatol. 2007 Dec;22(12):2330-7. LinksPlasma and gastric mucosal 5-hydroxytryptamine concentrations following cold water intake in patients with diarrhea-predominant irritable bowel syndrome.Zuo XL, Li YQ, Yang XZ, Guo M, Guo YT, Lu XF, Li JM, Desmond PV.Department of Gastroenterology, Qilu Hospital, Shandong University, Jinan, China.BACKGROUND AND AIM: The purpose of the present paper was to investigate the effects of cold water intake on 5-hydroxytryptamine (5-HT) and its metabolite 5-hydroxyindole acetic acid (5-HIAA) in diarrhea-predominant irritable bowel syndrome (d-IBS) patients, and to observe the relationship between 5-HT and symptomatology. METHODS: The plasma 5-HT/5-HIAA concentrations at 0, 30 min, 60 min, 90 min, 120 min, 150 min and 180 min following cold or warm water intake were investigated in 32 female subjects with d-IBS and 21 healthy female subjects. Gastric mucosal 5-HT under fasting conditions and following water intake were further investigated in 15 d-IBS patients and nine healthy subjects. Symptomatology was assessed throughout the study. RESULTS: The plasma 5-HT concentrations in IBS patients were significantly higher than those of controls at 30 min (P = 0.022), 60 min (P < 0.001), 90 min (P < 0.001), 120 min (P < 0.001) and 150 min (P = 0.001) after cold water intake. The peak plasma 5-HT/5-HIAA and area under the curve for 5-HT/5-HIAA were also higher in d-IBS patients (P < 0.001). Gastric mucosal 5-HT in d-IBS patients and controls did not show any significant differences both under fasting condition (P = 0.596) and after cold water intake (P = 0.426). Last, the d-IBS patients with symptoms had higher 5-HT concentration (P < 0.001) and there was a positive correlation (r = 0.714, P = 0.001)between the symptomatology and plasma 5-HT level. *CONCLUSIONS: These data suggest that symptomatology following cold water intake may be associated with increased plasma 5-HT concentrations in female subjects with d-IBS.*PMID: 18265445 Please read this thread very carefullyhttp://www.ibsgroup.org/forums/index.php?showtopic=80198you mentioned the duodenum, *proximal end of jejunum and terminal ileum*World J Gastroenterol. 2007 Dec 7;13(45):6041-7. LinksDecreased expression of serotonin in the jejunum and increased numbers of mast cells in the terminal ileum in patients with irritable bowel syndrome.Wang SH, Dong L, Luo JY, Gong J, Li L, Lu XL, Han SP.Department of Gastroenterology, Second Hospital of Xi'an Jiaotong University, 157, Xi 5 Road, Xi'an 710004, Shaanxi Province, China. [email protected]: To investigate if there are changes in serotonin (5-HT) levels, enterochromaffin (EC) cells and mast cells in small intestinal mucosa of patients with irritable bowel syndrome (IBS). METHODS: Diarrhea-predominant (IBS-D, n = 20), or constipation-predominant (IBS-C, n = 18) IBS patients and healthy controls (n = 20) underwent colonoscopy and peroral small intestinal endoscopy, and mucosal samples were obtained at the descending part of the duodenum, proximal end of jejunum and terminal ileum. High-performance liquid chromatography-electrochemistry and immunohistochemical methods were used to detect 5-HT content, EC cells and mast cells. RESULTS: (1) There were no differences in the number and distribution of EC cells between IBS patients and the normal group. (2) The mucosal 5-HT contents at the duodenum, jejunum and ileum in IBS-C patients were 182 +/- 90, 122 +/- 54, 61 +/- 35 ng/mg protein, respectively, which were all lower than those in the normal group (256 +/- 84, 188 +/- 91, and 93 +/- 45 ng/mg protein, respectively), with a significant difference at the jejunum (P < 0.05). There were no differences in the small intestinal mucosal 5-HT contents between IBS-D patients and the normal group. The mucosal 5-HT contents at the duodenum were significantly higher than those at the ileum in the three groups (P < 0.001). (3) The numbers of mast cells in patients with IBS-C and IBS-D at the ileum were 38.7 +/- 9.4 and 35.8 +/- 5.5/high power field (hpf), respectively, which were significantly more than that in the normal group (29.8 +/- 4.4/hpf) (P < 0.001). There was no significant difference in the numbers of mast cells at the other two parts between IBS patients and the normal group. The numbers of mast cells in IBS-C, IBS-D, and normal groups were all significantly higher at the ileum (38.7 +/- 9.4, 35.8 +/- 5.5, 29.8 +/- 4.4/hpf, respectively) than at the duodenum (19.6 +/- 4.7, 18.5 +/- 6.3, 19.2 +/- 3.3/hpf, respectively, P < 0.001). CONCLUSION: The changes in the 5-HT signaling pathway at the jejunum of IBS-C patients and the increase in mast cells in patients with IBS at the terminal ileum may offer evidence to explain the pathogenesis of IBS.PMID: 18023097 [PubMed - in process]Neurogastroenterol Motil. 2007 Aug;19 Suppl 2:25-31. Recent advances in understanding the role of serotonin in gastrointestinal motility in functional bowel disorders: alterations in 5-HT signalling and metabolism in human disease.Spiller R.Professor of Gastroenterology, Wolfson Digestive Diseases Centre, Nottingham, UK. [email protected] (5-hydroxytryptamine, 5-HT) is present in abundance within the gut, most stored in enterochromaffin cell granules. It is released by a range of stimuli, most potently by mucosal stroking. Released 5-HT stimulates local enteric nervous reflexes to initiate secretion and propulsive motility. It also acts on vagal afferents altering motility and in large amounts induces nausea. Rapid reuptake by a specific transporter (serotonin transporter, SERT) limits its diffusion and actions. *Abnormally increased 5-HT is found in a range of gastrointestinal disorders including chemotherapy-induced nausea and vomiting, carcinoid syndrome, coeliac disease, inflammatory bowel disease and irritable bowel syndrome (IBS) with diarrhoea (IBS-D), especially that developing following enteric infection. Impaired SERT has been described in IBS-D and might account for some of the increase in mucosal 5-HT availability. 5-HT(3) receptor antagonists inhibit chemotherapy-induced nausea and diarrhoea associated with both carcinoid syndrome and IBS. While IBS-D is associated with increased 5-HT postprandially, IBS with constipation (IBS-C) is associated with impaired 5-HT response and responds to 5-HT(4) agonists such as Prucalopride and 5-HT(4) partial agonists such as Tegaserod.*PMID: 17620085 If you are going to talk about inflammation in IBS you better be up to date about post infectious IBS as well as IBS itself and you have not demonstrated that with the information you have posted so far.Serotonin is strongly implicated in IBS one for the d and c and d/c and second because its the neurotramsitter that singals the brain there is pain and pain is a must for an IBS diagnoses.IBS patinets effectively demonstrate dysregulation of the serotonin system.I have been down this road many times now and have looked at all the information in regards to IBS as well as asked personally some of the top experts on IBS in the world. FOODS can be triggers, but are not the cause and fats, or gas vegetables or carbonation can trigger IBS regardless of any food alleries or food intolerences. There is still an underlying disorder, some people have it mild some moderate and some very severe.2007 IFFGD Symposium Summary Report, Very much worth reading/state of the art researchIn addition to that IFFGD, as well as the Rome Foundation, is looking to identify other areas of funding eventually to provide alternate means of support for investigators in the field. Defining functional GI and motility - People often ask, what is a functional GI disorder and what is a motility disorder. They are clearly interrelated. Motility disorders look primarily at altered motility, or movement within the gut; the functional GI disorders address the person and the symptoms. The differences between these relate, in part, to the fact that with functional GI disorders there can be other physiological factors that explain the symptoms in addition to motility. Many factors contribute to functional GI symptoms. The 5 major areas of investigation of the influences on functional GI disorders now include:• Inflammation• Motility• Altered bacterial flora• Visceral hypersensitivity (increasedsensitivity of the gut)• Brain-gut dysfunctionThe biopsychosocial model is a conceptual way to integrate multiple factors based on the mutual interaction of various physiological systems. Rather than looking at linear causality (a singe causeexplaining a disorder), we look at how these many factors interact at a single point in time and over time at different points throughout a person's life. In effect, the biopsychosocial model is the researchand clinical model to explain the complex determinants of the symptoms that patients experience, and what the doctors see in their patients. Within a given individual these factors can explain the remarkable variability of symptom experience between individuals with the same disorder, theirlevel of severity, and response to treatment. Research Areas Genetics - In terms of the research areas, there is a lot of interest on geneticinfluences. These include:• Genetic variations that effect motility, andthe body's response to inflammation• Changes in central nervous systempathways that effect the way a personperceives and responds to pain• Linkage to psychological or emotionalresponsesFor example, there are mutations of genes that result in making more or less of a given protein, which may lead to susceptibility to an infection or to stress or to one's bowel sensitivity. When triggerslike inflammation or stress are added to a genetic predisposition, these individuals are more vulnerable to the development or flare up of the functional GI disorder, while others under the same exposure are not. However, genetics is not going to be the sole answer, since they describe thepredisposition to developing a condition rather than the leading to the condition itself. The functional GI disorders are heterogeneous; in other words, many factors contribute to the very specificsymptoms of each functional disorder. In the future, we will probably identify subsets of patients where there are genetic influences to explain why one is more prone to get one set of symptoms overanother.*Pathophysiology - What are the physical and biochemical changes that lead to gut dysfunction? Research in the last few years has looked at changes in the way nerves transmit signals in the brain and the gut, and the role of hormonal responses, all of which can effect motility, secretion, andinflammation. Serotonin - Serotonin (5HT) is a neurotransmitter, a chemical that acts on other targets within the body. Ninety-five percent of serotonin in the body is in the GI tract. It is contained in cells inthe lining of the gut (enterochromaffin cells). When activated through a variety of stimuli it can cause increased motility or nerve sensitivity within the enteric nervous system - the autonomic nervous system within the walls of the digestive tract. Thus it affects gut function as well as influencesthe brain's experience of these symptoms as more or less painful. Serotonin may also have a role in our understanding some of the subtypes of IBS. For example, studies show that patients with IBS withdiarrhea tend to produce more serotonin in their blood after a meal while those with constipation have less serotonin in their blood, compared to controls. Additionally, after serotonin signals nerves in the gut, it has to be removed. This involves a process where a protein, called the serotonin reuptake transporter (SERT), removes the serotonin from the nerve cell space. In effect, we have a hugesponge in our gut for removing serotonin once it's released. We're finding that SERT activity may be different in the intestines of individuals with inflammation or who have IBS, where the sponge effect for serotonin is being lost. When serotonin sits around too long after release it can over-stimulatereflexes and it might also desensitize receptors so they stop responding. These shifts in serotonin signaling could underlie some of the changes in gut function. 5 6Mast cells - Mast cells are a type of immune cell. When activated, certain chemicals contained in packets in the cell are released (degranulated), thus exposing the bowel lining to these secretedsubstances that influence other cells. The mast cell and the effects of degranulation is an area of great interest in understanding IBS since it is involved with many regulatory functions of the intestines. Wehave known for many years that there are increased mast cells in certain areas of the bowel in patients with IBS. Increased mast cell activity is a feature of patients with IBS and we are beginning to better understand how this activity may have effects on the gut. For example it may stimulate nerves to become more sensitive and can increase permeability of the intestinal barriers, thus leading to invasion by bacteria and production of toxic substances. The increased sensitivity of the nerves within the gut (visceral hyperalgesia) can lead to pain or discomfort, even in response to normal events such as eating a meal. Permeability is essential, allowing the passage of fluids and nutrients from the intestines into the body. But too much permeability can be harmful, allowing unwanted substances, like bacteria and its components, to pass into the wall of the gut and lead to inflammation.Cytokines are one type of molecule involved with regulating our immune response (an inflammatory mediator) associated with mast cell activity in addition to other types of cells like lymphocytes. Interestingly, there are good and bad types of cytokines. The bad types are associated with greater inflammation and sensitization, and the good types of cytokines reduce that. We are seeingthat there are differences here in people with IBS compared to controls. Some IBS patients are seen to have more of the bad cytokines that increase inflammation. Bacteria - Another area being looked atis the bacterial flora - the ecology of the gut. There are bad bacteria, which can be associated with infection (inflammation), and there are good bacteria (probiotics) which can help prevent infection. These good bacteria may have other beneficial effects, not only on inflammation. For example, lactobacillus was recently reported to activate certain receptors which suggest that it may have effects on pain. Bifidobacterium, in a study of IBS treatment that compared it to lactobacillus and to placebo, was associated with improvement in symptoms related to normalization of the inflammatory response, similar to healthy volunteers. That favorable response did not happen in the groups treated with lactobacillus or placebo. Stress - We are finding that stress has an effect on the gut flora, permeability,and secretions. The normal gut flora provides a barrier within the intestines to inflammatory types of bacteria. Stress can cause changes in this epithelial barrier, which can allow greater access by theflora to the intestine and in turn lead to increased inflammation. Stress can also significantly modify the immune response to the gut flora. So these are factors that could be affecting the sensitization in IBS and the condition itself. Brain-gut - The brain plays a role as well. The brain and the gut are connected. Thinking and feeling can have affects, influencing release of proteins that interactwith the nervous system (neuropeptides), which can affect motility, secretion, blood flow, and inflammation. Stress may influence inflammatory pathways causing a dysregulation that can lead to emotional conditions and more stress - a vicious cycle. It is not a question as to whether thiscycle begins in the gut or in the brain. The problem is that both systems are effected concurrently thus producing a disturbance of the regulation between the brain and gut; a "vicious cycle" with no beginning or end. Understanding this will open the door to more specific treatments. We can see examples of brain-gut interactions by looking at post-infectious IBS (PI-IBS) or dyspepsia. A study done after a salmonella infection outbreak showed that 10-15% of patients continued with their symptoms of either dyspepsia or IBS after the initial infection subsided. Some recent studies show that this is associated with greater levels of immune cell activity. In IBS, the subgroup of patients with diarrhea as the predominant bowel symptom is the group where more of this inflammatory response is seen; there is also increased psychologic distress occurring at the time of the initial infection, which may be enabling the post-infectious response. In the gut we see infection followed by an inflammatoryresponse, altered motility, and increased sensitivity. But these factors alone are not enough - the brain has a role in regulating these factors. If there is psychological distress around the time of the initial infection, it can result in the expression of the post-infectious symptoms. Thus, the brain and the gut are interacting so with this disorder the brain can influence the inflammation in the bowel while the bowel inflammation can produce psychosocial - emotional and social - distress. Similarly the pain experienced may occur more when there is psychological distress. Both factors are predictive ofpost-infectious IBS. Since post-infectious IBS has inflammation in the intestine, it challenges the concept of functional vs. structural, since there are features here of both. This raises the question, how great are the distinctions between "functional" and "structural" disease? Perhaps not as great as we might think. To illustrate this, in addition to patients with post-infectious IBS, there is a subset of patients with inflammatory bowel disease called IBD/IBS. These are patients who have ulcerative colitis, for How great are the distinctions between "functional" and "structural" disease? Perhaps not as great as we might think. example, get treated, go into remission and have minimal or no inflammation in the rectum and the colon, but they still have severe pain and diarrhea. In these cases the entities of post-infectious IBS and IBD/IBS have some things in common. They're pain predominant, usually withdiarrhea; infection initially brings it on around a time of high emotional distress; there is minimal gross or microscopic inflammation found; and there seems to be activation of the immune system both inthe gut and in the brain. Thus with functional GI disorders, PI-IBS, and even IBD/IBS we see afeature of there being more pain in the presence of minimal disease, save for some microscopic inflammation. The evidence for this seems to be that it is the combination of central nervous systemdistress along with the inflammation that might lead to the pain syndrome and post-infectious IBS or IBD/IBS. It may essentially be that this all starts with having a genetic predisposition, which can increase susceptibility to getting the disorder. Furthermore, combined with factors that lead to immune system dysfunction, and with inflammation in the gut, exposure at a time when there are high levels of psychologic distress may be enough to lead to the development of the post-infectious IBS or IBD/IBS.Central regulation of visceral sensitivity: pain perception - A number of factors lead to the experience of pain. These involve mostly areas of the brain. When a pain signal is generated in the intestines,there is an ability of the brain to regulate this signal. We are learning that there are areas of the brain that stimulate or potentially cause more pain, which seem to be more associated with hypervigilanceand attention. Alternatively, there are areas of the brain that turn down the pain signal. This can be viewed on brain imaging. We are moving toward an understanding that patients with greater pain severity have a dysregulation not so much at the level of the gut, but at the level of the brain."*http://www.ibsgroup.org/forums/index.php?showtopic=92806


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## eric (Jul 8, 1999)

Ms.M this goes back to IgGThis is newer and it should be noted published in Clin Exp AllergyClin Exp Allergy. 2007 Jun;37(6):823-30.Alterations of food antigen-specific serum immunoglobulins G and E antibodies in patients with irritable bowel syndrome and functional dyspepsia.Zuo XL, Li YQ, Li WJ, Guo YT, Lu XF, Li JM, Desmond PV. Department of Gastroenterology, Qilu Hospital, Shandong University, Jinan, China.Background Post-prandial worsening of symptoms as well as adverse reactions to one or more foods are common in the patients with functional gastrointestinal diseases, such as irritable bowel syndrome (IBS) and functional dyspepsia (FD). *However, the role played by true food allergy in the pathogenesis of these diseases is still controversial and there are no well-established tests to identify food allergy in this condition.* Objective To investigate serum food antigen-specific IgG, IgE antibody and total IgE antibody titres in controls and patients with IBS and FD, and to correlate symptoms with the food antigen-specific IgG titres in IBS and FD patients. Methods Thirty-seven IBS patients, 28 FD patients and 20 healthy controls participated in this study. Serum IgG and IgE antibody titres to 14 common foods including beef, chicken, codfish, corn, crab, eggs, mushroom, milk, pork, rice, shrimp, soybean, tomatoes and wheat were analysed by ELISA. Serum total IgE titres were also measured. Last, symptomatology was assessed in the study. Results IBS patients had significantly higher titres of IgG antibody to crab (P=0.000), egg (P=0.000), shrimp (P=0.000), soybean (P=0.017) and wheat (P=0.004) than controls. FD patients had significantly higher titres of IgG antibody to egg (P=0.000) and soybean (P=0.017) than controls. *The percentage of individuals with detectable positive food antigen-specific IgE antibodies of the three groups did not show any significant differences (P=0.971). There were no significant differences between IBS patients, FD patients and controls in the serum total IgE antibody titres (P=0.978). Lastly, no significant correlation was seen between symptom severity and serum food antigen-specific IgG antibody titres both in IBS and FD patients. Conclusion Serum IgG antibody titres to some common foods increased in IBS and FD patients compared to controls. But there is no significant correlation between symptom severity and elevated serum food antigen-specific IgG antibodies in these patients.*PMID: 17517095 From Current Opinion in GastroenterologyDiet and Irritable Bowel Syndrome*Food AllergyIncreases in antigen-specific IgE antibodies can be found in most children under 5 years of age, but these antibodies do not remain in significant titer in later years.[18] Thus, true allergy to food is much more common in children than in adults, but does occur in adults, often without an increase in total IgE levels. Such an allergy needs to be identified in patients with a suggestive history, and the food withdrawn before a diagnosis of IBS can be made with confidence.* *Symptoms produced are commonly pain, bloating, and diarrhea, but the orofacial syndrome is the most common manifestation of food allergy, without accompanying bowel symptoms.[19] The oral allergy syndrome is usually seen in patients with allergic rhinitis and conjunctivitis and is triggered by tree, grass, or weed pollens. The oral syndrome following food is triggered by cross-reacting allergens in certain foods. The most common food allergens are proteins found in milk, eggs, fish, nuts, shellfish, soybeans, and wheat.[14] Diagnosis of food allergy has been suggested by skin prick tests, total serum IgE levels, and food-specific IgE levels identified in the radioallergosorbent (RAST) test. Skin atopy patch testing is a more recent method of allergy testing, but its advantage in food allergy over the skin prick test has yet to be established.[20*]**A recent study selected diets based on the presence of serum IgG antibodies against foods, and showed that IBS symptoms improved on such diets using a randomized, placebo-controlled study design.[21*] The diets of the two groups, however, were not comparable, in that only the treated group had diets restricted in yeast, milk, egg, and wheat, foods often associated with food intolerance in IBS patients. The specificity of the IgG test is still not documented by this and other studies.[20*] Desensitization trials based on the usual tests for diagnosis of food allergy have not shown a clear answer.[19] Results are rather more clear in peanut allergic patients, as the major peanut antigen produces a strong IgE response, and one that can be modified by infusion of anti-IgE antibodies.[22]**All that can be said at present about food allergy in IBS is that as yet unidentified antigens in food or the intestinal lumen might prove to be of importance in IBS.*Conclusion*The response to food in IBS patients appears to be multifactorial. This response includes food intolerances, food allergies, and very possibly an alteration in bacterial flora with consequent changes in intestinal function. Modulating these responses might be an underlying psychiatric framework that includes over-reporting, characterized by somatization or MCS. None of these factors likely occurs in all patients with the heterogeneous disorder known as IBS, nor is it likely that any or all of these factors occur in isolation in a given patient. For all these reasons it seems unlikely that dietary manipulation will improve symptoms in a consistent manner in groups of IBS patients. For the moment, until our understanding is better, it is best to discover and treat individual intolerances/allergies/sensitivities, recognizing that alteration in this aspect of the therapeutic program will likely cause only partial improvement, especially in patients who over-report symptoms.*You might also find this post interesting on all foods allergies and intolerences and a bigger picture of IBS. But this"ConclusionThe response to food in IBS patients appears to be *multifactorial*. This response includes food intolerances, food allergies, and very possibly an alteration in bacterial flora with consequent changes in intestinal function. "http://www.ibsgroup.org/forums/index.php?s...=food+allergiesIts also important that foods are only a part of all IBS research. Some immunology specialists might only look at one part of a system. The experts look at all of the information from all the different specialists, neurogastroenterology, gastroenterology, immunology and many other specialty areas combined for the bigger picture. Lastly it is well know in D IBSers that"The gastrocolic reflex, a partly neurogenic process, refers to an increase in colonic motility induced by feeding. Postprandial deviations from the normal motility patterns lead to altered bowel habits. For example, a spastic colon (eg, diarrhea-predominant IBS [D-IBS]) is characterized by an exaggerated motility response to food intake. This exaggerated postprandial response also occurs in response to intraluminal distention or to an injection of cholecystokinin (CCK -- a hormone released in the duodenum) in patients with IBS."This is about just the act of eating in IBS. The stomach signals to the sigmoid colon food is on the way and to make room. But in IBS the colon overacts to the hormone signals and the result is D. This is also why it can come on so fast. Also in the morning people might have more d when the gut wakes up from signaling hormones to wake it up. This is 15 minutes after eating in IBS and a healthy control and the gut pressure in the large colon.a normal person







IBS







so the large colon overreacts to just eating itself, regardless of the foods, although fats and the amount of calories are a big stimulus for the gastrocolic reflex. One reason to eat smaller meals more often.


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## Mike NoLomotil (Jun 6, 2000)

Well well well...it is nice to hear from some of my dietitians that the more things change here the more they stay the same. I was particularly amused by Sr. Shawn-Eric invoking my memory with disdain in recent post, and resorting to the ramblings of a widely discredited, non-practicing psychiatrist "OOOO QUACKWATCH" were the biggest quack is the quack who founded it. A non-practicing psychiatrist who obviously still never looked at the program and does not know any immunology at all is making a determination as to some treatments efficacy? Is that not the very definition itself of quackery? A person who has be affirmed a quack in the courts you use to somehow disparage the work of both our affiliated physicians and our affiliated Registered Dietitians in their effective treatment of irritable bowel syndrome patients over the years. I remain as ever amused by your behavior. Luckily life is too good these days to waste it bantering with you. However, you go too far this time with your antics so one does have to stop and speak up for healthcare professionals you are disparaging in front of patients. This is at best unethical and at worst defamatory.Oh yes and the continual posting of work from a myopic perspective, which remains opinion concerning putative mechanisms of a non-functional disease, the so-called irritable bowel syndrome, also persists...ever more vigorously! At least to Shawn-Erics credit, he is wise enough to qualify his thinly-disguised contempt for any actual credentialed healthcare practitioner (physician, dietitian , therapist or otherwise) who does not fall into step with his line of "thinking" or shall I say "assumption to know":"I am not a doctor. All information I present is for educational purposes only and should not be substituted for the advise of a qualified health care provider. Please make sure you have your symptoms diagnosed by a medical practitioner or a doctor."A very wise and sage piece of advice to offer any patients here who should read your missives, dismissing efficacious treatments of IBS which do not fit your paradigms!I assure you that there are several hundred qualified physicians and 100 or so (number keeps going up) of qualified Registered Dietitians who have treated enough patients with the LEAP program for a long enough time (since the year 2000 when the protocols were first solidified) to be able to tell that their patients recovery from their refractory IBS symptoms is not a placebo effect.Now as for my comments to add to this thread for any actual sick people looking for help in remediating their symptoms, and out of respect for the opinions and work of any physicians you may use in your citations or which the aforementioned Certified LEAP Therapist, who IS an actual REGISTERED DIETITIAN with some training in dietary therapeutics, I just thought after seeing some if the same silliness I used to see when I used to banter with people her before things got too busy with the work of actually coordinating the delivery of healthcare to hundreds of new patients every single month to spend my life here, this silly debate-aka-argument is still moot as it ever was.What the problem is "out here in the field" is that there is a plethora of research being done, and a huge amount of clinical work being done, on the symptom-set with which patients present which is used to define a SYNDROME. Rome I, II, II, Manning you name it are no different than the use of symptom sets to e=define any population with a series of common symptoms without an obvious single or even multiple obvious pathophysiology. That's why they are SYNDROMES not diseases by name.The fact is...the FACT IS... and you cannot change FACTS no matter how LOUD you speak or how HARD you stamp your ego...sorry...your feet and beat your gums, the fact remains the fact: if one has a broad enough and objective enough VIEW which is not dictated by your own personal BELEIF system and one recognizes he/she is predisposed to interpret that which one sees from the perspective of their own experiences, training and beliefs thus ones view is subject to innate bias, and one makes a practice of reading ALLLLLLL the literature worldwide in the overlapping areas of study which are related to the clinical presentation and symptom sets we associated with so called IBS, one will see that so called IBS is not a functional disease but a set of diseases whose pathophysiology is unique yet often overlapping. It does indeed involve various dysfunctions of the integrated gastroneuroimmunoendocrineexocrine systems...and there are subpopulations wherein the primary insult is x which leads to y set of consequences within the system. Neuroimmune activation occur locally, can occur centrally, can originate with altered oral tolerance, can originate with altered CNS function, or both can originate with altered HPA axis function...or not...I can go on long enough to waste another day of my life on nonsensical arguments over who is right when everyone and no on is right because there is no single answer....and all this hoo-haa about "this is the latest thinking" or "this is the latest research" and "you don't know anything" directed towards actual healthcare practitioners who actually treat people every day with an efficacious method would be wholly unethical if an actual trained healthcare practitioner were the source. But its not so it is tolerated here even as it continues still with impunity.You learn objectivity and open-mindedness when you train with our doctors and our dietitians, not bias and closed mindedness to things which do not fit your views. You also learn that no matter how anyone tries neither this expert or that expert has a corner on the so called 'IBS KNOWLEDGE"...no one...there are experts you quote who other experts as qualified would rebut with compelling evidence. I leave that to themBut if you wish to persist in your misguided beliefs that you then use to insult and debase qualified care givers with, you are the one posting false information because you take PUTATIVE MECHANISMS and phsyiology which is applicable and state that it is NOT when it IS because you do not understand that this is not a single disease. In the simplest terms that even a non caregiver can understand IBS is a symptom set which it is already shown represents the clinical presentation of more than one type of pathophysiologic abnormality. The one which eludes your understanding, the integrated immunologic process of oral tolerance to benign antigens, is one of the main elements in the non-homogenous population which is clinically diagnosed with so called "IBS".Spitting and spouting on about how "food allergy is not involved in IBS" is a fundamentally unsound proposition right out of the box because it is an innately meaningless term. "FOOD ALLERGY by its classic Gel & Coombs definition is defined as immediate hypersensitivity reactions to benign food antigens mediated by circulating IgE antibodies to benign antigens. DUH EVERYBODY KNOWS THIS IS NOT THE PROBLEM in any more IBS patients than it is within the general population (2%). The problem we have is that in the 21st century we have way more information than we have terminology with which to describe it which is standardized. To some food allergy also encompasses non-IgE mediated mechanisms because it is immunologic (such as the type of compromised oral tolerance which is manifest as Type IV or cell-mediated hypersensitivity)...or we have what some call intestinal allergy: lumenal antigen-specific IgE antibodies which degranulate gut mast cells in some people but can be present in others and do not degranulate gut mast cells when presented with the apparent sensitized antigen because some other lumenal mechanism blunts the response. If you actually want to LEARN anything about such processes and then how the mechanism are applicable to the clinical symptom set people call IBS then study the stuff. read some of Buenos excellent tutorials...note that all the studies you post about CECAL and ILEAL mast cells have zip to do with the site of insult: antigen processing in the small bowel, which can be and is compromised in many patients who are diagnosed with a SYNDROME when they have an actual immunologic dysfunction associated with antigen processing which cause mediator release in the lumen, or in the lymphatics and systemic circulation, or both, in response to antigens which are benign. It makes them ill and they present with the symptoms doctors are indoctrinated into calling IBS because "there is no visible cause and the colonoscopy is normal".Don't ignore it spewing "it has nothing to do with IBS" because it does. It helps eliminate a whole host of sick people from the population you call "functional bowel disease"! It helps define one of several patient populations...HUGE POPULATIONS...who are diagnosed with a so called functional disease based on the symptom based criteria du jour who do NOT HAVE a functional disease. They are treatable, their IBS symptoms can be relieved by oligoantigenic diet therapy.You and many people also presume that because neurogenic inflammation is a phenomenon, every time you see inflammatory patterns which fit the putative mechanism then that must be it! However people ignore the inverse, that the primary insult may be, for example, one or more forms of t cell activation and inflammatory cascade activation in response to ingested antigens which results in upregulation of, as you are fond of discussing in general terms "the little brain in the gut" AND. the big brain in your head" and all points in between. Conversely it is also possible for events with are neuronal in origin, or endocrine in origin, to alter antigen processing and thus alter the adaptive immune response to benign antigens in the lumen, systemically, or both and result in an unregulated TH1/[email protected] response when there should not be one. There is no single correct answer that it is always this way or always that way. The point is that the common ground clinically, whichever way it is, that we can use to TREAT PEOPLE AND HELP THEM FEEL BETTER without drugs and their side effects is that we can identify when such an aberrant response to benign antigen does occur and alter the diet immediately to avoid the response.This was presented by one of our physicians several years ago at the ACG annual scientific conference. We verified with quantitative analysis that of course the normal response to benign antigens is an inflammatory response which is immediately blunted normally. This is what occurs with intact oral tolerance. VERY SIMPLY benign antigens are presumed non-benign until one of several possible "memory mechanisms" innately designed into and developed as the human body grows identifies each antigen as benign, You see certain levels of pro and anti inflammatory cytokines in the plasma which are dynamic...they change with eating patterns and cycles of antigen uptake and processing. But at all times when oral tolerance is intact there is a range of normal values for specific cytokines and this is below the threshold at which symptoms appear.We also showed that in IBS patients the absolute values of specific cytokines are elevated, and their plasma levels vary in response to antigen challenge and symptoms trail along. Take a person diagnosed with IBS-D based on ROME du jour criteria if you like and place them on a diet which removes any and all antigens which an MRT assay shows precipitate a response outside the normal range of response to antigens for that patient. They can carry on asymptomatically. Now reintroduce those antigens to the diet and allow them to eat them freely. Their plasma cytokine levels begin to spike, some as much as 500%+ and within 24-48 hours their symptoms return. So do the symptoms which people constantly misinterpret based on their own opinions on how the immune response to antigens occurs in so called "allergy"...or lack therof. If the diet is altered to again remove the offending antigens the symptoms recede as the cytokine levels drop. And the ones of concern when you examine them have known physiologic effects which are specific to the symptoms the patients experience.THIS is why the LEAP PROGRAM is effective in relieving the symptoms of thousands of patients, and why doctors send us hundreds of new LEAP Program patients for our dietitians to treat every single month. Now using your logic, which is not actually flawed, we agree on this much: yes if hundreds of patients doctors are diagnosing them with IBS every single month (which very soon is going to be THOUSANDS we will be receiving every month) shows altered oral tolerance to certain antigens or chemicals by testing and then their symptoms are relieved by a diet YES YES YES THEY DO NOT HAVE A FRIGGING SYNDROME by your own definition...they have some other "disease" which is characterized by diminished oral tolerance and which is treated by dietary therapy. SO the IBS POPULATION IS REDUCED EVERY TIME WE DO THIS!!!GREAT! That is the idea. A condition is only functional until you discover some "marker" or pathology which we have.In fact, if the metrics we have seen over the last 8 years hold up in the clinical trials, we will likely end up proving that most patients diagnosed with so called IBS-D do not have a functional disease at all and that they should not be diagnosed with IBS anymore....and the ROME criteria du jour cannot differentiate these patients one from another. In fact, since most IBS diagnosis is made at the primary care level rather than the referred care level, most patients presenting with IBS symptoms don't need to be referred. The standards of diagnosis and treatment already say this, absent red flags, there is no benefit to referral for endoscopy and other procedures since the outcomes are no different and the cost is higher by about 1000%.So you see our interests are the same. This place and the nation in general is overflowing with people who are given a diagnosis of a so called functional bowel disease 'IBS" and often FAP patients as well, who have symptoms which arise from altered tolerance to benign antigens which leads to excess mediator release systemically...sometimes lumenally which has to be assessed another way... who can be TREATED WITH SUCCESS with oligoantigenic diet therapy.What the origin of the altered oral tolerance IS, is often the bone of contention...it can be impossible to pin down as yet since medicine is still in its infancy in understanding oral tolerance. CLINICALLLY it is less important to debate "gee is the origin specific to some t cell memory defect or is the origin central and the altered tolerance to antigen is secondary?" If you don't know who gives a flip? What you DO know is that the patients tolerance to certain benign antigens is compromised for some reason and she is unresponsive to standard treatments. However, placed on a patient specific oligoantigenic diet there is very high probability of a high degree of relief as measured both by self reporting symptoms, SF36 assessment, and if we have the huge sums to spend to do the analysis we can quantify the changes in plasma cytokines in response to treatment or antigen challenge. That is enough as a basis for treatment since even those whose thinking you ascribe as wholly-infallible, or as the only-source of any and all valid info regarding IBS all agree that what you are supposed to DO with an IBS patient after the diagnosis is confirmed is institute EMPIRICAL TREATMENT trials. So if the experts you cite recommend empirical treatment trials as the standard of care, and the ACG recommends dietary treatment as a primary treatment (published clinical guidelines) who are you to tell doctors and dietitians and patients that trying a dietary treatment based on at least a patient-specific assessment of antigen tolerance is NOT TO BE DONE? On what basis are you self appointed to determine which empirical treatments are appropriate and which are not?NO ONE can have it both ways...fortunately there are many people who are doctors and dietitians not only who believe this all makes sense clinically, they have so many cases in their practices of refractory patients now in remission they keep on sending more...whether the insurance pays or not...because they get results from us that they do not get from any other treatments anyone else has to offer they can easily implement.Rather than spending bandwidth piling on, as is your practice, all the pertinent references which YOU apparently don't know anything about nor have read nor if you did would understand, this is one which makes the point nicely that we are all actually saying the same thing. The only difference is we have seen the actual clinical evidence that the population of IBS patients who do "not have IBS" is not a minority of those diagnosed in primary care with IBS, it is the MAJORITY.When all is said and done you might be arguing over 2-3% incidence of an actual "functional disease"&#8230;not 15-30% (whose number do you want?)MikeNLLive WellEat WellFeel Swell


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## overitnow (Nov 25, 2001)

It is nice to read your voice again. It seems to me that you speak for numbers of us who have a bowel problem that is undiagnosable but can be mediated without messing with our serotonin operation. (And yes, I am sure that for some serotonin will provide the only handle they can find for symptomatic relief. What that percentage is would be difficult to know; but I just don't know why that mechanism would suddenly start working improperly without a cause.) I'm aware that the act of eating will set this off; but which of us hasn't seen a greater/quicker reaction to some foods than others? In my case, milk products would have been among the worst; yet now I consume them with impunity. Somewhere within the mechanism of my body there was a disfunction that brought on reactions to food, some more violent than others, resulting in continual indigestion and constant and chronic D. Whether it was from an inflammation, oxidized free radicals, brain perfusion and/or blockages or another function addressed by flavonoids I do not know. I believe I qualified as an Ibeezer under Rome I and II. Whether I still fit in under III is less clear. If Rome IV were to limit this to serotonin disfunction, I am sure any number of us could slip back into the darkness with an un-labelable syndrome. In the meantime, it is good to hear of your growing success amongst those of us who have something unnamable that makes the digestive process intolerable. Mark


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## ms.m (Jan 23, 2008)

I appreciate everyone's help & replies but I was wondering who had PERSONAL experience with whether or not these tests have helped them. Is there anyone? Not info on studies, because I've read A WHOLE LOT of it. And "Eric" your help is appreciated but I really am just an IBSer who wants to see if anyone else has done what I'm doing with any success. Arguing back & forth with people who are just trying to post helpful information isn't necessary and doesn't answer my question - at all.


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## eric (Jul 8, 1999)

Well well.First let me say I am not against food allergy testing in suspected patients. Nor am I in anyway against dietary manipulation in IBS. It should however be explain in the bigger picture of IBS.Secondly the symptoms of IBS discriminate between IBS and food allergies. But you don't tell anyone that part.Thirdly as mentioned Foods in IBS are multifactorial. This response includes food intolerances, food allergies, and very possibly an alteration in bacterial flora with consequent changes in intestinal function. "You don't ever seem to explain that part to anyone, only allergic reactions, which food intolerences are not and are also common in IBS. Not to mention the only focus on foods and its much bigger then that, or that the functional conditions can overlap like IBS and functional dyspepsia, both with altered motility, viceral hypersensitivity and brain gut axis dysregulation. You present such a narrow view it seems to make you blind to everything else or you don't want to mention other issues that have ALREADY been established. For one structural cell changes they have now found using more powerful microscopes.The above was from multinational working teams from many disiplines on IBS and functional disorders and the current state of research. Not one doctor.All you post about is food allergy and IBS and that is a problem, beause that is not the only mechansims involved for sure and that is a FACT!!!Also you don't ever seem to cvome up with any validaing research and then don't really keep up with IBS researchers who are actually doing the real research. It is a major problem when "healthcare" people come to a bb and post bad information on IBS.*American Academy of Allergy Asthma & Immunology*"1/29/*2008* RE: MRT/LEAP Test for Food Reactions I am a Registered Dietitian with a consult next week with an 80 year old gentleman that, after extensive testing, has received a diagnosis of severe IBS. He has tried many IBS drugs on the market with limited relief. He is being sent to me to evaluate his diet. On setting up this consult, he mentioned the Mediator Release Test, along with the LEAP protocol for food sensitivities. Can you provide guidance on the MRT/LEAP for IBS treatment? My research into the MRT/LEAP test fails to confirm its validity as a tool useful to evaluate patients with any form of food allergy. It claims to be able to help in the diagnosis of "non-IgE mediated food allergy." A search for this test as validated by any published study via PubMed failed to reveal a single reference to it, and an assessment of the web site, at least in my opinion, failed to validate its value in the diagnosis of adverse reactions to foods. Irritable bowel syndrome itself is not considered, in most instances, to be related to food allergy. Thus, my opinion is that this test would be of very little help.Thank you again for writing.Sincerely,Phil Lieberman, MD"http://www.aaaai.org/aadmc/ate/category.asp?cat=10069Funny also you should mentioned RAPDietary interventions for recurrent abdominal pain (RAP) and irritable bowel syndrome (IBS) in childhood."AUTHORS' CONCLUSIONS: There is a lack of high quality evidence on the effectiveness of dietary interventions. This review provides no evidence that fibre supplements, lactose free diets or lactobacillus supplementation are effective in the management of children with RAP."http://www.ibsgroup.org/forums/index.php?showtopic=93790New research on Rap, points more to brain processing abnormalities then gut abnormalities.Fibromyalgia and irritable bowel syndrome: How real must they be?"Second is the concept that these disorders are "nebulous" or poorly defined. Over the last two decades there has been an explosion in research in brain-body science, neurotransmitter function, and brain imaging that is precisely defining the location and mechanisms that explain these symptoms. This is probably the most exciting area in modern medical investigation, and many new drugs are being targeted to treat these mechanisms. "http://www.aboutibs.org/site/news-events/n...commentary#RealClinical Policy Bulletin:Allergy Testing and Allergy ImmunotherapyAetna considers the following tests for routine allergy testing *experimental and investigational as they have not been proven to be effective:*"Mediator release test (MRT)""Mediator Release TestThe mediator release test (MRT) (Signet Diagnostic Corporation) has primarily been used to detect intolerance to foods and additives in patients with irritable bowel syndrome. The MRT measures the aggregate release of inflammatory mediators from the patient's immunocytes in vitro after exposure to specific foods and food additives. The results of the mediator release test have been used to design a patient-specific diet to treat IBS by avoiding foods and additives that trigger significant inflammatory mediator release. For the mediator release test, the patient's blood sample is incubated with various extracts of foods and food additives and then analyzed for the presence and aggregate amount of release of inflammatory mediators from the patient's leukocytes. Results are compared to control samples of the patient's blood that have not been exposed to food extracts or additives The MRT-directed patient-specific diet is one component of the Lifestyle Eating and Performance (LEAP) Disease Management Program (Don Self & Associates, Inc., Whitehouse, TX). The LEAP program is based on the theory that symptoms irritable bowel syndrome and other certain conditions are caused by the physiological effects of non-IgE mediated immune reactions in response to sensitivities to specific foods and food additives. The LEAP program also includes patient selection tools, a self-directed stress reduction program, and outcomes assessment tools.* According to the manufacturer, *the LEAP program has been successful in reducing or eliminating symptoms in 84 percent of patients with irritable bowel syndrome, functional diarrhea, and related conditions. However, there is no evidence in the peer-reviewed published medical literature to substantiate these claims.The mediator release test has also been promoted for use in patients with chronic fatigue syndrome, metabolic conditions (e.g., diabetes, obesity), gastrointestinal disorders (e.g., gastroesophageal reflux disease, chronic ulcerative colitis, and Crohn's disease), neurologic disorders (e.g., migraine headaches, cluster headaches), rheumatologic disorders (inflammatory arthritis, arthralgias, fibromyalgia), otolaryngologic disorders (e.g., perennial rhinitis, chronic sinusitis, chronic otitis media with effusion), dermatologic conditions (e.g., eczema, urticaria, dermatitis), and in patients with behavioral conditions (e.g., attention deficit disorder, hyperactivity, frequent mood swings, inability to concentrate). *There are, however, no studies of the mediator release test reported in the peer-reviewed published medical literature that demonstrate improvements in clinical outcomes by incorporating the mediator release test and associated dietary modifications into the clinical management of patients with these conditions. Thus, the m*


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## eric (Jul 8, 1999)

Well well.First let me say I am not against food allergy testing in suspected patients. Nor am I in anyway against dietary manipulation in IBS. It should however be explain in the bigger picture of IBS.Secondly the symptoms of IBS discriminate between IBS and food allergies. But you don't tell anyone that part.Thirdly as mentioned Foods in IBS are multifactorial. This response includes food intolerances, food allergies, and very possibly an alteration in bacterial flora with consequent changes in intestinal function. "You don't ever seem to explain that part to anyone, only allergic reactions, which food intolerences are not and are also common in IBS. Not to mention the only focus on foods and its much bigger then that, or that the functional conditions can overlap like IBS and functional dyspepsia, both with altered motility, viceral hypersensitivity and brain gut axis dysregulation. You present such a narrow view it seems to make you blind to everything else or you don't want to mention other issues that have ALREADY been established. For one structural cell changes they have now found using more powerful microscopes.The above was from multinational working teams from many disiplines on IBS and functional disorders and the current state of research. Not one doctor.All you post about is food allergy and IBS and that is a problem, beause that is not the only mechansims involved for sure and that is a FACT!!!Also you don't ever seem to cvome up with any validaing research and then don't really keep up with IBS researchers who are actually doing the real research. It is a major problem when "healthcare" people come to a bb and post bad information on IBS.*American Academy of Allergy Asthma & Immunology*"1/29/*2008* RE: MRT/LEAP Test for Food Reactions I am a Registered Dietitian with a consult next week with an 80 year old gentleman that, after extensive testing, has received a diagnosis of severe IBS. He has tried many IBS drugs on the market with limited relief. He is being sent to me to evaluate his diet. On setting up this consult, he mentioned the Mediator Release Test, along with the LEAP protocol for food sensitivities. Can you provide guidance on the MRT/LEAP for IBS treatment? My research into the MRT/LEAP test fails to confirm its validity as a tool useful to evaluate patients with any form of food allergy. It claims to be able to help in the diagnosis of "non-IgE mediated food allergy." A search for this test as validated by any published study via PubMed failed to reveal a single reference to it, and an assessment of the web site, at least in my opinion, failed to validate its value in the diagnosis of adverse reactions to foods. Irritable bowel syndrome itself is not considered, in most instances, to be related to food allergy. Thus, my opinion is that this test would be of very little help.Thank you again for writing.Sincerely,Phil Lieberman, MD"http://www.aaaai.org/aadmc/ate/category.asp?cat=10069Funny also you should mentioned RAPDietary interventions for recurrent abdominal pain (RAP) and irritable bowel syndrome (IBS) in childhood."AUTHORS' CONCLUSIONS: There is a lack of high quality evidence on the effectiveness of dietary interventions. This review provides no evidence that fibre supplements, lactose free diets or lactobacillus supplementation are effective in the management of children with RAP."http://www.ibsgroup.org/forums/index.php?showtopic=93790New research on Rap, points more to brain processing abnormalities then gut abnormalities.Fibromyalgia and irritable bowel syndrome: How real must they be?"Second is the concept that these disorders are "nebulous" or poorly defined. Over the last two decades there has been an explosion in research in brain-body science, neurotransmitter function, and brain imaging that is precisely defining the location and mechanisms that explain these symptoms. This is probably the most exciting area in modern medical investigation, and many new drugs are being targeted to treat these mechanisms. "http://www.aboutibs.org/site/news-events/n...commentary#RealClinical Policy Bulletin:Allergy Testing and Allergy ImmunotherapyAetna considers the following tests for routine allergy testing *experimental and investigational as they have not been proven to be effective:*"Mediator release test (MRT)""Mediator Release TestThe mediator release test (MRT) (Signet Diagnostic Corporation) has primarily been used to detect intolerance to foods and additives in patients with irritable bowel syndrome. The MRT measures the aggregate release of inflammatory mediators from the patient's immunocytes in vitro after exposure to specific foods and food additives. The results of the mediator release test have been used to design a patient-specific diet to treat IBS by avoiding foods and additives that trigger significant inflammatory mediator release. For the mediator release test, the patient's blood sample is incubated with various extracts of foods and food additives and then analyzed for the presence and aggregate amount of release of inflammatory mediators from the patient's leukocytes. Results are compared to control samples of the patient's blood that have not been exposed to food extracts or additives The MRT-directed patient-specific diet is one component of the Lifestyle Eating and Performance (LEAP) Disease Management Program (Don Self & Associates, Inc., Whitehouse, TX). The LEAP program is based on the theory that symptoms irritable bowel syndrome and other certain conditions are caused by the physiological effects of non-IgE mediated immune reactions in response to sensitivities to specific foods and food additives. The LEAP program also includes patient selection tools, a self-directed stress reduction program, and outcomes assessment tools.* According to the manufacturer, *the LEAP program has been successful in reducing or eliminating symptoms in 84 percent of patients with irritable bowel syndrome, functional diarrhea, and related conditions. However, there is no evidence in the peer-reviewed published medical literature to substantiate these claims.The mediator release test has also been promoted for use in patients with chronic fatigue syndrome, metabolic conditions (e.g., diabetes, obesity), gastrointestinal disorders (e.g., gastroesophageal reflux disease, chronic ulcerative colitis, and Crohn's disease), neurologic disorders (e.g., migraine headaches, cluster headaches), rheumatologic disorders (inflammatory arthritis, arthralgias, fibromyalgia), otolaryngologic disorders (e.g., perennial rhinitis, chronic sinusitis, chronic otitis media with effusion), dermatologic conditions (e.g., eczema, urticaria, dermatitis), and in patients with behavioral conditions (e.g., attention deficit disorder, hyperactivity, frequent mood swings, inability to concentrate). *There are, however, no studies of the mediator release test reported in the peer-reviewed published medical literature that demonstrate improvements in clinical outcomes by incorporating the mediator release test and associated dietary modifications into the clinical management of patients with these conditions. Thus, the mediator release test is considered experimental and investigational."*http://www.aetna.com/cpb/medical/data/1_99/0038.html


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## eric (Jul 8, 1999)

FYI"IBS -- Review and What's NewAmy Foxx-Orenstein, DO, FACG, FACP Medscape General Medicine. *2006*;8(3) Â©2006 MedscapePosted 07/26/2006Abstract and IntroductionAbstractIrritable bowel syndrome (IBS) is a highly prevalent gastrointestinal motility disorder broadly characterized by abdominal pain/discomfort associated with altered bowel habits. The chronic and bothersome nature of IBS symptoms often negatively affects patient quality of life and activity level and places a substantial economic burden on patients and the healthcare system. Advances in research have led to a greater understanding of the underlying pathophysiology of IBS, particularly regarding the role serotonin plays in the gastrointestinal tract; the development of stepwise, symptom-based diagnostic strategies that allow for a diagnosis of IBS to be made without the need for extensive laboratory testing; and the development of treatment options targeting underlying pathophysiologic mechanisms that provide relief of the multiple symptoms associated with IBS. This review highlights recent advances in research and discusses how these findings can be applied to daily clinical practice.IntroductionIBS -- a complex, multifaceted condition broadly characterized by abdominal pain/discomfort associated with altered bowel habits -- is among the most prevalent gastrointestinal (GI) motility disorders. Prevalence estimates for IBS range from 3% to 20%, with most estimates in North America ranging from 10% to 15%.[1-3] Women are affected by IBS more often than men (2:1 in the community setting and 3:1 to 4:1 in the tertiary care setting).[2] IBS-related symptoms are often chronic and bothersome, negatively affecting patient activities of daily living (eg, sleep, leisure time), social relationships, and productivity at work or school.[4-6] Patients with IBS typically score lower than population norms or those with other chronic GI and non-GI disorders on measures of quality of life.[7-10] IBS also puts a heavy economic burden on patients, employers, and the healthcare system, resulting in more than $10 billion in direct costs (eg, from office visits, medications) and $20 billion in indirect costs (eg, through work absenteeism and reduced productivity) each year.[11-14]Advances in research during the past several decades have provided insight into the underlying pathophysiology of IBS, particularly the role of serotonin in the GI tract; the development of stepwise, symptom-based diagnostic strategies; and the development of targeted treatment options. This review discusses recent advances in research and explores how these findings can be applied in the clinical practice setting.""The Science of IBSGiven the lack of definitive organic markers for IBS, the absence of a unifying hypothesis regarding its underlying pathophysiology is not surprising. Nevertheless, important advances in research made during the past 50 years have brought us closer than ever to understanding the numerous putative etiologic factors involved in this multifaceted disorder, including environmental factors, genetic links, previous infection, food intolerance, and abnormal serotonergic signaling in the GI tract.Environmental InfluencesAlthough a patient's psychological state may influence the way in which he or she presents, copes with illness, and responds to treatment, no evidence supports the theory that psychological disturbances are the cause of IBS.[39,40] The biopsychosocial model proposed by Engel takes into account the interplay between biologic, psychological, and social factors.[41] This model proposes that there is an underlying biologic predisposition for IBS that may be acted on by environmental factors and psychological stressors, which contribute to disease development, the patient's perception of illness, and impact on treatment outcomes.[42,43]Studies evaluating the role of acute stress have shown that stress can result in release of stress-related hormones that affect colonic sensorimotor function (eg, corticotropin-releasing factor [CRF] and inflammatory mediators [eg, interleukin (IL)-1]), leading to inflammation and altering GI motility and sensation.[44] For example, CRF-1 receptors located in the central nervous system (CNS) and gut can affect colonic motility, epithelial water transport, and gut permeability.[45] Sagami and colleagues[46] determined that the peripheral administration of a nonselective corticotropin-releasing hormone (CRH) receptor antagonist improved GI motility, visceral perception, and negative mood in response to gut stimulation in patients with IBS. These findings suggest that CRH may play an important role in the pathophysiology of IBS.GeneticsStudies with twins have shown that IBS is twice as prevalent in monozygotic twins as in dizygotic twins.[47-49] Limited research on familial aggregation has found that individuals who have a family member (other than a spouse) with a history of abdominal pain or bowel disorder have more than 2-fold increased odds of having IBS. It is likely that environmental influences may help explain this finding (eg, awareness of the symptom status of family members may make sufferers more open to discussing their symptoms and seeking help for the condition).[50] Preliminary findings also suggest that IBS may be associated with select gene polymorphisms, including those in IL-10, G-protein GNb3, alpha adrenoceptor, and serotonin reuptake transporter (SERT).[47, 51-54] Despite these potential links, however, conclusive evidence for a genetic basis for IBS has not been established.Postinfectious IBSThe presence of postinfectious (PI)-IBS, referring to the development of IBS symptoms -- particularly abdominal pain and diarrhea -- shortly after an enteric infection, is based on research from prospective studies in which IBS symptoms developed in 7% to 32% of patients after they recovered from bacterial gastroenteritis.[52,55,56] Specific risk factors for the development of PI-IBS have been identified, including younger age, female sex, presence of severe infectious gastroenteritis for a prolonged period, use of antibiotics to treat this infection, and presence of concomitant psychological disorders (eg, anxiety).[39,52,55,57] Difficulty in downregulating intestinal inflammation in the colonic mucosa has been suggested as a potential underlying mechanism in this condition.[52] Also suggested as a potential underlying mechanism is the presence of colonic changes shown in patients with PI-IBS compared with controls, including increased gut permeability, increased mucosal enterochromaffin cell production, and increased concentration of mast cells and T lymphocytes in the gut mucosa.[39,52,55,57] Despite considerable evidence linking IBS with an inflammatory etiology (perhaps triggered by enteric infection), in a controlled trial of patients with PI-IBS, anti-inflammatory treatment with prednisolone was not more effective than placebo in improving patient symptoms.[58] The true role of prior infection as a key factor in PI-IBS remains to be established.[59]The use of probiotics (products containing live or attenuated bacteria that have a positive effect on the host) in alleviating symptoms in patients with PI-IBS is an area of recent focus.[60,61] The potential utility of probiotics in this setting stems from their antibacterial, antiviral, and immune-modulating properties; their ability to modify intestinal flora; and their potential to enhance intestinal mucus secretion or influence stool consistency or volume and gas handling.[60] The number of studies evaluating the efficacy of probiotic preparations in patients with IBS is limited but growing.[60-68] Because trials vary in study design, dose, and strain (Lactobacillus and Bifidobacteria alone or in combination; mixture of Lactobacillus, Bifidobacteria, and Streptococcus), direct comparison of results is challenging. Overall, some degree of IBS symptom improvement has been demonstrated in symptoms such as abdominal pain,[65,66] bloating,[63,66] gas,[66] and daily symptom scores.[62,65] O'Mahoney and colleagues[60] have recently demonstrated that results with the Bifidobacterium infantis strain are particularly promising. In a separate analysis, these investigators showed that the baseline characteristics of urgency and hard stool increased the odds ratio of response to this strain, whereas straining and alcohol consumption reduced the likelihood of response.[69,70] The ultimate place in therapy of probiotics in IBS remains to be elucidated.Small Intestinal Bacterial OvergrowthThe presence of a higher than usual population of bacteria in the small intestine (leading to bacterial fermentation of poorly digestible starches and subsequent gas production) has been proposed as a potential etiologic factor in IBS.[71] Pimentel and colleagues have shown that, when measured by the lactose hydrogen breath test (LHBT), small intestinal bacterial overgrowth (SIBO) has been detected in 78% to 84% of patients with IBS.[71,72] However, the accuracy of the LHBT in testing for the presence of SIBO has been questioned.[73] Sensitivity of the LHBT for SIBO has been shown to be as low as 16.7%, and specificity approximately 70%.[74] Additionally, this test may suboptimally assess treatment response.[75] The glucose breath test has been shown to be a more reliable tool,[76] with a 75% sensitivity for SIBO[77] vs 39% with LHBT for the "double-peak" method of SIBO detection.[74] In a recently conducted retrospective study involving review of patient charts for the presence of gastrointestinal-related symptoms (including IBS) in patients who were referred for glucose hydrogen breath tests for SIBO, of 113 patients who met Rome II criteria for IBS, 11% tested positive for SIBO.[78] Thus, results demonstrated that IBS symptoms are often unrelated to the presence of SIBO. Despite the controversy regarding the contribution of SIBO to the underlying pathophysiology of IBS and its symptoms, short-term placebo-controlled clinical studies with select antibiotics, including neomycin and rifaximin, have demonstrated symptom improvement in IBS patients.[61,72,79] Antibiotics may therefore have potential utility in select subgroups of IBS patients in whom SIBO contributes to symptoms. However, the chronic nature of IBS symptoms often leads to the need for long-term treatment. Given the fact that long-term use of antibiotics is generally undesirable, the place of antibiotics in IBS therapy remains to be established.[73]Food IntoleranceFood intolerance has been proposed as a potential cause of GI symptoms in some patients with IBS; however, this link is not well established. Although some patients associate onset of IBS symptoms with ingestion of particular foods, identification of a true food intolerance is challenging, and elimination diets are typically time-consuming and difficult to implement. Recent research involving exclusion of foods to which patients had immunoglobulin (Ig) G antibodies, which are associated with a more delayed response after antigen exposure than IgE antibodies, resulted in significantly better symptom improvement than in patients in the nonexclusion group.[80] Further research into the role of food intolerance in IBS is warranted.Serotonin Signaling*Of the putative mechanisms underlying the pathophysiology of IBS, the strongest evidence points to the role of serotonin in the GI tract. *The effect of serotonergic mechanisms in the manifestation of IBS symptoms has led to development of a new drug class for the treatment of IBS patients: the GI serotonergic agents.Normal GI function relies on a properly functioning brain-gut axis, which involves the coordinated interplay of the GI musculature, the CNS, the autonomic nervous system, and the enteric nervous system (ENS). The ENS contains millions of neurons embedded in the wall of the digestive tract and functions, at least in part, independently of the CNS. The size, complexity, and independent function of the ENS has resulted in application of the terms "the second brain" and "the mini-brain."[81] Impaired function or coordination of any of these systems, or the communication between these systems and the GI musculature, can lead to symptoms of dysmotility and altered sensory perception, which are characteristic of IBS and select other GI motility disorders.[82]The neurotransmitter serotonin (5-hydroxytryptamine [5-HT]) is a predominant signaling molecule in the ENS. Most (90% to 95%) of the body's serotonin is found in the gut, and smaller amounts are found in the brain (about 3%) and in platelets (about 2%).[83] In the GI tract, serotonin facilitates communication between the ENS and its effector systems (muscles, secretory endothelium, endocrine cells, and vasculature of the GI tract), thus playing a key role in normal GI tract functioning.[84] In addition, serotonin plays a role in the communication between the ENS and the CNS.In the gut, serotonin is synthesized by and stored in the enterochromaffin cells, which are located within the mucosa of the intestinal wall. When material passes through the lumen and the mucosa is stimulated, enterochromaffin cells release serotonin, which then binds to its receptors (primarily 5-HT1P receptors) on intrinsic primary afferent neurons, initiating peristalsis and secretion. Serotonin also binds to 5-HT4 receptors on interneurons, which augments the transmission of signals to motor neurons, resulting in enhanced peristaltic activity. In transgenic mice lacking 5-HT4 receptors, colonic motility is abnormally slow, confirming the role of these receptors in facilitating normal colonic motility.[85] By binding to 5-HT3 receptors on efferent sensory innervations coming from the vagus and the spinal nerves, serotonin mediates signaling between the ENS and the CNS and, thus, modulates pain perception.To regulate the signaling process, excess serotonin must be removed; this is accomplished by the SERT molecule expressed by intestinal epithelial cells.[86] Human studies have shown that defects in serotonin signaling contribute to the pathophysiology of IBS and, potentially, other GI motility disorders. In a recent study by Coates and colleagues,[87] biopsy specimens from patients with IBS showed significantly lower mucosal serotonin concentrations than those from healthy controls, potentially the result of lower mRNA levels for tryptophan hydroxylase (the rate-limiting enzyme in serotonin synthesis), which were also significantly lower in patients with inflammatory bowel disease.[87] There was no significant difference in the number of enterochromaffin cells or in the capacity of these cells to release serotonin under stimulated conditions. In another study, higher serotonin levels were observed in mucosal biopsy samples from patients with IBS with constipation (IBS-C) than in patients with IBS-D or in healthy volunteers.[88]Serotonin levels may also be affected by altering the amount or function of SERT. The study by Coates and colleagues[87] showed a significant decrease in the level of SERT mRNA and SERT protein expressed in the intestinal epithelial cells of IBS patients compared with that of healthy volunteers. In another study,[89] SERT expression and binding capacity in platelets were decreased in women with IBS-D compared with expression and binding capacity in healthy controls. Furthermore, Chen and colleagues[90] showed that mice with a SERT gene deletion had altered colonic motility. It is interesting to note that the mice thrived in laboratory housing conditions, indicating that other transporters could compensate for the lack of SERT. Additional studies have focused on SERT polymorphisms. Yeo and colleagues[91] showed an association between patients with IBS-D and the homozygous short polymorphism of the SERT gene promoter. This mutation results in lower levels of SERT gene transcription and reduced amounts of SERT protein available for reuptake of serotonin. In addition, Camilleri and colleagues[92] showed a possible link between the long promoter polymorphism and patient response to therapy.*Thus, a substantially large body of work shows that normal gut physiology is predicated on the interplay between the GI musculature and the ENS, autonomic nervous system, and CNS. One of the central mediators of this complex interplay is the neurotransmitter serotonin. Impairment or imbalance in serotonergic signaling, which can affect GI motility, secretion, and visceral sensitivity, may be affected by defects or deficiencies in serotonin production, specific serotonin receptors, or proteins such as SERT. These changes can manifest in symptoms associated with IBS, including abdominal pain, altered bowel habits (constipation, diarrhea, or alternation between these 2 states), and bloating."*http://www.medscape.com/viewarticle/532089_print Brand new videos from experts IN GI Research and IBSIncreasingly our understanding of IBS is that it is a heterogeneous disorder - that is, multiple factors contribute to the well defined symptoms of the disorder. One of these suspected underlying dysfunctions involves serotonin, which is a neurotransmitter or messenger to nerves. Most serotonin in the body is in cells that line the gut where it senses what is going on and through receptors signals nerves that stimulate a response. The serotonin must then be reabsorbed (a process called re-uptake) into cells. *This process appears to be disrupted in people with IBS.*Serotonin and SERTHow does serotonin affect gut function? An interview with Gary M. Mawe, PhD, Professor of Anatomy and Neurobiology, University of Vermont, Burlington, VT. Dr. Mawe is a basic scientist. http://www.aboutibs.org/site/learning-cent...orner/serotoninMore professional videosCauses and Treatmentshttp://www.aboutibs.org/site/learning-cent...o-corner/causesall videoshttp://www.aboutibs.org/site/learning-center/video-corner/


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## ms.m (Jan 23, 2008)

This is all so off topic. I've done research, I've read studies very similar to what you are posting Eric. I've never said nor ever believed that food allergies cause IBS. I just know that many researchers are saying they may play a part in aggravating one's IBS. *My post was asking if anyone had taken any sort of IgG Food Allergy test, and if so, did the elimination diet all of these tests suggest going on (once receiving your results) help*. I didn't want to discuss research because I've done a lot and am not hear to provide detailed information about IgG/delayed food allergies and the role they may or may not play in IBS. I'm not hear to try and educate people about them, I was speaking to those that ALREADY HAD PERSONAL EXPERIENCE with them. I wasn't out to discuss theories, research, etc. The point of my post wasn't to be an educational post, it was to see if anyone out there had been put on an elimination diet because of these tests and if it helped them. I've spent hours upon hours researching it, I wanted to hear if anyone had personal success stories or not. I'm not going respond to your posts "Eric" any longer because you're really just rude and not paying attention to the original question asked. If anyone has a personal story if eliminating foods they had a high reaction to on an IgG Food Allergy test helped or not, I would love to hear it. That's all I wanted and I would appreciate people's responses. Thank you.


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## eric (Jul 8, 1999)

" I've never said nor ever believed that food allergies cause IBS."I never said *YOU* did.I am sorry you feel the way you do. Perhaps others who have not done any of this research reading will be helped by all the information and not misguided.


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## eric (Jul 8, 1999)

Maybe you haven't seen this oneWhy IgG Testing for Food Intolerance Is Not As Simple As ABC or Doh Ray Mi http://breathspakids.blogspot.com/2007/02/...lerance-is.htmlBy the way Dr Whorwell in this article is a senior Gastro in England on IBS. There are also letters of communications going back and forth between these doctors on all this.""Food elimination based on IgG antibodies may be effective in reducing IBS symptoms and is worthy of further biomedical research," the authors write. "Many patients with IBS would prefer a dietary solution to their problem rather than having to take medication, and the economic benefits of this approach to health services are obvious. *It is well known that patients expend large sums of money on a variety of unsubstantiated tests in a vain attempt to identify dietary intolerances."*"Food intolerance is a perceived source of the condition and exclusion diets, which are time-consuming and labor intensive, have been used as a form of management. Conflicting results have been reported with elimination diets, *and attempts to eliminate food items based on IgE antibodies have been disappointing*, according to the authors of this study. "This is the whole study, its looks like they got 10% better at first and then 26% if they stayed on it.http://www.pubmedcentral.nih.gov/articlere...i?artid=1774223 What symptoms I can find yet.Food Elimination Based on IgG Antibodies Helpful in Irritable Bowel Syndrome http://www.medscape.com/viewarticle/489349MsM, I don't think there are a lot of people who have had IgG testing for IBS in general.I also appologize if I upset you.


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## ms.m (Jan 23, 2008)

Yeah I read that study, my doctor sent it to me. It was 26% for those who were fully compliant. To tell you the truth, that result isn't that great if you consider what a pain the elimination diet can be. Plus, they only used 150 outpatients for the study which is an incredibly low number of people. Also, elevated IgG levels can occur when one simply eats that food all of the time because your body produces those antibodies, but it doesn't necessarily mean you're having an allergic reaction. Which would make sense because almost everything I eat on a regular basis I had a reaction to. Whatever I didn't eat on a regular basis I didn't have a reaction to. My IBS has felt quite better lately but it started almost immediately after digestive enzymes and a fiber/herbal supplement. I don't really think it's the diet. Also what I kind of don't buy about these delayed allergies is that they claim the odds are good you may be able to add back the foods you had a high reaction to, back into your diet after not eating it for 6 months. It seems as if you're truly allergic to something you'll be allergic to it in six months, that it shouldn't just "go away." Plus most doctors say two weeks is long enough to go without eating something to tell if it irritates you or not. Not three months or more like the laboratories and doctors that issue IgG delayed allergy tests say.


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## eric (Jul 8, 1999)

Allergies are complex. Sometimes the more exposure to them you build up a tolerence.Some of the labs proported success rates and promotion don't add up in what they are promoting or saying in clinical studies or in IBS research. Dr Whorewell was very careful to say might reduce some symptoms in a subset of patients. Dr Whorewell is a leading IBS doctor in the UK involved in many IBS studies.For twenty years he has been studying Gut directed hypnotherapy, he was the first to use it. Then DR Pallson from the UNC center for functional GI disorders. These drs don't just study HT and IBS either, but are involved in all kinds of studies. I mention this because these are sources you can trust.It is a recommed IBS treatment by the ROME experts for IBS. Clinical studies have shown a high success rate. Not only that but a person can stay better years after treatment. Much of this is not well understood by many IBS patients.Why Consider Hypnosis Treatment for IBS?by Olafur S. Palsson, Psy.D.Hypnosis is only one of several approaches to treating irritable bowel syndrome and may not be the most suitable option for all patients (click here for discussion of treatment options for IBS). However, hypnosis treatment has some advantages which makes it an attractive option for many IBS sufferers with chronic and severe symptoms:- It is one of the most successful treatment approaches for chronic IBS. The response rate to treatment is *80% and better in most published studies to date. *- The treatment often helps individuals who have failed to get improvements with other methods (see for example: Whorwell et al., 1984, 1987; Palsson et al., 1997, 2000).- It is a uniquely comfortable form of treatment; relaxing, easy and generally enjoyable.- It utilizes the healing power of the person's own mind, and is generally completely without negative side effects. - The treatment sometimes results in improvement in other symptoms or problems such as migraine or tension headaches, along with the improvement in IBS symptoms.- The beneficial effects of the treatment last long after the end of the course of treatment. According to research, individuals who improve from hypnosis treatment for IBS can generally look forward to years of reduced bowel symptoms. http://www.ibshypnosis.com/whyhypnosis.htmlThere is a lot of research on all this.http://www.app.com/apps/pbcs.dll/article?A...50317/1006/LIFEThere are many ways it physically works on IBS, but because mast cells can be set off by the fight or flight, just as if they would from a food allergy, you can turn down the fight or flight responce. The mast cells release histimine onto the smooth muscle which is toxic and this can contribute to pain and d in IBS. An example of this is I use to teach IBS classes at a major hospital and we had hypnotherapist work with the group. In this case he got people relaxed and mentioned walking through a garden and smelling the flowers ect., and one of the women had an allergy reaction. Her eyes started watering and she was sneezing.Popcorn use to trigger my IBS every time I ate it. After HT it no longer does.Just posting this for the info.Evidence, claims and counterclaims*There are only two types of therapies for disease; those that have been proven to be effective, and those that are unproven. The plural of anecdote or testimonial is not good clinical evidence. *The medical literature is littered with the corpses of treatments previously claimed or thought to be effective on theoretical grounds, later discarded as unproven when subjected to careful study.Food allergyQuestions to ask unorthodox practitionersIn the absence of effective advertising or government regulation for unsubstantiated claims for unorthodox allergy testing or treatments, patients should ask the same questions they pose for any form of treatment before going ahead: What is the evidence it works? Has such evidence been published? If so, can I find it on Medline/Pubmed? What are the risks and benefits? What might happen if I do not undertake this form of treatment? How much does it cost? Are there any side-effects? What are the qualifications of the practitioner recommending the treatment? Why doesn't my own doctor suggest this type of treatment? Why can this one test of treatment detect or treat so many different problems?


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## eric (Jul 8, 1999)

MsMKind of off topic just to check outWhat the World Eats, Part Ihttp://www.time.com/time/photogallery/0,29...1626519,00.html


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## eric (Jul 8, 1999)

This was written for the IFFGD by the Dr Whorewell who actually was part of the IgG study on foods and IBS.with permissionIBS DietDiet, food and eating can affect symptoms in IBS. Many people with irritable bowel syndrome (IBS) notice that their symptoms appear to get worse following a meal. They may wonder if they have a dietary allergy or intolerance. More confusing, they may notice that a food seems to upset them on one day but not another. Among the most common questions IBS patients have is what food to avoid. This can drive a person to go looking for a diet or a test that might help sort all this out. A bewildering amount of often conflicting advice is available, especially on the Internet. Much of it is associated with a considerable cost.Diet and IBS symptomsThere are a variety of factors that affect IBS, and diet is just one of these. If other factors, such as stressors or hormonal changes, are more active on a particular day, then diet is more likely to push your symptoms "over the edge." There is no evidence that digestion of food is different in those with IBS compared to those without IBS. Diet, food and eating does not cause IBS. However, increased intestinal muscle reactivity and/or heightened sensitivity in IBS can cause the bowel to over-respond to stimuli. Even a normal event such as the act of eating itself, and not a particular food, may aggravate symptoms at times. When we eat, hormones are released that stimulate the gut.Cramping and diarrheaCertain foods are known to stimulate gut reactions in general, and in those with IBS eating too much of these might influence or worsen symptoms. Examples that may provoke symptoms of abdominal cramps and diarrhea include:Meals that are too large or high in fat Fried foods Coffee Caffeine Alcohol Eating too much of some types of sugar that are poorly absorbed by the bowel can also cause cramping or diarrhea. Examples include: Sorbitol - commonly used as a sweetener in many dietetic foods, candies, and gums Fructose - also used as a sweetener and found naturally in honey as well as some fruits Gas and bloatingSome foods are gas producing (e.g., beans, cabbage, legumes [e.g., peas, peanuts, soybeans] , cauliflower, broccoli, lentils, Brussels sprouts, raisins, onions, bagels) and eating too much may cause increased gaseousness, particularly since IBS can be associated with retention of gas and bloating.FiberIf fiber seems to be a problem, it is usually insoluble fiber (mainly found in cereals or whole grains) that is the offender. Soluble fiber, mainly found in fruits and vegetables, is less likely to be a problem. When adding fiber to the diet, it is best to do so slowly over a period of weeks, which helps avoid discomfort. If gas or distention occur, try reducing the amount of fiber and reducing consumption of gas-producing foods. For more on dietary fiber Go ».What to do about dietThe influence of diet is unique to each individual and there is no generalized dietary advice that will work for everyone. A physician can take a brief dietary history and with a 2-3 week diary of dietary intake, symptoms, and any associated factors (e.g., daily obligations, stressors, poor sleep, medications) can help identify dietary and/or other factors that may impact symptoms.For those with IBS who benefit from simple dietary modifications, it makes sense to adjust the diet and reduce intake of the offending food. It does not make sense to adopt unnecessarily limited diets, which can lead to reduced quality of life or even malnutrition.Physicians and patients need to talk about diet. Guidance needs to be provided by a knowledgeable health care professional (e.g., physician or registered dietician) who can assess individual circumstances while helping make sure that nutritional needs are being met through a balanced diet, and healthy eating habits.http://www.aboutibs.org/site/about-ibs/management/ibs-dietThere is a small charge for this one also written by Dr Whorewell.Dietary Aspects of Irritable Bowel Syndrome (IBS)Many patients with irritable bowel syndrome (IBS) comment that their symptoms appear to deteriorate following a meal. In many individuals this is merely a nuisance but in others it can be much more of a problem. Fortunately, it is usually reasonably easy to tackle the dietary aspects of IBS as long as you understand a few basic principles. For those who suspect food is a factor in their symptoms, there are 4 foods that most often seem to be involved.http://www.aboutibs.org/store/viewproduct/220Personal Daily Diary (Online version)Use this Personal Daily Diary for 2-4 weeks to help you get the most out of your next doctor visit.The objective of using this Daily Diary is to gain a better understanding of your bowel disorder.http://www.aboutibs.org/store/viewproduct/PDDThere is a relatively high percentage of IBSers who don't eat right, who have food phobias and other food issues in general. Not eating regularly is bad for the gut and stresses it out, because it somewhat shuts down when you don't eat and then the act of eating turns it back on, sometimes after a longer period of time. Say a person with d goes out somewhere to work for example and doesn't want to eat so they don't have d or pain or bloating and then goes the whole day without eating and comes home and eats a big meal, in part because their now really hungry. This physically can stress digestion out itself. Not eating right can also contribute to fatique and brain fog and possible malnutrition.


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## anmegrl (Jul 4, 2004)

Hi Ms. M:Sorry you got involved in this quagmire. I see things definitely haven't changed here. Kind of reassuring though, like being in a nice dysfunctional family I have been tested for IgG Food Allergies when I did my experiment with a Dr. that I won't mention lest Eric's head explodes. I was tested through GSDL so my results included IgE and IgG allergic foods. On the IgE side, I was only slightly allergic to crab (I don't like or eat crab so no big deal). However, like you I had lots a foods on the IgG side and like you I was skeptical about IgG "allergies". Let me preface this by saying that I was taking digestive enzymes, probiotics, and other supplements before I got tested. It seemed I was getting a bit better with the supplements but I still had a few pesky problems that remained therefore I went the extra step. Luckily for me, many of the foods weren't foods that I ate regularly so cutting them out entirely wasn't difficult. I restricted my diet accordingly and -from my own reading - devised a diet where I rotated foods so I never ate the same group of foods daily or even every other day. That was the hardest part but not impossible. You've probably heard or read about that already - making sure you don't eat the same foods over and over. I don't know if you did this too, if not it couldn't hurt. Since most my IgG allergies were listed as "very low" I had the option to include them, one by one, after a period of time if they didn't cause any problems. Honestly, I didn't notice an appreciable difference between eating what I ate before being tested and eating on the elimination diet. After I while I said "screw it" and went back to what I was eating before. I'm not sure how long I stayed on that diet but it was probably at least 3-4 months. I generally use a 1 month cut off date for prescription drugs - if I don't see ANY improvement I will stop. I use a 3 month cut off date for natural or alternative remedies. It may have been six months - it seemed like forever.Right now my diet is close to the one Heather has on her site . . . Funny that I had been naturally eating that way since I first started having IBS problems years and years ago but she made a book and a website out of it. Whatever pays the bills. Personally, I would just focus on the supplements and throw some Kundalini Yoga in from time to time. They'll probably give you more relief than the elimination diet. Just pay attention to how you feel. After you get stable with the supplements and you don't think you could get any better, you could always try the elimination diet again and see if it does push you over into Wellsville. Every person is different and sometimes other things must be up and running before you notice improvement with a particular technique. My ideology is if it doesn't cost you much money and won't harm you, give it a wholehearted try and see if it works. If it does, you'll definitely benefit. If it doesn't, at least you know you gave it your best shot and you don't have to try it again. I hate sitting around wondering whether I should have done something longer or different because someone I talked to or something I read made me quit midstream. Don't pay too much attention to studies unless they say something will be detrimental to your health. I find they just make me worry more than I should and that definitely doesn't help me get better.Either way, good luck. I hope I helped a little.


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## eric (Jul 8, 1999)

Its not my head will explode as much it is my heart sinks someone is giving really bad information.again from the allergy experts, this isn't even about IBS"The Australasian Society of Clinical Immunology and Allergy has issued this paper on Allergy testing and treatments."Unorthodox Techniques for the Diagnosis and Treatment of Allergy, Asthma and Immune Disorders *"Inappropriate use of Conventional TestingAdverse consequences may also arise if conventional laboratory tests are used in inappropriate clinical situations, or where results are presented in a manner amenable to misinterpretation. *Food specific IgG, IgG4Use: Diagnosis of food sensitivity / allergy. Method: Antibodies to food are measured using standard laboratory techniques. Evidence: Level II Comment: *IgG antibodies to food are commonly detectable in healthy adult patients and children, independent of the presence of absence of food-related symptoms. There is no credible evidence that measuring IgG antibodies is useful for diagnosing food allergy or intolerance, nor that IgG antibodies cause symptoms. In fact, IgG antibodies reflect exposure to allergen but not the presence of disease. *The exception is that gliadin IgG antibodies are sometimes useful in monitoring adherence to a gluten-free diet patients with histologically confirmed coeliac disease. Otherwise, inappropriate use of food allergy testing (or misinterpretation of results) in patients with inhalant allergy, for example, may lead to inappropriate and unnecessary dietary restrictions, with particular nutritional implications in children. Despite studies showing the uselessness of this technique, it continues to be promoted in the community, even for diagnosing disorders for which no evidence of immune system involvement exists. "http://www.allergy.org.au/pospapers/unorthodox.htmDo they tell you that when they want to test for IgG antibodies, I think not.


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## anmegrl (Jul 4, 2004)

Aren't you only supposed to be posting links rather than copying/pasting info?It makes it so hard to reply to peoples' threads when their original questions are buried in pages and pages of quotes.I don't think anyone here is saying that this is an IBS thing. And contrary to your belief, not everyone who comes to this place is a complete idiot. As she's proven, we can search and find scientific articles/studies via the internet or through real doctors. We don't need you to do that for us. In fact, many of us do the research first before they ask the question. It really isn't helpful to bombard a person with info she already knows or has when all they want are responses from people with PERSONAL experience on the topic. It isn't helpful to people who are looking at this thread out of curiosity either. Who the heck wants to read through your famously loooonng posts just to get a simple answer? It takes the humanity away. No one likes to be taught at or talked down to when all they want to do is connect with someone with similar experiences.I've said it before but I'll say it again. If you just have to post study after study, then put it on the section of the site where someone can easily locate it and refer to it months later when this post is hidden away and forgotten. Now that would be helpful to future users. Not piling on every single thing you have on your computer on each and every thread you ever reply to. I know old habits die hard but I could have sworn that Jeff already addressed your "problem."


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## eric (Jul 8, 1999)

Its totally legit to post what I posted there."I don't think anyone here is saying that this is an IBS thing"Yes someone was doing that please read the whole thread, not the orginal poster though.I am sorry to hear you think the information I posted from accurate sources is a problem. How do you know who its helpful to or not and others taking the time to read it and I am hoping it is helpful to those who are reading it all, which you may not agree with.If you think for a minute I don't have humanity for IBSers perhaps you should think again.


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## eric (Jul 8, 1999)

I could be wrong but"IgG Food Allergies when I did my experiment with a Dr."Was that Dr Dalman,* a chiropractor?*What kind of doctor was it really?


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## anmegrl (Jul 4, 2004)

Now you know exactly what type of Dr he was. What type of doctor are you?And if you paid any attention to my posts back then you would have also noted that I was working with my gastroenterologist and internist at the same time I was using his protocol and I told them exactly what I was doing at every step and asked whether they agreed or not or had any concerns. They didn't have any concerns and thought it was good for me to try it since (1) my previous doctors never eliminated many possible sources of my symptoms and (2) much of what he was doing wasn't any different from what other nutritionists or MDs were suggesting to IBS patients. But of course you knew more than they did







so I shouldn't have paid attention to any of their medical opinions.How do I know what you do is not helpful to other people or not? They tell me (in private messages). Plus, have you ever noticed that after you post, people stop responding as much or not at all. It scares them away. Of course I'm not talking about everyone but obviously a number of people get really tired of it after a while and just choose to not post.I'm sure you think you are helping . . . in your own way . . . but there is such a thing as overkill.Get away from the computer every now and then. You spend way too much time on this site.


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## eric (Jul 8, 1999)

I am glad to hear this"working with my gastroenterologist and internist at the same time "FYIDr. Dahlman has posted misinformation to this bb calling all gi symptoms, including inflammatory diseases IBS as well as other misinformation on IBS. IBS is a distint entity and its also classified as a functional disorder.They are further along in IBS research then he has information posted to his website and some things are down right false and not based on real research and much is left out. They already have strong research although incomplete on IBS. He also will treat people over the internet without seeing them and their is a question of how ethical that is, because its important to see the person in person.He does not actually do any IBS research.He bases his treatments on his own alternative beliefs and not on the actual research on IBS.He is also expensive and offers advise most people could do themselves. So I personally believe buyer beware, be very aware.I also believe, there are a lot of really bad websites on the internet about IBS and personally believe this is a good example really.His nine variables"The Nine Variables1. Altered levels of beneficial bacteria (probiotics)2. Possible presence of bad bacteria, yeast or parasites3. Lack of digestive enzymes (especially if you have lost your gall bladder)4. Imbalanced bowel chemistry5. Intolerances to dairy products6. Intolerances to fructose containing foods7. Intolerances to gluten containing foods8. Celiac Disease (a gluten problem, but different than a gluten intolerance)9. Possible food allergies (different than intolerances, it's an immune response)"There is evidence that bacteria may play a role in IBS and in fact already does in Post infectious IBS, but that infection resolves. There are many reason bacteria can play a role in IBS.IBS is NOT cause by yeast or parasites!!!!!!IBS is NOT caused by digestive enzymes!!!!!Imbalanced bowel chemistry has been found in IBS and more then just the bowel, but he does not address here what they have found at all. IT is much more complicated in reality.Fructose is not IBS!!!!Gluten is not IBS.Celiac sprue is celiac spruce are not IBS.Food allergies DO NOT CAUSE IBS!!!!This is outdated and sometimes totally false information.If you had a good workup by a gi doctor then some or all of those conditions would have been ruled out because some cause symptoms IBS does not for one, but there are other reasons major reasons.He is " Dr. David Dahlman, a Chiropractic Physician with a degree in Nutrition" and not a gastroenterologist or neurogastroenterologist or specialist in IBS or the actual enteric nervous system and brain gut axis. Not all states will let "alternative doctors" practice this way. anmegrl, I am sorry you feel none of the information I posted to this thread was helpful to you in anyway what so ever or to anyone. I had already applogized to MsM in the thread.


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## ms.m (Jan 23, 2008)

Okay, awhile back I said I wasn't going to reply to Eric's posts but I just have to say a few things. I have privately messaged people about this topic, and also received private messages due to the fact that we cannot come on this forum and talk about the original issue. The reason we can't is because you, Eric, do not stick to the topic, and you antagonize people. I posted this topic because I wanted to hear PERSONAL STORIES about people's PERSONAL EXPERIENCES with IgG Food Allergy testing. Whether they were a patient or doctor I didn't care but I wanted personal stories. Not just study after study copy and pasted. I wasn't asking for research, I've done a lot. So what you post isn't relevant. I suggest if you want to merely discuss what you've researched you should post a separate topic.Also, we're all on this site because we suffer from IBS. It's an annoying, unpleasant, and at times can be debilitating and painful. It's stressful enough that we all have this horrible condition. And what would be nice if we could all come on here and support one another, help one another, and listen to one another. Putting up post after post that is off topic (doesn't offer any PERSONAL experience story which is what my original post asked for) and just acting like you know it all when in fact you don't even know how to stay on topic - is not necessary. We should all feel welcome on these forums. But due to Eric's constant antagonizing I and other people on this topic are privately messaging each other. We want to stay on topic and be supportive. This forum should be a place of comfort not arguing and stress. And I've noticed that you, Eric have close to 25,000 posts. Over a period of many years but still, that's a lot. I've found that not focusing on my IBS constantly, not talking about it constantly helps. Discussing it is good, healthy, and helpful. And I'm glad I've found this site. But if I was constantly discussing my IBS on this site all the time, I'd start to dwell on my problems. And if your other posts are anything like the ones you've posted on this topic, you're not helping people. That may be your intention, but it's not helping. So I will continue to PRIVATELY respond to people's messages so we can support each other and stay on topic. Which is a shame because more people would be helped if they could see all of our conversations out in the open, but unfortunately you make that a hassle to do. If anyone has a question to ask me, or wants to respond to my original topic - please feel free to send me a message.


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## eric (Jul 8, 1999)

"The reason we can't is because you, Eric, do not stick to the topic, "What I have posted is on topic on IgG foods as well as IBS and the information is from professionals."I wanted to hear PERSONAL STORIES about people's PERSONAL EXPERIENCES with IgG Food Allergy testing."*You did not post you only wanted personal experiences *and *there are spammers posting to this thread giving inaccurate information.*"So what you post isn't relevant." Again what I posted is very relevant.


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## ms.m (Jan 23, 2008)

This is what I said in my original post. - "I just wanted to know if anyone has had *experience* with these tests and the elimination diets you're placed on after you find what your allergies are. Thanks!" So yes, I did ask for personal experience.Whatever. I just got ANOTHER personal message saying they feel the same way as me. I'm done responding to anything by you now, big waste of time.


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## eric (Jul 8, 1999)

To anyone who has not seen this might find this discussion helpful on this topic. Not one of these doctors believes foods cause IBS and that foods are multifactoral in triggering synmptoms.This trial did not actually test IgG testing John O Hunter (23 December 2004) IgG anti-betalactoglobulin in children with IBS symptoms: a valid aid to decide for the elimination Antonio Carroccio, Calogero Scalici, Lidia Di Prima, Giuseppe Iacono (8 December 2004) Author's reply Peter J. Whorwell, Wendy Atkinson and Trevor A. Sheldon (6 December 2004) Food elimination in IBS: the case for IgG testing remains doubtful John O Hunter (1 December 2004) Author's reply Peter J. Whorwell, Kathryn J. Bentley, Wendy Atkinson and Trevor A. Sheldon (5 November 2004) IgG food antibodies should be studied in similarly treated groups W A Carrock Sewell (19 October 2004) IgG antibodies to foods in IBS Joel E Mawdsley, Peter M. Irving and Richard J. Makins (18 October 2004) --------------------------------------------------------------------------------"The problem with the current trial is that its ambiguities allow it to be used to promote IgG testing to the general public, who are being informed that these results provide unequivocal support for such testing procedures in all IBS patients."http://gut.bmj.com/cgi/eletters/53/10/1459That was happening on this thread by Mike no lomo and Texas mom who work for Leap food allergy testing.


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