# IBS, Migraines and Food



## AnnieOCFP (Jan 9, 2001)

I've had IBS for years. Stress is my main contributing factor, as evidenced by IBS symptom relief when taking 10 mg. of Paxil daily. However, food can trigger an episode as well.This week, I had an unusual episode. After eating a half cup of cottage cheese and a stick of string cheese (both of which I can normally eat with no problem), I experienced a violent attack of diarrhea, followed by the worst migraine headache imaginable.My question is this: Can IBS and Migraine be linked? Can both be caused by a food intolerance?I've done some research, and discovered that a migraine can be triggered by aged cheese (perhaps the string cheese was old??) as it contains tyramine. Migraine sufferers should avoid tyramine, artificial sweetners, MSG, and processed meats. These are often the things that trigger my IBS.Relationship?? Link?? Clue??


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## Mercedes . (Apr 4, 2003)

I can relate to part of your problem, I was convinced I didnt have ibs, and discovered I didnt really, but I do have loads, and I mean loads of food intolerances, if I eat something I shouldnt I get a really bad headache, and feel sick, but if I drink something (Anything) I feel less sick, but the headache has to go away by itself (Eventually) - Dont know if thats any help but I thought I would say it anyway!!


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## Julia37 (May 9, 2001)

Food intolerance can cause both digestive problems and migraines, as well as congestion, asthma, hives, and any other condition usually considered an allergic reaction.I've copied one of Mike NoLomotil's posts here that references several dicussions of food sensitivity. He's busy with other projects and doesn't have as much time to come here as he used to, he taught me and several others about managing food sensitivity, and his company has a diagnostic and treatment program.Dr. Brostoff's book "Food Allergies and Food Intolerance A Complete Guide...", written for lay people, is excellent and explains all the symptoms and reactions known to date.







Happy reading!







Julia---------------------------------"Considerable confusion is now arising over the relationship between food intolerance and the Irritable Bowel Syndrome (IBS). Although the name has been hallowed by long usage, IBS is not a distinct entity but merely a collection of disorders which are characterized by abdominal symptoms but no obvious organic pathology. G.W. Thompson forecast in 1985: 'the IBS is organic; that is all sufferers will eventually be found to have measurable, unique pathologic defects.' When that happy day arrives, the term 'IBS' will no longer be used, and each patient will receive a more precise diagnosis. Until then it is sufficient to appreciate that food intolerance represents an important proportion of the conditions which together make up IBS."John Hunter, MD, FCRPDirector or Gastroenterology and Consultant PhysicianAddenbrooke's HospitalCambridge, United KingdomFrom"Food Allergy and Food Intolerance" Second Edition 2002J. Brostoff, MDS. Challacombe, MDSaunders ___________________________Indeed, the one specific statement set forth by Dr. Drossman in the post above which no one does or would disagree with, is that food intolerance is no more the causal basis of the pathogenesis of the group of conditions currently called 'IBS" than chronic stress is.It is, however, known by many and is the basis for effective treatment of many IBS patients, to be a major set of symptom-generating mechanisms among the subpopulation of diarrheic-prone people diagnosed with "IBS".There is ample evidence of this in the literature, sufficent even to result in inclusion of it in the Merck Manual of Diagnosis and Therapy:________________________________"Page 1051 of the hard copy of the Merck Manual, and online Merck Manual at http://www.merck.com/pubs/mmanual/section1...ter148/148b.htm "Recently Food Intolerance was found to be responsible for symptoms of some patients with the IRRITABLE BOWEL SYNDROME, confirmed by double-blind food challenge.An increase in rectal prostaglandin levels was noted when a reaction occurred.Preliminary information suggests the same phenomenon may take place in patients with chronic ulcerative colitis."___________________________In actuality the discovery of this mechanism is not all that recent....it sates back over 23 years to when it was first obserevd nad has been studied in vivo with invasive jejunal segmantal isolation studies which quantifiy inflammatory mediator release in the isolated small bowel of patients with so called "IBS" per the Rome criterai (food allergy ruled out) since about 1994. It can also be duplicated in vitro since about 1997.If one is seeking the most experienced and qualified experts on pscyhophysiology as it mat realte to IBS one should look to UNC and their work.If one is seeking expertise in fod allergy and intolerance one must begin at the top of the order, with Professors Brostoff, Challacombe and perhaps the 100 authors whoc contributed to the following new medical text on the subject...and for in vivo assays of immune response in food intolerance induce GI and systemic symptoms Prof Ulf Bengtsson has donw the most work to date in that area...____________________________Books written edited or contributed by Professor Jonathan Brostoff:FOOD ALLERGY AND INTOLERANCE, Professor Jonathan Brostoff, MD, Stephen Challacombe, MD (NEW 2002) http://www.amazon.com/exec/obidos/ASIN/070...product-details http://www.greenleaves.com/bookcat/by_brostoff_jonathan.html Asthma: The Complete Guide to Integrative Therapies- by Jonathan Brostoff, Linda GamlinThe Complete Guide to Food Allergy and Intolerance- by Jonathan Brostoff, Linda GamlinFood Allergies and Food Intolerance : The Complete Guide to Their Identification and Treatment- by Jonathan Brostoff, Linda GamlinImmunology- by Ivan Roitt(Editor), Brostoff et alThe Allergy Bible : Understanding, Diagnosing, Treating, Allergies and Intolerances- by Reader's Digest(Editor), et alAutoimmune Disease : Aetiopathogenesis, Diagnosis and Treatment : Essays in Honour of the Retirement of Professor Ivan Roitt Frs- by Peter M. Lydyard(Editor), Jonathan Brostoff(Editor)Case Studies in Immunology- by Jonathan Brostoff, et alCase Studies in Immunology: Companion to Immunology, Fifth Edition- by Jonathan Brostoff, et alClinical Immunology- by Jonathan BrostoffClinical Immunology : An Illustrated Outline- by Jonathan Brostoff, David K. MaleImmunology- by Ivan M. Roitt, et alImmunology : Interactive 2.1- by David Male, et alThe Complete Guide to Hay Fever : The Latest Research & Techniques for Coping With Hayfever- by Jonathan BrostoffFood Allergy and Intolerance- by Jonathan Brostoff, Stephen J. ChallacombeImmunology- by Ivan Maurice Roitt, et alInmunologia Clinica- by Jonathan Brostoff, et alIntroducing Immunology- by Norman A. Staines, et al__________________________Also, a good tutorial on the mechanisms (multiple) of food reactivity and how they marshall IBS symptoms in the food intlerant patients would be this one:Alimentary Pharmacology and Therapeutics Vol. 15 Issue 4 Page 439 April 2001 Food hypersensitivity and irritable bowel syndrome S. Zar, D. Kumar, M. J. Benson http://www.blackwell-synergy.com/servlet/u...36.2001.00951.x To gain some eprspective into the effectiveness of isolating and prophylactically treating food and chemical intolerance in IBS and related conditions these discussions would also be useful: http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000407#000002 http://www.ibsgroup.org/ubb/ultimatebb.php...=4;t=000286;p=4 http://www.ibsgroup.org/cgi-local/ubbcgi/u...0286;p=3#000106 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000364 http://www.ibsgroup.org/cgi-local/ubbcgi/u...=4&DaysPrune=30 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000286 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000285 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000331#000001 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000302 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000287 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000364 http://www.ibsgroup.org/cgi-local/ubbcgi/u...f=5&t=000313&p= http://www.ibsgroup.org/cgi-local/ubbcgi/u...0293;p=2#000069 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000276 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=5;t=000073 http://www.ibsgroup.org/cgi-local/ubbcgi/u...f=5&t=000356&p= http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000320#000016 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000383#000010 http://www.ibsgroup.org/cgi-local/ubbcgi/u...f=5&t=000126&p= http://www.ibsgroup.org/ubb/ultimatebb.php...c;f=17;t=000033 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000363#000002 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=028290#000001 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000335#000009 http://www.ibsgroup.org/cgi-local/ubbcgi/u...f=1&t=028290&p= http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000353 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000389 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000427#000006 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000421 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000427#000015 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=030178#000003 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000476 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=029840#000027 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000478 (NEW testimonial by Bobby&#8230;good) http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000488 (OHNOMETOO One year anniversary) http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000478 In general this is like any other area of medicine...everyuone posesses some information in any given area, and the most specialzied information will be found among those whsoe specialty area is devoted to a particular area. There are many centers of excellence on the subject of food and chemical intolerance mechansism and therapy which go beyond the common boundaries simply due to the fact that it is their focus, so it is usually helpful to seek out specialized information at the acknoweldged source of the specialty.I do beleive that the 2002 edition of Brostoff 7 Challacome remains the ONLY medical textbook yet published on the subject of this particular thread.The more patient-specific one can make the assessment of any patients food and chemical tolerance, or lack thereof, the greater the degree of remission one can achieve. This is not easily done in most centers, as most centers do not make use of the most current methodologies in this specialized area, or do not approach the issue from the perspective that a specialist in that area would.But a study of broader information would make it apprant that there is broader informatio available upon which to base treatment. MNL--------------------Eat Well. Think Well. Be Well. http://www.nowleap.com --------------------------------------------------------------------------------


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## AnnieOCFP (Jan 9, 2001)

Whoa, Julia!! What a wealth of information! I shall be busy reading all day! Thank you!!!


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## Mike NoLomotil (Jun 6, 2000)

Thanks for covering in my absence Julia...Mom in hospital and all its impossible to come round much.here us a link where this subject was addressed quickly today http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=1;t=034076 MNL


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## Mike NoLomotil (Jun 6, 2000)

The link between the conditions was already proven sufficiently for this to have been published by the British Royal Society of Medicine over 10 YEARAS ago.In fact they bemoan the lack of an effective tool for isolating food intolerance reactions in the conditions cited, as of 1992.That "technology problem" has been alleviated, at least. __________________________________________Journal of the Royal Society of Medicine 1992 Sep;85(9):560-4Food ï¿½Allergyï¿½--Fact or Fiction: a Review.Finn R.Royal Liverpool Hospital.Food sensitivity is a common condition presenting with various clinical syndromes including Migraine, Urticaria, Gluten Enteropathy, Crohn's disease and Irritable Bowel Syndrome. It is a heterogeneous condition affecting different organ systems and is also aetiologically diverse with subgroups due to allergy, pharmacological reactions, enzyme deficiencies and psychological causes. Clinical acceptance of food sensitivity has been delayed by the use of dubious diagnostic techniques by a minority of practitioners and the lack of laboratory diagnostic tests, but several double blind studies have now fully validated the existence of food sensitivity syndromes. More widespread recognition of food sensitivity would be cost effective for the National Health Service.Publication Types: ï¿½	Review ï¿½	Review, Tutorial _____________________________MNL


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## Julia37 (May 9, 2001)

Your welcome Mike! I hope your Mom feels better.


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## Mike NoLomotil (Jun 6, 2000)

a little dittie on Migraine...The recommended prophylactic, abortive, or analgesic treatments for Migraine described in the Merck Manual of Diagnosis and Therapy are exclusively pharmaceutical interventions. The medical literature contains ample references to general dietary guidance of foods to counsel the patient to avoid which may contain endogenous chemicals believed to potentially trigger migraine in affected patients. However, the first weakness of dietary prophylaxis is that this advice is not patient specific, while food triggers are highly patient specific and difficult to detect from standard dietary intake monitoring methods. In addition, the literature contains evidence that some standard dietary guidance based on the reputed effects of endogenous chemicals is at best equivocal as to its relevancy. For example, studies have shown such disparities as chocolate, a commonly accepted dietary trigger, being no more likely to provoke migraine than a placebo of carob. On the other hand the literature has also shown what was believed to be a ï¿½placebo response to blind oral challengeï¿½ was actually an immunologic reaction to the gel capsules used to contain and administer the placebo. The literature clearly confirms the relative lack of involvement of actual food allergy (specific IgE antibody) as a common causal basis for symptoms, except as an occasional comorbidity. On the other hand, it is not widely recognized that the literature also contains ample evidence that some other, as yet not fully elucidated, abnormal non-allergic (cell mediated) immunologic response to staple foods on a patient-specific basis is involved in the symptom generation of many migraine sufferers wholly separate and apart from the influence of any food-endogenous chemicals upon the patient. Food challenge results in the systemic release of proinflammatory and proalgesic mediators from circulating immunocytes in the absence of any specific antibodies to the provoking staple food.For example, from ï¿½Disruption of the Immunopeptidergic Network in Dietary Migraine.ï¿½Headache. 1993 Nov-Dec;33 (10):524-7. Martelletti P, Stirparo G, Rinaldi C, Frati L, Giacovazzo M.ï¿½ This investigation is devoted to the study of the time-course of a cytokines panel (IL-4, IL-6, IFN-gamma, GM-CSF) in plasma samples from migraine patients. The data obtained during challenged migraine crises was compared to the baseline values. Time-data series analysis showed a fall after a challenge test for IL-4 and IL-6 plasma levels and an opposite trend (increase) for gamma-IFN and Granulocyte Macrophage Colony Stimulating Factor (GM-CSF) levels. ï¿½The literature also contains evidence that a patient-specific Oligoantigenic Diet is highly effective at reducing symptoms in a substantial subpopulation of pediatric and adult migraine sufferers. However, typical Oligoantigenic Dieting is NOT patient specific due to a lack of any available method to correctly isolate patient-specific staple foods that provoke the release of mediators leading to symptom generation. The cell-mediated mechanisms involved have made detection extremely difficult. Reactions are both delayed onset and dose dependent; ergo ï¿½trigger monitoringï¿½ may not only be misleading, but non-revealing of any perceivable patterns. This often leads to the belief that diet plays little or no role in the patientï¿½s condition. Also as a consequence, effective diets have been restricted primarily to research milieu, since to be effective they need to be ï¿½few foods dietsï¿½ (elimination of a wide range of foods in the hope of inclusion of the actual offending foods). Such diets, while effective at reducing frequency and intensity of episodes, are by nature nutritionally unsound and clinically impossible for the patient to follow long term.The purpose of this summary is to provide a selection of references that explain the basis, both physiologic and technologic, for an effective new approach to Disease Management of Migraine via Patient Specific Oligoantigenic Dieting that is integrated with the patientï¿½s existing prophylactic, abortive, or analgesic treatment. This Protocol improves prophylaxis and can reduce or even eliminate the need for abortive and/or analgesic pharmacotherapy.Reports from physicians adopting this new protocol into the care of their Migraine patients have been extremely positive. Contact information for such physicians is available. This summary will provide an explanation of the basis for this experience of improved therapeutic outcomes in the treatment of their Migraine patients.As far back as 1979, Oligoantigenic Dietary Therapy has shown clinical promise as an effective means of reducing Migraine symptoms, with the limitation that a relatively large number of staple foods, often associated with regular ingestion by the patient, needed to be removed to ensure effectiveness over a wide range of patients. This typically leads to recidivism, or at best dietary imbalance. _______________________________Lancet. 1979 May 5;1(8123):966-9Food allergies and migraine.Grant EC.60 migraine patients completed elimination diets after a 5-day period of withdrawal from their normal diet. 52 (87%) of these patients had been using oral contraceptives, steroids, tobacco, and/or ergotamine for an average of 3 years, 22 years, and 7.4 years respectively. The commonest foods causing reactions were wheat (78%), orange (65%), eggs (45%), tea and coffee (40% each), chocolate and milk (37% each), beef (35%), and corn, cane sugar, and yeast (33% each). When an average of ten common foods were avoided there was a dramatic fall in the number of headaches per month, 85% of patients becoming headache-free. The 25% of patients with hypertension became normotensive. Chemicals in the home environment can make this testing difficult for outpatients. Both immunological and non-immunological mechanisms may play a part in the pathogenesis of migraine caused by food intolerance._________________________________________________However, by 1983 it had been shown that advocacy of food allergy (specific antibody reactions) as the basis for Food Induced Migraines was misplaced, as no distinction could be drawn between antibody profiles of patients vs. asymptomatic controls.________________________________J Neurol Neurosurg Psychiatry 1983 Aug; 46 (8):738-42Food Related Antibodies in Headache Patients.Merrett J, Peatfield RC, Rose FC, Merrett TG.Highly sensitive and specific methods for assaying IgE and IgG4 for antibodies in serum have been developed in order to test a recent suggestion that food allergy is a major cause of migraine. Sera were collected from 208 adultsï¿½74 with dietary migraine, 45 with non-dietary migraine, 29 with cluster headache and 60 controls. No significant differences were identified between any of the groups with the one exception that cluster headache patients had significantly raised levels of total serum IgE: this difference may be explained by the high proportion of smokers. Mean IgG4 titres to cheese, milk and chocolate were very similar in the dietary and non-dietary migraine patients and the control subjects, though lower in the cluster headache patients.There was, therefore, no evidence that the food intolerance often associated with migraine headaches is associated with a conventional allergic mechanism._________________________________________However, success with oligoantigenic diet trials not only was often confirmed, but other co-morbid symptomology was relieved as well, as was the tendency for physical phenomena or stressors to provoke episodes in subjects.__________________________________________Lancet 1983 Oct 15;2(8355):865-9Is Migraine Food ï¿½Allergyï¿½? A Double-Blind Controlled Trial of Oligoantigenic Diet Treatment.Egger J, Carter CM, Wilson J, Turner MW, Soothill JF.93% of 88 children with severe frequent migraine recovered on oligoantigenic diets. The causative foods were identified by sequential reintroduction, and the role of the foods provoking migraine was established by a double-blind controlled trial in 40 of the children. Most patients responded to several foods. Many foods were involved, suggesting an allergic rather than an idiosyncratic (metabolic) pathogenesis. Associated symptoms which improved in addition to headache included abdominal pain, behaviour disorder, fits, asthma, and eczema. In most of the patients in whom migraine was provoked by non-specific factors, such as blows to the head, exercise, and flashing lights, this provocation no longer provoked migraine while they were on the diet.Publication Types: ï¿½	Clinical Trial ï¿½	Controlled Clinical Trial ï¿½	Randomized Controlled Trial ____________________________________The role of cell-mediated immune response to foods in Migraine was further suggested by this 1994 study, using the immunomodulator (cell-stabilizer) Cromolyn Sodium to relieve symptoms in confirmed food provoked migraines in the absence of specific immunoglobulins to the provoking foods, thus eliminating food allergy but suggesting other immunologic mechanisms which could be blunted._____________________________________Lancet 1984 Sep 29;2(8405):719-21Migraine Is a Food ï¿½Allergicï¿½ Disease.Monro J, Carini C, Brostoff J.Foods which provoked migraine in 9 patients with severe migraine refractory to drug therapy were identified. The patients were then given either sodium cromoglycate or placebo orally in a double-blind manner, with foods previously identified as provocants. Sodium cromoglycate exerted a protective effect, thus confirming that it can prevent a hypersensitivity mechanism as well as the symptoms of migraine. Immune complexes were not produced in those patients who were protected by sodium cromoglycate. These observations confirm that a food-sensitivity reaction is the cause of migraine in this group of patients.Publication Types: ï¿½	Clinical Trial ï¿½	Controlled Clinical Trial ______________________________________Subsequent clinical use of Cromolyn Sodium revealed the propensity of the patients to develop tolerance and tachyphylaxis to such treatment. This rules it out as a long-term prophylactic solution, but continued experimentation with oligoantigenic elimination and challenge diet reconfirmed the role of food intolerance or sensitivity in the milieu of migraine. However, while the dietary protocols were successful under the controlled conditions of study, the methods were not very practical as yet for clinical use by the caregiver. The methods are exceedingly time consuming, require a high degree of patient compliance with a highly restrictive initial elimination diet, and precision and patience is required in subsequent sequential reintroduction challenges to isolate offending foods with accuracy. In addition, nutritional support is essential during the protracted phase of elimination and serial challenge as the diets were very nutritionally deficient due to the narrow range of foods consumed to achieve the remission necessary to begin serial oral challenge (lamb, rice, pear protocol for example). The only solution at the time was to eliminate only (10) common foods, to produce partial remission in a portion of the subjects. This was a compromise which was still non-patient-specific, and that still hindered clinical results. Outcomes could be improved upon if a method were developed to more easily identify offending foods based on detecting the actual reactions in vitro.Yet results remain positive and the need for a method to translate this into a practical clinical approach was clear. The absence of this solution has led over time to the widely held beliefs concerning the lack of a role of food intolerance, other than endogenous chemical offenders.Examples of the fast and challenge results were published.______________________________Annals of Allergy 1985 Jul; 55 (1): 28-32Migraine: a Diagnostic Test for Etiology of Food Sensitivity by a Nutritionally Supported Fast and Confirmed by Long-Term Report.Hughes EC, Gott PS, Weinstein RC, Binggeli R.A diagnostic procedure during a nutritionally supported fast week followed by conventional food sensitivity management achieved major improvement for 80% of a migraine panel. This procedure gave a reliable (0.8 correlation coefficient) prognosis on the substantial value of this approach for selection of the treatment of migraine. The study gave two lines of evidence which indicate that migraine has an etiology of food sensitivity.______________________________________ [Article in Italian: abstract translated]Recenti Prog Med 1989 Feb; 80 (2):53-5[Migraine and Food]Pacor ML, Nicolis F, Cortina P, Peroli P, Venturini G, Andri L, Corrocher R, Lunardi C.The frequency of migraine with suspected adverse reaction to foods has been studied in adult patients. Migraine was present in 41 out of 300 patients (13.6%). 38 of these 41 subjects have been treated with elimination diet; 25 (65.7%) obtained a significant improvement of migraine and subsequently, performed challenge tests. 24 of 25 (96%) of oral challenged patients were affected by food intolerance and only (1) one by food allergy. The remaining 13 non-responder subjects suffering from migraine have been subsequently submitted to pharmacological treatment._____________________________________Investigation of migraines induced by cow milk challenge by assessing potential markers of cell mediated immune response was an early quantification of this mechanism.____________________________________Headache 1989 Nov;29(10):664-70Evidence For an Immune-Mediated Mechanism in Food-Induced Migraine from a Study on Activated T-cells, IgG4 subclass, anti-IgG Antibodies and Circulating Immune Complexes.Martelletti P, Sutherland J, Anastasi E, Di Mario U, Giacovazzo M.Various immunological studies have revealed controversial outcomes on pathogenetic mechanisms of food-induced migraine. In order to better define the immune status of this disease we studied 21 patients (cow milk provoked migraines) for circulating immune complexes (CIC). Six out of them were also studied for lymphocyte subpopulations, IgG4 and anti-IgG antibodies, before oral challenge (TO), 4 hours after oral challenge (T4), and 72 hours after oral challenge (T72) with 250 ml of cow milk. The ClqSp assay was used to determine CIC. Lymphocyte subpopulations were defined by the following monoclonal antibodies (Mab): OKT3, OKT4, OKT8, 4F2, H366, TAC, 5E9, L.243 and DA6.231. IgG4 subclass was assessed by using a mouse specific Mab. Anti-IgG antibodies were determined by using HPLC. No significant variation was observed in the study of the expression of DR antigens (L.243 and DA6.231) at the three times. IgG4 and anti-IgG antibodies values showed no variation in their time-course.However, the results showed an increased incidence (3x) of CIC (28.6%) when compared to the control group (10%). Total T-cells (OKT3+) showed a marked increase at T4 (p less than 0.01) and a subsequent decrease at T72 (p less than 0.02). Interestingly, T-activated cells (4F2+ and TAC+) showed a parallel trend at T4 (respectively p less than 0.02 and less than 0.01) and a subsequent decrease at T72 only for the Tac+ cells (p less than 0.05). Also K and NK cells (H366+) showed an early increase at T4 (p less than 0.05). All of which suggest an aberrant cell-mediated immune response to the food antigen challenge.____________________________________At the same time very positive results to Oligoantigenic Dietary therapy were reported for pediatric patients with comorbid Migraine and Epilepsy, and remission was verified by subsequent positive response to oral challenge of the antigenic foods.___________________________________Journal of Pediatrics 1989 Jan; 114 (1): 51-8Oligoantigenic Diet Treatment of Children with Epilepsy and Migraine (Comorbid)Egger J, Carter CM, Soothill JF, Wilson J.Department of Neurology, Hospital for Sick Children, London, U.K..We studied the role of oligoantigenic diets (ï¿½few foodsï¿½ diet) in 63 children with epilepsy; 45 children had epilepsy with migraine, hyperkinetic behavior, or both, and 18 had epilepsy alone. Of the 45 children who had epilepsy with recurrent headaches, abdominal symptoms, or hyperkinetic behavior, 25 (56%) ceased to have seizures and 11 (24%) had fewer seizures during diet therapy.Headaches, abdominal pains, and hyperkinetic behavior ceased in all those whose seizures ceased, (56%) and in some of those whose seizures did not cease. Foods provoking symptoms were identified by systematic reintroduction of foods, one by one; symptoms recurred with 42 foods, and seizures recurred with 31; most children reacted to several foods. Of 24 children with generalized epilepsy, 18 recovered or improved (75%) including 4 of 7 (57%) with myoclonic seizures and all with petit mal, as did 18 of 21 children with partial epilepsy (86%). In double-blind, placebo-controlled provocation studies, symptoms recurred in 15 of 16 children, (94%) including seizures in eight; none recurred when placebo was given. The Eighteen other children, who had epilepsy alone, were similarly treated with an oligoantigenic diet; none improved.Publication Types: ï¿½	Clinical Trial ï¿½	Controlled Clinical Trial______________________________________Further study of non-allergic cell mediated reactions to staple foods in migraine subjects again confirmed that cell-mediated reactions were associated with symptomology in the subjects. It was becoming clear that if a simple means of reproducing these cell-mediated responses in vitro could be developed, then the offending foods could be easily isolated without the need for strict and protracted elimination-challenge regimens. Patients could move directly to an oligoantigenic diet specific to their needs and experience reduction in symptoms._______________________________Acta Neurol (Napoli) 1991 Oct;13(5):448-56[Italian]T cells Expressing IL-2 Receptor in Migraine (Food Induced).Martelletti P.Centro Cefalee, Universita La Sapienza, Roma, Italia.We studied a group of migraine patients for circulating immune complexes, lymphocyte subpopulations, IgG4 and anti-IgG antibodies, before, after 4 hours and after 72 hours a specific challenge test. We found an increased incidence of circulating immune complexes. Total T cells showed a marked increase after challenge test. The most important finding was the presence of T-activated cells. Also K and NK cells showed an early increase after the challenge. In commenting on the outcomes of this investigation, it must be stressed that the evidence of an early lymphocyte activation after the challenge test indicates an involvement of interleukin-2 related receptor in food-induced migraine. The results have reinforced the idea of immune mechanism involvement in food-induced migraine, but it seems to be a different mechanism from that previously hypothesized, with the involvement of the ï¿½complex cytokinesï¿½ network.Publication Types: ï¿½	Review ï¿½	Review, Tutorial ________________________________________Over 10 years ago, the following position was set forth in the Journal of the Royal Society of Medicine, United Kingdom, concerning the role of food intolerance in certain conditions including Migraine, and recommending the National Health Service accept this condition and pursue means of diagnosis and treatment to reduce healthcare costs and improve outcomes.They bemoan the lack of any accurate assay at the time which could identify the offending foods which provoked the symptoms of the conditions listed including Migraine and IBS.__________________________________________Journal of the Royal Society of Medicine 1992 Sep; 85 (9):560-4Food ï¿½Allergyï¿½--Fact or Fiction: a Review.Finn R.Royal Liverpool Hospital.Food sensitivity is a common condition presenting with various clinical syndromes including Migraine, Urticaria, Gluten Enteropathy, Crohn's Disease and Irritable Bowel Syndrome. It is a heterogeneous condition affecting different organ systems and is also aetiologically diverse with subgroups due to allergy, pharmacological reactions, enzyme deficiencies and psychological causes. Clinical acceptance of food sensitivity has been delayed by the use of dubious diagnostic techniques by a minority of practitioners and the lack of laboratory diagnostic tests, but several double blind studies have now fully validated the existence of food sensitivity syndromes. More widespread recognition of food sensitivity would be cost effective for the National Health Service.Publication Types: ï¿½	Review ï¿½	Review, Tutorial ______________________________________Am J Med 1992 Apr;92(4):363-7Comorbidity of Fibromyalgia with Medical and Psychiatric Disorders.Hudson JI, Goldenberg DL, Pope HG, Keck PE, Schlesinger LBiological Psychiatry Laboratory, McLean Hospital, Belmont, Massachusetts 02178.PURPOSE: Patients with fibromyalgia have been reported to display high rates of several concomitant medical and psychiatric disorders, including migraine, irritable bowel syndrome, chronic fatigue syndrome, major depression, and panic disorder. To test further these and other possible associations, we assessed the personal and family histories of a broad range of medical and psychiatric disorders in patients with fibromyalgia. PATIENTS AND METHODS: Subjects were 33 women (mean age 42.1 years) who each met American College of Rheumatology criteria for fibromyalgia and presented to a rheumatologist at a tertiary referral center. They received the Structured Clinical Interview for DSM-III-R (SCID); a supplemental interview, in SCID format, for other medical and psychiatric disorders, including migraine, irritable bowel syndrome, and chronic fatigue syndrome; and an interview for family history of medical and psychiatric disorders. RESULTS: Patients with fibromyalgia displayed high lifetime rates of migraine, irritable bowel syndrome, chronic fatigue syndrome, major depression, and panic disorder. They also exhibited high rates of familial major mood disorder. CONCLUSIONS: The finding that migraine, irritable bowel syndrome, chronic fatigue syndrome, major depression, and panic disorder are frequently comorbid with fibromyalgia is consistent with the hypothesis that these various disorders may share a common physiologic abnormality.___________________________In 1993 the Headache Center at Rome University expressed their particular interest in food-provoked migraine and evidence from prior studies of cell mediated reactions to foods by assessing post-challenge mediator release. This resulted in the discovery of T Cell activation and macrophage stimulation mediator release, as well as a reduction in mediators, which would normally inhibit macrophage production. All signs that an immunologic response to foods paralleling an immunologic response to pathogens occurred in dietary migraine victims. This parallels findings the next year in Sweden using jejunal isolation techniques on IBS patients which revealed a not understood, but clear dysfunction in the Oral Tolerance mechanism, appears in both conditions, whether comorbid or not.____________________________________Headache. 1993 Nov-Dec; 33 (10): 524-7.Disruption of the Immunopeptidergic Network in Dietary Migraine.Martelletti P, Stirparo G, Rinaldi C, Frati L, Giacovazzo M.Headache Centre, Rome University La Sapienza, Italy.This investigation is devoted to the study of the time-course of a cytokines panel (IL-4, IL-6, IFN-gamma, GM-CSF) in plasma samples from migraine patients. The data obtained during challenged migraine crises was compared to the baseline values. Time-data series analysis showed a fall after a challenge test for IL-4 and IL-6 plasma levels and an opposite trend for *gamma-IFN and **GM-CSF levels. The implication of this phenomenon in dietary migraine is not readily evident. There may possibly be an activation of this cytokine network together with the well-known impairment in the neuropeptidergic system, considering the close links between interleukins and other cytokines and the neuro-mediators of pain, such as histamine and 5-HT._________________________________________________Further confirmation of the lack of a role for conventional food allergy mechanisms was set forth by investigation specifically seeking to confirm or rule out food specific antibodies as implicated in food induced migraine. The conclusion was again confirmed that whatever the immune mechanism was, it was not allergy.________________________________________Cephalalgia 1994 Oct;14(5):365-7 Immunocyte Enumeration in Duodenal Biopsies of Migraine Without Aura Patients With or Without Food-Induced Migraine.Pradalier A, de Saint Maur P, Lamy F, Launay JM.Service de Medecine Interne, Hopital Louis Mourier, Colombes, France.The possibility of an IgE-mediated (allergic) mechanism in food-induced migraine remains controversial. Twenty consecutive migraine patients, 11 with food-induced migraine, 9 without, were investigated for determination and counting of immunocyte populations (IgA, IgM, IgE, IgG containing cells) by biopsies at duodenum level. Conventional histology and plasmocyte populations were not significantly different between the two groups of migraine patients. This study does not support the existence of an IgE-mediated allergic mechanism in food-induced migraine.__________________________________________Even using relatively crude and narrowly focused food challenges, a population of patients with staple food induced migraines was confirmed via release of proinflammatory mediators post challenge. If a wider range of foods had been used for challenge the frequency would have been higher, as we now know._________________________________________________Allergy 1995; 50 (20 Suppl):78-81Mechanisms in Adverse Reactions to Food. The Brain.Anderson JA.Division of Allergy & Clinical, Henry Ford Hospital, Detroit, Michigan, USA.Specific chemical mediator release such as histamine and the prostaglandins (PG2a or PGD2) associated with headaches has been found in a few patients who were repeatedlychallenged with specific foods, using Double Blinded Placebo Controlled Food Challenge techniques._________________________________________________Subsequent published findings have demonstrated that PGD2 plays a significant role in the regulation of cerebromicrovascular function and stability. (J Auton Nerv Syst. 1994 Sep; 49 Suppl: S123-7. ï¿½Vasoactive Peptides and Prostaglandin D2 in Human Cerebromicrovascular Endothelium.ï¿½ Spatz M, Stanimirovic DB, Uematsu S, McCarron RM). Further studies continued to reiterate the presence of non-allergic pathways to mediator release and migraine provocation from staple foods (Rev Neurol 1996 May;24(129):534-8, ï¿½Diet and Migraineï¿½; Leira R, Rodriguez R.; Servicio de Neurologia, Hospital General de Galicia Clinico Universitario, Santiago de Compostela). The understanding that cell mediated reactions are key in food-induced non-allergic conditions continued to be clarified throughout the 1990ï¿½s (especially those involving T Cells). This led to the development of new technology in 1997 which could and would accurately detect abnormal reactivity of any circulating immunocyte regardless of the non-allergic pathway by detecting the common end point action of all cell mediated reactions: antigen uptake and subsequent mediator release. In the last several years the improtance of aberrations in T Cell response to what should be innocuous food antigens has led to an understan ding of the validity of this approach to assaying cell mediated response to innocuous antigens in vitro.______________________________________Current Opinion in Immunology 1998 Dec;10(6):620-7T cell Immunity to Oral Allergens.MacDonald TT.Department of Paediatric Gastroenterology St Bartholomews and the Royal London School of Medicine and Dentistry St Bartholomews Hospital London EC1A 7BE UK.Considerable light has been thrown on the mechanisms of oral tolerance (or, more correctly, orally-induced systemic tolerance) in the past 12-18 months. While it is very clear that T cell anergy and apoptosis can occur after being fed antigen, a major pathway that has been described in different models is the induction of regulatory T cells which secrete transforming growth factor beta. These cells have been designated Th3 cells but their relation to the in-vitro-generated Tr cells, which inhibit tissue-damaging T cell responses in the gut mucosa, is not known. An important discovery is that food antigens have major systemic effects on T cells, similar in many ways to those seen following intravenous injection of soluble antigens. This conceptually moves us away from the notion that there is something special about mucosal (compared to systemic) lymphoid tissue to the notion that it is the type of antigens seen in the gut (i.e. digested, soluble polypeptides) which dictates the types of response seen there. __________________________________________Lancet 2000 Jul 29; 356 (9227): 400-1Relation Between Food Provocation and Systemic Immune Activation in Patients with Food Intolerance.Jacobsen MB, Aukrust P, Kittang E, Muller F, Ueland T, Bratlie J, Bjerkeli V, Vatn MH.Section of Gastroenterology, Rikshospitalet, University of Oslo, N-0027 Oslo, Norwayb Section of Clinical Immunology and Infectious Diseases, Rikshospitalet, University of Oslo, N-0027 Oslo, Norwayc Section of Endocrinology, Rikshospitalet, University of Oslo, N-0027 Oslo, Norwayd Medical Department and Research Institute of Internal Medicine, Rikshospitalet, University of Oslo, N-0027 Oslo, Norwaye Medical Department, Vestfold Sentral Hospital, Tï¿½nsberg, Norway We found that food provocation in food intolerant patients was characterized by a general and systemic immune activation accompanied by an increase in systemic symptoms. Our findings might be important for the understanding of the mechanisms involved in the pathogenesis of food intolerance._________________________________________________Curiously, looking at another aspect of food intolerance regardless of sysmptom set, is the so called "placebo response" to oral challenge. Recent experiments may explain why patients report migraine onset even from placebos: the gelatin capsules have been shown to provoke a migraine via reactivity to the gelatin itself (an ï¿½animal proteinï¿½). An examination was done by a researcher on himself, knowing his migraine foods, after observing that 18% of subjects receiving placebo experienced migraine from the placebo (encapsulated)._______________________________________Clin. Exper. Allergy 2000 May;30(5):739-43Why Do Some Dietary Migraine Patients Claim They Get Headaches from Placebos?Strong FC 3rd.Departamento de Ciencia de Alimentos, Faculdade de Engenharia de Alimentos, Universidade Estadual de Campinas, SP, Brasil.BACKGROUND: In six double-blind studies involving 182 tests of dietary migraine patients sensitive to tyramine and beta-phenylethylamine, 18% reported headaches from placebos which were all concealed in gelatin capsules. OBJECTIVE: The purpose of this research was to test a hypothesis: gelatin is partially hydrolysed animal protein; (partially) hydrolysed vegetable protein (PHVP) is known to cause migraine; perhaps the gelatin caused some of the headaches. METHOD: The author tested this hypothesis on himself because he suffers from dietary migraine. He proved this in a double-blind test with tyramine hydrochloride (TYH). The amount required for the test was so small (1 mg) that it was tasteless and capsules were unnecessary. The author then undertook tests with a gelatin capsule, vegetable protein (PHVP), monosodium glutamate (MSG) aspartame (a dipeptide) and TYH, adjusting quantities to give a moderate headache. Samples were mixed with foods to simulate normal eating and administered double-blind: the capsule with potato chips, aspartame with orange juice and the rest with cottage cheese or ricotta cheese. Times were measured from ingestion (1) to start of the headache and (2) to maximum headache intensity. Each experiment was repeated three times. The headaches were relieved with caffeine. RESULTS: Of eight double-blind test samples, the author identified correctly the two placebos and five of the six samples containing tyramine. Quantities giving moderate headaches were: 1 gelatin capsule, 400 mg MSG, 118 mg PHVP, 4.0 mg aspartame and 1.0 mg TYH. Typical times for the three repetitions of the two time periods were 8, 9 and 11 and 17, 19 and 22 min. CONCLUSIONS: Capsules may give headaches to dietary migraine patients that are similar to those from foods. This would explain some of the headaches of patients from placebos. The double-blind test and the repeatability of the time measurements demonstrated the validity of the experiments. ______________________________Pediatric Neurology 2003 Jan;28(1):9-15The diet factor in pediatric and adolescent migraine.Millichap JG, Yee MM.Division of Neurology; Children's Memorial Hospital; and Northwestern University Medical School;, Chicago, Illinois, USADiet can play an important role in the precipitation of headaches in children and adolescents with migraine. The diet factor in pediatric migraine is frequently neglected in favor of preventive drug therapy. The list of foods, beverages, and additives that trigger migraine includes cheese, chocolate, citrus fruits, hot dogs, monosodium glutamate, aspartame, fatty foods, ice cream, caffeine withdrawal, and alcoholic drinks, especially red wine and beer. Underage drinking is a significant potential cause of recurrent headache in today's adolescent patients. Tyramine, phenylethylamine, histamine, nitrites, and sulfites are involved in the mechanism of food intolerance headache. Immunoglobulin E-mediated food allergy is an infrequent cause. Dietary triggers affect phases of the migraine process by influencing release of serotonin and norepinephrine, causing vasoconstriction or vasodilatation, or by direct stimulation of trigeminal ganglia, brainstem, and cortical neuronal pathways. Treatment begins with a headache and diet diary and the selective avoidance of foods presumed to trigger attacks. A universal migraine diet with simultaneous elimination of all potential food triggers is generally not advised in practice. A well-balanced diet is encouraged, with avoidance of fasting or skipped meals. Long-term prophylactic drug therapy is appropriate only after exclusion of headache-precipitating trigger factors, including dietary factors._________________________________________________RES IPSA LOQUITUR._________________________________________________January 20, 2003To Whom It May Concern,I have been asked to comment regarding my experience with the L.E.A.P. (Lifestyle, Eating and Performance) Program. We have been performing these tests for well over a year now and have had phenomenal results.Our most impressive results have come with Irritable Bowel Syndrome and Fibromyalgia, though we have had very impressive results as well with other conditions such as Migraine, Depression, and Gastroesophageal Reflux Disease.Our experience has been a 95% or better success rate, in that this percentage of persons have either become completely symptom free or have improved in their symptomology. Reimbursement is excellent and easily obtained from private insurance companies. Signet Laboratories has been very easy to work with and are very aggressive about keeping us well stocked on supplies for these tests. Overall, our experience has been a tremendous success and I would highly recommend it to any physician who deals with any of these problems.Sincerely,W. Brad Wilson, M.D.1602 East Starr AvenueNacogdoches, Texas 75961 _________________________________...and so the Migraine Story continues to unfold...







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