# Brostoff takes fungal-type dysbiosis and Leaky gut seriously



## bonniei (Jan 25, 2001)

The great Professor Brostoff who Mike cites regularly takes Fungal- type dysbiosis and Leaky gut seriously. There is a whole chapter in his book Food Allergies and Intolerances meant for docs. He says fungal type dysbiosis might include bacterial dysbiosis / For e.g some moulds require the presence of contaminating bacteria for their healthy growth. I wonder if this is what Mike has been talking about- the dysbiosis studiesIn this chapter he makes a reference to Leaky Gut syndrome but in a serious manner.Is there such a thing as intestines being permeable to macromolecules because of the incompetence of tight junctions? And he gives this as a reason for malabsorption of nutrients like B12(which I have) by giving the example that if proteins are not broken down into amino acids or peptides, they may be able to enter the body intact and by competitive inhibition diminsh the absorption of micronutrients. Is this possible?There is a whole chapter on Altered Gut Permeability in which he says increased permeability is in some instances a consequence of disease like Celiac.Is what he says true? He does state though that it remains to be determined if increased intestinal permeability leads to inflammatory responses.Any comments anyone? meckle and kel will be thrilled, I am sure. flux would have a field day dissecting these chapters and MikeNL would have a field day expounding on the chapter. I don't know what to make of this frankly. I would have thought fungal type dysbiosis and Leaky Gut belong in the realm of quackery but the revered Brostoff has taken this seriously. I am so disturbed.


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## flux (Dec 13, 1998)

Nobody takes him seriously though


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## misummer nightmare (Feb 14, 2003)

I am loathe to enter into any confrontation with you flux but I have been to see Prof Brostoff myself and found him to be enormously helpful and extraordinarily intelligent. I am also aware of many London doctors sharing Mike's (and my) enthusiasm. I think it is dangerous to dismiss him so lightly (and arrogantly).


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## ohnometo (Sep 20, 2001)

FluxYou have to be the most negative person I have even come in contact with !!!! How does your family see you







Do you ever have friends? Do you enjoy life ? What makes you tick ?Dr Brostoff has alot of knowledge ...That man has helped me more that I can ever thank him...Flux ..Have you ever been a patient at Saint Elizabeths hospital







Bonnie How in the world could you have be head over hills for someone like him ?


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## bonniei (Jan 25, 2001)

Well folks it is disturbing when you hear something which the medical community has derided is taken seriously by anyone. I myself was wondering if Brostoff should be taken seriously. I would be interested in knowing from Mike if my perception was correct, that Brostoff does consider these conditions seriously in the book. I could have got it wrong! Unless he was merely trying to cover the topic from the point of view of being complete in a book of Food Allergies and Intolerances. But he didn't dismiss it outright.


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## bonniei (Jan 25, 2001)

flux, thanks for the comment







It is a reality check for me


> quote:How in the world could you have be head over hills for someone like him ?


It was all in my mind.


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## SteveE (Jan 7, 1999)

midwinter madness--telling us that you were helped enormously isn't specific enough to convince those of us who are more inclined to buy into flux's short, yet mainstream position statements. What kind of improvement did you experience by seeking the advice of this man of extraordinary intelligence? Were you cured? 80% improvement? My $.02:I have no reason to doubt that dysbiosis could be the cause for many of us experiencing IBS. However, everyone on this board will be six feet under the Earth before they figure-out what to do about dysbiosis. Why? Because there are hundreds of organisms in your gut--HUNDREDS! Nobody knows for certain what the correct amounts are for each organism for you or me or anyone else. Even if they did know, how would they know how to put them into the appropriate balance once they're out of balance? If you use an antibiotic, that's similar to using a pesticide in a corn field. Sure, you may kill some bugs, but there are environmental consequences. If you add a preditory bug to kill the original bugs, there are environmental consequences.I haven't read Brostoff's book, but unless his extraordinary intelligence can unravel the complexities of balancing complex ecosystems--then it would be a waste of anyone's time. If he is capable of balancing complex ecosystems, then his time is being wasted. He should figure out how to fix global warming before dealing with our pesky problem.


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## meckle (Mar 5, 2003)

let me put it this wayI am no longer interested in discussing the ins and outs of unanswerable questions with people who have fixed view-points.So you people go on discussing - and suffering from your IBS.Me - I've gotten rid of mine - that's all the convincing I need.


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## bonniei (Jan 25, 2001)

To be fair I just realized that that chapter on fungal-type dysbiosis was written by K. Eaton from Biolab UK. Isn't that the lab which has been touted on the board by meckle? I read the preface and it says that that chapter is a critical review of fungal type dysbiosis. How can someone who has written papers on the subject do a critical review of it? It would seem he would have a vested interest.The other thing which occurs to me is that all these labs including Enterolab seem to be coming up with these alt med theories and seem to be investigating the immunological aspects.They do have access to samples. But is this a common practice that labs notice a certain trend in samples of a certain subset of patients and this is how they come up with new ideas in gastroenterology?


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## meckle (Mar 5, 2003)

Er - I wasn't touting any lab.All I said was I ahd tests done there. Other people picked up the argument then. I don't presume to have sufficient knowledge to judge one lab over another.


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## eric (Jul 8, 1999)

FYI http://www.nickmorgan.net/html/food_tests.html


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## bonniei (Jan 25, 2001)

I stand corrected meckle. The article eric posted really makes me wonder because the panel of tests with Enterolab include milk, yeast and wheat. Hey what else is left in the Ameruican diet if you eliminate wheat, egg and and yeast. Meat, chicken and fish. So moral of the story: might as well have started out on the basic elimination diet. But it is so tempting to get a diagnosis through a test!


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## Fachtna (May 22, 2002)

Hey meckle, I never heard back from you after my last email?!


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## trbell (Nov 1, 2000)

I think Mike NML would agree that FDA approval is very important here as is publication of research in a peer reviewed journal like the info eric posted on hypnosis.tom


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## bonniei (Jan 25, 2001)

I think FDA is only for food. There is a different agency for labs if you were regerring to labs.


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## bonniei (Jan 25, 2001)

Well it seems that the medical library book by Brostoff has only been edited by him. The book that Mike keeps referring to, the paperback for the layperson, which has actually been written by Brostoff arrived in the mail today and there he says if Candida had been present in the intestines we would have seen it in the stool by now. And in this book he selects K Eaton's statement that Nystatin may work because of gut wall stabilizing properties that it has rather than its action on Candida


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## trbell (Nov 1, 2000)

no, the FDA is the Federal Drug Agency for drugs an laboratory tests. they also have some regulatory authority for advertising claims but it's much too weak obviously because anyone can claim anything on the net. tom


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## meckle (Mar 5, 2003)

yeah good link on the intolerance tests eric. Clearly these tests are not scientific.Bonniei - when I speak of having intolerances myself - I mean ones I ahve discovered myself through an elimination diet - I didn't have any tests. I don't have genuine food intolerances - I just have problems with certain foods temporarily as my gut lining is irritated. I am taking l-glutamine and whey to heal my gut lining.


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## misummer nightmare (Feb 14, 2003)

Meckle, you say you've gotten much better, sorry if you've already done a post on this but I'd be really interested to find out what helped you. Steve, Admittedly I am not cured, far from it, nor am I trying to convince anyone of Brstoff's capabilities, I only recently had an appt with him andI will have to see, but so far I've found him to be, as I said, very helpful, caring and intellingent, he will not provide my 'cure' as I'm not just dealing with a simple case of food intolerances and dybiosis but I do believe that is part of the problem. The reason I replied intially to this post was simply because I was suprised that anyone (Flux) could be so dismissive, I'm not interested in having a heated debate, I just want to get well, I'll leave those who want to get fired up. Good Luck to you all.


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## ohnometo (Sep 20, 2001)

GO AHEAD ERIC SHOW YOUR TRUE COLORS.....


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## kel1059 (Feb 28, 2003)

I believe that these issues are highly complicated; and any time you have a disorder that can contain so many different variables, it can be incredibly difficult to sort out.I am trying to tackle the problem from several different angles and I am having a lot of success, but at the same time I have a ways to go.I used to be extremely reactive to almost everything especially odors like perfume and petrochemicals. However, now that i am much better, most of that is gone. I am still highly reactive to most foods though. I am still very reactive to foods that have a high yeast, mold, fungus content.As far as dysbiosis goes, I don't have a good answer for that. All I can do is continue to take probiotics and hope for the best. I take a slew of antibacterial /fungal/ parasitic herbs and garlic and it seems to give me considerable relief from some symptoms. However, i wish I did not have to take these herbs because I think they may be just keeping symptoms down.I think it would help if they knew why some people have an intolerance or a bad reaction to so many foods. I think it could be multifactorial. I think that people who have CFIDS have multiple factors all of which depress their immune system. There has been a lot of evidence that antifungal drugs can take a substantial load off of CFIDS patients. I know that when I was on the drugs, I had regained tolerance to certain foods. However, there is more to my problem than just fungal issues.I think the fungal issues may be just a factor that has caused a more serious or worsening of problems.


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## Fay (Jan 11, 2001)

Dr. Brostoff books are used as reference material for study in the UK (when we still needed sitters (2 years ago), one of them was a university student and she saw my copy of Dr. Brostoff's 'The Complete Guide to Food Allergy and Intolerance' and she told me she had studied that and it was supposed to be one of the best in its field. She was studying dietetics amongst other things.). Fay


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## Mike NoLomotil (Jun 6, 2000)

Iranian proverb: ___________________________"Be sure the mud you throw will fall on your own head".Examples of indiscrete mud slinging... ______________________________"Nobody takes him seriously though " ______________________________and the following _____________________________"FYI http://www.nickmorgan.net/html/food_tests.html _______________________________Some things to consider.FOOD ALLERGY AND INTOLERANCE, Professor Jonathan Brostoff, MD, Stephen Challacombe, MD (NEW 2002) http://www.amazon.com/exec/obidos/ASIN/070...product-details ï¿½	Hardcover: 1120 pages ï¿½	Publisher: W B Saunders Co; ISBN: 0702020389; 2nd edition (August 9, 2002) ï¿½Book DescriptionIn the 15 years since the first edition of Food Allergy and Intolerance was published, the subject has become the focus of intense public interest. Not only are more people aware of the phenomena involved, but new evidence and practices are constantly being introduced, and there has been an unprecedented growth of the field. The second edition encompasses the rigor and depth of the first, whilst incorporating all the changes required to produce the definitive guide to the subject for all those involved. The symptoms of a food allergy or intolerance impacts not only on all allergists, immunologists, nutritionists, gastroenterologists, and pathologists, but doctors of respiratory medicine, dermatologists, general practitioners, pharmcologists and all those in environmental medicine. Book InfoKing's College, London, UK. Provides information on food allergy and intolerance. Topics include immune response, animal models, mediators in food allergy, enzyme deficiency, abnormal nutrition, foods as allergens, migraines, and epilepsy. For primary care physicians, clinicians, pathologists, and pharmacologists. Includes detailed halftone images. Previous edition: c1987.ï¿½ _________________________The new edition of this textbook for physicians has (70) chapters, 1,000 pages and about 100 contributing authors from all fields from around the world. So if no one else does, at least these 100 medical professionals consider the physician in question of sufficient veracity to associate themselves formally with him to further the advancement of the understanding of the subject matter...as well as those who purchase such textbooks and use them to further their understanding. Rather than entering into a repeat of more pointless circular debate over that which is not subject to debate as it is fact, or over such things as putative mechanisms of various immune dysfunctions, which are no more or less valid or useful than setting forth putative mechanisms of any symptom generating pathways, as often set forth by anyone else doing research on any subject, it would be best to become more familiar with the subject at hand before misleading sick people seeking help into believing that the work and investigations of the physicians and researchers in the field of food allergy and food intolerance (immunologic and otherwise), and rapidly emerging subspecialty area in immunology focusing on the bodies Oral Tolerance mechanisms, is any less credible than those whose work does not focus on, deal with, or take into account the work of others whose findings might conflict with or even refute their own theories or belief systems.[End of Worlds longest run-on sentence]As far as Mr. Morgans "musings", we have here the astoundingly authoritative figures of a chef using a reporter to cast an implicit, indeed explicit, pall of suspicion not only over obsolete technologies which indeed suffer limitations as to their usefulness, and which are rarely if ever discussed in this forum (I do not know anyone proposing kinesiologic assessment of food intolerances here, nor anyone suggesting IgE methods are applicable to IBS, nor have I ever seen anyone suggesting with any regularity here that the old ALCAT assay is a solution to their IBS problems...or hair analaysis or whatever else is inlcuded in the reference posted), but to also imply that there is something unsavory or untoward about a technology or technologies (such as invasive jejunal isolation and challenge techniques, for example which are the new gold standard for food intolerence physiologic studies) which is not mentioned nor evaluated in the journalists article. "Guilt by association" is a very elementary tactic. As such and as usual it all lacks veracity and is a mere reflection of biased and selective thinking consistent with such persistent behavior as this, which is often witnessed in this forum and on this subject. Indeed taken in proper context the journalist makes some fair points about certain technologies referred to in the article. These are the very reasons that many of those techologies do not provide an adequate basis for disease management of affected IBS victims and why work has moved on and beyond such methods in the last few years. So it is not even pertinent to anything that is discussed here anyway, though it may be pertinent elsewhere...Keep in mind if one wants the best information about the brakes on one's car talk to the brake expert, one does not rely heavily on the transmission man...or the guy who makes his lunch for that matter. Medicine is no different, and the debates between the various specialists who work with IBS patients (from gastroenterologists to pschologists to allergists and immunologists) is no different, than is the situation with other conditions and the debates between other specialists (re: the perspectives of a board certified pulmonologist towards a given asthmatic may differ from the perspectives or paradigms of a board crtified allergist).By way of comment directly to the members of IBS Self Help Group who are actual victims, patients, of bowel dysfucntion and who come here seeking help, as a healthcare worker with 30+ years in patient care and eduction let ne advise you of a reality of forums like this.The most imprtant thing to realize as you review what people post ehre or what they refer you too, far too much weight is given in this forum to various debates (past and present) between specialists who work with IBS patients or do IBS investigations by people who are not healthcare providers themselves. This is because they do not have the personal experiential base which comes from working side by side with physicians and other healthcare workers taking care of and educating the sick so as to comprehend the dynamic of such debates, differences in views, perspective ,paradigms, and the specific personal agendas of various medical experts and thus are not able to place them in their proper perspective. Its not a crtiicism it is a fact thats all. ANd one does not know often what another means about some experience until one experiences it oneself...then the bulb blinks on "oh now I see what he meant."This situation sometimes misleads patients who come here into thinking that there is somewhere at this time some one center, or some one specialist, or some perspective of some specialty, which has all the valid answers about so called IBS to the exclsusion of all other peoples studies finidings experiences or treatments. This is simply not the case.This is not only unfair to the patients here but is in fact unethical...even for laypeople. When one are sets oneself forward (regardless of any words of disclaimer to the contrary which may accompany any posting) to be a person whose intent is to provide information objectively, when one provides advise or counsel and assumes the posture of being some authority figure on the subject, one has assumed de facto the role of care-giver and is obligated to behave accordingly. This means that your first order of ethical begavior becomes "PRIMUM NON NOCERE", or "First Do No Harm." It would do people well to remind themesleves of this obligation when they set finger to keyboard and click ADD REPLY.It is at least nice to see some people taking an objective approach, and trying to come to an understanding of the subject, before commenting.for example: ___________________________________"I have no reason to doubt that dysbiosis could be the cause for many of us experiencing IBS. However, everyone on this board will be six feet under the Earth before they figure-out what to do about dysbiosis." ___________________________________Indeed researchers who finally developed a means of studying the oral tolerance mechanisms and how their locus of function in the small bowel and circulation can be elucidated with new invasive methods (whereas old methods which were ineffective due to their inapplicability to the mechanisms had kept an understanding of oral tolerance in the dark, at least until 1994 when jejunal isolation and challenge methods were first pioneered at a major medical center in Sweden)would probably express at this point similar frustration as Steve.While it is now possible, and is ongoing, to study the oral tolerance mechanisms and loss of oral tolerance through direct means, even though it is clear that one of the prerequisites of normal oral tolerance function is for the subjects gut flora to be intact, it is so far not very practical to form clear judgements about the state of dysbiosis or lack thereof in any subject...be it a pathogenic dysbiosis or simpkly a deficieny in some commensul organisms essential to proper digestion thus proper oral tolerance.Some of these links lead to tutorials relative to flora, so one can understand the veracity of Steves concern...how the flora develops, why it is so patient specific and potentially diverse, and if one understands that and how induction of oral tolerence occurs as the human organism grows and the interplay between the GI tract and immune function begins to develop concurrent with the establishment of the subjects flora one can see then why we may understand the impact of dysbiosis but have still no practical clinicalmeans of assessing it with any patient-specificity...thus of course treatment is diffult when you cannot quantify what to treat. http://www.gsbs.utmb.edu/microbook/ch006.htm http://www.ccfa.org/weekly/previous/wkly0723.htm http://www4.ncbi.nlm.nih.gov/htbin-post/En...83059595&Dopt=r http://www4.ncbi.nlm.nih.gov/htbin-post/En...81119781&Dopt=r http://www.canceralt.net/Bowel%20I%20Alter...l%20Ecology.htm The exception is that at least in some European centers experimentation with various antibiotic regimens continues with certain subpopulations of subjects who present with diarrheic-IBS symptoms....and the results being seen do show some promise.I do know that at Kings College Medical Center the Immunoloists and Gastroenterologists are working together on people with diarrheic IBS to try to deternine with specificity the a workable clinical diagnostic protocol, follwoed up with an effective antibiotic treatment protocol, for selecting and treating the subpopulation of IBS victims whose symptomology can be eliminated by treatment for pathogenic dysbiosis.So it is an area where the preliminary successes have been significant enough that physicians are continuing the work clinically to learn how to isolate the affected population and then once identified how to treat those with this type of reversibility.For an intersting slide show which descibes in some detail some of what is now known about the Oral Tolerance Mechanisms. this slide show from Medical University of Sunderland, U.K., may be of interest to those who sincerely do wish to learn more about it....SLIDE SHOWORAL TOLERANCEUNIVERSITY OF SUNDERLAND, U.K. http://www.sunderland.ac.uk/~hs0acu/lec01.ppt Note it is 41 pages when it opens to the first slide simply click your mouse and each time you do some info will fly in from the left to fill out the slide...then click to the next one etc. until end of show.Oh one other clarification... _______________________________________" think Mike NML would agree that FDA approval is very important here ..." ______________________________________There is great misunderstanding among the public about whjo regulates what in medical devices and medical services.Simply stated if you want to sell a medical device you need either a 510K from the FDA stating it is substantially equivalent to another device already approved for sale (say a pacemaker or a stent or a a hematolgy machine you wnat to sell to other labs) or a PMA (Premarket Approval) for a new device you intedn to sell.However, if you have what would be called a "custom device" which is either not for commercial sale and/or whic is used on the order of a physician for a specific patient, or is a device which does some tests but the service is for sale not the device, then the device is exempt from FDA jurisdiction sicne it is not a commerical medical device. However if you use a device, say, a custom lab device which no one else has but you to provide some lab service on ordr of a physician, then your lab has to be inspected and approved under federal guidelines origianlly developed by HRS and its subagencies to reguklate laboratories, and which each state has a stae agency to implement, inspect, regulate, control etc commercial lab services.For example as in the case of Mediator Release Testing done by our lab the licensing data showing fukll compliance with all regulatory requirments isHCFA/CLIA Lab License #10D0914974Florida License # L80010492Certificate #33704This approval is only gaiven after full complicance is achieved determined by applications and periodic visula inspections of the laboratory, its devices, procedure manulas, quality control systems to ensure accuracy of reporting results, staffing qualifications, etc etc.Aslo I do not think anyone debates the value of peer reviewed journals, and one must conisder that there are many means of establishing efficacy of any medical protocol or procedure and that new technologies, protocols, Disease Management Programs, go through developmental phases that do almost univerally end up with one or more publications in such journals. tyhe first one concenrning the technology upon which our Disease Managment programs' Oligoantigenic Diet protocol is based was published in a European peer reviewed journal sevral years ago (1997) and the technology advances and description were published before our peers in Laboratory journals as part of a series on the new technologies in 1999.The first formal clinical reports on the outcomes of the LEAP Disease Managment Programs for Iritable Bowel Syndrome, prepared by several centers which have been using LEAP for some time, will be distributed to the attendees as the upcoming DMAA (Disease Management Association of America) 5th Annual Leadership Conference in Chicago, Oct 12-15 2003. These clincial reports of LEAP outcomes are scheduled to be submitted to the peer reviewed journal Disease Management either concurrent with their release at this upcoming meeting or just prior to.The data are being compiled now, though the final patient assessments will be completed August 30, 2003 to get the longest followup timeline possible on the patients being examined...so that the report carries more weight of course than simple 30-60- or 90 day outcome assessments.Hey if you are at the Conference come by the booth and meet us and our head dietician. Several doctors who have been actively using the Program to treat their IBS and Migraine patients will also likely be at the conference to answer questions for other physicians and for the Utilization Management staff of the various health insurance plans who also attend seeking new DM programs to investigate and implement.There ar about 300 now that have reimbursed so it is time to start looking at in-network contracts, so the outcoem data being accumulated will show this Program to be far more successful at reducing symptomology than almost any other DM program for chronic disease states currently available.Next year should see the achievement of the next phase of this "developmental progression" that new things go through early in their life.In the emantime there is plenty of open discussion on the subject including actual early patients in the program, some of whom were from this community, now hundreds of new ones a month from all over the United States are being out on the program by affiliated physicians who have seen the results for themslves. When a doctor has a patient whose disease symptoms have been refractory under his/her care and you provide a treatment plan which produces success that the physician was unable to achieve before...well nothing speaks as loudly to that doctor. That doctor KNOWS that patient and KNOWS he/she had no solution previously, and now does, and has done it herself/himself. Its quite compelling. http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=1;t=033220 Oh this comment is also very apt as regards Dr. Brostoff: ____________________________________"...very helpful, caring and intellingent..." _____________________________________Indeed he is among the most patient-centric and caring physicians, especially for an admitted academician, that I have ever met in the last 30+ years. Many of his peers hold him in high regard as well.







MNL


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## bonniei (Jan 25, 2001)

Mike I apologize if you were offended by any of my comments. Thanks for your comments. The two books by Brostoff are different perhaps because he has only edited the one with Challacombe. That was the book I read first.


> quote:He studied the longevity of Bulgarians and provided strong evidence that certain bowel microbes played important roles in preserving health and promoting longevity among them. He named the microbe he thought was most prominent in this field as Lactobacillus bulgaricus


from http://www.canceralt.net/Bowel%20I%20Alter...l%20Ecology.htm I think I will load up on the Bulgaricus.


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## eric (Jul 8, 1999)

Foods are a trigger in IBS.IBS is not caused by loss of oral tolerence to foods!!!American Family PhysicanManagement of irritable bowel syndrome."DIETARY RECOMMENDATIONSWhile no specific dietary advice has been shown in trials to be efficacious, many authors advocate having patients limit alcohol, caffeine, sorbitol, and fat intake. 6 Lactose should be eliminated only in those with proven lactase deficiency. If a patient believes a particular dietary substance is exacerbating the symptoms, then a trial of eliminating that substance is warranted. However, in general, there is no association between IBS and food intolerance.""Etiology and PathophysiologyThe etiology of IBS remains unclear. Theories have ranged from purely psychologic to more recent proposals about postinfectious alterations in GI tract neuromuscular function. IBS may best be viewed as a biopsychosocial disorder in which altered GI motility, GI hypersensitivity, and psychosocial factors all interact to predispose someone to the syndrome.Patients with IBS have an exaggerated gastrocolic reflex, altered gastric emptying, increased small bowel contractions, and increased small intestinal transit, all of which are exacerbated by food intake or stress. 7 However, more than 50 percent of healthy individuals report similar symptoms during increased stress. 8 Therefore, other factors likely play an important role in the patient who develops IBS.One such factor may be the involvement of neurotransmitters such as serotonin, which may stimulate intestinal secretion and peristalsis in addition to visceral pain receptors via 5-HT3 and 5-HT4 pathways. It is at neurotransmitter receptors such as these that new and investigational therapeutic agents are targeted."Side note on motility of IBSAmerican College of Gastroenterology 67th Annual Scientific Meeting | IBS/Functional Dyspepsia & Pancreatic Disease "PathophysiologyAltered Serotonin Signaling?The pathogenesis of IBS remains obscure, and in particular, an explanation for alternating diarrhea and constipation has been elusive. In arguably one of the most important papers presented during this year's meeting, Moses and colleagues 21 studied potential deregulation of the gut's serotonin transporter in IBS. It is known that serotonin 5-hydroxytryptamine or 5HT is released from enteroendocrine (or enterochromaffin cells in response to either chemical or mechanical stimulation of the gut mucosa. Serotonin in turn initiates peristalsis, and then the serotonin released is taken up in health by a highly selective serotonin transporter SERT. One potential mechanism that could explain altered bowel function in IBS is an abnormality in the serotonin transporter itself. The study authors evaluated this hypothesis in patients with IBS with constipation and IBS with diarrhea compared with patients with ulcerative colitis and healthy controls. They were able to convincing show on blinded review that SERT immunoreactivity was less intense in patients with IBS with constipation and patients with ulcerative colitis. If these findings are indeed correct, they represent a landmark observation. The findings suggest that patients with constipation and IBS may have a reduced capacity to reuptake serotonin, leading to excess free serotonin and then desensitization of these receptors, thus reducing motor function. In contrast, in the setting of diarrhea, serotonin uptake was normal. If the underlying abnormality in serotonin transporter function alternated, then this would in turn explain alternating constipation and diarrhea. These data strongly suggest that IBS is a "real" gut disease and a potential diagnostic disease marker. They also suggest that it is valid to subdivide IBS into constipation and diarrhea symptom subgroups. This study also provides additional rationale for the use of serotonin-modulating agents in IBS and provides a new target for drug modulation. Confirmation of these very exciting initial findings in larger patient samples is awaited with great interest." http://www.medscape.com/viewarticle/444514 Psychosocial factors also play an important role in the development of IBS and may be the most important factors in terms of who manifests IBS and how severe it becomes. 9 For example, traumatic life events such as a history of physical or sexual abuse have been shown to correlate with the development of IBS and the severity of its symptoms. 10 Studies have repeatedly shown a higher incidence of anxiety, hypochondriasis, and depression in IBS patients. 11 A multicomponent model Figure 1 has been proposed that shows the relationship of psychosocial cognitive, behavior, emotional and physiologic components of IBS. 7" http://www.findarticles.com/cf_0/m3225/10_...+bowel+syndrome Dr Drossman, Head of the Rome criteria to 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. "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-but 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 " http://www.ibshealth.com/ibs_foods_2.htm "TIPS ABOUT FOOD ALLERGIES AND FOOD INTOLERANCEAlthough relatively rare, food allergies to certain foods can also mimic or exacerbate symptoms of functional GI disorders. Allergies can also lead to more generalized symptoms involving skin rashes, asthma, and swelling.Food intolerance occurs when the body cannot adequately digest a portion of a particular food, usually because of a chemical deficiency. For example, people with lactose intolerance have difficulty digesting milk because of a deficiency of the enzyme lactase.If you suspect you are intolerant to certain foods or that you have a food allergy, talk to your physician or consult a registered dietitian before making any drastic changes in your diet. You want to make sure you are maintaining proper nutritional balance in your diet and not disrupting your quality of life by needlessly eliminating certain beneficial foods.""A food allergy is an immune system response by which the body creates antibodies as a reaction to certain food. Symptoms similar to those of IBS include diarrhea and abdominal pain. Other symptoms can include vomiting, hives, itching, swelling of the lips, tightness in the throat, and wheezing. Allergic symptoms usually occur within a few minutes to an hour after ingesting the causative food. Eight foods cause 90% of all allergic reactions: milk, egg, wheat, peanut, soy, tree nuts (almonds, walnuts, pecans, etc.), fish, and shellfish.In response to a mailed consumer questionnaire that surveyed 5,000 representative Americans, 16% reported conditions that they felt were food allergies. However, studies show that true food allergies are present in only 1-2% of adults. In people with IBS, reactions to food are rarely allergic reactions. If a food allergy is suspected, the offending food should be eliminated from the diet and then reintroduced. If the symptoms improve on the elimination diet, and then consistently recur when the food is introduced back into the diet, formal allergy testing should be performed. Sometimes an elimination diet to exclude all known allergens can help distinguish food allergy from other symptoms. Studies have shown that the onset of symptoms in a person can be influenced by even a mistaken belief that they have food allergies. Therefore, allergy testing is done to make a definitive diagnosis." http://www.aboutibs.org/Publications/dieta...delines.html#FA American College of Gastroenterology 67th Annual Scientific Meeting | IBS/Functional Dyspepsia & Pancreatic Disease Digestive Disease Week 2003"Diagnostic Markers in IBSThe search continues for objective diagnostic markers in IBS, although at this time, symptom-based criteria remain the "gold standard." Minor inflammatory change seems to persist in a subset of patients with IBS.2,3 Simren and colleagues 4 evaluated stool samples from 17 healthy controls, 18 patients with IBS with diarrhea, and 7 patients with IBS with constipation, based on the ROME II criteria. They found small increases in eosinophil protein X in patients with IBS with diarrhea. These investigators also surprisingly found higher levels of myeloperoxidase in healthy controls than in patients with IBS and constipation. There were no group differences observed in tryptase levels. Thus, although low-grade inflammation may be involved in the pathogenesis of a subset of patients with IBS, this initial study did not demonstrate any convincing alterations in eosinophil, neutrophil, or mast-cell markers in feces. More careful selection of patient subsets eg, postinfectious vs not postinfectious) may yield different results; additional work in this area may be productive.Another approach to identifying new diagnostic tests involves searching for potential genetic markers in IBS. Kim and colleagues 5 postulated that polymorphisms of the alpha-2 adrenoreceptors, norepinephrine transporter, and serotonin transporter promoter would be associated with IBS. Genetic variation in these mechanisms may in turn alter lower gastrointestinal tract function and hence promote the expression of IBS. The investigators applied a validated bowel disease questionnaire and selected a number of candidate genes to test for polymorphisms by PCR-based restriction fragment length polymorphisms that were confirmed by direct sequencing. The results of this study, however, were largely negative. There was no association of polymorphisms of the serotonin transporter or of the norepinephrine transporter with functional bowel disease overall. One of the alpha-2 adrenergic receptor polymorphisms Nci1 was associated with an increased risk of IBS with constipation compared with controls, and there was a trend for another alpha-2 adrenergic receptor polymorphism Msp1 to also be associated with IBS and constipation -- but these results require validation in another, larger sample. It has yet to be shown that polymorphisms of the serotonergic or adrenergic pathways are relevant to the pathophysiology of IBS, and at this stage, no genetic markers have been convincingly demonstrated to be linked to IBS. Such studies are difficult because defining the phenotype remains crucial, and in a heterogeneous syndrome such as IBS, associations may be overlooked unless rigorous attention is applied."Irritable Bowel Syndrome: Taking Concepts Into Clinical Practice CME Chairperson: Michael D. Gershon, MD; Faculty: Kevin W. Olden, MD; Walter L. Peterson, MD; Nicholas J. Talley, MD, PhD; Gervais Tougas, MD, CM, FRCPC"We know that in terms of its phenomenology, IBS is a condition that's associated with altered brain-gut communication. Pain plays a major role so that we have alterations, or at least generation of abnormal sensation within the gut. Emotions can modulate these symptoms to a large extent, but at the end they also have alterations of function characterized in general by either constipation or diarrhea. This is largely due to alterations of neuromodulation at the level of the enteric neurons and also at the level of central and autonomic pathways."American Gastroenterological AssociationAmerican Gastroenterological Association medical position statement: Irritable bowel syndromePathophysiology of IBS symptoms The symptoms of IBS have a physiological basis. Although no specific physiological mechanism is unique to, or characterizes IBS, there are at least 3 interrelated factors that affect symptoms to varying degrees in individuals with IBS: 1 altered gut reactivity motility, secretion in response to luminal e.g., meals, gut distention, inflammation, bacterial factors or provocative environmental psychosocial stress stimuli, resulting in symptoms of diarrhea and/or constipation; 2 a hypersensitive gut with enhanced visceral perception and pain; and 3 dysregulation of the brain-gut axis, possibly associated with greater stress-reactivity and altered perception and/or modulation of visceral afferent signals. Brain-gut axis dysregulation may also play a role in the subgroups of patients who have gut inflammatory and immune factors persisting following infection or inflammation of the bowel. Further studies are needed to characterize the precise role of these factors in IBS and to identify physiological subgroups more amenable to specific treatments." J Gastroenterol Hepatol. 1998 Oct;13 10:980-9. Related Articles, Links Mast cells: a possible link between psychological stress, enteric infection, food allergy and gut hypersensitivity in the irritable bowel syndrome.Gui XY.University of Sydney Department of Medicine, Royal North Shore Hospital, St Leonards, New South Wales, Australia.Intestinal mast cell activation degranulation, which results from previous enteric infection and/or intestinal allergy, may play a central role in the gut hypersensitivity in both motor response and visceral perception in the Irritable Bowel syndrome. This occurs through various mediators acting on enteric neurons and smooth muscle cells. Psychological stress may trigger this sensitive alarm system via the brain-gut axis.Publication Types: Review Review, Tutorial PMID: 9835312Ann Allergy. 1988 Jul;61 1:47-9. Related Articles, Links The irritable bowel syndrome and food hypersensitivity.Zwetchkenbaum J, Burakoff R.Evans Memorial Department of Clinical Medicine, University Hospital, Boston University School of Medicine, MA.Ten patients with irritable bowel syndrome were evaluated for food hypersensitivity with skin testing IgE and IgG serum antibodies (RAST panel to common food antigens. Patients also underwent an open elimination diet for 2 weeks followed by a 48-hour challenge of each food that was considered to be suspicious from patients diary, positive skin prick test, and/or positive IgG antibodies. Six patients had positive skin scratch test results and only one patient had RAST IgG food antibodies greater than 3,000 cpm which is a marked increase above normal. None of the patients however had an exacerbation of their irritable bowel symptoms with a food challenge. We conclude therefore that positive skin testing and IgG serum antibodies are not reliable indicators of food hypersensitivity in irritable bowel syndrome and that food hypersensitivity does not seem to play a role in the symptoms related to the irritable bowel syndrome.PMID: 3389571 DDW 2003"The gastrointestinal (GI) complaints commonly associated with reactions to food include dyspepsia, heartburn, bloating, excessive gas, diarrhea, and constipation. The exact dietary factors that contribute to these symptoms in functional GI disorders, such as IBS, are poorly understood. Clearly, there is a need for more research to examine the relationship between food intake and functional GI symptoms.However, a substantial amount of research has been done to determine the relationship between food and other digestive diseases. This article will examine five such diseases that affect the GI system: gastroesophageal reflux disease (GERD), celiac disease, food allergies, lactose intolerance, and eosinophilic gastroenteritis.The possible presence of these five diseases should be considered in the diagnosis of a functional GI disorder. Not only can some of the symptoms associated with these diseases be found in functional GI disorders, but some of these diseases can coexist with, or be confused with, a functional GI disorder. *These diseases do have distinguishing characteristics that, upon investigation, differentiate them from functional GI disorders."* http://www.aboutibs.org/Publications/dieta...delines.html#FA The symptoms of IBS are produced by abnormal functioning of the nerves and muscles of the bowel. In IBS there is no evidence of an organic disease, yet, something -- a "dysregulation" between the brain, the gut, and the central nervous system -- causes the bowel to become "irritated," or overly sensitive to stimuli. Symptoms may occur even in response to normal events. IBS is not caused by stress. It is not a psychological or psychiatric disorder. It is not, "All in the mind." Because of the connection between the brain and the gut, symptoms in some individuals can be exacerbated or triggered by stress -- whether physical, emotional, or environmental. Dietary and hormonal factors can affect symptoms of IBS. http://www.aboutibs.org/characteristics.html


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## bonniei (Jan 25, 2001)

> quote: Minor inflammatory change seems to persist in a subset of patients with IBS.2,3 Simren and colleagues 4 evaluated stool samples from 17 healthy controls, 18 patients with IBS with diarrhea, and 7 patients with IBS with constipation, based on the ROME II criteria. They found small increases in eosinophil protein X in patients with IBS with diarrhea. These investigators also surprisingly found higher levels of myeloperoxidase in healthy controls than in patients with IBS and constipation. There were no group differences observed in tryptase levels. Thus, although low-grade inflammation may be involved in the pathogenesis of a subset of patients with IBS


Let's celebrateThis coming from eric means end of debate between the two, I think.







More research is necessary for sure because foods which provoke inflammatory responses if eliminated do produce results. It is just the right tests may not yet have been conclusively established


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## ohnometo (Sep 20, 2001)

First let me say that I am not in a very good mood today...and NO ONE has ever said that food intolerance causes IBS...I get so sick of hearing about UNC and Drossman and they didnt discover Rome in one day....You know what Eric if you got your IBS from where ever you did in Mexico it looks like you would have somewhat more of a open mind...You have never read or learned about the books that Brostoff has wrote so how can you say the stuff about the books that you do ???????These idoits in the world that goes by the guide lines to this Rome Criteria stuff makes me sick







Hypnosis is not always the answer to IBS.. Will you ever accept the fact that there is new ways of approaching IBS...FOOD does not, does not,does not,does not, does not, does not causes IBS and no one said it did


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## Fay (Jan 11, 2001)

I thought this article in Medscape from a hwile ago was interesting. Note who wrote it and note how a diet based on the results of an IgG antibodies test is said to be a treatment with potential clinical benefit in patients with IBS.From Medscape: http://www.medscape.com/viewarticle/456987 *The Brain, the Gut, the Food, and the Bacteria? Update on Treatment of Functional Gastrointestinal Disorders*DisclosuresYehuda Ringel, MD Douglas A. Drossman, MDIntroductionDespite being the most prevalent gastrointestinal (GI) disorders seen in gastroenterology practice, functional gastrointestinal disorders (FGIDs) continue to be difficult conditions to understand and manage, for both clinicians and patients. The latter relates to the complex, multifactorial nature of these disorders, the limited understanding of the pathophysiologic mechanisms that underlie them, and the lack of effective comprehensive treatments. Given these circumstances, it has not been surprising to note the ongoing increase in interest in FGIDs, as reflected by the number of high-quality abstracts submitted and presented at this year's Digestive Disease Week (DDW) meeting, as well as by the number of attendees at sessions focusing on these disorders.Presentations during this year's meeting proceedings covered the wide spectrum of intensive research that is ongoing in the field, and provided interesting new data about various aspects of these disorders. The latter included discussion of new data on the epidemiology, clinical characteristics, possible pathophysiologic mechanisms, diagnosis, and management of FGIDs.This overview focuses on those key presentations that provided updates and new information about the effect and efficacy of available and commonly used treatment options for functional GI and motility disorders.The BrainAntidepressants have been commonly used for the treatment of irritable bowel syndrome (IBS) and other FGIDs, and recently published American Gastroenterological Association guidelines recommended their use for the pain associated with FGIDs, particularly when first-line therapies fail.(1) However, despite this recommendation and their long-standing availability and use in clinical settings, the evidence for efficacy of antidepressants in the treatment of FGIDs has been relatively weak. This has been, in part, due to the quality of the trials and the small sample sizes.During DDW 2003, Drossman and colleagues(2,3) presented the results of a 7-year, 2-site, randomized, double-blind, placebo-controlled, treatment trial in patients with moderate-to-severe functional bowel disorders (FBDs; ie, chronic functional abdominal pain, IBS, painful constipation, and unspecified FBD). The investigators from the University of North Carolina and the University of Toronto randomized 431 patients into 2 treatment arms: medication (antidepressants vs placebo)(2) and psychological (cognitive behavioral therapy vs education).(3)Medication ApproachIn the medication arm,(2) 216 patients were randomized to receive either desipramine* up to 150 mg/day, and averaging 100 mg/day (dosage adjustment was based on side effects), or placebo. Responders were determined by an averaged satisfaction with treatment score of greater than 3.5 on a 0-5 scale range. The results on the intention-to-treat analysis (includes all patients who started the medication treatment) showed no statistically significant difference between the active and placebo groups (response rate of 60% vs 47%, respectively; P = .128). However, in the per protocol analysis of study completers (excluding 25% [30% desipramine, 17% placebo] drop outs and 12 subjects with nondetectable desipramine blood levels), there was a significant effect (response rate of 73% vs 49%, respectively; P = .006) and a number needed to treat of 4.3. It is interesting to note that desipramine was found to be more effective in nondepressed patients, as well as in those with moderate disease severity, predominant diarrhea, and a history of abuse.Psychological ApproachThe other arm of this study was presented in poster form. In this psychological treatment arm,(3) 215 patients were randomized to receive either cognitive behavioral treatment (CBT) or education for 12 weeks. Responder rates were determined, similar to the medication arm, by an averaged satisfaction with treatment score of greater than 3.5 on a 0-5 scale range. In the intention-to-treat analysis, CBT was found to be more effective than education (P = .0001), with a response rate of 70% vs 37% (P smaller than .0001) and a number needed to treat of 3.1. These results held also in per protocol analysis after 21% (18% on CBT, 29% on education) dropped out. CBT was found to be effective for patients with moderate or severe FBD and for individuals with or without abuse history, but was not different from EDU in efficacy for patients with severe depression.Commentary. The study authors concluded that CBT is statistically and clinically effective for treatment of FBD (including IBS) and that desipramine, although not significant in the intention-to-treat analysis, appears effective for patients who stay on treatment and who can tolerate the side effects (if present). However, certain clinically meaningful subgroups (eg, patients with depression, patients who appear less responsive) may be amenable to combination treatments using both modalities.The GutVery few medications have been specifically approved for treatment of FGIDs. Therefore, it is not surprising that the US Food and Drug Administration-approved serotonin active agent, tegaserod, has gained noticeable interest during this year's meeting. Tegaserod, a 5-HT4 partial agonist, has been shown to be more effective than placebo in alleviating IBS global and associated symptoms in women with IBS with constipation. Because of its promotility/prokinetic effects on various parts of the GI tract, clinicians have been prompted to use this medication for various non-IBS-related GI motility disorders as well. Several studies were presented during DDW 2003 that offered new information about the use of tegaserod in these settings.Dyspepsia and GastroparesisTougas and colleagues(4) investigated the effect of different doses of tegaserod* in 163 patients with dyspeptic symptoms who also had delayed gastric emptying. Subjects were randomized to receive tegaserod at 6 mg twice daily (n = 38), 6 mg thrice daily (n = 24), 12 mg twice daily (n = 38), or placebo (n = 63), and gastric emptying was quantitated by scintigraphy before and after treatment. The investigators reported statistically significant improvement in gastric emptying with the 18 mg and 24 mg per day dosages of tegaserod.Commentary. Several limitations of this study make it difficult to assess the clinical significance and relevance of these findings, such as that the currently approved dose of 12 mg daily did not show a significant effect; the patient population did not meet criteria for dyspepsia or other defined disorders; and information was not available about the symptom response or patients' quality of life (QOL) with this treatment. This is particularly important since it is well known that the correlation between dyspeptic symptoms and gastroparesis is poor. Therefore, at this time, the role of tegaserod in the treatment of dyspepsia and gastroparesis is not yet defined and additional investigation is warranted.Chronic ConstipationJohansen and colleagues(5) reported the results of a double-blind, placebo-controlled multicenter study that examined the efficacy of tegaserod* 2 mg twice daily (n = 450), 6 mg twice daily (n = 451), or placebo (n = 447) in patients with chronic constipation. They found that tegaserod, 2 mg twice daily and 6 mg twice daily, given for 12 weeks, was superior to placebo in increasing spontaneous bowel movements per week (response was defined as an increase of greater than 1 spontaneous bowel movements/week compared with baseline), either after 4 weeks (response rate, 41.4%, 43.2%, and 24.9%, respectively; P smaller than .0001 vs placebo) and 12 weeks (40.3%, 44.8%, and 26.9%, respectively; P smaller than .0001 vs placebo). This response was also associated with improvement in other functional GI symptoms.Commentary. The study authors concluded that tegaserod (2 mg twice daily and 6 mg twice daily) is effective in the treatment of chronic constipation and its related symptoms. However, it should be noted that patients with IBS whose predominant symptom was constipation were not excluded from this study. Patients with IBS with constipation are already known to benefit from tegaserod; therefore, not identifying this subgroup in the study population may have made it difficult to assess the efficacy of this agent in this setting. It would have been helpful to divide the patients in this study into 2 treatment groups -- those with chronic constipation with IBS and those with chronic constipation without IBS -- and to have looked at the treatment response rate in each subgroup. Thus, although these data are encouraging, additional investigation is warranted to assess the efficacy of tegaserod in treating chronic functional constipation.*The FoodNutritional factors have been suspected to contribute to the symptoms and clinical presentation of FGIDs. Exacerbation of symptoms such as diarrhea, dyspepsia, and nausea are commonly reported postprandially. Many patients attribute some of their symptoms to certain types of food, and therefore avoid those food items. However, recommendations for elimination of specific food items in FGIDs is usually done in variable ways. That is, there are no available guidelines' evidence for the efficacy of this approach to managing these disorders.Atkinson and colleagues(6) presented an interesting approach to this issue by assessing the efficacy of an exclusion diet based on testing for the presence of IgG food antibodies in unselected (all subtypes) patients with IBS. Patients (n = 150) were tested for the presence of IgG antibodies in a variety of food items and were then blindly randomized to receive either a diet excluding all foods to which they were found to be sensitive (IgG antibody titers greater or equal to 3:1) or a sham diet excluding the same number of foods, but not those to which they were sensitive.They found that the true diet was significantly more effective than the sham diet in reducing symptom severity scores (average reduction, 34; 95% confidence interval (CI): 17.3, 68.6; P = .049) in the intention-to-treat analysis (considering all patients who were offered the treatment). When accounting for the patients' adherence to the number of foods to which they were sensitive, the reduction in symptom scores was even higher (average reduction, 89; 95% CI: 41, 137; P smaller than .001). The adherence to the diet affected the response observed in patients on the true diet, but not patients on the sham diet (P = .038). These findings further supported the potential clinical benefit of food-elimination diets based on IgG food antibodies in patients with IBS.*The BacteriaSeveral studies have suggested a potential beneficial effect of certain probiotics in reducing some of the symptoms of IBS.(7)Probiotics vs AntibioticsIn a small (n = 44) study, Faber(8) examined the effect of probiotics* alone (n = 20) and in combination with antibiotics (n = 24) on GI symptoms and QOL in an uncontrolled trial of unselected (all subtypes) patients with IBS. Antibiotic treatment included ciprofloxacin* 500 mg twice daily per week, and probiotic treatment included Lactobacillus acidophilus NCFM (10 billion/g) and Bifidobacteria infantis (10 billion/g) daily for 4 weeks. Both groups showed significant improvement following treatment: In the probiotic/antibiotic group, a decrease in symptom frequency index scores from 35 to 18 (P smaller than .001) and an increase in IBS-QOL scores from 67.6 to 87.8 (P smaller than .001) were seen; in the probiotic-only group, a decrease in symptom frequency index scores from 39 to 17 (P smaller than .001) and an increase in IBS-QOL scores from 69.3 to 86.4 (P smaller than .001) were seen. The predominant IBS type did not alter the response to therapy.Commentary. As a small uncontrolled study, these results may reflect, at least in part, a placebo response. Nevertheless, the findings emphasize the need for additional clinical studies to evaluate the role of probiotics and antibiotics in IBS patients.Mechanisms of ProbioticsAlthough the efficacy and role of probiotics in the treatment of IBS remain uncertain and require confirmation, several studies presented during this year's meeting examined possible mechanisms for their effects on GI motor, sensory, and immune function.Lamine and colleagues(9) investigated the effect of treatment with Lactobacillus farciminis bacteria on the nociceptive response to colorectal distension in basal conditions and after TNBS (2,4,6-trinitrobenzene sulfonic acid)-induced colonic inflammation in rats. They found that L farciminis treatment significantly reduced (P smaller than .05) abdominal nociceptive response for all distending pressures in both the noninflamed-treated group compared with the noninflamed controls and in the TNBS-induced inflamed hypersensitivity treated group compared with the nontreated group. These researchers attributed this antinociceptive effect to the known ability of L farciminis to produce nitric oxide (NO). Indeed, hemoglobin (an NO scavenger) infusion resulted in reversing this organism's antinociceptive effect. These investigators concluded that a 3-week treatment with L farciminis can reduce visceral pain induced by colorectal distension in basal and inflammatory conditions, and that this effect depends on the NO released by these bacterial strains into the colonic lumen.In another study, the same group of investigators reported a protective effect of the NO producing-L farciminis against TNBS-induced colitis in rats.(10) Rats that were treated with this organism for 3 weeks prior to induction of colitis showed significantly lower inflammation, as expressed by reduction in macroscopic damage score, MPO (myeloperoxidase) activity, and inducible NO synthase activities. As with the previous study, hemoglobin reversed the beneficial effect of L farciminis on the inflammation activity in the colitic rats.Commentary. These studies suggest a role for NO-producing bacteria in protecting against inflammatory and hypersensitivity conditions. However, these findings in animal models deserve additional investigation in humans in order to confirm beneficial effects.Another possible mechanism mediating the effects of probiotic bacteria on GI function has been proposed by Verdu and colleagues.(11) They investigated the effects of probiotics on intestinal muscle dysfunction in a mouse model of postinfective Trichinella spiralis IBS. Study mice groups were treated with Lactobacillus paracasei, Lactobacillus johnsonii, Bifidobacterium longum, or B lactis. Additional mice received heat-inactivated L paracasei or bacteria-free L paracasei spent culture medium (SCM). At 21 days post infection, L paracasei, but not L johnsonii, showed significant attenuation of hypercontractility to carbachol stimulation, compared with the control group (P = .01). The 2 bifidobacteria strains tended to decrease the hypercontractility; however, this trend did not reach statistical significance (P = .09). The attenuation of muscle hypercontractility was paralleled by a 2-fold decrease in the secretion of interleukin-4 (P smaller than .0001), mRNA for transforming growth factor-beta (P = .0001), and cyclooxygenase-2 (P = .001) in longitudinal myenteric plexus preparation and by modulation of genes involved in innate defenses such as RANTES and cryptdin, as evaluated by gene array analysis.Commentary. It is interesting that the normalization of the postinfection contractility was independent of L paracasei presence in the mucosa-associated flora -- thus indicating that the improvement in intestinal muscle dysfunction by L paracasei and free-L paracasei SCM is likely due to attenuation of cytokine and inflammatory mediator production in the muscularis externa and modulation of innate defense genes in the small intestine. In addition, this effect is strain-dependent.The importance of the strain-specific effect has also been suggested by findings from other studies.(12) The clinical implication for this strain-specific effect has been shown in an interesting abstract presented by Drisko and colleagues.(13) These investigators examined 5 commercially, commonly available probiotic products. They used polymerase chain reaction (PCR) gel electrophoresis and amplicon excision with DNA sequencing to determine the bacterial strain content of these 5 products and compared their findings against what was reported in the respective product labeling information.These investigators found that with a single exception, all bacterial species that were tested were detected in the probiotic samples by PCR analysis and confirmed by DNA sequencing. Bifidobacterium bifidum was not detected in 2 of the 5 samples reporting its presence. In contrast, Lactobacillus spp. were detected in 2 of the 5 product samples for which the species was not listed as an "ingredient."Commentary. Although cultures of commercially available probiotics closely resemble their labeling information overall, there are some differences. Because emerging data suggest that the beneficial effect of probiotics is strain-dependent, a better regulation of dietary supplements may be necessary to ensure proper preparation and marketing standards.Concluding RemarksThe above discussion is intended to bring to the fore the current state of knowledge regarding the multifactorial nature of FGIDs. Within this context, new insight may be gained with respect to the clinical and therapeutic implications for patients with these disorders, with a view toward the effect and effectiveness of available and commonly used treatment options.* The United States Food and Drug Administration has not approved this medication for this use.


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## trbell (Nov 1, 2000)

yes, it would be great if the FDA could regulate this but as long as they are not advertised as medication I don't think the FDA can do anything. That's why naltrexone is important as they are developing it for a patent for the FDA.tom


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## eric (Jul 8, 1999)

Right Fay, foods are a trigger in IBS. And no one argues that in the slightest, but watch how its presented that loss of oral tolerence is what causes d in IBS and that is not it. *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. * Thats the point exactly and it should be talked about first that many things are triggers to IBS.Not implied that loss of oral tolerence is the cause of d in IBS, it is only *a* trigger, so its important to understand all triggers, in regards to IBS not just one, especially in something that causes d from the * ACT OF EATING*, which many people do not understand and certain people who talk about foods all the time, don't talk about.Why not talk about this first."How Does Diet and Stress Affect Irritable Bowel Syndrome?The potential for abnormal function of the colon is always present in people with IBS, but a trigger also must be present to cause symptoms. The most likely culprits seem to be diet and emotional stress. Many people report that their symptoms occur following a meal or when they are under stress. No one is sure why this happens, but scientists have some clues. Eating causes contractions of the colon. Normally, this response may cause an urge to have a bowel movement within 30 to 60 minutes after a meal. In people with IBS, the urge may come sooner with cramps and diarrhea. *Patients with IBS have an exaggerated gastrocolic reflex* The strength of the response is often related to the number of calories in a meal and especially the amount of fat in a meal. Fat in any form animal or vegetable is a strong stimulus of colonic contractions after a meal. Many foods contain fat, especially meats of all kinds, poultry skin, whole milk, cream, cheese, butter, vegetable oil, margarine, shortening, avocados, and whipped toppings.-what this means is the lower colon over reacts FROM EATING- especially if there is a lot of fat in the meal and dumps the food in it- Taken with the excess release of serotonin in the gut in d predominate IBS which also over activates the colon and causes d from the act of eating-"A:Irritable bowel syndrome is now recognized as a disorder of serotonin activity. Serotonin is a neurotransmitter in the brain that regulates sleep, mood depression, anxiety, aggression, appetite, temperature, sexual behavior and pain sensation. Serotonin also acts as a neurotransmitter in the gastrointestinal tract.Excessive serotonin activity in the gastrointestinal system enteric nervous system is thought to cause the diarrhea of irritable-bowel syndrome. The enteric nervous system detects bowel distension expansion on the basis of pressure-sensitive cells in the bowel lumen opening. Once activated, these pressure-sensitive cells promote the release of serotonin, which in turn promotes both secretory function and peristaltic function (the contractions of the intestines that force the contents outward). At least four serotonergic receptors have been identified to be participants in the secretory and peristaltic response.Patients with diarrhea-predominant IBS may have higher levels of serotonin after eating than do people without the disorder. This recognition led to the development of the first drug used specifically to treat diarrheal symptoms of IBS, alosetron also known as Lotronex. Alosetron blocked the specific serotonin receptors responsible for recognizing bowel distention. In doing so, it blocked the effects of serotonin and reduced both bowel secretions and peristalsis. Constipation was the most common side effect seen. Note: Alosetron was removed from the market by the manufacturer after repeated reports of a dangerous condition known as ischemic colitis became known. Tegaserod Zelmac is another drug under development and under review by the U.S. Food and Drug Administration for approval. Tegaserod is indicated for the treatment of constipation-predominant IBS and works to increase enteric nervous system serotonin activity.So, increasing serotonin activity in the enteric nervous system produces increased bowel secretions and peristalsis and potentially diarrhea, whereas depressing serotonin activity produces reduced secretions and reduce peristalsis and potentially constipation. Increasing serotonin activity in the brain would increase awareness and, in higher doses, produce anxiety, insomnia and restlessness."Maybe that should be talked about first in regards to food.Stress also stimulates colonic spasm in people with IBS. This process is not completely understood, but scientists point out that the colon is controlled partly by the nervous system. Stress reduction relaxation training or counseling and support help relieve IBS symptoms in some people. However, healthcare providers are quick to note that this does not mean IBS is the result of a personality disorder. IBS is at least partly a disorder of colon motility. " The inflammation is not understood either and a lot of evidence for neurogenic inflammation without a pathogen is coming to light in IBS.Dr Wood is an expert in food allergy and also the brain connections"Jack Wood, PhDProfessor of Physiology and Internal MedicineChairman Emeritus, Department of PhysiologyThe Ohio State University College of Medicine Dr. Wood was the first to use microelectrodes to record the electrical and synaptic behavior of neurons in the enteric nervous system. He coined the term "brain-in-the-gut" in view of emerging evidence that the enteric nervous system had neurophysiological properties like the brain and spinal cord. In recent years he has focused on signaling interactions between the enteric immune system and the brain-in-the-gut during infectious enteritis and food allergy. In this lecture he shows how the central nervous system, enteric nervous system and intestinal immune system are integrated during physical and emotional stress to produce irritable bowel symptoms of diarrhea and abdominal pain and discomfort."Douglas Drossman, MDProfessor of Medicine and PsychiatryCo-Director, UNC Center for Functional GI and Motility DisordersUniversity of North Carolina at Chapel Hill Recently, the irritable bowel syndrome IBS has gained a great deal of prominence within the field of Gastroenterology. An explosion of basic and clinical research has advanced our understanding of the pathophysiology of this condition. We now understand the IBS not only as a disorder of motility, but also as one associated with visceral hypersensitivity with brain-gut modulation. This new knowledge has been associated with the development of symptom-based criteria for diagnosis, and has led to new forms of treatment. Dr. Drossman, is a nationally recognized investigator and clinician in the field of functional gastrointestinal disorders. He presents an update using an integrated Biopsychosocial approach that applies our new knowledge of the pathophysiology of IBS in order to develop a practical approach to diagnosis and treatment." Dr Gershon is helping in IBSMichael Gershon, MDChair, Department of Anatomy and Cell BiologyColumbia University College of Physicians And Surgeons Dr. Gershon's earliest work involved investigations of the function of serotonin in the bowel, but it soon also came to involve studies of the cellular and molecular basis of intrinsic reflex control and ontogeny of the ENS. Dr. Gershon's work has been vital in the rediscovery of the unique ability of the enteric nervous system ENS to function independently of CNS input, and he has become the acknowledged world leader in research in enteric neuronal development. In this lecture he shows how and why blocking signals from the brain to the gut with alosetron, a potent, long-lasting and specific 5-HT3 antagonist, relieves many of the symptoms of IBS. This lecture also includes a discussion of the 5-HT1P, 5-HT4 and 5-HT3 receptors. ""Nigel Bunnett, PhDUniversity of California School of MedicineDepartment of Surgery and PhysiologyAccumulating evidence indicates that sensory nerves play a major role in inflammation of multiple tissues, and that communication between the nervous system and mast cells is of particular importance. Dr. Bunnettï¿½s lecture will highlight recent experimental evidence that mast cell proteases signal to sensory nerves through novel receptors that couple to the release of proinflammatory peptides, and that defects in this mechanism result in uncontrolled inflammation and disease. Dr. Bunnett will present evidence that therapies designed to block signaling by neuropeptides and proteases are attractive treatments for inflammation.""Esther Sternberg, MDChief, Section on Neuroendocrine Immunology and BehaviorDirector, Molecular, Cellular and Behavioral Integrative Neuroscience ProgramNational Institute of Mental Health, National Institute of HealthA pioneer in the field of neural-immune interactions, Dr. Sternberg will present the scientific evidence proving molecular, neuroanatomical and hormonal links between the brain and immune system and will discuss the role that disruptions of such links play in inflammatory/autoimmune disease. ""Bruce Naliboff, PhDCURE Digestive Disease Research CenterDepartment of Medicine, Physiology and PsychiatryIt is increasingly recognized that Irritable Bowel Syndrome is a common and diagnosable disorder that has a significant impact on Quality of Life. Dr. Naliboff is a leading authority on the interplay between psychological, behavioral, and biological factors in IBS. His research includes perceptual, autonomic, and brain imaging studies of visceral sensitivity, as well as studies of psychosocial variables that impact Quality of Life and symptoms in IBS. His lecture will review the most recent data on the broad range of intestinal and extra-intestinal symptoms in IBS, the overlap of IBS with psychiatric disorders, and the role of both symptoms and psychosocial factors in determining Quality of Life for IBS sufferers."You can view there lectures here. http://www.conference-cast.com/ibs/Lecture...dRegLecture.cfm The evidence by the way in IBS for the "low-grade inflammatory response" is more on the chronic stress side then foods. Besides"An increase in inflammatory mediators alone is insufficient to explain the pathogenesis of IBS" http://www.med.unc.edu/medicine/fgidc/infl...rymediators.htm They don't know everything that causes IBS, although they are closer on the motiliy problem of d and c and d/c associated with serotonin, but they have clues more now then ever.Maybe there is a high percentage of food phobia in IBS because when a person eats they get pain. Hence people think foods cause pain, but in actuality the pain is not caused by foods and if the person didn't have IBS they might not have food problems when they eat, foods are a trigger to the underlying problem and that is very important in IBS to know and why they cause pain through the brain gut axis.


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## bonniei (Jan 25, 2001)

eric while food intolerance may not be the cause I think you dismiss too often that food is a factor by debating with mike.Just want to add that Brostoff's book with Challacombe had 33 MD's and 22 FRCP's contributing to it.


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## eric (Jul 8, 1999)

Bonnie, I have had IBS for over thirty years, I know food is a factor for sure. However, fats are one of the biggest triggers to the colon and there are other foods that set of IBS for purely chemical reasons, not from loss of tolerence to them. How come that is not the first parts of information shared here in regards to foods and IBS?Since the digestive system in IBS reacts to and is sensitive to *all * stimuli its important to understand that and not just the role and focus on foods. People may think a food is causing a flare when in fact it might not be at all, many factors come into play to cause the symptoms.How many people know the cells lining the GI tract are pressure sensitive? There is some basic information that should be presented first and reasons for d, other then loss of oral tolerence and they should be presented also in regards to IBS, that is the whole picture, not just foods, thats the point. A lot of information is left out in regards to IBS.Not to mention comorbid food problems discussed for the conditions they are, like lactose intolerence or fructose or celiac ect. Not one big lump of problems label food intolerence and then suggested IBS!!!Or the overlap to other functional gi conditions like dyspepsia which is found in a lot of IBS patients, upper gi functioning problems.You can trigger IBS symptoms from both the gut and the brain. Thats very important to understand! The weather can trigger the symptoms, heat, cold, emotions, foods, and from the work being done in Fibro and cfis and the comborbid association with IBS, there is strong evidence and reasons to suspect these conditions are interelated and there is convergence through the nervous systems. Also why do more women have IBS? Does it have to do with the fact they have more serotonin then men and a different stress responce? Or hormones?Why does it wax and wane?Why is there the sensation of incomplete evacuation and rectal sensitivity?How about these foods that trigger IBS."Fatty foods like french fries Milk products like cheese or ice cream especially in people who have trouble digesting lactose, or milk sugar Chocolate Alcohol Caffeine found in coffee, tea, and some sodas Carbonated drinks like soda Sorbitol, a sweetener found in dietetic foods and in some chewing gums Gas-producing foods including beans and certain vegetables like broccoli or cabbage. "How about some basic food advise, starting here first to see if someone gets better after eliminating these know trigger foods first, since the gut reacts to them in IBS.Even if you were to eliminate loss of intolerent foods would not these foods still provoke symptoms do to their chemical nature and effect on the gi trat in IBS since "The potential for abnormal function of the colon is always present in people with IBS"How about explaining that foods are not the only triggers and that the digestive system reacts to all stimuli.This is not about being tested for food problems, it never was and I have said that many times, its about the presentation of the role of food problems in IBS that is the problem. There is a much bigger picture.I am all for diet and stress reduction as the first line of treatment in IBS. Stress/ anxiety and emotions also play a major role in IBS and is way underestimated on the bb here in regards to how it triggers IBS, just like foods can. In fact they are probably a bigger part of the picture from the research on IBS. This should also be presented in the whole picture in IBS, because its also extremely important. Not just dismissed so easily."Recent studies have led to a better understanding of the gastrointestinal GI tract and how it is "wired." This, in turn, has led to a better understanding of many GI illnesses, IBS being one. The lining of the intestine has pressure-sensitive cells, which detect the amount of digested material. *Once activated by the quantity of food you eat* , these cells promote the release of a neurotransmitter called serotonin, which promotes both digestive secretions and a mechanical function that propels food through the digestive tract called peristalsis. Patients with diarrhea-predominant IBS have higher levels of serotonin after eating than do people without this disorder. It is assumed that this higher level of serotonin leads to excessive activity of the intestine, including diarrhea."The research above on this is much newer then this article from Harvard."Can J Gastroenterol. 2003 Mar;17 3:191-6. Sex differences of brain serotonin synthesis in patients with irritable bowel syndrome using alpha-11Cmethyl-L-tryptophan, positron emission tomography and statistical parametric mapping.Nakai A, Kumakura Y, Boivin M, Rosa P, Diksic M, D'Souza D, Kersey K.Fukui Medical University School of Medicine, Fukui, Japan.BACKGROUND: Irritable bowel syndrome IBS is the most common functional bowel disorder and has a strong predominance in women. Recent data suggest that the brain may play an important role in the pathophysiology of IBS in the brain-gut axis. It is strongly suspected that serotonin 5-HT, a neurotransmitter found in the brain and gut, may be related to the pathophysiology of IBS. It is reported that a 5-HT3 antagonist is effective only in female patients with diarrhea-predominant IBS. OBJECTIVE: In the present study, 5-HT synthesis was measured using positron emission tomography, with alpha-11Cmethyl-L-tryptophan as the tracer, in patients with IBS. The aim of the present study was to compare 5-HT synthesis in the IBS patients with that in the controls, and to compare 5-HT synthesis between male and female IBS patients. METHODS: Six male and six female nonconstipated IBS patients were scanned. Age-matched healthy volunteers were scanned as controls. Eighty minute dynamic scans were performed. Functional 5-HT synthesis images were analyzed using statistical parametric mapping. RESULTS: 5-HT synthesis was greater only in the female IBS patients in the right medial temporal gyrus multimodal sensory association cortex compared with the female controls P<0.001. CONCLUSIONS: The greater brain 5-HT synthesis in the female IBS patients than in the controls may be related to the pathological visceral pain processing of the IBS patients, a larger female predominance of the disorder, and the sex difference of the efficacy of the 5-HT3 antagonist in treatment.PMID: 12677270The symptoms of d and c and d/c in IBS are just symptoms of motility to a larger picture. Serotonin does not explain the whole picture either, but part of the motility end and pain end and emotional end.Aliment Pharmacol Ther. 2003 Jan;17 1:43-51. Related Articles, Links Systematic review: serotonergic modulators in the treatment of irritable bowel syndrome--influence on psychiatric and gastrointestinal symptoms.Kilkens TO, Honig A, Rozendaal N, Van Nieuwenhoven MA, Brummer RJ.Department of Psychiatry, University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, The Netherlands.BACKGROUND: Both central and peripheral serotonergic modulators are used in the treatment of irritable bowel syndrome. The majority of patients with irritable bowel syndrome presenting to a gastroenterologist demonstrate affective dysregulation. Serotonin may play a regulatory role in both gastrointestinal motility and sensitivity, as well as in affective dysregulation, in irritable bowel syndrome. AIM: To analyse, systematically, randomized controlled trials studying the influence of serotonergic modulators on both gastrointestinal and psychiatric symptoms in irritable bowel syndrome, in order to elucidate baseline irritable bowel syndrome symptomatology and possible differential effects of serotonergic modulation on this symptomatology. METHODS: A standardized qualitative analysis was performed of studies investigating the influence of serotonergic modulators on both gastrointestinal and psychiatric symptoms in irritable bowel syndrome using a blind review approach. The studies were ranked according to their total quality score maximum 100 points. RESULTS: Eleven studies fulfilled the entry criteria, six of which scored above 55 points. An association between gastroenterological and psychiatric changes was present in five of the six studies. CONCLUSIONS: The results strengthen the serotonergic association between gastroenterological and psychiatric symptoms. Adjusted guidelines for combined gastrointestinal and psychiatric assessments are recommended in order to further elucidate the serotonergic interaction between gastrointestinal and psychiatric symptoms.Publication Types: Review Review, Academic PMID: 12492731 Am J Gastroenterol. 2003 Jan;981:135-43. Related Articles, Links Irritable bowel syndrome patients show enhanced modulation of visceral perception by auditory stress.Dickhaus B, Mayer EA, Firooz N, Stains J, Conde F, Olivas TI, Fass R, Chang L, Mayer M, Naliboff BD.University of California, Department of Medicine, Los Angeles UCLA/CNS: Center for Neurovisceral Sciences & Women's Health, VA Greater Los Angeles Healthcare System, Los Angeles, California 90073, USA.OBJECTIVES: Symptoms in irritable bowel syndrome IBS patients are sensitive to psychological stressors. These effects may operate through an enhanced responsiveness of the emotional motor system, a network of brain circuits that modulate arousal, viscerosomatic perception, and autonomic responses associated with emotional responses, including anxiety and anger. The aim of this study was to test the primary hypothesis that IBS patients show altered perceptual responses to rectal balloon distention during experimentally induced psychological stress compared with healthy control subjects. METHODS: A total of 15 IBS patients nine women and six men and 14 healthy controls seven women and seven men were studied during two laboratory sessions: 1 a mild stress condition dichotomous listening to two conflicting types of music, and 2 a control condition relaxing nature sounds. The stress and relaxation auditory stimuli were delivered over a 10-min listening period preceding rectal distentions and during the rectal distentions but not during the distention rating process. Ratings of intensity and unpleasantness of the visceral sensations, subjective emotional responses, heart rate, and neuroendocrine measures norepinephrine, cortisol, adrenocorticotropic hormone ACTH, and prolactin were obtained during the study. RESULTS: IBS patients, but not healthy controls, rated the 45-mm Hg visceral stimulus significantly higher in terms of intensity and unpleasantness during the stress condition compared with the relaxation condition. IBS patients also reported higher ratings of stress, anger, and anxiety during the stress compared with the relaxing condition, whereas controls had smaller and nonsignificant subjective responses. Heart rate measurements, but not other neuroendocrine stress measures, were increased under the stress condition in both groups. CONCLUSION: These findings confirm the hypothesis of altered stress-induced modulation of visceral perception in IBS patients.PMID: 1252694So why would it be important to understand and discuss the whole picture? For a better ways to treat it perhaps, from all angles?Donna, sorry you had a bad day and no need to be angry at the UNC or me or anyone for that matter, one anger upsets IBS and is a trigger and the UNC and UCLA and Mayo and many others researching IBS around the world, are trying to solve the mystery and help people/US with functional gi disorders, such as IBS and the relationships to other gi problems, even food relationships.I don't think holding it against them that it is so complex is the answer either. They have reasons for what they do and say as experts in the different fields way beyond our comprehension in regards to how the gut and the brain work together.This is not a competition between the brain and the gut, both are players in IBS!History of Functional Disorders Douglas A. Drossman, MDCenter-Co-DirectorMelissa Swantkowski New York UniversityPrintable formatTHE PASTHISTORICAL PRECEDENTSHistorians and physicians have documented the presence of Functional GI disorders throughout recorded human history. However, until recently, limited attention has been granted to these disorders due to the lack of identifiable pathology and the absence of a conceptual framework to understand and categorize them. Systematic investigation of functional GI disorders did not begin until the middle of the 20th century, and prior to this time, only occasional reports of functional GI symptoms were published, the first appearing only 200 years ago. Over the past 25 years, scientific attention to understanding and properly caring for patients with functional GI disorders has grown progressively. With the understanding comes the rationale for use of medications directed at intestinal receptors as well as psychopharmacological, behavioral, and psychological forms of treatment. Additionally, there has been an increase in the rate of scientific publications and greater media exposure to the public through television, radio, and Internet. To understand the historical classification of these disorders, two differing theories relating to the interaction between the mind and body should be considered.Holism: a theory built upon the foundation that the mind and body are integrated and utterly inseparable. Dualism: a theory that proposes a separation between the mind and the body. Greek philosophers Plato, Aristotle, and Hippocrates first proposed the principle of holism about 3,000 years ago, and later in the 12th century; Jewish physician and philosopher Maimonides reexamined this philosophy. Based on holism, the study of medical disease must take into account the whole person rather than merely the diseased part. However, societal concepts of illness and disease drastically shifted when European philosopher Rene Descartes offered the divergent theory of dualism in the 17th century. Prior to the notion of dualism, the church discouraged human dissection on the premise that the spirit resided in the body. The acceptance of dualism paved the way for the emergence of scientific investigation and new medical discoveries by lifting the prohibition of human dissection. This shift in medical thought was congruent with the societal changes of the 17th century: the shift towards a separation in church and state. IMPLICATIONS FOR FUNCTIONAL GI DISORDERSBased on the concept of dualism, disease was now understood in terms of structural abnormalities. Therefore, the validity of a disease rested with the observation of morphological abnormalities. Medical conditions occurring in the absence of such morphological abnormalities and symptoms were not considered legitimate, and were often viewed as psychiatric, consistent with the concept of dualism. The concept of dualism had other effects with regard to treatment. For example, this would include all the functional GI disorders and other somatic syndromes, such as fibromyalgia. Until the latter part of the 20th century, a medical illness was considered amenable to scientific inquiry and treatment. However, patients with psychiatric disorders were interred in insane asylums and considered to no longer be treatable by medical physicians. Unfortunately this concept leads to a clinical dilemma. Specific diseases explain only about 10% of medical illnesses seen by physicians. Furthermore, people with structural i.e. organic diagnosis such as inflammatory bowel disease or cancer show considerable variation in their symptom presentation and clinical behavior. Gastroenterologists as well as other health care practitioners are all too familiar with the poor correlation between structural findings on endoscopy and their patient's symptoms. Although efforts to find morphological or even motility etiologies for functional GI disorders in the latter part of the 20th century were unsuccessful, the assumption that functional GI disorders must be psychiatric has developed and has permeated current thinking. However, in the face of current scientific research, this is being seriously challenged. Studies have shown that persons with irritable bowel syndrome who do not seek health care are psychologically much like healthy subjects. THE PRESENT CONCEPTUAL BASES FOR THE STUDY OF FUNCTIONAL GI DISORDERSThe recent acceptance of functional GI disorders as legitimate medical entities is based on the following three developments: The concept of the Biopsychosocial model of illness and disease The development of new investigative methods for studying disease The development of the Rome Criteria Biopsychosocial ModelIn 1977, the publication of the concept of the Biopsychosocial model by George Engel, and its later demonstration specifically for gastrointestinal disorders, marked an important change in thinking. A biopsychosocial model of illness and disease provides the needed framework to understand, categorize, and treat common GI symptoms. These symptoms are the integrated product of altered motility, enhanced visceral sensitivity, and brain-gut dysregulation and often are influenced by psychosocial factors. Figure 1 illustrates the proposed relationship between psychosocial and physiological factors with functional GI symptoms and the clinical outcome. Early in life, genetics and environmental influences family attitudes toward bowel training or illness in general, major loss or abuse history or exposure to infection may affect one's psychosocial development susceptibility to life stress, psychological state, coping skills, social support or the development of gut dysfunction abnormal motility or visceral hypersensitivity. Additionally, the presence and nature of a functional GI disorder is determined by the interaction of psychosocial factors and altered physiology via the brain-gut axis. In other words, one individual afflicted with a bowel disorder but with no psychosocial disturbances, good coping skills and adequate social support may have less severe symptoms and not seek medical care. Another having similar symptoms but with coexistent psychosocial disturbance, high life stress, or poor coping skills may frequent his physician's office and have generally poor outcome. Development of New Investigative Methods The second concurrent process has been the expansion and refinement of investigative methods that allow the study of functional GI disorders in terms of biological, cultural, and psychosocial i.e. brain influences. These developments include:the improvement of motility assessment, the standardization of the barostat to measure visceral sensitivity, the enhancement of psychometric instruments to determine psychosocial influences, the introduction of brain imaging PET, fMRI to determine CNS contribution to symptoms, and the molecular investigation of brain-gut peptides, which provide insight into how these symptoms become manifest. In less than ten years, these methods have produced new knowledge of the underlying pathophysiological features that characterize the age-old symptoms we now define as functional GI disorders. Rome CriteriaThe Rome Criteria is an international effort to characterize and classify the functional GI disorders using a symptom-based classification system. This approach that has its precedents with classification systems in psychiatry and rheumatology. The rationale for such a system is based on the premise that patients with functional GI complaints consistently report symptoms that breed true in their clinical features, yet cannot be classified by any existing structural, physiological or biochemical substrate. The Rome Criteria was built upon the Manning Criteria, which was developed from discriminate function analysis of GI patients. The decision to develop diagnostic criteria by international consensus was introduced as part of a larger effort to address issues within gastroenterology that are not easily resolved by usual scientific inquiry or literary review. By 1992, several committees had met to discuss the criteria, which ultimately resulted in the publishing of many articles in Gastroenterology International and a book detailing the criteria titled "The Functional Gastrointestinal Disorders Rome I". Elaboration of the Rome I criteria led to a second edition of the Rome criteria titled Rome II in 2000 as well as the publication of a supplement to the journal Gut in 1999. Recently the Rome Coordinating Committee has met to begin Rome III, expected to be published in 2006. To learn more about the Rome Committees and to see a summary of the Rome II book: go to www.romecriteria.com.PRESENT PATHOPHYSIOLOGICAL OBSERVATIONS Despite differences among the functional gastrointestinal disorders, in location and symptom features, common characteristics are shared with regard to:motor and sensory physiology, central nervous system relationships, approach to patient care. What follows are the general observations and guidelines. MotilityIn healthy subjects, stress can increase motility in the esophagus, stomach, small and large intestine and colon. Abnormal motility can generate a variety of GI symptoms including vomiting, diarrhea, constipation, acute abdominal pain, and fecal incontinence. Functional GI patients have even greater increased motility in response to stressors in comparison to normal subjects. While abnormal motility plays a vital role in understanding many of the functional GI disorders and their symptoms, it is not sufficient to explain reports of chronic or recurrent abdominal pain.Visceral HypersensitivityVisceral hypersensitivity helps to account for disorders associated with chronic or recurrent pain, which are not well correlated with changes in gastrointestinal motility, and in some cases, where motility disturbances do not exist. Patients suffering from visceral hypersensitivity have a lower pain threshold with balloon distension of the bowel or have increased sensitivity to even normal intestinal function. Additionally, there may be an increased or unusual area of somatic referral of visceral pain. Recently it has been concluded that visceral hypersensitivity may be induced in response to rectal or colonic distension in normal subjects, and to a greater degree, in persons with IBS. Therefore, it is possible that the pain of functional GI disorders may relate to sensitization resulting from chronic abnormal motor hyperactivity, GI infection, or trauma/injury to the viscera. Brain-Gut AxisThe concept of brain-gut interactions brings together observations relating to motility and visceral hypersensitivity and their modulation by psychosocial factors. By integrating intestinal and CNS central nervous system activity, the brain-gut axis explains the symptoms relating to functional GI disorders. In other words, senses such as vision and smell, as well as enteroceptive information i.e. emotion and thought have the capability to affect gastrointestinal sensation, motility, secretion, and inflammation. Conversely, viscerotopic effects reciprocally affect central pain perception, mood, and behavior. For example, spontaneously induced contractions of the colon in rats leads to activation of the locus coeruleus in the pons, an area closely connected to pain and emotional centers in the brain. Jointly, the increased arousal or anxiety is associated with a decrease in the frequency of MMC activity of the small bowel possibly mediated by stress hormones in the brain. Based on these observations, it is no longer rational to try to discriminate whether physiological or psychological factors produce pain or other bowel symptoms. Instead, the Functional GI disorders are understood in terms of dysregulation of brain-gut function, and the task is to determine to what degree each is remediable. Therefore, a treatment approach consistent with the concept of brain-gut dysfunction may focus on the neuropeptides and receptors that are present in both enteric and central nervous systems. The Role for Psychological FactorsAlthough psychological factors do not define these disorders and are not required for diagnosis, they are important modulators of the patient's experience and ultimately, the clinical outcome. Research on the psychosocial aspects of patients with functional GI disorders yields three general observations: Psychological stress exacerbates gastrointestinal symptoms in patients with functional GI disorders and can even produce symptoms in healthy patients (but to a lesser degree. Psychological disturbances modify the experience of illness and illness behaviors such as health care seeking. For example, a history of major psychological trauma e.g. sexual or physical abuse is more common among patients seen in referral centers than in primary care and is associated with a more severe disorder and a poorer clinical outcome. Additionally, psychological trauma may increase pain-reporting tendency. Having a functional GI disorder has psychological consequences in terms of one's general well-being, daily functional status, concerns relating to control over symptoms, and future implications of the illness e.g. functioning at work and home. APPROACH TO TREATMENTThe approach to treatment for all functional GI disorders is founded on a therapeutic physician-patient relationship. The basis for implementing a strong physician-patient relationship is supported by evidence that patients with functional GI disorders have anywhere from a 30 to 80% placebo response rate regardless of treatment. Because functional GI disorders are chronic, it is important to determine the immediate reasons behind each visit, after which treatment can be based on severity and nature of symptoms, physiological and psychosocial determinants of the patients illness behavior, and the degree of functional impairment.These factors can separate patients into mild, moderate, and severe categories.Patients with mild symptoms: usually seen in primary care, do not have major impairment in function or psychological disturbance and can maintain normal activity. These patients have concerns about their condition but do not need to make many visits to their physician. Regarding treatment, these patients require education about their disorder and its symptoms as well as information regarding a proper diet and the kinds of medication that can have adverse effects. Patients with moderate symptoms:seen in both primary and secondary care facilities and experience intermittent disruptions in activity on account of their symptoms. may identify a close relationship between symptoms and inciting events such as stress, travel, or dietary indiscretion. For these patients, symptom monitoring to record time, severity, and presence of associated factors can help to identify inciting factors and give the patient a sense of control over the disorder. Additionally, pharmacotherapy directed at specific symptoms, particularly those that impair daily function, can be helpful, as can psychological treatments relaxation, hypnosis, cognitive-behavioral therapy, and combination treatments in reducing anxiety and encouraging health promoting behaviors. Patients with severe symptoms: have trouble functioning daily, find their disorder to be disabling and debilitating in nearly every facet of life, have a high frequency of associated psychological difficulties, make frequent visits to their physicians , and may hope for a magical cure. In these cases a long-term physician-patient relationship, which sets realistic treatment goals such as improved quality of life rather than elimination of all pain is necessary. The focus for these patients needs to shift from treating a disease to coping with a chronic disorder, where much of the responsibility is place on the patient, himself. Furthermore, antidepressants have proven useful to control pain and alleviate associated depressive symptoms. THE FUTUREFuture studies will identify pathophysiological subgroups, each having its own set of determinants and treatment. Examples are as follows::Some patients will develop their disorders or exacerbate symptoms via sensitization of afferent transmission from infection, enhanced motility, or trauma to the gut. They may respond to the newly developing neurotransmitter blocking agents. Patients with more painful and severe symptoms may prove to have "abnormal perception of normal gut function" rather than abnormal function. This dysfunction in the central regulation of incoming visceral signs may be remedied with a psychopharmacological treatment approach. The symptoms of some patients could be attributed to genetic factors, which result in abnormalities in central reactivity to stress, in which case genetic manipulation strategies would prove beneficial. Early learning within the familial structure and socio-cultural influences has been demonstrated to affect symptom perception and illness behavior. Future studies are also likely to identify psychological and behavioral interventions that are targeted for this subgroup. While it is likely that there are potent new treatments that will follow our growing pathphysiologic knowledge of these disorders, it is unlikely that they will replace some of the fundamental clinical principles: active listening, careful decision making, an effective patient-physician relationship, and patient centered biopsychosocial plan of care.


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## eric (Jul 8, 1999)

By the way the foremost thing I believe helps people with IBS is education on it first.


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## meckle (Mar 5, 2003)

I agree with you on the education thing eric.And I would say that the next thing that would definitely help is the education of the non-sufferers who we have to live and work with everyday.


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## Mike NoLomotil (Jun 6, 2000)

Hi Bon Bon ____________________________ï¿½Mike I apologize if you were offended by any of my comments.ï¿½ ___________________________Hmmmm....Bonnie, you did not say anything offensive as I recall. Don't read that anything I wrote was addressed to you... it is not.







it is addressed to styatment like this which are counterproductive to the optimal treatment of many patients who suffer from IBS: _____________________________ï¿½Foods are a trigger in IBS.IBS is not caused by loss of oral tolerence to foods!!!ï¿½ ____________________________Sadly, I am again reluctant to advise that such statements are fundamentally unsound. This statement is out of date, obselete, incorrect, and is derived from references which do not include all aspects of investigation into patients who present with IBS symptoms. ______________________________ï¿½Right Fay, foods are a trigger in IBS. And no one argues that in the slightest, but watch how its presented that loss of oral tolerence is what causes d in IBS and that is not it.ï¿½ _____________________________Buzzzt. Wrong again. This is a fundamental problem in some IBS victims. But feel free to do as was suggested, and watch and see how theorum and putative and possibility and conjecture is morphed and woven into fact by selective thinking. Happens all the time so why should today be any different?Let me speak very precisely so there is no equivocation to try to interpret. What is factual, is that it has been shown that there is a subpopulation of patients, an apparently large one, many of whom come to this forum seeking help, who are diagnosed with IBS by their doctors based on their clinical presentation and symptoms per one of the recommended Symptom Based Diagnostic Criteria, such as the ROME II criteria (example)and in whom differential disgnosuis reveals nothing obvious.However, when investigators take patients diagnosed with IBS via these "approved" symptom based criteria and whom have a diarrheic component to their symptoms and then rule out food allergy by checking for it (often by multiple methods), and then isolate the jejunum with a multi-lumen double cuffed nasogatsic tube and perform serial direct blind oral challenges to the jejunum with various staple foods, these patients all release proinflammatory mediators in response to some of the foods and not to others. Normal controls do not. They tolerate staple foods as they should. Their gastroimmune system isable to discriminate normally. However the subjects have lost this ability with crtain foods. This can also now de duplicated in vitro.The offending foods are patient-specific and include an array of staple foods (meats, vegetables, fruits, grains, dairy productsï¿½all the things that people eat and which are benign in the normal asymptomatic control subjects). The offending foods which provoke mediator release vary from patient to patient. There is no set pattern.The mediators (and other markers of cell mediated immune reactions) captured from the jejunal washings are from various types of immunocytes involved in the mechanism known as Oral Tolerance, both mucosal and systemic.In addition, more recently, rather than just collecting the jejunal washings and analyzing them for proinflammatory and proalgesic mediators (whose presence then qauntitatively accounts for the upregulated state of the diarrheics bowels since it is well known what each of the mediators does and to what structures) full thickness biopsy of these subjects reveals the specific inflammtogenic reactions and cell types which have been activated.The findings correspond exactly to other investigators findings, widely revealed, published, discussed and often cited here by others, who have found such things in the lamina propria as specific cellular infilatrates and mucosal cell changes which vary by IBS subtype. Often those other findings, evaluated in a vacuum from having tried to assess by jejunal challenge if the inflammatory response can be provoked or subsided via food challenge, the fini=dings are interpreted solely in the context of the fact that it is known that chronic stress can alter immune fuunction among other things, so this is postukated to be the probable mechanism. this then becomes dogma aming those who have not taken into account the other possibilities...indeed other studies of what happens in the upper bowel of people presenting with IBS symptoms.C-types do not show these inflammatory changes, only diarrheics with or without a history of enteritis as a precursor to their symptoms. This was also indepdnently confirmed and I am sure is posted elsewhere among all the mass of clippings as evidence in support of some other postulate.Anyway It is proved already that all these things, these events, these abnormal responses are fact. They have been under study since at least 1994, and are under continued investigation as we sit here and debate that which is not debatable instead of that which is.....WHY does this happen? Curiously, when the investigators remove from the subjects diets the foods which provoked the jejunal reaction, the reactions cease, the mediator release ceases, and the patient symptoms subside. All of their symptoms. However They can be provoked at any time through food challenge. How mystical! How abhorrent to some peoples belief systems!This is very different from the concept of triggers. Trigger= challenge with rapid response. Most of the mechanisms of lost oral tolerance are dose dependent and elayed onset, so thats very different form things which trigger. Triggers are things, liuterally anything, which provoke an already-upregulated bowel to further respond to that stimulus.This word confuses patients when it is used as if it refers to the same thing as I am describibng, Nope. Different deal.In these food intolerant IBS subjects, primary events have ocuurred which result in upregulation of the gut and thus making it susceptibel to the so called "trigger elements" be they fods, chemicals, events, emotions, ad nauseaum. But when the foods or additives are removed from the diet which provoke the original primary reaction (the ones to which the subject has lost oral tolerance for some reason), the gut no longer responds abnormally to ï¿½triggersï¿½ as it did before, especially those which did not involve any form of immune response or digestive enzyme deficiency (other pathways not discussed here but which also occur comorbidly...the subject is being simplified here so as to limit confusion).In fact this established that there is a supopulation of IBS victims who are from a symptom based diagnostic criteria, defined as being among the 2/3 with diarrheic symptoms, who suffer loss of oral tolerance to staple foods. Some may be secondary to persistent eleveted inflammatory response following a history of enteritis, some subjects lose oral tolerance for other reasons that are as yet unclear as the mechanisms do not follow the rules of traditional Gel & Coombs immune response classifications.So one may continue to try to make those facts disappear as they conflict with ones beliefs or paradigms but that does not make the patients who suffer from this and who are diagnosed by their doctors as being IBS sufferers disappear from the IBS population. The way to make them disappear is to isolate foods and additives to which they have lost oral tolerance and remove them from the diet on a patient specific basis, as part of an integrated multidisciplinary Disease Management approach to getting the best therapeutic outcomes possible. As the literature universally recommends, an integrated treatment program begins with a solid physician-patient relationship, evaluation and implementation of patient specific dietary and lifestyle changes, and evaluation of the patients psychological state and implementation of psychological support treatments such as HT or CBT as are appropriate and which are accepted by the patient and will be followed.Oh this is always intriguing wherever it appears: _________________________________________________ï¿½Irritable bowel syndrome is now recognized as a disorder of serotonin activity.ï¿½ _________________________________________________when this is written it reflects the authors viewpoint, which may or may not be consisitent with everyones viewpoint. In this case it is not. This is merely an act of morphing one putative mechanism into proof that it is the sole base mechanism of all that follows with IBS. It's not a true statememt thatï¿½s allï¿½ï¿½now recognizedï¿½ï¿½ suggests that everyone agrees that some mystical serotonin dysfunction is what causes all IBS symptoms. Nope. Far be it from me however to waste more time debating the obvious. If one looks at all the literature objectively and inclusively without selectivity and bias, and all the material and all the subjects diagnosed with so called IBS it is clear this is a belief system being expressed, not a physiologic fact. If one actually read the findings of those researching the disease from this angle ("Serotonin Solution", paraphraing the OZman, Prince of Darkness) and actually looks at the words used to express the investigators findings one would understand what I mean. Words like ï¿½appearsï¿½ and ï¿½suggestsï¿½ and ï¿½is consistent with the possibilityï¿½ and all other such hedging is necessary and is used by even the most beguiled scientists as they know ethically and physiologically that to state more would be inaccurate at this time.Indeed while the literature is quite clear that 5HT and 5HT [x] receptors and 5HT agonists and antagonists all play a role in the regulation of gut function and in supportive treatment of the IBS subject, the literature also shows if one takes a more inclusive view of the big picture that there are many other mediators than serotonin which are in play in the various IBS subpopulations, ranging from prostaglandins to leukotrienes, cytokines, heck there are up to 100 known proinflammatory and proalgesic mediators which can participate in symptom generation in IBS victims. But you have to go look for them to know they are there. So when they are looked they are found, and a relationship between their presence, what elicits their presence and their effects on the bowel structures is simplistic to understand once you accept that there are investigators doing that kind of work on people who meet the same selection criteria as everyone else.Now what will be interesting will be the eventual understanding of WHY some people lose oral tolerance with no history of an inflammatory event, for example, which can accoun for a persistent oral tolerance dysfunctionï¿½like many findings of observed events in ISB patients you know WHAT happens but it remains unclear WHY it happens so work continues. In the meantime, though, if you can AVOID it happening if it is something that results in the patients symptoms then it behooves you to DO SO.It is unfortunate that investigatory findings happen faster than they are eventually all accumulated, integrated, assimilated and then appear in tutorial literature such as that posted. It is quite easy to find tutorials about IBS that are not current with all that is recently discovered about some diseases, including syndrome like IBS. It behooves one to try to look further and more inclusively if you want to really know as much as you about what is known at any given time. It could be easy for me to dredge up and postal kinds of things investigators and authors have concluded about certain treatment modalities widely touted as ï¿½highly effective for IBSï¿½ as if they are a panacea and in so doing inflame their advocates top fits of apoplexy. That might be fun but it would not contribute anything positive to the lives of those who are ill seeking relief here.At least what I describe here has been known long enough for the Merck Manual to attempt to alert physicians to the fact that food intolerance of the type I described above is the cause of symptoms in some IBS patients. Newer work seems to suggest that the number is larger than is implicit in the word ï¿½someï¿½.Like I said before, at one time asthma was firmly believed and taught in medical literature to be a psychological dysfunction and the standards of treatment set forth were on that basis. The actual causal basis was discovered and discussed long and hard in the literature, at conferences, at the bedside, on grand rounds, and around tall mugs of stout at late night pub debates among doctors before all the literature was updated. So the situation with IBS is no different. This happens with syndromes all the time it is the nature of the literature that what is known and what is printed in tutorials are often out of synch. This does not remove new facts or new realities from existence.As much as it may pain some people that these things are true, they never the less remain true.enjoy!







MNL


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## bonniei (Jan 25, 2001)

Insightful analysis of eric's articles Mike- that the scientists are hedging and not saying unequivocally the things eric claims them to be saying.MikeNL, why do certain foods produce proinflammatory mediators in IBS patients? I assume the body is seeing those foods as toxic in some way. Have they discovered why this happens? It is too bad foods have to be eliminated from the diet. That is no way to live.


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## trbell (Nov 1, 2000)

Once again I'm having trouble figuring out what the argument is about here. "IBS is recognized as a disorder of serotonin functioning" Th same can be said of depression and anxiety."Like I said before, at one time asthma was firmly believed and taught in medical literature to be a psychological dysfunction and the standards of treatment set forth were on that basis. The actual causal basis was discovered and discussed long and hard in the literature, at conferences, at the bedside, on grand rounds, and around tall mugs of stout at late night pub debates among doctors before all the literature was updated. So the situation with IBS is no different. This happens with syndromes all the time it is the nature of the literature that what is known and what is printed in tutorials are often out of synch. This does not remove new facts or new realities from existence."Once again you can substitute depression and anxiety for 'asthma' in the above. The interesting thing is that therapy and hypnosis can chang serotoni levels probably through the immune system and can do the same for asthma again through the immune system although no psychologist who knows anything wil tell you it's the onl thing.tom


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## Blair (Dec 15, 1998)

Erics right about fat making IBS worse. I think as well as imediate triggers it also gets bile moving, too much for my poor old irritable colon to deal with.


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## kel1059 (Feb 28, 2003)

Eric,I am very glad that you show your true intelligence in the way you construct your sentences and the way you choose words. this is a very important clue that you are not very sharp. however, i am not putting you down. It is okay to have average intelligence. But, if you have average intelligence then you must quit acting like the all-knowing pervader of IBS knowledge.It is very clear that MNL clearly outclasses you in understanding and explaining the true role of food and its relation to IBS.You are clearly the most stubborn and narrow-minded person I have ever encountered.It seems that your entire problem is that you have this preconceived idea of what IBS is and isn't. This "idea" of yours is very dangerous because whenever you encounter anything that does not fit your "idea" then you seem to automatically reject it.You also seem to cling to the findings of the doctors at UNC far too closely. These doctors are not only somewhat biased in their beliefs but they don't seem to be too concerned with the role of the immune system in IBS. They probably ignore this factor because they do not understand it very well.


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## trbell (Nov 1, 2000)

too bad we have to talk about people here instead of the facts. I agree with Mike's approach.tom


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## eric (Jul 8, 1999)

Kel,"In this world, Elwood" - she always called me Elwood - she'd say "In this world, Elwood, you must be oh, so smart or oh, so pleasant." For years I was smart. I recommend pleasant. You may quote me."Jimmy Stewart in "Harvey"


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## eric (Jul 8, 1999)

"Causes of IBS This is an exciting time for IBS because we are now understanding more and more about the disorder. Many years ago, physicians believed this to be a psychosomatic illness. More recently, we have discovered that there seems to be increased sensitivity in the gut i.e., increased perception of pain in patients with IBS. This is accompanied by increased motor activity in the gut and a dysregulation between the *central nervous* system and the *enteric nervous system* , involving the small and large intestine. The enteric intestinal nervous system is a key mediator. It connects the cells lining the gut to the various nerve networks in our spinal cords and, finally, to our brains. This enteric nervous system controls not only the motion of the intestine and the perception of pain, but also the ability of our intestines to secrete various substances involved in digestion via chemicals called neurotransmitters. One of the most important of these seems to be 5-hydroxytryptamine (5-HT), also known as serotonin. Serotonin seems to be particularly important in IBS, and studies indicate that patients with diarrhea-predominant IBS secrete more serotonin after a meal than people without IBS. It is also suggested that this high level of serotonin stimulates increased movement of the intestine. Further studies with PET Positron Emission Tomography scans of the brain indicate that when patients with IBS undergo rectal distention with a balloon, the signals for pain perception actually fail to go to the part of the brain that modulates this kind of pain in people without IBS. It goes instead to an area of the brain that makes them perceive more pain." http://fdhn.healthology.com/focus_article....owel#Who%20Gets


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## kel1059 (Feb 28, 2003)

> quote: MikeNL, why do certain foods produce proinflammatory mediators in IBS patients? I assume the body is seeing those foods as toxic in some way. Have they discovered why this happens?


This is the million dollar question. I wish i knew the answer. I once read that babies who are not breast fed (such as me) can end up with a compromised immune system due to the highly allergenic protein that is found in milk. This may only be one of several factors that can happen. It is not the sole reason because a lot of people were breast fed and they develop lost oral tolerance.


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## bonniei (Jan 25, 2001)

Re: the topic of increased gut permeability. Also to talk about gluten sensitivity(which I have) and something of personal significance to me. I would appreciate all comments even though I realize this is not something you all usually read up on. It seems by Brostoff's medical book that subsets of schizophrenics have increased gut permeability perhaps leading to increased absorption of exorphins. . And there maybe decreased catabolism by genetically deficient enzymes. One scientist proposed that wheat consumption is linked to schizophrenia based on epidemiological reasons like mental illness improves during famine and differences in wheat consuming population and non wheat consuming populations. 10% of schizophrenics underwent remission on gluten free diets by one study. Please comment seriously people.


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## kel1059 (Feb 28, 2003)

> quote: One scientist proposed that wheat consumption is linked to schizophrenia based on epidemiological reasons like mental illness improves during famine and differences in wheat consuming population and non wheat consuming populations


I completely believe this to be true. I experience nervous type disorders when i eat foods that are highly symptom provoking.This is entire issue of lost oral tolerance seems to be completely missed by medical professioals. They do not care if 5 to 15% of schizophrenics could have dramatic symptom reduction based on an altered diet. A psychiatrist can actually become fairly wealthy by treating symptoms instead of getting to the root cause. That may seem cynical but modern medicine too often misses these connections. They deal in drugs and surgery not food --- even if food can cure.


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## bonniei (Jan 25, 2001)

It was scary reading Brostoff's book because now I am seriously considering giving up gluten though without fructose and wheat I am going to be constipated and I haven't found a suitable remedy as yet. Jan had recommended sugar free pectin type fiber to me when I had brought it up a year ago but I was unable to find it.


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## eric (Jul 8, 1999)

Something to ponder."Inflammation Moderator: Robin Spiller MD; Panel: Jackie Wood PhD, Mary Perdue MD, Robin Spiller MD The last few years have led to a greater understanding of the role of inflammation in influencing intestinal hypersensitivity in the functional GI disorders. For example, a well-defined subgroup up to 25% of IBS patients appear to develop their IBS after an infectious illness. Jackie Wood from Ohio State University, discussed how inflammation alters the neurophysiology of the enteric nervous system ENS by activating nerves within the ENS. There are a variety of ENS neurons that can direct responses within the body leading to altered motility, sensation and secretion, and ultimately, symptoms of diarrhea, constipation, and pain. Mary Perdue from McMaster University, Ontario discussed the importance of the epithelial intestinal barrier to maintain immune tolerance to potentially harmful matter, such as bacteria, ingested when we eat or drink. Everything that enters the human body must pass through an epithelial layer. Various types of epithelial tissues line not only the body cavities, blood vessels, and most organs, but also our outer surface-our skin. Within the intestines, epithelial tissue forms an intestinal barrier involved with absorption, secretion, sensation, contractility, and protection. Studies in animal models show that psychological stress can disrupt this barrier, leading to the penetration of bacteria into the gut, inflammation, an immune system response inflammatory cytokines, and ultimately sensitization of neural signals from the gut to the brain that can heighten the perception of pain. Robin Spiller from the University of Notingham, UK brought this basic information to the human model of post-infectious IBS. The predictors of post-infectious IBS include increased life events and psychological distress, female sex, and longer duration of diarrhea episode. In response to bacterial infection, there is an increase in certain gut enterochromaffin secretory cells 5HT producing and inflammatory cells cytokine producing leading to prolongation of pain and diarrheal symptoms, and this may be aggravated by the presence of psychological stressors. These findings suggest ways in which infection-induced inflammation might interact with chronic stress to produce long lasting bowel dysfunction. They also suggest possible treatments that need study. Who is DR WoodJackie D. Wood, Ph.D.Professor, Departments of Physiology and Cell Biology, and Internal MedicineSomething majorally missing here is the neuro immune connections in the debate, you cannot discuss the gut immune system, with out the neuroimmunology as a big part of the picture. http://ngsp.osu.edu/wood.htm Who is Dr SpillerThe leading expert on Post infectious IBS.Bonnie and Kel, why don't you read through these because they will help.4th International Symposium on Functional GI Disorders, 20013rd International Symposium on Functional GI Disorders, 19992nd International Symposium on Functional GI Disorders, 19971st International Symposium on Functional GI Disorders, 1995 http://www.aboutibs.org/Publications/symposium.html#1 Type in "loss of oral tolerence and foods and IBS" into pubmed The national library of medicine, also.


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## lflower (Jun 23, 2003)

OK, here is my profound opinion (two cents worth). I classify this disease as a "modern day" disease. I look at the everything medically in terms of adaptations and natural selection (I like to think of myself as a behavioral evolutionist). For 50 million years (but before agricultural) our bodies were in tune, and designed for getting a lot of excercise and eating very little fat. So with us with IBS, when we get the "fight or flight response", we just sit and stew when we should be fighting or flighting. I think that we are more "flighters". Our gut churns away and tangles itself up. Our body says "don't eat now you fool, run!" It's much easier to run when you've got an empty gut. If you're a "flighter" its easier to run away if your gut is empty. Animals in the wild often deficate before they run off in fear. With some people their response to stress (fight or flight) is to have their blood pressure go way up and FIGHT! That quick burst of energy. To me these people are the michilin-man type A personalities that are really good at comebacks and being in your face. The "flighters" are more the pear shaped bodies that go with the flow, pent it up, stew it, when they should be running! The type B personalities, that tend to procastinate. This is why I promote lots of excercise for this disease, reduce the stress if you can. Cavemen never had to worry about mortgage payments, retirement accounts or their teenager's driving habits or the stock market crashing or terrorism and nuclear war in the news. The only stress caveman had to worry about was "is this animal going to charge at me? If so, should I run, or should I fight? I must decide.. mmmmm.. quick! We've got caveman bodies in a modern world.


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## bonniei (Jan 25, 2001)

I typed in Schizophrenia and Gluten sensitivity in pubmed. I found these two studies which were referred to in Brostoff's book Jenner FA, Vlissides DN. Related Articles, Links Gluten sensitivity in schizophrenia.Br J Psychiatry. 1987 Apr;150:559. No abstract available. PMID: 3664144 [PubMed - indexed for MEDLINE] 2: Sengh MM, Kay SR. Related Articles, Links Gluten sensitivity in schizophrenia.Br J Psychiatry. 1987 Jan;150:130-1. No abstract available. PMID: 3651664 [PubMed - indexed for MEDLINE] The first study was about 10% of schizophrenic patients recovering in a double blind gluten free trial.The second study claimed a pathogenic involvement of gluten in schizophrenia following a blind challenge with gluten after previously excluding both gluten and casein from their diets. I apologize for discussing schizophrenia but I hope you will forgive me as I have been pretty good sticking to the problem of IBS over the years. And think of it as relevant to IBS , as a comorbid condition for some. Also a scientist, Dohan, drew attention to the possible biochemical similarities between schizophrenian and celiac. Hmmm, maybe I should post this in the Celiac forum.I suffer from a delusional disorder and I have recently found I am gluten sensitive so I would so appreciate comments on this topic,eric , flux, Mike


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## bonniei (Jan 25, 2001)

eric, ok let me tie it into this discussion you are trying to have. If schizophrenia which is clearly affected by meds ,which have serotonin and the like, is rare if grain is rare, it is very possible that IBS, a milder disease in terms of the mind, could be linked to food.Is Schizophrenia Rare if Grain is rare?


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## eric (Jul 8, 1999)

I cannot comment on Schizophrenia and Gluten sensitivity. Those abstracts seem to be pretty old though."Some people have suggested that schizophrenia might be made worse, or even caused, by an abnormal sensitivity to gluten. But although a number of studies have been carried out, the precise causes of schizophrenia arenï¿½t clear." http://www.foodstandards.gov.uk/healthiere...luten?version=1 There is this however."The similarities between the two nervous systems may also mean that they are vulnerable to similar toxins and disease processes. For example, in both Parkinson's disease and Alzheimer's, the degenerative processes seen in brain nerve cells are also seen in the neurons of the enteric system."Gut ThoughtsThough few know about it, humans have a second brain that handles most of the body's digestive functions. Study of the enteric nervous system is a rapidly growing specialty, offering insight into malfunctions of the "gut brain" as well as the more complex cranial brain. Digestion is such a prosaic function that most people prefer not to think about it. Fortunately, they don't have to ï¿½ at least not with the brain in their heads. Though few know about it, humans and other animals have a second brain that handles most digestive functions. Deep in your gut lies a complex self-contained nervous system containing more nerve cells than the spinal cord, and indeed more neurons than all the rest of the peripheral nervous system. There are over 100 million nerve cells in the human small intestine alone. Malfunctions of this "gut brain" may be involved in irritable bowel syndrome IBS, a condition that affects an estimated 20 percent of the U.S. population and is believed to be responsible for $8 billion in health care costs alone in the United States each year, according to the International Foundation for Functional Gastrointestinal Disorders. Patients with IBS suffer bouts of chronic diarrhea, constipation, or sometimes both alternately. IBS is the most common diagnosis made by gastroenterologists. The study of the enteric nervous system is a rapidly growing specialty known as neurogastroenterology. "What the gut has to do is extremely complicated," says Michael Gershon, chair of the department of anatomy and cell biology at the Columbia University College of Physicians and Surgeons and author of The Second Brain Harper Perennial, 1999. "If the brain had to control that, it would have to run huge cables and have a huge number of cells devoted solely to that purpose. It makes great evolutionary sense to separate these functions and essentially use a microcomputer that is independent rather than a central processing unit." In fact, researchers believe that the gut brain evolved first ï¿½ because digestion came before locomotion in multicellular creatures. In mammals, the two systems originate near each other in the outer layer of the early embryo. Like many poorly understood organs, the gut brain was discovered by classical anatomists in the 19th century and then ignored. "No one knew what it did," says David Wingate, emeritus professor of gastrointestinal science at Queen Mary, University of London. "When you'd ask what it was for in medical school, they'd say, 'Let's move on.' " In 1899, physiologists studying dogs found that unlike any other reflex, the continuous push of material through the digestive system now called the peristaltic reflex continued when nerves linking the brain to the intestines were cut. By the 1970s, a society for the study of gastrointestinal motility had been set up ï¿½ but how this motility was controlled remained unclear. The vagus nerve, for example, sends some fibers from the brain to the gut; however, it connects directly with only a tiny minority of cells there. In 1965, Gershon published a paper in Science suggesting that serotonin might act as a neurotransmitter in the gut. At the time, acetylcholine and norepinephrine were accepted as transmitters in the peripheral nervous system, but serotonin was seen as a centrally acting transmitter used by some nerves to modulate the action of others. The peripheral nervous system wasn't supposed to use such controls ï¿½ only the brain and spinal cord were believed to process information through "interneurons" such as those containing serotonin. At a meeting of the Society for Neuroscience in 1981, however, Gershon and others marshaled enough data to finally convince skeptics that serotonin was indeed a key transmitter in the gut. In fact, it is now known that 95% of the body's serotonin is used by the gut ï¿½ and the enteric nervous system contains every neurotransmitter and neuromodulator found so far in the brain. "We now know quite a lot about the library of programs run by the gut brain," says Jackie Wood, professor of physiology and cell biology and of internal medicine at Ohio State University. "For example, when the bowel is empty, one particular program runs." Called the migrating motor complex MMC, this involves a series of movements running from the stomach to the end of the small intestine, which is believed to function in keeping the potentially dangerous bacteria stored in the colon from moving upwards rather than out. At least 500 different species of deadly bacteria have been found to inhabit a person's colon at any given time; "traveler's diarrhea" often results when this mix is changed through exposure to new pathogens. If this happens, the gut runs a program designed to expel as much of its contents as quickly as possible ï¿½ unpleasant for the vacationer, but much better than a fatal infection. "Another program involves a flood of serotonin throughout the entire circuit, which produces the digestive pattern that mixes and stirs the contents," says Wood. Because the gut brain is smaller and more accessible than the brain itself, understanding it could offer insights about how to parse the more complex organ. "That idea was what lead me to begin my research when I was a fledgling neuroscientist," says Gershon. "I looked at the brain and found it daunting, and I still do, so I looked for a simpler nervous system to study." He adds, " 'Simple nervous system,' of course, turned out to be an oxymoron." Unlike the cranial brain, however, the gut brain doesn't seem to be conscious ï¿½ or at least, in health, it doesn't impinge much on consciousness. "The gut is not an organ from which you like to receive frequent progress reports," says Gershon. For most digestive processes, no news is good news. The problem in IBS, in fact, may be that the enteric nervous system becomes overly sensitive to normal functioning and reports to the brain when it shouldn't. Or, the brain may overreact to normal bowel signals. Normally, the brain may avoid conscious awareness of most gut activity. But in IBS, says Wingate, one theory is that "the barrier to information being projected into consciousness is lowered." As in many heterogeneous conditions defined by symptoms rather than specific pathology, different subgroups of patients may have different causes or varying levels of contributions by different factors. In some cases, IBS may be an autoimmune problem ï¿½ something like multiple sclerosis of the gut, where immune cells attack nervous tissue. "If you catch it early enough," says Wood, "You can use steroids to treat it in such cases." High doses of steroids shut down immune activity and prevent immune cells from causing harm, but they don't help once damage has been done. The gut is, in fact, a major immune organ, containing more immune cells than the rest of the body combined. The enteric nervous system interacts intimately with the immune system, and can affect mood and behavior by signaling the central nervous system. Further, the gut brain may in fact be the only system that can refuse central signals. Says Gershon, "The gut brain can say no to the big brain, absolutely. In fact, there are nerve fibers that project towards the CNS, and if the bowel doesn't like the message, it can turn it off or cancel it." Indeed, the vagus nerve mostly carries information from the enteric nervous system to the brain ï¿½ for every one message sent by the brain to the gut, about nine are sent in the other direction. And recent research has found that stimulating this nerve can have antidepressant and even learning-enhancing effects ï¿½ so "gut feelings" could genuinely be more than just a metaphor. The similarities between the two nervous systems may also mean that they are vulnerable to similar toxins and disease processes. For example, in both Parkinson's disease and Alzheimer's, the degenerative processes seen in brain nerve cells are also seen in the neurons of the enteric system. This link could also help explain the connection between psychological problems and gut problems ï¿½ and could put to rest the myth that problems such as IBS are simply "neuroses" because they so often occur in people with other psychological disorders. It may be that the real reason that bowel disorders often accompany psychological problems is that both brain and gut neurons are suffering simultaneously ï¿½ in addition to the fact that having to spend a significant portion of one's life attending to bathroom functions is in itself depressing. Simultaneous effects of drugs on both systems also account for the gastrointestinal "side effects" of Prozac and other drugs that act on serotonin metabolism ï¿½ which actually may have more effect on the bowel than on the brain, because serotonin predominates in the bowel and the drug moves through the digestive system before reaching the brain. Fortunately, in most people, the bowel quickly develops tolerance to these drugs, and gastrointestinal side effects usually subside within a few days or weeks of the start of treatment. In fact, low doses of SSRI selective serotonin reuptake inhibitor drugs may actually help patients with IBS. And since different serotonin receptors predominate in the brain and in the gut, new drugs may be developed to affect certain subtypes but not others. "What's exciting," says Wingate, "is getting away from essentially anecdotal ways of categorizing patients by symptoms and being able to study their Problems in a very systematic biological way." http://www.kiwiterapi.dk/whiplash/frames/gutthoughts.htm


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## trbell (Nov 1, 2000)

Bonniei, i don't think anyone reputable would even think of giving you an answer to your question as there are a lot of different kinds of schizophrenia and disagreements about the many kinds of causation. also dignostic criteria are constanty being updated so any research you come up with that's more than a few years old is probably misleading. But if you can post or send me bc a research article (not just the abstract which can be misleading) I'll comment on the research methodology. I realize this doesn't answer your question but it's a complicated question.tom


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## bonniei (Jan 25, 2001)

That abstract was old because the data is old. With westernization that kind of data is hard to produce these days.If you want new abstracts New Abstract 1 of Celiac and schizophrenia 2nd new abstract of Celiac and Schizophrenia IgA antibodiies and schizophrenia While my disorder is under control with serotonin type meds wouldn't it be better to control it through diet? And without the stigma? _edited_ to change 2nd link


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## bonniei (Jan 25, 2001)

tom, I don't have access online to the articles. Like eric said some are old so they aren't available online. I'll see if I can get access to the newer articles but take a look at the abstract and remember I have been found gluten sensitive


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## trbell (Nov 1, 2000)

bonniei, I'd be willing to comment on reaearch but I'd like the whole article. abstracts can lead to misinterpretations and confusions. as for your other comment what can be done through serotonin can sometimes be done through exercise, diet, or therapy as research has shown in depression but your right the problem is a societal one here where we tend to stigmatize the ill?tom


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## kel1059 (Feb 28, 2003)

Bonniei,I believe that you are definitely on the right track. I also, deeply suspect that there is a connection between mental symptoms and gut symptoms. eliminating dozens of foods has helped me to a very large extent. however, I think I may have discovered this too late and now i think there may be some permanent damage. wheat was one of my worst foods and i read that an autoimmune type reaction can take place after years of heavy wheat intake among certain people. I also think that yeast, sugar, grain, dairy, and just about any other food can cause symptoms in people. *This is why i wish eric would quit downplaying the role of food.* Every time he downplays it, he is hurting people who are in this subgroup.


> quote: In some cases, IBS may be an autoimmune problem - something like multiple sclerosis of the gut, where immune cells attack nervous tissue. "If you catch it early enough," says Wood, "You can use steroids to treat it in such cases." High doses of steroids shut down immune activity and prevent immune cells from causing harm, but they don't help once damage has been done. Indeed, the vagus nerve mostly carries information from the enteric nervous system to the brain - for every one message sent by the brain to the gut, about nine are sent in the other direction. And recent research has found that stimulating this nerve can have antidepressant and even learning-enhancing effects This link could also help explain the connection between psychological problems and gut problems


This is one of the better pieces of info that eric has posted. I enjoy reading this kind of material.i really think that the role of serotonin is very important but I think that equal weight should be given to prostaglandins, leukotrienes, cytokines and other mediators.I have a feeling that serotonin is just a "middle player" in all of this. I have read that the immune system (prostaglandins) actually will direct serotonin and control its behavior.However, a possible treatment would be to try and get both systems in balance.


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## kel1059 (Feb 28, 2003)

I am convinced that the Ibsacol is helping me because of its strong role in balancing out the immune system. No other product or method of treatment has given me a greater overall reduction in symptoms than Ibsacol.However, it remains to be seen if Ibsacol will continue to provide relief. Also, it is not a cure-all because when I eat a bad food-- i do get symptoms (just not as bad --and i recover quicker).I believe that eric's dislike and negative attitude towards Ibsacol is either due to the fact that he tried it and it does not work for him or he has not tried it and is just jumping to conclusions. If he did try it and it failed then eric's problem may not be immune related at all. if that is the case then it is easy to see why he ignores the immune system.It is remotely possible that eric is having serious reactions to a number of foods and he is unaware of it or can not fathom the idea of giving up these cherished foods. but maybe not-- who knows.


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## bonniei (Jan 25, 2001)

Tom I found one of those articles online but there is restricted access to it and it is in PDF format so I can't copy and paste and email it to you And take a look at this abstract for genetic infoGenetically similar regions for celiac and schizophrenia kel, I really hope there is this food link. I don't know what to think. For years I lived on bread and tomatoes diet as my staple diet being a vegetarian at home before I developed this disorder.


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## kel1059 (Feb 28, 2003)

> quote: While my disorder is under control with serotonin type meds wouldn't it be better to control it through diet? And without the stigma?


Bonniei,You and I are in the same boat. The things you are talking about fascinate me because I am investigating the same set of phenomena.I wish I knew what portion of this is genetic. I wish I knew exactly how to go about getting treated correctly. I think eric's post mentioned possible steroid treatment and I have wondered about this but i don't like steroids. i have experimented with licorice because it keeps cortisol elevated which decreases inflammation but the results are unpredictable. In other words, the Ibsacol provided far more conclusive results.I am trying very hard to add some herbs such as cat's claw (antiinflammatory) to my regimen but i need to be very careful because i don't want to add too many variables. ....besides, cats claw is suppossed to be immune stimulating (just like astragulus) and astragulus caused severe trouble for me. I am left groping in the dark because modern medicine is so far beyond where they should be in terms of lost oral tolerance and immune regulation in IBS symptoms.


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## kel1059 (Feb 28, 2003)

> quote: For years I lived on bread


Bingo!So did I. I lived off of whole wheat bread and pasta for 2 years. It was after that that I became highly symptomatic.I am guessing that I screwed up my immune system due to the wheat. i think milk played a role as did too much sugar (bacterial and yeast dysbiosis was the icing on the cake).Genetic factors have also contributed.Therefore my concentration needs to be focused on the immune system, prostaglandins, leukotrienes, cytokines etc.


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## bonniei (Jan 25, 2001)

kel, Enterolab does a gene test for Celiac and gluten sensitivity. I am going to pass on this genetic info I found out about schizophrenia and am going to get them a schizo genetic test too. I think if you have the genes which predispose you to such things you develop these illnesses with the wrong type of diet.eric, "Based upon the increased pretest probability of celiac disease, routine performance of serological tests for celiac disease may be useful in this patient population, though additional study is needed in this area. " Abstract saying more celiac testing is recommended for IBS'ers Given this, don't you think you have a responsibility to talk about wheat and Coeliac and gluten sensitivity?


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## kel1059 (Feb 28, 2003)

> quote: In some cases, IBS may be an autoimmune problem - something like multiple sclerosis of the gut, where immune cells attack nervous tissue. "If you catch it early enough," says Wood, "You can use steroids to treat it in such cases." High doses of steroids shut down immune activity and prevent immune cells from causing harm, but they don't help once damage has been done


I need to know more about this.eric, are you aware of any studies that have tested the hypothesis of IBS and curtailing the immune system?I hesitate to ask because I think that since your mind is made up about IBS you won't think it is important or relevant to your model of IBS.by the way, I think it is ridiculous to get "hung up" on such incredibly strict definitions of IBS. It hurts everyone when we focus on a label (IBS) verse symptom sets and patient's complaints.


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## bonniei (Jan 25, 2001)

I agree with kel that it is totally ridiculous to get hung up on such narrow definitions of IBS. eric, do answer the question posed in my earlier post.


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## kel1059 (Feb 28, 2003)

> quote: by the way, I think it is ridiculous to get "hung up" on such incredibly strict definitions of IBS. It hurts everyone when we focus on a label (IBS) verse symptom sets and patient's complaints. I agree with kel that it is totally ridiculous to get hung up on such narrow definitions of IBS


I think that if eric could ever come to accept this then I would have a powerful ally in discovering and digging for relevant info.however, that will never happen because I deeply suspect that there are some fundamental differences between eric's causation and my causation. ----and according to "eric's law" --if your causation is different than eric's then "you don't have IBS".Once again ---there is that awful label that screws everything up.thank god for sane and intelligent people like MNL whom recognizes this.


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## trbell (Nov 1, 2000)

boniei, that's a good lead but remember that they are still finding out a lot about gene mapping as we speak and I remember seeing somewhere they have been doing some now on IBS and they've done a lot of depression which shows IBS is a subtype of depression based on studies of genetic inheritance. I'm not really qualified to comment on the study you mention as far as the content goes but caution you not to read to much into one study. You really need to have about ten studies like this from published sources before you can say anything for sure.I'm sure you and kel have realized that you can "prove" anything by searching for studies or through the web. That's why the combination of articles eric posted is important and why the things (more than one) that Mike has posted on the immune system are important.tom


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## flux (Dec 13, 1998)

> quote:So with us with IBS, when we get the "fight or flight response", we just sit and stew when we should be fighting or flighting. I think that we are more "flighters". Our gut churns away and tangles itself up. Our body says "don't eat now you fool, run!" It's much easier to run when you've got an empty gut. If you're a "flighter" its easier to run away if your gut is empty. Animals in the wild often deficate before they run off in fear.


I don't get it. You want an empty gut whether you run *or* fight.


> quote:eliminating dozens of foods has helped me to a very large extent. however, I think I may have discovered this too late and now i think there may be some permanent damage. wheat was one of my worst foods and i read that an autoimmune type reaction can take place after years of heavy wheat intake among certain people. I also think that yeast, sugar, grain, dairy, and just about any other food can cause symptoms in people. This is why i wish eric would quit downplaying the role of food.


But the role of food in this is to a good degree psychological. It's not the food hurts your gut. It's the brain thinking it does (i.e., lactose intolerance), which can lead to symptoms.


> quote:I need to know more about this.eric, are you aware of any studies that have tested the hypothesis of IBS and curtailing the immune system?.


It wouldn't be relevant for most people with IBS, however. Only rarely does IBS turn into pseudoobstruction, which is what this is referring to.


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## trbell (Nov 1, 2000)

stress apparently curtails the immune system and can lead to some tpes of IBS - read the thread on caretaker stress from yesterday.tom


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## eric (Jul 8, 1999)

Irritable Bowel Syndrome: How far do you go in the Workup? Testing celiac and IBS http://www.romecriteria.org/reading1.html


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## bonniei (Jan 25, 2001)

I think people don't go beyond endoscopy for Celiac. I need to see old posts of yours where you have put this link. Have you posted this link before, eric.? And now there are genes for gluten sensitivity. Did you know that? Not just the expression of HLA-DQ2 alleles DQA1*050/DQB1*0201.Please refer to my EnteroLab test thread in the Products section. I know I for one will improve on a wheat free diet.


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## bonniei (Jan 25, 2001)

> quote:But the role of food in this is to a good degree psychological. It's not the food hurts your gut. It's the brain thinking it does (i.e., lactose intolerance), which can lead to symptoms.


Did you know there is a test for milk sensitivity based on IgA antibodies? What do you think of that? Quite apart from lactose maldigestion (where I have proved to you that that a difference of 2.5 farts/day can mean quite a lot for some), and reaction to fat in milk.


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## trbell (Nov 1, 2000)

The question I would have is do the treatments to improve the immune system in IBS differ from those to improve the immune system in celiac disease?tom


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## bonniei (Jan 25, 2001)

Celiac is treated by gluten free diets. And from what MikeNL says, elimination diets are the way to go for IBS.


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## trbell (Nov 1, 2000)

the immune system seems to control the body's response to foods so if you strengthen the immune system you can deal with foods. Mike's posted abou this and you can ask him.tom


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## kel1059 (Feb 28, 2003)

> quote: the immune system seems to control the body's response to foods so if you strengthen the immune system you can deal with foods. Mike's posted abou this and you can ask him.


Yes, I am hoping that this is the case. In fact i have actually witnessed it. When i was at my sickest level, I was experiencing the most severe symptoms-- chemical sensitivity and other factors. Now that i am getting healthier and healthier I am actually regaining tolerance to some foods. however, anything with mold or yeast continues to cause severe reactions. I wonder if it is more of a case of getting the immune system to straighten out as opposed to making it stronger. I was told by my doctor that i have an extremely strong immune system. It seems to be far too aggressive and it needs to be "modulated" not necessarily strengthened. i think that this is why Ibsacol has been able to help me. It reverses the good/bad prostaglandin ratios among other things.****************************I completely disagree with flux's assertion that the role of food is a psychological issue. at least in my case it is not psychological. I had read about the role of food so many times in the past but I kept dismissing it as not pertaining to me (i was in denial; i could not stand the thought that i would have to give up milk, wheat, and other foods that I had strong cravings for). However, after several years I decided to try the elimination diet and sure enough I was able to identify several troublesome foods. Wheat was a food that gave me some of my most violent cramps. Milk caused bloating so did corn.Once again this shows how screwed up flux can get when it comes to the facts. he makes claims that are sometimes flat out incorrect. If he fails to understand this issue on food after all the good data provided by MNL then it is hopeless that he will ever understand it.However, it does seem that we finally got him to understand the role of yeast hypersensitivity and how fungus can cause a strange "immune reaction" in certain vulnerable people. he has been denying that for years --it was good to see him admit he was wrong. He is very slow but on some things he will come along. ---slow, dense, and irrational but not completely beyond hope.


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## eric (Jul 8, 1999)

Bonnie, yes I have posted that link many times.I am going to say this again for the 1,000,000,000 time.The immune system is governed by the brain and the hpa axis is hard wired to certain areas of the brain that also deal with stress, emotions perceptions and anxiety.If the brain perceieves a threat, like where is a bathroom or will this food triger my IBS or will I have pain again today or can I leave my house or numerous other fight or flight responces we have everyday in life and living with IBS, especially with IBS a chronic pain condition and bowel problems it releases chemicals to the gut in responce to the threat and can cause inflammation without a pathogen."When the brain senses a threat, real or imagined, it sounds the alarm by flooding the body with adrenaline and another hormone called CRF short for corticotropin-releasing factor. "It also can tell what the threat is so it view everything as a threat.The inflammation in IBS is more from previous enteric infection that causes inflammation and then goes away but the brain still sends the chemicals to the gut anyway, even after resolution of the intial problem and that is still causing very minute inflamations, however inflammation is not the entire picture. There is still that fact that serotonin as a signaler and the FACT it intiates peristalsis and receptors in the gut that are *known* not to be functioning right send messages to the brain from the gut. The prefrontal cortex is a big part of this as well in emtions and anxiety as well as the ACC which is a major part of pain processing in the brain where all pain is processed, the brain is also not functioning the way it should be in IBS, like it does in normals. IBSers have different scans then normals or fibro or cfs or IBD ect.."What is irritable bowel syndrome?Irritable bowel syndrome (IBS) is a condition characterised by a mixture of symptoms which are believed to be due to a disorder of intestinal motor function. It is the commonest condition seen by gastroenterologists. The normal gut moves contents along the gut through muscular contractions propulsion, but also has areas of hold-up segmentation. The combination of propulsion and segmentation is called peristalsis, and when it is working normally, one is completely unaware of it. The control of peristalsis is complex and the best way to regard irritable bowel is as a loss of co-ordination of these muscular contractions. In addition, there is evidence that patients with irritable bowel syndrome have increased sensitivity to stimuli arising within the gut." "In addition to the intestinal symptoms, psychological factors are commonly involved. This is not to say that the symptoms are not real they are, but irritable bowel syndrome is often the outcome of a complex interaction between psychological and physical factors.The disorder of gut function can affect the gut anywhere from the mouth to the anus, which accounts for the diversity of symptoms seen in this condition." http://www.netdoctor.co.uk/diseases/facts/irritablecolon.htm "Postenteritis IBSCurrently, another area of major interest in IBS is the prognosis of postenteritis IBS.19 It is now well recognized that up to 1 in 5 cases of IBS will occur after infection, and a low-grade inflammatory process has been documented in some of these cases, although histologically the colonic mucosa is normal.1,19 In a study by Spears and colleagues,20 patients with acute infectious enteritis were administered standardized questionnaires 3 months after infection as part of a repeat evaluation. Although a small study, the investigators observed that 2 patients with IBS 3 months after infection also had depression. In contrast, the remaining 9 patients who did not develop postenteritis IBS were negative for depression on the patient health questionnaire. These results are consistent with the literature, which suggests that psychological factors may identify a vulnerability to the development of postinfectious IBS.1 The latter may in turn reflect disturbed central down-regulation of visceral afferent signals from the gut that may be genetically determined." www.medscape.com/viewarticle/444514Gut Feelings: The Mind-Body Connection Chris WoolstonCONSUMER HEALTH INTERACTIVE Below: ï¿½ Listening to your gut ï¿½ The stress alarm ï¿½ Functional disease in a dysfunctional world ï¿½ Setting your mind on relief If you've ever felt your insides twist in knots before a big speech, you know the stomach listens carefully to the brain. In fact, the entire digestive system is closely tuned to a person's emotions and state of mind, says William E. Whitehead, PhD, a professor of medicine and an adjunct professor of psychology at the University of North Carolina. People with irritable bowel syndrome often suffer flare-ups during times of stress and anxiety, and even perfectly healthy people can worry their way to stomach pain, nausea, diarrhea, constipation, or other problems. Even if a doctor can't find anything physically wrong, the misery is real. In the past -- back when scientists believed the mind and the body operated as separate entities -- some physicians wrote off digestive distress with no sign of organic disease as being "all in the head." But in recent years, that wall has crumbled. Doctors now see intricate links between the nervous system and the digestive system. The two realms constantly exchange streams of chemical and electrical messages, and anything that affects one is likely to affect the other. The connections between the two systems are so tight that scientists often refer to them as one entity: the brain-gut axis. (The brain-gut axis is a hot topic in medicine. In the summer of 2001, more than 100 researchers from around the world gathered in Los Angeles for a convention called "2001: A Brain-Gut Odyssey." For people suffering from persistent digestive troubles unconnected to disease, such research suggests that reducing stress, depression, and anxiety may go a long way toward calming the gut. Listening to your gut It may surprise many people to learn that the gut actually contains as many neurons nerve cells as the spinal cord. In an article in the medical journal Gut, author J. D. Woods and colleagues compare this network -- known as the enteric nervous system, or ENS -- to a "local mini-brain" storing a library of programs for different patterns of gut behavior." Woods and colleagues compare the ENS to a microcomputer with its own independent software, "whereas the brain is like a larger mainframe with extended memory and processing circuits that receive information from and issue commands to the enteric computer."With all these messages, the connection between the brain and the digestive system is a busy two-way street. The central nervous system releases chemicals acetylcholine and adrenaline that tell the stomach when to produce acid, when to churn, and when to rest. Similar signals help guide the movements of the intestines. The digestive system responds by sending electrical messages to the brain, creating such sensations as hunger, fullness, pain, nausea, discomfort, and possibly sadness and joy.As strange as it sounds, our guts just might help shape our moods, says Emeran Mayer, MD, a gastroenterologist and the chairman of the new Mind-Body Collaborative Research Center at the University of California at Los Angeles. Mayer points to the vagus nerve, essentially a large electrical cable that runs between the brain and the digestive system. "Doctors once believed the nerve's main job was controlling acid production in the stomach," Mayer says. "But 95 percent of the fibers go the other direction -- from the gut to the brain."Nobody knows exactly what messages travel along this cable, but scientists have found that stimulating the nerve at different frequencies can cause either anxiety or a strong sense of well being. Perhaps the term "gut feeling" isn't just a figure of speech after all.Mayer suggests another intriguing possibility: Prozac and similar antidepressants may actually work on the gut, not the brain. Drugs known as SSRIs short for selective serotonin reuptake inhibitors ease depression by enhancing levels of serotonin. Most experts assume it's the extra serotonin in the brain that helps improve mood. But 95 percent of the serotonin in the body actually lies within the digestive system. Perhaps, Mayer says, SSRIs do their job by boosting serotonin in the gut and changing the signals along the vagus nerve. The stress alarm Whatever messages may be passing back and forth, they can easily become garbled in times of stress. When the brain senses a threat, real or imagined, it sounds the alarm by flooding the body with adrenaline and another hormone called CRF short for corticotropin-releasing factor. These hormones trigger the "fight or flight" response -- helpful back in the days when humans had to run from lions, but a potential liability when we lose a job or go through a divorce.If you suffer from frequent emotional distress -- perhaps because of extreme stress, depression, or anxiety -- the unrelenting flood of adrenaline and CRF will take a toll on your digestive system. For one thing, the hormones can make the cells in the stomach and intestines extra-sensitive to pain. As a result, normal contractions and movements can become excruciating. The new signals can also disrupt the motion of the intestines, causing bouts of constipation or diarrhea. Functional disease in a dysfunctional world Because of the close connection between the brain and many abdominal disorders, a multinational team of investigators, specialists, and federal research agencies convened in the mid-1980s to develop criteria for diagnosing more than 20 digestive disorders known as "Functional Gastrointestinal Disorders," or FGIDs. A "functional" disease, in this case, means a disturbance in GI function that it isn't related to any injury, infection, or other obvious physical problem. These criteria, which include persistent constipation, diarrhea, bloating, abdominal pain, or irritable bowel syndrome unrelated to diagnosable physical disorder, was recently updated by an international team known as the Rome II Committee, which called for a classification system of these disorders based on clusters of common symptoms.Among the disorders the committee examined is irritable bowel syndrome IBS, a very common and perplexing malady often characterized by painful cramps, bloating, and constipation alternating with diarrhea. If you have "functional" IBS, you may feel that "dysfunctional" is a much more apt term.Emotional distress alone can't cause IBS -- the source of the disorder is still unknown -- but stress or a mood disorder may worsen the symptoms. In fact, few other conditions provide such a clear illustration of the link between the mind and the body. One recent Australian study found that chronic distress -- arising from such traumas as divorce, lawsuits, serious illnesses, or job troubles -- accounted for 97 percent of all changes in IBS symptoms. Interestingly, short-term swings in mood don't seem to have much effect on IBS, which explains why many people still suffer symptoms on relatively calm, relaxing days.In a similar manner, strange messages along the gut-brain axis also seem to be a major cause of "functional" dyspepsia, or indigestion. People with dyspepsia often experience the discomfort of constant ulcer pain without actually having ulcers. Stress definitely makes the symptoms worse, but the effect isn't nearly as dramatic as with irritable bowel syndrome. If adding stress to functional dyspepsia is like throwing woodchips on a fire, combining stress with IBS is like dousing a blaze with gasoline.The influence of the mind on the gut goes beyond functional diseases. For instance, people with Crohn's disease or ulcerative colitis -- two conditions with clearly physical origins -- often suffer flareups during times of emotional stress. And in a recent survey, 68 percent of people with basically healthy digestive systems said stress gives them stomachaches. Setting your mind on relief So what can you do if your mind and your digestive system aren't getting along? One thing you shouldn't do is suffer silently. Ask your doctor if you would be a good candidate for cognitive behavioral therapy, interpersonal therapy, relaxation therapy, or another form of counseling. In several studies, these treatments have been shown to give IBS patients more relief than standard medical therapies. You might even consider hypnosis or self-hypnosis.While rarely used in the United States, hypnosis is a popular -- and apparently effective -- treatment for IBS in Europe, Whitehead says. Preliminary studies suggest it may also help ease functional dyspepsia.It's worth noting that Prozac and other SSRIs may help calm the stomach. Small doses of a tricyclic antidepressant -- too small to affect mood -- can lessen stomach pain, presumably by blocking pain messages.There's another reason to go to the doctor: Simply hearing you're not crazy or gravely ill may be a great source of comfort. "Reassurance from a physician is probably the most effective treatment for IBS," Mayer says.Supportive docs will never go out of style, but even better treatments for IBS and other functional disorders may soon be on the way. Researchers are currently studying medications designed to block the release of CRF, the hormone that helps translate stress into stomach trouble. Mayer says the medication may be available in a little more than a year.But you don't have to wait that long to get better. Do what you can to avoid stress and work closely with your doctor. With a little luck, your gut feelings will be much more pleasant.-- Chris Woolston, M.S., is a health and medical writer with a master's degree in biology. He is a contributing editor at Consumer Health Interactive, and was the staff writer at Hippocrates, a magazine for physicians. He has also covered science issues for Time Inc. Health, WebMD, and the Chronicle of Higher Education. His reporting on occupational health earned him an award from the northern California Society of Professional Journalists.Science & Ideas 4/3/00The wisdom of the gutThose butterflies in your stomach are not just in your mindBy Rachel K. Sobel In 1917, German scientist Paul Trendelenburg huddled over a test tube in his three-story laboratory, prodding a small section of tissue submerged in the body's natural juices. Forced to stay home from the war because of tuberculosis, this budding pharmacologist poured his energies into designing the experiment that would prove what his scientific forefathers had suspected for years. Embedded within the wall of the gut, he would show, was a self-contained, self-regulating nervous system that could function on its own, without the help of the brain or the spinal cord. The gut, in short, had a mind of its own. For reasons that still mystify researchers today, the stunning results of this experiment went into hibernation for nearly half a century and are only now receiving fresh validation. Indeed, no one in medicine paid attention again until a fledgling neurobiologist began touting its clinical value in 1965. "The idea that the gut can be operating its own nervous system was shocking," recalls Michael Gershon, now chair of the department of anatomy and cell biology at Columbia University and author of The Second Brain, a 1998 account of the acceptance of this scientific idea. Since the 1980s, Gershon's colleagues have zealously embraced the notion of "the little brain in the gut," as it's affectionately known. "What Mother Nature had done, rather than packing all of those neurons in the big brain in the skull and sending long lines to the gut, is distribute the microcomputer, the little brain, right along with the gut," says Jackie Wood, a neurobiologist at Ohio State University.Now a full-blown renaissance in neurogastroenterologyï¿½the nine-syllable code word for the study of the nerves entrenched in the lining of the esophagus, stomach, small intestine, and colonï¿½has researchers probing the depths of the digestive nervous system with feverish intensity and surfacing with remarkable insights. This new breed of neuroscientist, 300 strong, and counting, is shaping a novel notion of the gut and deriving innovative ways to treat its ailments. Last month, for example, the first drug ever designed for irritable-bowel syndrome IBS, called Lotronex, arrived in doctors' offices. It's based on this new understanding of the sentient gut and may, in fact, change the way physicians handle this and related disorders.Daily chores. By peeling away the layers of padding that surround the digestive tract, scientists have indeed unearthed some of the buried secrets of the little brain. This miniature central processing unit, whose 100 million-plus nerves number more than those in the spinal cord, carries out many of its daily chores without guidance from the brain. "Suppose the gut gets a message that the pressure is up in the stomach. The brain doesn't get its hands dirty with that kind of nonsenseï¿½so the gut takes care of it," explains Gershon. Not only does the gut direct its own show, he adds, but its spidery projections trickle into neighboring organs, commanding the pancreas and gallbladder to aid with digestion.Though able to run itself, the little brain does stay in close touch with the big brain via 1,000 or so nerve fibers. Scientists studying this relationship have discovered that the gut-brain connection is at the heart of some of the most visceral human emotions. A "gut feeling," for example, isn't just a poetic conceit used to convey intuition. It arises from the biological interplay between these two intimately connected brains, says Emeran Mayer, a gastroenterologist and professor of physiology at the University of California-Los Angeles. When faced with an anxiety-ridden situation, the big brain sends urgent messages to the little brain, which begins orchestrating a physical response, read as gurgling or "butterflies" in the stomach. These sensations are recorded in an "emotional memory bank" residing in the big brain, says Mayer, and the next time the big brain makes a decision in a similar situation, it's not based on some intellectual calculation. Rather, it's instantaneously formulated from this catalog of previous bodily responsesï¿½"gut feelings"ï¿½stored in the brain. Why some people feel the burden of stress in their gutï¿½and not for instance, in their heartï¿½can also be explained by the close communication between the brain and the gut. When the big brain consciously perceives a stressful situation, it calls on its fraternal twin through specialized cellsï¿½called mast cellsï¿½embedded in the gut's lining. These mast cells secrete a chemical called histamine, which activates the nerves controlling the gut, telling the muscles to contract. Hence, the cramps and bathroom trips so often associated with bouts of stress.The complex circuitry in the gut not only operates like a brain; it looks uncannily similar to one, too. Just like the nerves in the brain and spinal cord, those in the gut are naked, lacking an insulating sheath that wraps around the rest of the body's nerves. Swishing among the gut's nerves are serotonin, nitric oxide, carbon monoxide, and at least 30 other neurochemicalsï¿½the same ones sloshing around in the skull. Curiously enough, as healthy brains in the head and gut resemble each other, so too do diseased ones. Scientists have found that some Alzheimer's and Parkinson's patients accumulate the same type of tissue damage in their bowels as they do in their skulls, raising the possibility that these disorders might someday be diagnosed by routine rectal biopsy.No-brainer. The fact that the two brains share so much of the same biology can explain why psychiatric medications have side effects in the gut. Antidepressants like Prozac, for instance, increase the presence of serotonin in the spaces where nerves talk to each other in both brains. While this neurochemical shift settles the big brain emotionally, it causes the gut to squirm, leading to side effects like abdominal cramping and diarrhea. Many investigators are taking their cues in treating gut disorders from drugs that have worked on the brain. For example, Michael Camilleri, a gastroenterologist at the Mayo Clinic, is treating a variety of gastrointestinal disorders with Clonidine, a drug sometimes used in psychiatry. Another medication called Imitrex, customarily used to soothe the pangs of migraine headaches, has effectively healed the gut in two studies by Belgian teams. And Lotronex, the recently released treatment for irritable-bowel syndrome, came from an anti-anxiety drug. If the arrival of Lotronex signals a new era in treatment, it also goes a long way in debunking the popular notion that IBS is "all in the head." Though IBS is a relatively common disorder, affecting as many as 1 in 5 people, it is difficult to diagnose with conventional methods. The chronic abdominal pain, discomfort, and irregular bowel movements leave no trace in the lining of the gut because such abnormalities presumably occur at the level of the nerves tucked inside the gut. This lack of physiological evidence has led many doctors to dismiss patients' complaints as psychosomatic. It's now hypothesized that the nerves lining the gut are oversensitive and overreact to gas and food passing by, thus causing pain and cramping. "Lotronex suggests that there is a mechanism that is malfunctioning either in the big brain or the little brain, or both, or someplace in between," says Wood. "IBS is not imagined." http://www.ibsgroup.org/other/usnews000403.htm "When the big brain consciously perceives a stressful situation, it calls on its fraternal twin through specialized cellsï¿½called mast cellsï¿½embedded in the gut's lining. These mast cells secrete a chemical called histamine, which activates the nerves controlling the gut, telling the muscles to contract. Hence, the cramps and bathroom trips so often associated with bouts of stress."This is tied into the immune system and IBS and foods.Think about this long and hard, because its very important even to foods!!!Peripheral Inflammatory Response Enhanced In Post-Gastroenteritis Irritable Bowel SyndromeA DGReview of :"Increased rectal mucosal expression of interleukin 1beta in recently acquired post-infectious irritable bowel syndrome"Gut03/21/2003By Elda HauschildtPatients with acute gastroenteritis who develop irritable bowel syndrome IBS have an enhanced peripheral inflammatory response in comparison with infected patients who do not develop IBS.An international team of researchers from Singapore, Canada and the United Kingdom say that the observed higher expression of interleukin-1beta IL-1beta messenger RNA mRNA is in keeping with clinical observations that patients with more severe infective gastroenteritis are more likely to develop post-infectious IBS PI-IBS. At the same time, the response contrasts with previous work that suggested behavioural factors predicted the development of PI-IBS, say the investigators, led by Dr. K-A. Gee of National University Hospital in Singapore.The pathways may not be mutually exclusive, say the researchers: "On the contrary, there is growing evidence that behavioural and peripheral inflammatory processes converge to influence disease expression, and supporting examples are available in animal-based studies."Approximately 25% of patients with infectious diarrhoea develop chronic bowel disturbances that resemble IBS, they explain. Expressions of IL-1beta and its receptor antagonist IL-1ra were measured in eight patients who developed PI-IBS and in seven patients who did not. The aim was to see if an inflammatory process underpins the pathogenesis of PI-IBS. A group of 18 healthy volunteers who had not had acute gastroenteritis in the previous two years acted as normal controls.Sequential rectal biopsy samples were taken during and three months after acute gastroenteritis. Reverse transcriptase-polymerase chain reaction was used to assay IL-1beta and IL-1ra gene expressions. The level of expression was quantified by optical densitometry.PI-IBS patients had significantly greater expression of IL-1beta mRNA than did patients who returned to normal bowel habits aster infection. As well, increases in IL-1beta mRNA was seen in the PI-IBS patients three months post-infection.Patients who did not develop PI-IBS did not have significantly different IL-1beta mRNA expression from healthy controls at three months. Patients who developed PI-IBS did.There were no significant changes in IL-1ra expression in any of the three groups at three months, the investigators note. Gut 2003;52:4:523-526. "Increased rectal mucosal expression of interleukin 1beta in recently acquired post-infectious irritable bowel syndrome"


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## eric (Jul 8, 1999)

Mike and the Full-thickness biopsy of the jejunum reveals inflammation and enteric *neuropathy* in irritable bowel syndrome.Full-thickness biopsy of the jejunum reveals inflammation and enteric neuropathy in irritable bowel syndrome.Tornblom H, Lindberg G, Nyberg B, Veress B.Karolinska Institutet Department of Medicine, Huddinge University Hospital, Stockholm, Sweden. hans.tornblom###gastro.hs.sll.seBACKGROUND & AIMS: Irritable bowel syndrome IBS is regarded as a functional bowel disorder. Few studies have looked for histopathologic changes in the gut and only then in biopsy specimens from intestinal mucosa. Because bowel function is governed mainly by nerve plexuses in the bowel wall, we have investigated full-thickness bowel biopsy specimens in patients with severe IBS. METHODS: We used a laparoscopy-assisted technique to obtain full-thickness biopsy specimens from the proximal jejunum. Tissue specimens were investigated with light microscopy using routine stainings and immunohistochemical techniques. Horizontal sectioning was done to visualize large areas of the myenteric plexus. Fifteen autopsy specimens were used as controls regarding the myenteric plexus. Colorectal adenoma controls with terminal ileum biopsy specimens and full-thickness jejunal biopsy specimens from patients with degenerative enteric neuropathy were used as control groups for intraepithelial lymphocyte counts. RESULTS: Ten patients 2 males, 8 females were studied. In 9 patients, we found low-grade infiltration of lymphocytes in the myenteric plexus. Lymphocytes had peri- and intraganglionic location. The mean number of lymphocytes per ganglion ranged from 1.9 to 7.1 per patient, with an overall mean of 3.4. No intraganglionic lymphocytes were found in the control group and only a few periganglionic lymphocytes mean, 0.2. Four patients had concomitant intraepithelial lymphocytosis. Neuron degeneration was evident in 6 of 9 patients with and 1 patient without ganglionic lymphocyte infiltration. CONCLUSIONS: Our findings indicate that inflammation and neuronal degeneration in the myenteric plexus are involved in the pathogenesis of IBS.PMID: 12454854Neuropathology of IBS?Robin C. Spiller The irritable bowel syndrome IBS is currently diagnosed on the basis of a characteristic cluster of symptoms in the absence of objective abnormalities of structure. This lack of objective measures has considerably hampered further understanding of IBS because it forces us to lump together patients whose widely differing symptoms suggest differing underlying pathologies. Several investigators have attempted to develop more objective tests by which to categorize patients, including measurement of intestinal transit,1,2 colonic,3,4 and small bowl motility,5,6 as well as threshold for discomfort during rectal balloon distention.7 Although differences have been shown between IBS patients and healthy controls, these tests have not been adopted into routine practice because they are either poorly reproducible or impractical. By contrast, psychological measures of anxiety, hypochondriasis, and concern about the meaning of symptoms are easy to use and have shown much greater consistency since, with a nonfatal condition like IBS, they are the main determinants of whether an individual with symptoms ever sees a doctor. This has led to the perception that psychological factors predominate, when in reality it simply reflects the crudeness of the tools we have available to detect other factors such as disorders of the enteric nervous system. The study in the current issue of GASTROENTEROLOGY by Tornblom et al.8 is a valiant attempt to redress this imbalance. *The study is somewhat audacious in obtaining full-thickness small bowel biopsy specimens in 10 cases of disabling IBS. Patients had already undergone a full work up including small intestinal manometry with inconclusive results. * The biopsy specimen provided the unique opportunity to examine changes in the myenteric plexus, an area inaccessible to mucosal biopsy, yet critical to controlling small bowel motility. *Three of these IBS patients were diarrhea-predominant, 2 of which had a clear postinfectious onset of their symptoms; the remainder were described as having alternating * 5 or constipated 2 bowel habit. The main findings were that all patients had some neural degeneration in the ganglia of the myenteric plexus, associated in 9 of 10 with an infiltrate of CD3-positive T lymphocytes, which were not seen in the control autopsy specimens. The authors also reported longitude muscle hypertrophy in all, although the numerical data were not provided. Four cases were reported to have increased numbers of interstitial cells of Cajal and 2 had decreased numbers focally around the myenteric plexus, but again, the numerical values are not given. Intraepithelial lymphocyte IEL counts were above their upper limit of normal 26/100 epithelial cells in 4 of 10 cases. They argue that inflammatory damage to the neural structures leads to dysmotility and secondary longitude muscle hypertrophy. *The raised IELs suggested to the authors that in some subjects the inflammation was driven by luminal factors, but this was not found in 6, suggesting that even within this extreme group there remain important differences in underlying mechanisms.* *Plainly, it is impossible to relate the observed pathology to other factors like symptoms, concomitant drugs, or diseases because the numbers are so small. This must therefore be regarded as a pilot study that needs repeating with much larger numbers* . *Although undoubtedly important, we should be cautious before accepting these findings at face value. * The use of autopsy controls, as a comparison for a laparoscopically obtained small bowel, raises several concerns. Although the patients studied had a mean age of 40 years range, 23ï¿½57, autopsy material might be expected to come from a much older age group, but this is not specified in the report. Older people have fewer mucosal-associated lymphocytes and a decreased response to infection, which might account for some of the differences. Furthermore, autolysis of autopsy material may well have reduced the ability to detect the subtle changes reported. A further important difference between the patients and autopsy controls is the manipulation of the small bowel through the tiny incision used in laparoscopy. Whether this could induce inflammation within the myenteric plexus is unknown, but in animals, merely handling the bowel activates macrophages within a matter of hours.9 A final issue is the wisdom of scoring the ganglia with the most lymphocytes. This introduces an unknown effect because most other studies use random sampling to ensure a fair representation of the whole tissue. Since the pathologist who scored the biopsies was blinded as to the clinical details, this would not account for the finding of a difference between IBS and controls, but it might have the effect of exaggerating any difference. If we accept the validity of the findings, then what are the implications? If some cases of severe IBS are caused by inflammatory damage to the enteric nervous system, this could arise by several mechanisms. The most common precipitant is likely to be a bacterial infection damaging the mucosa, activating the immune response, and indirectly damaging the myenteric plexus. Alternatives include direct damage by neurotropic viruses10 such as Herpes zoster, Epstein-Barr virus, cytomegalovirus, or an autoimmune attack initiated by exposure to cross-reacting antigens. Of course, inflammatory bowel disease is associated with neural damage including nerve trunk hypertrophy,11 alteration in neuropeptide profile,12,13 and receptor expression14; however, these cases are unlikely to be confused with IBS. IBS can certainly begin acutely after bacterial enteritis15,16-18 and symptoms can persist for at least 6 years.19 The changes in mucosal histology have been described in some detail20 following Campylobacter infection, which has the highest incidence of postinfectious IBS.17 An acute increase in lamina propria CD3-positive lymphocytes, IELs, and serotonin-containing enteroendocrine cells were described together with an influx of activated macrophages. Simultaneously, a decrease in neural staining with PGP9.5 was observed,21 suggesting an acute damage to mucosal nerves. These human studies used mucosal biopsy specimens and so were unable to examine changes in the myenteric plexus. However, in experimental animals, a chemically induced colitis induces infiltration of the myenteric plexus with eosinophils within 6 hours,22 whereas the mild trauma induced by rubbing the colon with a cotton wool wad activates macrophages within 3 hours.9 It also induces the production of the intracellular adhesion molecule ICAM-1, recruits circulating blood monocytes, and induces epithelial cells to produce cytokines, particularly interleukin IL-8. Inflammatory cells and altered permeability allows access of colonic bacterial products, especially endotoxin, which induces secondary responses including IL-1 production by glial cells surrounding afferent nerve terminals.23 These experimental data make it quite plausible that an acute bacterial enteritis might initiate an inflammatory response in the myenteric plexus. Why this might continue for months and years is unclear but may relate to either continued exposure to antigen or genetic differences in immunoregulation. Thus, high producers of IL-10, an anti-inflammatory cytokine, are less likely to develop IBS, suggesting that down-regulation of inflammatory response might be protective.24 This would also fit with the reduced risk of developing postinfective IBS in those aged >65 years17 in whom immune responsiveness is reduced. Autoimmune damage to peripheral and autonomic nerves25 can develop after bacterial infection if the organism has a cross-reacting antigen such as Campylobacter, whose lipopolysaccharide26 mimics the GM1 ganglioside found on peripheral nerves. Whether a lesser form of this response might explain the postinfectious IBS following Campylobacter or other infections is unknown. Viral-induced injury is of a different nature because viral gastroenteritis usually heals with little residual inflammatory injury to the gut mucosa. However, neurotropic viruses can easily enter enteric nerves without significant mucosal damage. One such virus, Herpes zoster, has been associated with damage to the myenteric plexus and the development of pseudo-obstruction in immunocompromised patients.27 Other investigators have found evidence of residual viral DNA in the myenteric plexus and lamina propria in patients with chronic idiopathic pseudo-obstruction.10 The viruses included cytomegalovirus and the Epstein-Barr virus. The latter has also been associated with an acute cholinergic dysautonomia and marked gastrointestinal dysfunction, although in this case the colonic myenteric plexus was normal.28 Cytomegalovirus infection after liver transplantation has been shown to be associated with chronic gastrointestinal symptoms, including delayed gastric emptying,29 and the same infection in an immunocompromised host has also been associated with delayed gastric emptying and disordered small bowel manometry.30 Ganglionitis, or inflammation limited to the myenteric plexus as reported in the present paper,8 has been associated with pseudo-obstruction that can be paraneoplastic, autoimmune, or idiopathic in origin. The mechanism in some cases of paraneoplastic syndrome associated with small cell lung cancer appears to be a neoantigen, the Hu protein expressed in the cancer, which induces an immunological reaction antibodies and cytotoxic T cells that cross-reacts with and damages the myenteric plexus. Antineuronal antibodies cross-reacting with the Hu antigen have also been reported in autoimmune diseases such as Sjï¿½rgren's syndrome and are associated with intestinal dysmotility.31 These immunoglobulin G antibodies have been shown to passively transfer motility disturbances when injected into immunosuppressed rats.32 Similarly, antibodies cross-reacting with myenteric nerves have been observed in achalsia.33 Of special relevance to the present study, chronic ganglionitis has been reported in a number of patients without cancer or autoimmune disease34-36 with severe intestinal dysmotility, 2 of whom had autoantibodies cross-reacting with the same Hu antigen.34 Three of these patients with severe pseudo-obstruction34,36 and 1 with intractable vomiting35 were responsive to immunosuppressive therapy. This chance of reversing what would otherwise be a lifelong disability makes identifying such cases potentially very important. Cases of pseudo-obstruction are unlikely to be confused with IBS, but they could represent a tip of the iceberg, and it is possible that there are many less severe cases of ganglionitis who never undergo small bowel biopsy and who are currently diagnosed as IBS. It is important to note that the histological picture may depend on when the biopsy specimen is taken. *Both Smith et al.34 and Di Giorgio et al.36 found that obvious ganglionitis was replaced by a picture of aganglionosis without any evidence of the previous inflammation when the biopsy was repeated some years later. Because the IBS patients reported by Tornblom et al.8 had put up with symptoms for many years before having biopsies performed, evidence of the initiating inflammation may well have subsided, possibly accounting for the low-grade inflammation observed. This is analogous to insulin-dependent diabetes mellitus, in which the clearest evidence of inflammation, both histological and serological (anti-islet antibodies), is seen early on but fades with time. Increased apoptosis is another mechanism that might account for ganglion cell loss without inflammation, and decreased expression of the antiapoptotic proto-oncogene bcl-2 has been found in some such cases,37 although the significance of this finding is unclear. * The authors' idea that neurological dysfunction leads to functional obstruction and subsequent muscular hypertrophy is interesting, but equally, cytokines and growth factors induced by tissue damage may well be responsible because these changes are seen in many different models of experimental inflammation.38,39 The increase in IELs has parallels with other studies recently published.20,40 While clearly it can be a residue of previous infection,20 it could also be part of an allergic response to luminal antigen as is seen in celiac disease. Determining exactly what these cells are reacting to would be most informative. It is clear that this study is preliminary and needs repeating. Furthermore, it only considers very severe examples of IBS and may only be relevant for a tiny minority. However, it is important because it suggests that there may be a small subgroup of IBS patients who might respond to anti-inflammatory treatment. Furthermore, it adds increasing weight to the argument that in IBS, both central and peripheral components need careful consideration. Previous disappointment in attempts to show disordered gut function has led to the current emphasis on central components, particularly the emotional reaction to visceral stimuli, which are undoubtedly important. However, the pendulum may have swung too far in that direction, something the current study should help to correct. http://www2.us.elsevierhealth.com/scripts/...16508502004857&


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## eric (Jul 8, 1999)

It should be noted again what those patients symptoms were since they did not all have d IBS."Three of these IBS patients were diarrhea-predominant, 2 of which had a clear postinfectious onset of their symptoms; the remainder were described as having alternating 5 or constipated 2 bowel habit. "Only three did.


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## eric (Jul 8, 1999)

And just for the information. Just one more reason for HT in IBS or any relaxation techniques for that matter, but still not the only reason HT works on IBS, there are many many others. Relaxation itself gives your body time to heal, lowers anxiety , reduces muscle tension and has many other very practical benefits in IBS as well as good health.







*Self-Hypnosis Can Cut Stress and Boost Your Immune System* A number of studies have suggested stress can hinder the body's immune system defenses. Now researchers say people may be able to fight back with the stress-relieving techniques of self-hypnosis.In a study of medical students under exam-time stress, investigators found that those who received "hypnotic-relaxation training" did not show the same reduction in key immune system components that their untrained counterparts did.The researchers looked at 33 medical and dental students during relatively low-stress periods and around the time of the first major exam of the term. Half of the students attended sessions where they learned to relax through self-hypnosis.The investigators found that during exam time, the self-hypnosis students launched stronger immune responses compared with students who did not learn the technique. And the more often students practiced the relaxation strategy, the stronger their immune response.In previous studies, the researchers found that stressful times may impair the body's wound-healing process and response to vaccination. They and other researchers have also found that relaxation techniques may combat these effects by relieving stress and boosting the immune system.The data from this study provide encouraging evidence that interventions may reduce the immunological dysregulation associated with acute stressors.Journal of Consulting and Clinical Psychology 2001;69


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## eric (Jul 8, 1999)

Also by the way, in responce to Bonnie and Kel and their comments to me on foods. I am more concerned first for IBSers not eating period and malnutrition and food phobias in IBS and a better rounded approach to understanding foods in IBS first. Which is very hard when any food information on this bb is regarded in IBS as loss of oral tolerence to them, instead of the trigger foods they know effect the gut function and the altered gastro colonic responce, which is seriously downplayed here, by people who want others to believe there d is caused only by loss of oral tolerence to foods in IBS and that is not the case. The gut-brain axis is already not working right and foods and stress can set it off and they do not know the cause of IBS yet or do they have a biological marker for it.


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## kel1059 (Feb 28, 2003)

> quote: PMID: 12454854Neuropathology of IBS?Robin C. Spiller Thus, high producers of IL-10, an anti-inflammatory cytokine, are less likely to develop IBS, suggesting that down-regulation of inflammatory response might be protective.24 This would also fit with the reduced risk of developing postinfective IBS in those aged >65 years17 in whom immune responsiveness is reduced. However, it is important because it suggests that there may be a small subgroup of IBS patients who might respond to anti-inflammatory treatment


Eric,the last abstract that you posted is brilliant--- i hope you keep posting it. i don't agree with your view of things but you do come up with a few good abstracts. I am ecstatic that these clowns are finally finding hardcore evidence of physical differences between IBSers and normal people. This will not only lead to more treatment options such as the use of immunomodulators (Ibsacol --for some people) but it also will let these doctors know that we are not crazy. THERE REALLY ARE PHYSICAL DIFFERENCES IN THE NERVE PLEXUS.However, I am still firmly convinced that foods like wheat, corn, fungus, cow's milk, ..... can cause a lot of the immune response such as eosinophils.......You even stated that IBS can be caused by a shock to digestion. that can be bacterial or food related among several possible causes.Yours was bacterial, and then all the antibiotics worsened your problems and then you ended up with a fungal problem. You are probably experiencing a strange "immune reaction" to the fungus in your gut. we all have it in us.anyway, I am convinced that some of this lymphocytic/ ganglion activity is due to bacterial overgrowth, eating junk food, allowing yeast to over grow, wheat or dairy or corn allergy/intolerance, antibiotic or other drug toxicity, and many other factors.Food plays a very strong role for some of us.


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## bonniei (Jan 25, 2001)

eric, what is your point? You are surely not saying that people with Celiac(which is proving to be an immunological disease) as well as Crohn's will get cured with hypnotherapy?


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## bonniei (Jan 25, 2001)

eric, as far as malnutrition goes, I think people might naturally avoid veggies fruits, milk or and wheat because they instinctively know they are a problem without all the fancy tests. I think a better way of communicating needs to be developed. And what is your solution to the problem of malnutrition? Ignore food problems and eat healthy. Well if you eat wheat and have the gene for Celiac, you could develop Celiac. If you are yeast sensitive and load up on yeast you could develop Crohn's. I don't see you addressing these questions.


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## Mike NoLomotil (Jun 6, 2000)

I can see everyone had an amusing time engaging in the usual and customary repartee' over the holiday.Suddenly, the barbecue grill whose leg broke in the middle of cooking an array of 100% oligoantigenic foods for my brood, spewing tasty burgers and sauce-slathered demised chicken parts all over the tiled floor of the screened patio seems like the experience I would rather relive than slogging through this thread.But what is past is indeed past...and at least the kids did not step in a pile of red ants this year during the fireworks display like last year.Speaking of fireworks, I tried but I just cannot bring myself to waste any more bandwidth on debates about that which cannot be debated, as we cannot debate facts, only whether we choose to accept them or not.There are, I see, a couple of very key statements or questions set forth by the less emotionally-invested participants in this wondrously wandering thread, which do lead me to what should be characterized as my fundamental point...the foundation of everything I try to convey to ï¿½Les Miserablesï¿½ who suffer symptoms of what their doctors have elected to tell them is so called Irritable Bowel Syndrome.I was first struck with interest by Bonnie, who stuck her neck out and asked this question.... _______________________________________"MikeNL, why do certain foods produce proinflammatory mediators in IBS patients? I assume the body is seeing those foods as toxic in some way. Have they discovered why this happens? It is too bad foods have to be eliminated from the diet. That is no way to live" ________________________________________As I was about to begin the answer of ï¿½yesï¿½.ï¿½ and explain further what I laid out briefly in my previous post, I stopped to gather any more questions that might be there. I started wandering down again through another morass of attempts to rationalize and justify some persistent selective and biased reasoning plus the selective use of references to support an argument, or assertion, rather than an attempt to convey an objective desire to help sick people get better. Sigh for the sick.







But just before clicking-out without answering any more at all with a sense of ï¿½why bother with a stoneï¿½ I reminded myself that there is fruit among the stones here and retraced my steps.This is because I was struck by this statement from Tom, among several others he made which were also very appropriate: ________________________________"The interesting thing is that therapy and hypnosis can change serotonin levels probably through the immune system and can do the same for asthma again through the immune system although no psychologist who knows anything will tell you it's the only thing." ______________________________________You know, if the ALL the reader(s) and writers of reputed credibility, and those experts-of-choice from whom they derive their opinions, on all sides of the IBS milieu could only step back, set aside all biases, personal agendas, belief systems, selection or biases as applied to their personal rankings of data as "important and pertinent" or not important and not pertinent" and consider the following, maybe we could all get past certain barriers to understanding I will try mightily reduce it to (3) key things, FACTS, that any healthcare researcher or provider or any person seeking to act in the capacity of one (disclaimers to the contrary, you are what you act like not what you say you are) MUST ACCEPT to be able to view all perspectives of the subject for which this entire community was created...advance the understanding and self-help of people suffering from a particular set of symptoms which are used to define a SYNDROME arbitrarily called (latest name) Irritable Bowel Syndrome. Think these things through carefully.1. Based solely upon the assignment of the diagnosis of IBS by various doctors of all kinds to their patients, and extrapolations from that population of what the possibly affected population in the USA is, nobody has any clue whatsoever as to exactly how many people suffer the symptoms we call IBS...but it is SWAG'ed at anywhere from 15% to 25% of the population depending upon whose SWAG you want to believe. A greater % seems to either be affected, or perhaps just emerges, each year.2. In spite of the fact that IBS is defined by ï¿½opinion leadersï¿½ as a SYMPTOM BASED diagnosis, and published diagnostic guidelines exist for symptom based diagnosis, and several protocols of differential (exclusionary) diagnosis exist, surveys have shown that (again pick one) as many as 80% of physicians rendering IBS diagnosis do not FOLLOW the published guidelines and protocols when rendering the diagnosis of IBS. It is also estimated that (again depends who you talk to) only 20-25% of physicians rendering IBS diagnosis are even familiar with those protocols and standards. You can find these estimates in several places.3. The best way to express the third point is to quote a section of a good tutorial, you can read the whole thing on line I will give you the link, which establishes the key concept that is at the root of most pointless debate that is perpetuated about IBS, both here and in the HIGH PLACES one can be shat-upon from, where The Opinion Leaders Of Different Medical Specialties Dwell On High.I will BREAK it DOWN for emphasisï¿½_________________________________"ï¿½It should not be surprising that the nervous system and the immune system function in close relation. The immune system functions as an internal sensory network of sorts. The reciprocal communications and interactions among the endocrine, nervous, and immune systems maintain homeostasis. The CNS may interact with the immune system via the HPA and through peripheral innervation of the lymphopoietic organs, and through the release of neurotransmitters into the blood. Of these three potential mechanisms, the HPA axis appears the most influential pathway for CNS effects on the immune system. The HPA axis has well described inputs as mentioned above. The reciprocal communication from the immune system may be in the form of immunoglobins, lymphokines, or other molecular mediators which may cross the blood-brain-barrier. ï¿½ http://www.uams.edu/m2004/Behavioral%20Sci...ress%20text.htm from Biology of StressTim Kimbrell, M.D.University of Arkansas School of Medicine ______________________________This must alllllll be accepted as fact because it is. These facts MUST be taken into account whenever assessing the possible or actual mechanisms of symptom generation in the symptom-defined Syndrome of IBS. Medicine is not like picking a religion, where a person selects the philosophy and its supporting scriptural basis that pleases him or her to the exclusion of allll else as heresy and devils'-work. You have to accept all the facts, the whole magilla, or your position henceforth is intrinsically flawed and as such lacks veracity. It does not matter if you are Jose Fufufnee, floor polisher, or Medical Director of the AMA. The same rules apply to reality for both people.These body systems are 100% integrated and co and cross dependent and influential. The integrated system does not only function in one direction, thus justifying a hypothesis of the CNS and HPA being responsible for all abnormal gut function and immune function and all such dysfunctions being interpreted only in the context of how stress may effect the function of those organs. That is as foolhardy as the opposite view would be if held.Again note: ____________________________ï¿½The reciprocal communication from the immune system may be in the form of immunoglobins, lymphokines, or other molecular mediators which may cross the blood-brain-barrier. ï¿½ __________________________In kind, to maintain homeostasis, the complex elements of the immune system communicate with and modulate the function of the CNS, HPA, and all other organs systems as well, not just the GI tract or the pulmonary system.The biggest barrier to coming to an understanding of the problems suffered by millions of people diagnosed with IBS based upon ALL MANNER of degrees of diligence in ruling out other conditions before deciding to assign a label of IBS to the patient is the failure to acknowledge these (3) facts AS the FACTS they are.There is ample evidence which suggests that patients suffer symptomology interpreted as IBS due to dysfunction of the gatroneuroimmunoexoendocrine system which may originate at some point or points on the neurologic side and may even have a basis in prior history of stress related events (from child abuse victimology to neuroses) and symptoms may be the result of a primary dysfunction of this type, including altered overall gut response, sensory response and even immunoendocrine response.On the other hand, the problems the patient presents have also been shown to at times originate on the immunologic side of the system, current understanding of those mechanisms so far is sufficient to demonstrate that allergy in the classic sense can be ruled out yet loss of oral tolerance (or what is now being called by some ï¿½intestinal allergyï¿½ or ï¿½enteric allergyï¿½ or some other such term du jour for the moment) and it is clearly a primary mechanism. The psychosocial consequences of living with symptoms induced by these mechanisms up to and including behavioral and CNS changes can be a consequence of chronic local and systemic inflammatogenic activity, and amplification of dysfunction, thus symptoms, occurs as a consequence.If you look at the diagrams in the above tutorial, esp. the one describing adaptive responses to stress via the HPA, and take note of ALL the myriad codependent systems, maybe one can visualize the complexity of the physiologic loops in question. On the other hand maybe ones scotomas will not allow one to. Ok, so what, that does not change the facts.So in summary, to dogmatically adhere to ANY proposition which commands that ï¿½What is IBSï¿½ be restricted to anyoneï¿½s specific definition here or elsewhere is a fundamentally unsound proposition. For the first reason, IBS subpopulations can now be seen to be defined by the presence (diarrheics) or absence (constipators) of an aberrant inflammatory response in the small bowel, it is clear that there are pathologies which differentiate supopulations. The pathogenesis needs to be further pursued.Second, to presume that everyone diagnosed with IBS and who comes either here or to your daughters wedding or to the bar stool next to you professing to have been diagnosed IBS fits some specific diagnostic definition or protocol is preposterous as it is common knowledge among the well informed that they do not, based on how IBS is diagnosed IN THE REAL WORLD of primary and specialty medical care.If a person cannot grasp these fundamental truths and accept them into their belief set, and then study, learn, advise, correspond and discourse in accordance with those realities one cannot contribute effectively to science and medicine. Nor to the sick public eventually coming to a real comprehension of all the different reasons people get the symptoms they get which their doctors diagnoses as IBS then sent then on their way with a prescription, a fiber-change diet, and a CYA-type laundry list of foods a mile long to try and guess at which ones are safe to eat and which ones are not.This is not only true on our side of the equationï¿½us ï¿½civiliansï¿½, exercising our fingers and meager understanding of physiology here, BUT it is even truer of the Opinion Leaders in Medicine, who exist in BOTH worlds of bias in viewing IBS through their own Board Certified Scotomascopes !One guy over here interprets all that is observed clinically or in research through the perspective of his specialty, his Scotomascope, while the specialist on the flip side interprets all that he sees or reads or observes through HIS Board Certified Scotomascope unique to his board certification and practice or research area.Indeed they are out there, debating each other with the same or greater fervor you see expressed in threads like this and others in this place of humble expression. Yet they are in a far better position to comprehend, accept and integrate the simple realities I have tried to set before you here. Until that happy day arrives that ï¿½everyone can get together and combine their notes, assimilate the big picture, and develop an INTEGRATIVE diagnostic and treatment approach to ALL the different populations of people who are being diagnosed with IBS using all manner of disparate and diverse criteria and protocols, the fate of the sufferers (the patients) will remain as it is for now:







ï¿½Look at the bright side, at least itï¿½s not COLON CANCER and it wonï¿½t kill you. Calm down, get a hobby, do meditation, take these pills ï¿½til you find one that helps, eat more fiber unless you get pain and gassy then eat less, donï¿½t eat spicy/fatty/big meals unless they don't bother you, drink more water, eat more fruit but donï¿½t eat fruit it if gives you gas, donï¿½t eat dairy it it bothers you, avoid ï¿½trigger foodsï¿½ if you can figure them out- here is a laundry-list, see a shrinkï¿½[ï¿½These IBS patients are really head casesï¿½]ï¿½go see another specialist, tell your husband to help you more, maybe you need to get your mother-in-law out of your house!







WHAT-ever.







If ï¿½weï¿½ can actually read those realities set forth above in plain English and in black and white and still persist with the same old tired arguments and selective use of references, often from professionals who suffer the same selective and biased thinking on ANY side of the issue of IBS (they are not limited to any one side of the issue) and keep yodeling and parroting the same old ï¿½this is IBS and this is notï¿½ and ï¿½this causes IBS and this does notï¿½ and ï¿½I am right and you are a quack and a hereticï¿½ then ï¿½weï¿½ are doing ourselves and the millions who suffer from IBS and the thousands who come here for advice a gross and unethical disservice.On the other hand, if EVERYONE could just step back and consider those realities, and maybe make a slight adjustment to ï¿½ourï¿½ paradigms, rather than expending essential brainpower and energy trying to ï¿½win a debate over the undebatableï¿½ , we could advance the science and art of the diagnosis and treatment of all those millions of the poor people (like ourselves) staggering around in the wilderness of healthcare like the Lost Tribe of Israel. Except they are lost in the erroneous belief they have a disease with no physiologic basis and for which there is no certain solution. Maybe we could improve the quality of all their lives, not just the select few who get lucky enough to stumble into a protocol or modality which happens to fit their needs to the exclusion of others whose needs the protocol or modality does NOT fit.Maybe.







Maybe there IS a Santa Claus, too, MNL!







Bye, and I mean it when I sayHave a DFD, eat well, think well, be wellï¿½alllll of you!







MNL


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## bonniei (Jan 25, 2001)

> quote:as many as 80% of physicians rendering IBS diagnosis do not FOLLOW the published guidelines and protocols when rendering the diagnosis of IBS.


Wow! No physician asked me, for one , questions based on Rome Criteria. They did the routine colonoscopy and endoscopy. That was it! The 80% number is something you should keep in mind, eric!


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## trbell (Nov 1, 2000)

yes, bonniei, it appears that hypnosis can be effective in any disorder that involves the immune system since the immune system is the body's reaction to substances.tom


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## trbell (Nov 1, 2000)

and MNL you are right. It's a tendency for people to prefer being right to getting better. I have to admit I get into this myself.tom


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## bonniei (Jan 25, 2001)

Well, Surprise, surprise! I did a search on infotrieve.com and found that there was one study which said that hypnosis was a promising cure for Crohn's. Interesting.


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## trbell (Nov 1, 2000)

yes, hypnosis is a promising cure for a lot of things. i tink eric and chrisgeorge might be able to give you more information on this.tom


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## eric (Jul 8, 1999)

Bonnie, I never said anything about hypnosis and celiac or any other conditions other then IBS and dyspepsia period,I said it boosted the immune system, nor did I ever say cure, do you guys read the threads and links or just make comments out of the blue. And some of the comments are even past way out of the blue boarding the atmosphere. All relaxation boosts the immune system and you guys just don't understand the system, so learn about it first. Because it is also part of why foods effect the gut in IBS and since your so interested in them , read up and quite being subjective to only what you want to hear, which is what I keep being accused of here LOL, like I wrote the artciles myself or created IBS personally, read who wrote them and who they are and why there saying what they are saying. I am trying to present a more rounded picture to the problem and things they do know and ways to help even with foods.When you can't stay with the subject you bash HT. Like that helps anything and its already PROVEN EFFECTIVE in IBS. Read the whole thread over a couple times!!!!!!!Its not about HT its about foods and IBS and the immune system itself.*Hypnosis is effective in IBS and this is an IBS bb.* Mike saying the abstract he posts constantly and uses it to say that loss of oral tolerence is a major cause of d in IBS, not from the abstract he posted its not although he has been applying it here for years as proff of some sort, read the follow up very carefully. And its a very very small minority as well. Noticed he say's nothing about it either that only a couple people in that study had d and there may have been reasons for that even and the inflammation went away. Extremely weak and undocumented information and evidence on what he is saying and everyone knows its possible for a problem with foods as triggers, but it still doesn't add up to IBS.Nor was this about diagnoses which I do now a lot about by the way.This is on IBS and hypnotherapy, regardless of what causes IBS and is solid evidence for IBS."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.html Overview of research on Hypnotherapy for IBS http://www.ibshypnosis.com/IBSresearch.html Hypnosis Treatment of Irritable Bowel Syndrome By: Olafur S. Palsson, Psy.D., Research Associate, Department of Medicine, University of North Carolina at Chapel Hill http://www.aboutibs.org/Publications/HypnosisPalsson.html Hypnotherapy for Functional Gastrointestinal DisordersBy: Peter J. Whorwell, M.D., University Hospital of South Manchester, England http://www.aboutibs.org/Publications/hypnosis.html The Effects of Hypnosison Gastrointestinal ProblemsOlafur S. Palsson, Psy. D.Research Associate, UNC-CHAPEL HillDepartment of MedicinesHypnosis is a treatment method, which still carries an aura of mystery,that unfortunately continues to be promoted by misrepresentations in movies and stage shows for entertainment. In reality, there is little mysterious about hypnosis anymore. It is a well-researched clinical technique which was formally accepted as a treatment method by the American Medical Association and the American psychological Association over thirty years ago. Clinical hypnosis is currently used by thousands of clinicians in the U.S. to treat both psychological and medical problems.Until recently, the possibilities of using hypnosis to treat gastrointestinal problems had received little attention. In the last 15 years, however, research has shown that hypnosis can influence gastrointestinal functioning in powerful ways, and that in particular, it is effective in helping patients with irritable bowel syndrome and to control nausea and vomiting.How Hypnosis Works:Hypnosis is a special mental state in which a person's focus of attention becomes narrow and intense like the beam of a bright flashlight in a dark room. This state is usually created with the aid of a hypnotist,who guides the person systematically to relax, focus only on one thing, and to allow things to happen by themselves.Whatever the mind focuses on while in this special mental state of hypnosis holds the entire attention. Therefore, people tend to experience things they think of, imagine or remember, more vividly and clearly than under usual circumstances. This is why people can sometimes recall things from their distant past under hypnosis even though unable to do so in the normal waking state (research has shown, however, that such hypnotically enhanced recall can be highly contaminated by the person's imagination). The narrow hyperfocus of this mental state is also why therapists using hypnosis are frequently able to help people make strong positive changes in their emotions and physical functioning. Hypnosis can work like a magnifying glass on the mind's effects on the body and emotion.Clinical hypnosis relies on suggestions, imagery, and relaxation to produce its therapeutic effects. Hypnotic suggestions are things that the hypnotist verbally suggests may happen while the person is under hypnosis. Due to the focused and receptive state of the hypnotized person, these suggestions happen almost automatically and without conscious decision or effort. If you, for example, receive the suggestion under hypnosis that your arm may be getting heavy, you will very likely feel it becoming heavy, without trying to do anything to make it happen. This "automaticity", the feeling of things happening by themselves, is by some considered the hallmark of hypnosis, and is often surprising to people experiencing hypnosis for the first time.Hypnotic imagery consists of picturing mentally events or situation or place in a way that has a desired positive physical or mental effect. For example, patients undergoing surgical or dental procedures are sometimes taught to enter a hypnotic state and go to a pleasant place in their mind. When successfully applied, the person gets completely engrossed in the vivid enjoyable imagery and is therefore happily unaware of the unpleasantness of the procedure.The hypnotic state is naturally accompanied by relaxation, and the physical relaxing effects are often deliberately strengthened further by clinicians through suggestions and relaxing imagery. Some of the benefits that come from hypnosis treatment are likely to result partly or entirely from the fact that hypnosis is a powerful relaxation method.Over decades of research and clinical experience, hypnosis has proven to have many valuable therapeutic uses. In psychotherapy, hypnotic techniques can speed the therapy process in various ways - for example by facilitating patients' self-understanding, extinguishing unfortunate habits, uncovering repressed or forgotten memories, reducing anxiety and phobias, and helping people to adopt a new and more adaptive outlook. In medicine and health psychology, hypnosis is used to reduce pain and discomfort associated with medical procedures such as childbirth, treatment of burns, and surgery where chemical anesthesia cannot be used effectively. It is also used to treat chronic pain and psychosomatic problems and counter unhealthy habits that contribute to illness. In dentistry, hypnotic analgesia is an effective needle-less alternative to topical anesthetic drugs, reduces bleeding and discomfort in oral surgery, and is used to treat teeth grinding and temporomandibular disorder. In recent years, the effects of gastrointestinal functioning and GI symptoms have been studied extensively.The Effects of Hypnosis on Gastrointestinal Functioning:The hypnotic state itself, without any particular suggestions, seems to slow down the gut, and clear-cut and specific changes in GI functioning can be induced in individuals by directing thinking or inducing specific emotional states under hypnosis.For example, one study 1 found that when healthy volunteers were hypnotized and simply instructed to relax, the orocaecal transit time the time it takes material to pass through the GI tract from the mouth to the first part of the colon was lengthened from 93 to 133 minutes. Another study 2 found that being in a hypnotic state decreases muscle movements in the stomach. The same study demonstrated that the emotional state of happiness, created under hypnosis, suppresses gastric muscle activity but anger and excitement increase muscle movement in the stomach . A pair of other studies 3 showed that when volunteers were guided to use imagery of eating a delicious meal while they were under hypnosis, gastric acid secretion was increased by 89%, and that acid production of the stomach could also be deliberately decreased during hypnosis using hypnotic instructions.Close to fifty published studies have reported on the therapeutic effects of hypnosis on nausea and vomiting problems related to chemotherapy, after surgery, and during pregnancy. Overall, this substantial body of literature indicates that hypnosis can be a powerful aid in controlling nausea and vomiting.Hypnosis may also be helpful in preventing gastrointestinal problems from recurring after they have been treated with medication: One study 4 of thirty patients with relapsing duodenal ulcers who had been successfully treated with a course of medication, found that only 53% of the patients who received preventive hypnosis treatment had a relapse within one year. In contrast everybody 100% in a comparison group receiving no hypnosis relapsed in the same period of time.In 1984, researchers in Manchester in England published a study 5 report in the journal Lancet, showing that hypnosis treatment dramatically improved the symptoms of IBS patients who had failed to benefit from other treatment. The researchers had randomly divided patients with severe IBS problems into two groups. Fifteen patients were treated with seven hypnosis sessions. Fifteen comparison patients were treated with seven sessions of psychotherapy, and those patients also received placebo pills pills with no medically active ingredients which they were told were a new research medication for IBS symptoms. Every patient in the hypnosis group improved, and that group showed substantial improvement in all central symptoms of IBS. The control group showed only very modest improvement in symptoms.Partly due to these dramatic results with treatment-refractory patients, a dozen other studies have followed, including three U.S. studies. The general conclusions from most of these studies are that hypnosis seems to improve the symptoms of 80% or more of all treated patients who have well-defined "classic" IBS problems, especially if they do not have complicating factors such as psychiatric disorders. The improvement is in many cases maintained at least for a year after the end of treatment. What is particularly remarkable is that this high rate of positive treatment response is seen even in studies where the participating patients all have failed to improve from regular medical care.The dramatic response of IBS patients to hypnosis treatment raises the question of exactly how this kind of treatment influences the symptoms in such a beneficial way.Four studies to date, two in England and two in the U.S., have tried to discover how hypnosis treatment affects the body of IBS patients. Since it is well known that many people with IBS have unusual pain sensitivity in their intestines, which is thought to be related to the clinical pain they experience, much of the focus of these studies has been on assessing the impact of this kind of treatment on intestinal pain thresholds. The two English studies both measured intestinal pain sensitivity with balloon inflation tests. The second study also measured muscle tone, to see if hypnosis relaxes the smooth muscles of the GI tract. No overall changes in pain sensitivity were detected, and gut muscle tension was also unchanged after treatment except a subgroup of unusually pain-sensitive patients had lessened pain sensitivity in the second study 7.. In 1995-1996, during my post-doctoral fellowship in the Division of Digestive Diseases and Nutrition at UNC-Chapel Hill, we conducted the first U.S. study 8 on hypnosis for IBS under the direction of Dr. Whitehead. We evaluated the effects of a highly standardized treatment protocol, delivered verbatim following written scripts, on rectal pain thresholds and muscle tone. Seventeen out of the 18 patients we treated with hypnosis showed significant improvement in their clinical symptoms. However, we found, like the English researchers, that gut pain thresholds and muscle tension were unchanged after treatment. In a second study 9, which I conducted with co-investigators at the Eastern Virginia Medical School, we used the same treatment protocol but this time measured autonomic nervous system functioning and blood levels of a gut hormone called vasoactive intestinal peptide. These are regulators of GI functioning in the human body, and the aim was to see if they would change due to treatment. Again, we found no changes in our physical measures after treatment with the exception of reduction in sweat gland reactivity even though 21 out of 24 treated patients were clinically improved. It should be noted, though, that in both our studies, we found clear improvement in the psychological well-being of our patients after treatment.In summary, it is clear from our work and other research that hypnosis treatment substantially improves all the central symptoms of IBS in the majority of patients who receive such treatment see the effects of our two studies on clinical symptoms in the Figure. What happens in the body of these patients to cause such improvement, however, remains a mystery.Future prospects:In light of the many studies which have shown hypnosis treatment to be effective for such problems as IBS and nausea and vomiting, the question may be raised why this kind of treatment is not more widely available or generally offered to patients with such GI problems.One limitation is the fact that not everybody is equally hypnotizable. Research has consistently shown that at least 15% of people are practically non-hypnotizable, and even those who are able to enter a hypnotic state vary greatly in how well they respond. Interestingly, the ability to be hypnotized is a stable mental trait. In other word, if you are highly hypnotizable now, you will most likely be so also in thirty years. Fortunately, the majority of people are sufficiently hypnotizable to have a potential for enjoying at least some of the medical and psychological benefits of clinical hypnosis.Furthermore, the idea of being hypnotized does not agree with all people. Even individuals who are sufficiently hypnotizable, may not like the idea of "letting go", may have difficulty trusting a therapist to guide them in hypnosis, or may have other concerns about the hypnosis experience. Fortunately, other forms of psychological treatment for gastrointestinal problems - in the case of IBS especially cognitive-behavioral therapy -- have also been found to be effective and are good alternatives.Finally, an obstacle which has barred many patients from receiving help for gastrointestinal disorders with hypnosis is the fact that in the U.S. the technique is more commonly used by psychologists and other mental health professionals than by physicians. Many mental health professionals who use hypnosis are not accustomed to treating gastrointestinal disorders, and therefore reluctant to take on treatment of such problems.As the reliably beneficial effects of hypnosis on gastrointestinal functioning become better known both to health professionals and the general public, this benign and comfortable form of treatment will hopefully become a more popular treatment option for GI patients - especially for those who have not received much relief from standard medical management. As far as IBS is concerned, we have been making an effort in the last two years to encourage clinicians across the country who have adequate training in hypnosis to provide such treatment for IBS. We have done this by providing them, free of charge, with the complete standardized treatment protocol which has proven effective in our research. To date, more than eighty licensed health professionals, practicing in almost all states, are started using our protocol, making it a little bit easier for patients in many geographical locations to receive help with hypnosis.webmdHypnosis for Irritable Bowel http://my.webmd.com/content/article/34/1728_87469 Aliment Pharmacol Ther. 2003 Mar 1;17 5:635-42. Related Articles, LinksGut-focused hypnotherapy normalizes disordered rectal sensitivity in patients with irritable bowel syndrome.Lea R, Houghton LA, Calvert EL, Larder S, Gonsalkorale WM, Whelan V, Randles J, Cooper P, Cruickshanks P, Miller V, Whorwell PJ.Academic Department of Medicine, University Hospital of South Manchester, UK.BACKGROUND: We have previously shown that hypnotherapy alters rectal sensitivity in some patients with irritable bowel syndrome. However, this previous study used incremental volume distension of a latex balloon, which might be susceptible to subject response bias and might compromise the assessment of compliance. In addition, the study group was symptomatically rather than physiologically defined. AIM: To assess the effect of hypnotherapy on rectal sensitivity in hypersensitive, hyposensitive and normally sensitive irritable bowel syndrome patients using a distension technique barostat that addresses these technical issues. METHODS: Twenty-three irritable bowel syndrome Rome I patients aged 24-72 years were assessed before and after 12 weeks of hypnotherapy in terms of rectal sensitivity, symptomatology, anxiety and depression. Normal values for sensitivity were established in 17 healthy volunteers aged 20-55 years. RESULTS: Compared with controls, 10 patients were hypersensitive, seven hyposensitive and six normally sensitive before treatment. Following hypnotherapy, the mean pain sensory threshold increased in the hypersensitive group P = 0.04 and decreased in the hyposensitive group, although the latter failed to reach statistical significance P = 0.19. Normal sensory perception was unchanged. Sensory improvement in the hypersensitive patients tended to correlate with a reduction in abdominal pain r = 0.714, P = 0.07. CONCLUSION: Hypnotherapy improves abnormal sensory perception in irritable bowel syndrome, leaving normal sensation unchanged.PMID: 12641511Am J Clin Hypn. 2002 Jul;45 1:31-7. RelatedHypnotherapy and refractory irritable bowel syndrome: a single case study.Galovski TE, Blanchard EB.State University of New York at Albany, USA.The current study describes the successful administration of hypnotherapy with a subject suffering from refractory Irritable Bowel Syndrome IBS and Generalized Anxiety Disorder GAD. The subject had suffered from IBS for 30 years and had unsuccessfully pursued multiple psychological treatments, both traditional and non-traditional. He was referred to the Center for Stress and Anxiety Disorders and commenced hypnotherapy directed primarily at the IBS symptoms. After 6 treatment sessions, his IBS symptomatology had improved 53%. He stopped treatment at that point and continued autohypnosis with the aid of treatment audiotapes provided by his therapist. Follow-up at 6 months indicated continued improvement 70%. A 2-year follow-up revealed an improvement of 38% in IBS symptomatology. Concurrent levels of depression and anxiety had also substantially decreased. Hypnotherapy is shown to be a viable, palatable, and enduring treatment option for an individual who had been refractory to many previous therapies.PMID: 12116613Am J Gastroenterol. 2002 Apr;97 4:954-61. Related Articles, LinksHypnotherapy in irritable bowel syndrome: a large-scale audit of a clinical service with examination of factors influencing responsiveness.Gonsalkorale WM, Houghton LA, Whorwell PJ.Department of Medicine, University Hospital of South Manchester, United Kingdom.OBJECTIVES: Hypnotherapy has been shown to be effective in the treatment of irritable bowel syndrome in a number of previous research studies. This has led to the establishment of the first unit in the United Kingdom staffed by six therapists that provides this treatment as a clinical service. This study presents an audit on the first 250 unselected patients treated, and these large numbers have also allowed analysis of data in terms of a variety of other factors, such as gender and bowel habit type, that might affect outcome. METHODS: Patients underwent 12 sessions of hypnotherapy over a 3-month period and were required to practice techniques in between sessions. At the beginning and end of the course of treatment, patients completed questionnaires to score bowel and extracolonic symptoms, quality of life, and anxiety and depression, allowing comparisons to be made. RESULTS: Marked improvement was seen in all symptom measures, quality of life, and anxiety and depression all ps < 0.001, in keeping with previous studies. All subgroups of patients appeared to do equally well, with the notable exception of males with diarrhea, who improved far less than other patients p < 0.001. No factors, such as anxiety and depression or other prehypnotherapy variables, could explain this lack of improvement. CONCLUSIONS: This study clearly demonstrates that hypnotherapy remains an extremely effective treatment for irritable bowel syndrome and should prove more cost-effective as new, more expensive drugs come on to the market. It may be less useful in males with diarrhea-predominant bowel habit, a finding that may have pathophysiological implications.PMID: 12003432Dig Dis Sci. 2002 Nov;47 11:2605-14. Related Articles, LinksHypnosis treatment for severe irritable bowel syndrome: investigation of mechanism and effects on symptoms.Palsson OS, Turner MJ, Johnson DA, Burnelt CK, Whitehead WE.University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7080 USA.Hypnosis improves irritable bowel syndrome IBS, but the mechanism is unknown. Possible physiological and psychological mechanisms were investigated in two studies. Patients with severe irritable bowel syndrome received seven biweekly hypnosis sessions and used hypnosis audiotapes at home. Rectal pain thresholds and smooth muscle tone were measured with a barostat before and after treatment in 18 patients study I, and treatment changes in heart rate, blood pressure, skin conductance, finger temperature, and forehead electromyographic activity were assessed in 24 patients study II. Somatization, anxiety, and depression were also measured. All central IBS symptoms improved substantially from treatment in both studies. Rectal pain thresholds, rectal smooth muscle tone, and autonomic functioning except sweat gland reactivity were unaffected by hypnosis treatment. However, somatization and psychological distress showed large decreases. In conclusion, hypnosis improves IBS symptoms through reductions in psychological distress and somatization. Improvements were unrelated to changes in the physiological parameters measured.Publication Types:Clinical TrialRandomized Controlled TrialPMID: 12452403Appl Psychophysiol Biofeedback. 1998 Dec;234:219-32. Related Articles, LinksThe treatment of irritable bowel syndrome with hypnotherapy.Galovski TE, Blanchard EB.University of Albany, State University of New York, New York, USA.Previous research from the United Kingdom has shown hypnotherapy to be effective in the treatment of irritable bowel syndrome IBS. The current study provides a systematic replication of this work in the United States. Six matched pairs of IBS patients were randomly assigned to either a gut-directed hypnotherapy n = 6 or to a symptom monitoring wait-list control condition n = 6 in a multiple baseline across subjects design. Those assigned to the control condition were later crossed over to the treatment condition. Subjects were matched on concurrent psychiatric diagnoses, susceptibility to hypnosis, and various demographic features. On a composite measure of primary IBS symptoms, treatment was superior p = .016 to symptom monitoring. Results from the entire treated sample n = 11; one subject was removed from analysis indicate that the individual symptoms of abdominal pain, constipation, and flatulence improved significantly. State and trait anxiety scores were also seen to decrease significantly. Results at the 2-month follow-up point indicated good maintenance of treatment gains. No significant correlation was found between initial susceptibility to hypnosis and treatment gain. A positive relationship was found between the incidence of psychiatric diagnosis and overall level of improvement.Publication Types:Clinical TrialPMID: 10457813Z Gastroenterol 2003 May;41 5:405-12Hypnosis in gastroenterologyArticle in GermanHauser W.Medizinische Klinik I, Klinikum Saarbrucken gGmbH, Saarbrucken. w.haeuser###klinikum-saarbruecken.deHypnosis is one of the oldest remedies against physical diseases and mental disorders of mankind. The term hypnosis is used for the description of a technique as well as for the description of an altered state of consciousness which is induced by this technique. Hypnosis is a scientific tool in psychophysiological studies of gastrointestinal functions secretion, motility, visceral sensitivity and their processing in the central nervous system. Hypnosis is an empirically validated treatment of the irritable bowel syndrome even refractory to medical treatment which is recommended by international expert groups Rome II and the British Society of Gastroenterology. In diagnostic upper gastrointestinal endoscopy the relevance of hypnosis as an alternative of intravenous sedation needs to be clarified. Hypnosis cannot be recommended as an alternative for intravenous analgosedation in painful endoscopic therapeutic procedures of the gastrointestinal tract.PMID: 12772053Gastroenterology. 2002 Dec;123 6:1778-85. Related Articles, LinksComment in:Gastroenterology. 2002 Dec;123 6:2132-5.Long-term improvement in functional dyspepsia using hypnotherapy.Calvert EL, Houghton LA, Cooper P, Morris J, Whorwell PJ.Department of Medicine, Wythenshawe Hospital, Southmoor Road, Manchester, United Kingdom.BACKGROUND & AIMS: We have shown hypnotherapy HT to be effective in irritable bowel syndrome, with long-term improvements in symptomatology and quality of life QOL. This study aimed to assess the efficacy of HT in functional dyspepsia FD. METHODS: A total of 126 FD patients were randomized to HT, supportive therapy plus placebo medication, or medical treatment for 16 weeks. Percentage change in symptomatology from baseline was assessed after the 16-week treatment phase short-term and after 56 weeks long-term with 26 HT, 24 supportive therapy, and 29 medical treatment patients completing all phases of the study. QOL was measured as a secondary outcome. RESULTS: Short-term symptom scores improved more in the HT group median, 59% than in the supportive 41%; P = 0.01 or medical treatment 33%; P = 0.057 groups. HT also benefited QOL 42% compared with either supportive therapy 10% P < 0.001 or medical treatment 11% P < 0.001. Long-term, HT significantly improved symptoms 73% compared with supportive therapy 34% P < 0.02 or medical treatment 43% P < 0.01. QOL improved significantly more with HT 44% than with medical treatment 20% P < 0.001. QOL did improve in the supportive therapy 43% group, but 5 of these patients commenced taking antidepressants during follow-up. A total of 90% of the patients in the medical treatment group and 82% of the patients in the supportive therapy group commenced medication during follow-up, whereas none in the HT group did so P < 0.001. Those in the HT group visited their general practitioner or gastroenterologist significantly less median, 1 than did those in the supportive therapy median, 4 and medical treatment median, 4 groups during follow-up P < 0.001. CONCLUSIONS: HT is highly effective in the long-term management of FD. Furthermore, the dramatic reduction in medication use and consultation rate provide major economic advantages.Publication Types:Clinical TrialRandomized Controlled TrialPMID: 12454833 I am done with this thread its a waste of my time and efforts.


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## bonniei (Jan 25, 2001)

As hard as it is we do read the countless studies you post in response to our questions eric. My comment wasn't out of the blue


> quote: The influence of the mind on the gut goes beyond functional diseases. For instance, people with Crohn's disease or ulcerative colitis -- two conditions with clearly physical origins -- often suffer flareups during times of emotional stress. And in a recent survey, 68 percent of people with basically healthy digestive systems said stress gives them stomachaches


And Celiac is proving to be immunological in nature.


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## bonniei (Jan 25, 2001)

And you said hypnotherapy boosts the immune system.


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## bonniei (Jan 25, 2001)

And while I don't want to argue with you, eric, I consider you to be my friend, sometimes it is hard for us to see the point of your countless studies. You might want to summarize the point before you post the study or we will see whatever point we can see and let you wade through the studies to see the connection.


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## trbell (Nov 1, 2000)

bonniei, you might want to look at the crohn's forum for leads or ask chrisgeorge. i think he's got some background in hypnosis for other conditions in addition to ibs.tom


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## bonniei (Jan 25, 2001)

Tom, who is chrisgeorge?


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## trbell (Nov 1, 2000)

he's a Canadian hypnotherapist who sometimes visits the hypno forum and the anxiety forum These would be other places you could also ask about hypnosis, I think.tom


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## kel1059 (Feb 28, 2003)

> quote:On the other hand, the problems the patient presents have also been shown to at times originate on the immunologic side of the system, current understanding of those mechanisms so far is sufficient to demonstrate that allergy in the classic sense can be ruled out yet loss of oral tolerance (or what is now being called by some "intestinal allergy" or "enteric allergy" or some other such term du jour for the moment) and it is clearly a primary mechanism. The psychosocial consequences of living with symptoms induced by these mechanisms up to and including behavioral and CNS changes can be a consequence of chronic local and systemic inflammatogenic activity, and amplification of dysfunction, thus symptoms, occurs as a consequence.


The above quote is from MNL and it is brilliant. (p.s. eric, the abstract that you posted (Neuropathology of IBS? Robin C. Spiller) on the immune system was a very good abstract and it ties in nicely with what MNL seems to be saying)(where is the link, i want a copy) quote _have also been shown to at times originate on the immunologic side of the system_ This is what I think has happened to me. I believe it started on the immunological side. So eric, why do you seem to be so blind to this mechanism of IBS? It is truly unbelievable that someone can be so blind to something that is fairly obvious. Blockhead or what?You make stupid claims that you are, "....more concerned that people are going to get malnourished or phobic....." Give me a break!!!Unbelievable!!! Eric, just because you may not suffer from lost oral tolerance does not mean that others don't. ....and this lost oral tolerance can cause every single IBS symptom listed and then some. It can cause lung, sinus, joint, and brain problems. This is why some people experience "psychosocial" problems.To continue to deny this aspect of IBS (or the cause of IBS-symptoms) is the sole reason I look down on you as being intellectually inferior. I hate to sound cruel because you are probably a very nice person (but you are probably more stubborn than a bull on a hot muggy day in Texas).I don't consider flux to be intellectually inferior. Instead, I consider him to mentally disturbed in some manner (he needs treatment or correct treatment--he deserves some understanding based on his disorder). However, you don't have an excuse because --despite your mental problem you appear to "be all there". Therefore, I conclude .....some type of "denseness".Anyway, I think that the role of the immune system in symptoms of IBS is fascinating and I know that food is a big problem for me. removal of foods has helped me considerably. However, I continue to struggle because my immune system is still off kilter. I am hoping that things straigten out within the next 12 months. I believe that yeast was definitely causing problems and Ibsacol has also shown great promise.


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## eric (Jul 8, 1999)

again, luminal factors can trigger IBS from the gut end and it says nothing about foods, there are tons of things that can trigger it, although they can also, but all kinds of things can in IBS, not just foods, IBS can also be triggered by the brain end.I have known and studied the immune system end in IBS for years now and have been constantly posting abstracts on it, which were ignored it seems.However, the immune system is by no means the whole picture. There are neuromuscular problems and issues that are also conmnected the immune system in IBS that are in and of themselves problems. The immune system is probally activated because of them in IBS.Kel, until you understand the brain's control of the immune system and not just the gut we will get nowwhere.The brain runs the entire show.To summarize: * Thoughts and even subtle emotions influence the activity and balance of the autonomic nervous system ANS. * The ANS interacts with our digestive, cardiovascular,immune and hormonal systems and is therefore ideally suited to translate mind states into organ functions/dysfunctions * Negative reactions create disorder and imbalance in the ANS. * Positive feelings such as appreciation and a state of relaxation create increased order and balance in the ANS, resulting in increased hormonal and immune system balance and more efficient brain function.It has been shown in a number of studies that during mental or emotional stress and physical stress, there is an increase in sympathetic activity and a decrease in parasympathetic activity. This results in increased strain on the heart as well as on the immune and hormonal systems. Increased sympathetic activity is associated with a lower ventricular fibrillation threshold and an increased risk of fibrillation, in contrast to increased parasympathetic activity, which protects the heart. http://ibs.med.ucla.edu/Newsletters/Summer02ANS.htm Bonnie, take HT out of the equation and replace with relaxation which helps boost the immune system, so yes any stress related or chroninc snydromes or even diseases can BEnefit from relaxation techniques. The CNS-Brain- is connected to the ANS-gut- and runs the show, even thought the ans has the ability to function on its own its still run by the brain if your head is still attached.


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## trbell (Nov 1, 2000)

eric, I think mind/body people and IBS researchers might say that the brain doesn't run verything? The second brain has some say, don't you think? tom


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## bonniei (Jan 25, 2001)

> quote:take HT out of the equation and replace with relaxation which helps boost the immune system, so yes any stress related or chroninc snydromes or even diseases can BEnefit from relaxation techniques.


I fail to see the difference between relaxation techniques, self hypnosis and hypnotherapy. It just seems to be a matter of intensity. If relaxation can boost the immune system, HT will do it even more, being a more intense form of relaxation, I would think.


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## bonniei (Jan 25, 2001)

Kel if eric and flux didn't have a mental disorder they would have got it now with your style


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## trbell (Nov 1, 2000)

there are pretty significant differences between hypnosis and hypnotherapy. You can probably find out more about this in the HT forum?tom


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## kel1059 (Feb 28, 2003)

> quote:Kel, until you understand the brain's control of the immune system and not just the gut we will get nowwhere.The brain runs the entire show.


Oh eric, eric, eric... the brain runs the entire show -hmmmmn. Bzzzzt. Wrong again! The brain does not run the whole show. The immune system runs just fine by itself. When the immune system encounters some nasty bacteria it does not need any information from the brain to do its work.However, that is not to say that extreme, severe stress or a severe mental disorder will not have an impact on the immune system --- it most certainly is capable of doing so. However, you are guilty of putting far too great of an emphasis on it. The idea of treating seasonal allergies by sitting on a shrink's couch or by listening to an audio recording of a hypnotist is ridiculous. Might it help some?? sure--it could help to some degree. Would it help a person who is incredibly reactive to aflatoxin from peanuts??? NO!!!!!!!How do you explain the tens of thousands of babies who need to be switched to a different formula due to constant spitting up of their existing formula??? Aaaah, the baby is really, really, really, really stressed out and had a really, really bad baby day. i think we should start putting these babies on Zoloft or Xanax --- or better yet let's get them some CBT or HT.


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## kel1059 (Feb 28, 2003)

> quote: again, luminal factors can trigger IBS from the gut end and it says nothing about foods


"luminal factors" ----what you are saying by luminal factors is either----- bacteria, fungus, yeast, protozoa, amoeba, other parasites or microorganisms ( and/or their metabolites), drugs, alcohol, and *FOOD* . .....because there is not much else in the way of "luminal factors".So where do you get this statement of "it says nothing about food". who says? you!I would like for you to have to spend a few days with me locked up in a small room after I eat bleu cheese. ....and then you tell me IT HAS NOTHING TO DO WITH FOOD.


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## trbell (Nov 1, 2000)

yes, some people can't be helped by therapy. i don't think eric ever said it sould work for you so why the argument?tom


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## kel1059 (Feb 28, 2003)

> quote: IBS can also be triggered by the brain end.


This is true. it is also more true for some than others. I tend to be much more of a reactor to foods, and FAT ain't one of them. Unless it is the cheapy transfatty, hydrogenated, unnatural garbage from fast food joints which I have not eaten in about a decade. Now that I think about it, the fact that I don't react to any "natural" fat --including ghee, tells me that I am NOT in the IBS subgroup of people who are fat-sensitive. Instead i am in the subgroup of people who are more likely to be atypically allergic to various proteins in foods. *It is immunological* . This explains why I am helped by ibsacol. You, Shawn eric Case, dismiss this valid treatment because it does not match up with your type of IBS. This just goes to show how narrow minded you are. MNL on the other hand not only endorses the methods that you espouse such as cbt and ht but he recognizes the validity of immunomodulators. Therefore, he is more well rounded than you and his methods reach out to greater numbers than your ridiculously narrow approach. Eric, is it starting to register yet??? It is about helping people not clinging to theories and narrow models.Eric, you are dead wrong when you make blanket statements such as, " any type of food can cause the release of serotonin and/or the enterochromaffin cells are pressure sensitive.....blah, blah, blah".I do NOT react this way!!!!!!!!! Neither do a lot of people here. What does that tell you? It tells you that the mechanism of action is either an atypical allergy to a protein or some microorganism is going to town on either the carb or protein content of the ingested food.


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## bonniei (Jan 25, 2001)

tom since you seem to frequent the hypnotherapy forum, why don't you tell me the difference between hypnosis and hypnotherapy. I don't know why you are being so directive. If you can educate me do so. Please don't tell me to go somewhere to learn. Is that the only useful thing you can contribute? I have no interest in digging up scores of threads in the hypnotherapy forum to figure out the difference.


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## trbell (Nov 1, 2000)

I'm sorry if I seem directive. what I am saying is a suggestion, not a directive. you can follow it or not. I'm not saying you have to do it. I find that suggestion works better for most than direction. but sorry. The difference between hypnosis and hypnotherapy is that hypnosis is the technique and hypnotherapy is it's use by a hypnotherapist in a clinical setting. I also suggested you go to the foru because it's smething you can learn better from eric or other people using the technique than fro me. I'm not the authority on everything.tom


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## flux (Dec 13, 1998)

> quote:the brain runs the entire show -hmmmmn. Bzzzzt. Wrong again! The brain does not run the whole show. The immune system runs just fine by itself. When the immune system encounters some nasty bacteria it does not need any information from the brain to do its w


Well, it's true, the brain doesn't really run moment to moment function in the immune system, but the brain is involved in its workings (e.g, fever).The brain technically doesn't run the gut. A lot of it self-running, but the brain is involved.


> quote:luminal factors" ----what you are saying by luminal factors is either----- bacteria, fungus, yeast, protozoa, amoeba, other parasites or microorganisms ( and/or their metabolites), drugs, alcohol, and FOOD . .....because there is not much else in the way of "luminal factors"


Luminal factors do include foods, but this doesn't mean there is anything wrong with the food, though.


> quote:" any type of food can cause the release of serotonin and/or the enterochromaffin cells are pressure sensitive".


These statements, however, are accurate.


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## bonniei (Jan 25, 2001)

Thanks Tom. I was having a conversation with the expert himself I thought. Anyway I accept your apology.


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## bonniei (Jan 25, 2001)

As far as the differences between hypnotherapy and self hypnosis go, duh, I got that much! I was talking about relaxation experience of the person being hypnotized - that it was a matter of intensity.


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## kel1059 (Feb 28, 2003)

> quote: but the brain is involved in its workings (e.g, fever).


bzzzzt! wrong again! the brain produces fever? not according to my understanding. fever is due in part to the immune system sending out IL-1 which creates that run-down feeling and possibly fever. if not IL-1, then any number of other chemicals that induce fever.You will need to supply some clear and hardcore evidence to prove that the brain initiates fever.


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## kel1059 (Feb 28, 2003)

> quote: Eric, you are dead wrong when you make blanket statements such as, " any type of food can cause the release of serotonin and/or the enterochromaffin cells are pressure sensitive.....blah, blah, blah".


To avoid confusion, I was referring to eric's incorrect assertion that a person WILL experience reactions to foods solely based on this mechanism of action (serotonin release upon pressure).This is simply nothing more than a blanket statement to try and explain away our reactions to food as due to this mechanism. complete foolishness.First, it assumes everyone has diarrhea which is not the case. second it fails to explain why only certain foods are symptom provoking.Flux, you are about as clueless as clueless comes on this subject so butt out.


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## trbell (Nov 1, 2000)

actually, bonniei, the hypnotic state I think is a paradoxical state in that the harder you try to relax the less likely it is that you will relax hypnotically speaking. it's certainly not an intense state. i also don't proclaim myself an expert on hypnosis even though I use it. I tend to let people hypnotize themselves. the old idea of the hypnotist as master or Svengali is pretty dated. I've asked before not to be treated as an expert on the bb so please let me just be a fellow ibs sufferer.tom


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## bonniei (Jan 25, 2001)

tom, when I said expert, I was referring to eric.







I was having a conversation with eric. I have tried all three techniques and I found the deepest experience I experienced was through hypnotherapy when I tried to give up smoking. Maybe we should wait for a reply from eric?


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## chrisgeorge (Feb 28, 2003)

Hi Bonniei,I'm wading in here! You asked what the difference was between relaxation and hypnosis. Relaxation, which can be accomplished through a variety methods such as yoga, sitting by the lake, reading a book, even deep breathing etc all give the physical sensation of well-being, simply by quietening the mind through the focusing of thought. Its a physical feeling.Hypnosis on the other hand is a tool/technique that allows us to "bypass the critical faculty and implant suggestive thinking". That quote was from Dave Elman, a U.S. hypnotist that taught the medical community in the late 60's, 70's and 80's and is perhaps the best definition of hypnosis. Relaxation is a by-product of hypnosis, in other words its not what we set out as our main goal, its a "freebe" along the way.One's a physical sensation the other a technique.Getting out of the water now.P.S.The critical faculty that Elman was referring to was our senses. If everyone reading this, just close your eyes - you can open them again! You've just by-passed your critical faculty ( probably relaxed yourself as well). Is this hypnosis? No, for hypnosis to happen you have to by-pass your senses ( or occupy your conscious mind - move it aside so to speak) and then implant suggestive thinking.Using a progressive relaxation induction such as Mike's tapes, you close your eyes ( again the by-pass) and the selective suggestions are: your eyes are getting very tired, relaxing etc. Which together allows you to go into this altered state of consciousness, we call hypnosis.By the way, speaking as a hypnotherapist (hypnotist) you allow yourself to enter this state. We ( ie hypnotists) don't put you into this state. All hypnosis is self-hypnosis and the role of the hypnotist is only to create the environment that allows you to enter.


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## bonniei (Jan 25, 2001)

Thanks for sharing your expertise, chrisgeorge.


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## Mike NoLomotil (Jun 6, 2000)

And the beat goes onï¿½.First as an aside I would have to agree that Fluxes Threesome above is indeed accurate.The first is a given re: the role of the CNS (esp. les brain) in regulation of body systems. That is kind of the point of some of the diagrams we see in the link to the tutorial I posted.These bear some slight expansion:_______________________________________________ï¿½Luminal factors do include foods, but this doesn't mean there is anything wrong with the food, though.ï¿½______________________________________________Indeed this a very simple concept which is very difficult even for some very sophistciated people to comprehend as there are so many possibilities. There are indeed times when there IS ï¿½something wrong with the foodï¿½ itself which provokes some form of intolerant responseï¿½some foods have endogenous chemicals of various types that even normal people with normal gut function tolerate to varying degrees. Just because some person is less tolerant of histaminic foods, for example, does not or should not translate by itself into say ï¿½Oh she has IBSï¿½.ï¿½. On the other hand the most basic innocuous staple food with no endogenous or otherwise innate reason for someone to not tolerate it can, in affected persons, prompt a chain reaction which results in the release of all manner of unwelcome proinflammatory and proalgesic mediators, again on response to something perfectly safe.ï¿½and all points in betweenï¿½ï¿½__________________________________quote: " any type of food can cause the release of serotonin and/or the enterochromaffin cells are pressure sensitive". "These statements, however, are accurate."_________________________________Indeed, the same answer applies as above. Do not be misled at times, however, that serotonin is some sole mystical God of all alterations in bowel motility and/or sensorial changes. It is one of the principal "mediators of concern" (ie: usual suspects) and due to the various types and effects of 5HT[x] receptors it/they make a convenient target for investigation into new pharmacotherapies for all manner of bodily dysfunctions.On the contrary a wide array of proinflammatory and proalgesic mediators are available within the array of mucosal and circulating immunocytes which serve as part of the sentinel-response-protective system integrated with the bowel and digestive functions which can be inappropriately liberated by not only innocupus foods but my central neurologic and endocrine ï¿½eventsï¿½. Unfortunately the simple-picture is what has led to so much confusion and misunderstanding or misinterpretation of observed physical phenomena.Ooooooo







the meat is again on the tableï¿½..______________________________________ï¿½Mike saying the abstract he posts constantly and uses it to say that loss of oral tolerence is a major cause of d in IBS, not from the abstract he posted its not although he has been applying it here for years as proff of some sort, read the follow up very carefully. And its a very very small minority as well.ï¿½_______________________________________Oh, andï¿½_________________________________________ï¿½Extremely weak and undocumented information and evidence on what he is saying and everyone knows its possible for a problem with foods as triggers, but it still doesn't add up to IBS.ï¿½__________________________________________Oh and this takes the cake all the way to bar mitzvah:_________________________________________ï¿½Kel, until you understand the brain's control of the immune system and not just the gut we will get nowwhere.The brain runs the entire showï¿½ ___________________________________________Oh golly gee I am so shocked at all this! I knew that the fun would continue! Sure, why not I got 15 minutes to kill.







OK. Best One word Response: Hogwash. Swill. Oh thats 2. Sorry.







No, I take that back. At some point you just have to call a spade a spade. If that is all you have to put to print after reading what I posted above, I am left with no alternative but to quote that famous philosopher and student of human behavior, Groucho Marx:_________________________________ï¿½A child of 5 could understand this. Send someone to fetch me a child of 5.ï¿½_________________________________It takes patient study of over 25 years of investigations and related studies coming at the symptom sets associated with IBS from all perspectives to get that side of the picture to which you so disdainfully make reference. No single study is used as the sole evidentiary basis. And any that is, IS precisely pertinent for the exact reasons I described. So all we have is another clumsy attempt to deflect attention from the facts via the use of pseudofact. Not unexpected at all. Followed by the usual retreat into a subject you are more familiar with: Hypnosis, and in which your vested interest lies. You have no oligoantigenic dietary solution for the patient therefore you must devalue it wherever it appears.For example, the monograph that physicians are provided to come to understand the role of food intolerance in their patients with symptoms of functional bowel disorders is 35 single-spaced typewritten pages using highly condensed selections from the literature so as to keep it short enough that physicians can find time to read it. That monograph is not posted here as it is several megabytes in file size, though as I offered many times in the past, members who wanted a copy of it to see what physicians review to base a decision as to whether to try the Integrated Disease Management Program we developed on their diarrheic IBS patients, received copy be emailing me with where to send it.So far majority of physicians treating IBS patients with the currently available methods who have met with a program consultant and reviewed it, perhaps along with some powerpoint slide shows on the subject, perhaps even speaking with other doctors who use the Integrated DM Protocol we provide, have become regular users of the program and all its elements for the patients who fit the profile of those who can benefit from it. Since there are trained consultants working in but (5) states so far (just started bringing it out to physicians in a formal manner during the last 10 months or so and it takes time to train consultants)) then the present base of useage growth is in those presently-served 5 states. But new consultants are trained each month and by the end of next year the protocol should be available an in use by physicians who choose to nationwide. In fact we have (12) new folks coming to Orlando for training from several other states at the end of this month to begin representing us in their areas in August.I should point out that this developing base of successful physician providers is not restricted to primary care providers. Several board-certified gastroenterologists very familiar with all the current literature, all the theories and putative mechanisms of so called IBS, and all the various medication and treatment options available as are often discussed here, have seen fit to try this DM approach as the material made sense to them. Now they may just be dumb doctors who need to be reeducated by such a worthy person on what to pay attention to and what to ignore, but I suspect they are capable of determining if something placed before them makes sense relative to their patients needs or not.In fact one of the physicians who will be in attendance at the upcoming Disease Management Association Leadership Conference in Chicago in October, to be available to speak to other physicians and insurance utilization review managers, will be a board certified gastroenterologist whose patients are enjoying excellent symptomatic relief as a result of all this silly oligoantigenic dieting therapy stuff integrated with stress reduction ï¿½which has nothing to do with IBSï¿½ allegedly. The Poor misguided souls.







Again I see however that if one cannot ï¿½win an argumentï¿½ about the specific subject we must, however, experience this constant need to the use that as another invitation to segue to aggressively assert to the readers that hypnotherapy somehow is "THE treatment of choice for IBS" at every opportunity...as if someone has said it is NOT an efficicious modality?







In spite of this somewhat bizarre behavior at times, I have as a professional courtesy refrained for several years now from really engaging in any of the repartee over HT, especially with one who markets HT tapes. It is understandable that one thus must assert their effectiveness to market them as anyone must assert effectiveness of their tools if they expect to move the inventory. Got no problem with that hence my perpetual presence on the sidelines of such discussions except to occassionally try to insert some objectivity about single-modality treatment vs. multi-modality treatment.I have also refrained from engaging in a more careful examination of the claims for HT as a "proven principal modality" since we use it as part of the LEAP DM Program. There is nothing really to debate if one uses a modlity one must consider it beneficial.Indeed our physicians and dieticians are aware enough of the potential helpfulness of such programs as modalities in an integrated DM program that we include along with all the other patient trainign materials, test results and dietary plans, an HT Program on CD developed by a gastroenterologist and clinical psychologist. http://www.specialistsingastro.com/IBS/index.html So inferences to the contrary, just as oligonatigenic dieting protocols are proven to be efficacious in the majority of IBS patients properly selected, so to are most HT and CBT protocols shown to be efficacious. I am unclear still as to who seems to be asserting otherwise.My only point would be that which it always is. To get the best outcomes with IBS victims you need to use an integrated treatment approach. There is no single modality which is a silver bullet for all IBS victims. If there was why is everybody here???The issue is that the more patient specific you can make each modality, and the more the patient values the modality thus actually uses it, the higher the success rate and the greater the overall degree of remission of any population. Anyone who would argue that point does not know anything about patient care.Now I do not know how many people realize, for example, that it makes a difference if the patient is male or female who undergoes hypnotherapy as a treatment, or if they realize that it makes a difference if the treatment is done personally by a therapist or via a self-administered audio program. Or that all the studies done are not done using the same protocol or programs or therapists or tapes or cdï¿½s. This has to be taken into account.Or that some studies showed that it makes a significant difference in the degree of remission if the program was done by the therapist or if it was done using tapes, as the subjects using tapes success rate was significantly less impressive than the therapist success rates. Anyway what was the measure of ï¿½successï¿½ in the first place?All kinds of aspects on that topic of HT which have a bearing on the outcomes which could be and would be discussed if one wanted to really assess the modality have not been borached by tyour truly. First before I go further, I challenge anyone to find any posts from me on the HT Board, or other than this one specific post for that matter on this board, pointing out any of the constant, inherent , misleading bias in the way the studies on this modality are presented to people so as to paint the field of hypnotherapy with the broadest possible brush with the intent to suggest that the outcomes are consistent, highly predictable, and all studies are applicable to all HT protocols. I will just say these things, just this once, for the sake of inserting objectivity since the subject was brought upï¿½.againï¿½in the midst of a different topic. Do not drain the swamp lest the alligators issue forth.Another thing that the average patient does not understand nor is advised of when abstracts are slathered all over a board like so many handbills, is that to understand if a study is applicable to you as a patient, you also have to understand how the subjects were selected, as the criteria are not uniform, and what was used to asses their baseline condition (and was it symptom based, quality of life base, or both), what degree of change in either behavioral field and in how many subjects, how many recidivised and after how long, what was considered significant enough to be counted as so called ï¿½effectiveï¿½ or ï¿½Successfulï¿½ï¿½. What is the investigators definition of "effective" or "successful". This is not uniform either. ï¿½Effectiveï¿½ is about as meaningful as talking to people who are drought-stricken and proclaiming ï¿½I made it rain!ï¿½. Ok bravo. Where, on whom, how much, did it make difference, who gave up and left before the rain came?This concept, this proposition, this presumption, that HT for IBS is somehow generic is misleading. As is the way the investigations are presented to people so as to persuade them that this modality is for them and that it is somehow Universally Accepted as a SOLE MODALITY for IBS treatment. I think this is no more the case than CBT is generic and universally effective as a sole modality nor any single drug protocol is universally efficacious nor any single diet is universally effective.Also, I can never tell which study or studies of all the studies posted as generic studies of HT, and whose protocols vary as much as dietary protocols can vary, are specific to the specific audio program being constantly recommended to everyone and for which the promulgator of same is granted a captive forum wherein to discuss it at any length that may be of pleasure? A place I again point out where I do not make any effort to even enter at all, to interfere with nor to refute anything claimed, no matter how vigorously stretched the assertions may be, how hypothetical the mechanisms may be, or whether or not I feel it is well supported.Ah, now this is an intriguing side-bar turn of events. I see that now single case studies as well are acceptable as proof of efficacy of the modality, as long as it is an HT single case study. Other modalities I assume then no longer require the higher burden of proof so loftily demanded. Hmmmï¿½.I wonder how long to type up and submit 200 , 300, 400 single case studies. Oh, no, one is enough.One also has to be careful not to get carried away with oneï¿½s own hype, not unlike the quarterback who must caution against falling in love with his arm.







"ANY" chronic diseases or syndromes can "benefit"? ï¿½Boosts the immune systemï¿½? Sheesh, talk about claims that sound like they came off the jar of $14 supplement of zebra tooth extract at the health food store!You know, at some point a tout who gets irritated and bombastic on a daily basis at the slightest provocation, or at any other persons words or actions which look at all remotely like a reasonable proposition that something else may be effective for the sick as well, needs to step back and do a little self examination. At least as much as he spends wagging his finger at everyone else who be might be so presumptuous as to offer an alternative.It will be, to me, intriguing to see ï¿½where it all ends upï¿½ out there in the real world, in the field of actual live mass healthcare over the next 2 years, rather than here in this microcosm of the cyber-health world.Off to da beach!Ya'll have good time with it now, hear?







MNL


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## flux (Dec 13, 1998)

> quote:bzzzzt! wrong again! the brain produces fever? not according to my understanding. fever is due in part to the immune system sending out IL-1 which creates that run-down feeling and possibly fever. if not IL-1, then any number of other chemicals that induce fever.










Ever heard of the hypothalmus?


> quote:I was referring to eric's incorrect assertion that a person WILL experience reactions to foods solely based on this mechanism of action (serotonin release upon pressu


They usually do.


> quote:it assumes everyone has diarrhea which is not the case.


Not necessarily.


> quote:second it fails to explain why only certain foods are symptom provoking


It is based on the idea that *al*l foods provoke at least some reaction. No serotonin, and your gut would be at a standstill.


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## trbell (Nov 1, 2000)

So, Chris would it be fair to say that hypnosis is like any other treatment in that there are different kinds depending on the patient and it's really nothing for people to get defensive about since it's not for evryone?tom


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## trbell (Nov 1, 2000)

So, Mike. are you saying you'd be happier if the hypno forum were opened up to include all kinds of hypnotherapy? if there were a food intolerance forum should it be restricted to the LEAP program or include other programs?tom


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## kel1059 (Feb 28, 2003)

The hypothalumus does indeed control body temperature. However, we are talking about what the "INITIATING" mechanism is. ....and the hypothalumus does not -out of the blue- just decide to create a fever.there is something sending signals to this gland and other glands.Eric's claim that the "brain runs the whole show" is still very much incorrect. When it comes to typical and atypical allergy, intolerances, and hypersensitivities --- the brain is not the director. it is the target.


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## chrisgeorge (Feb 28, 2003)

Tom,Hypnosis is only a part of the package. It's an adjunct and complements other modalities. In the right hands, it can be a very helpful, and a very powerful tool.But the one thought I'd like to make known, which was so eloquently stated by Mike, the advice been given by some members on this BB on hypnosis comes with a disguised agenda. In fact the advice comes not from a hypnotist or hypnotherapist.Within the hypnosis community (those who have studied and trained in it), words like cure and hypnosis are never linked together. As hypnotherapists, we realize that hypnosis is not the panacea for all that ails. But again, coupled with other treatment strategies can provide a formidable arsenal for health practitioners.And to answer your question, its not for everyone.


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## trbell (Nov 1, 2000)

right. people tend to forget about the role of the body in mind/body interventions and that's probably a key to why HT works for many. it bypsses the brain.tom


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## bonniei (Jan 25, 2001)

Well I was trying to read up papers on the role of inflammation in IBS and guess what- they spoke about serotonin under the topic of role of inflammation. That was news to me! I thank you for piquing my interestest in inflammation and leading me down this path."Although colonic biopsy specimens are normal in patients with this disorder, in those who have also had a bout of Campylobacter enteritis, an increase in rectal mucosal lymphocytes has been reported.79,80 Small-bowel permeability has also been shown to be greatly increased,79 but these findings need replication in other centres. Inflammation is associated with production of mediators including prostaglandins, bradykinins, nerve growth factors, adenosine, and 5-hydroxytryptamine. These mediators induce visceral hypersensitivity, exaggerated motor responses, and increased intestinal secretions81 (figure 2), which could contribute to episodic diarrhoea. Inflammation also increases availability of 5-hydroxytryptamine by raising enteroendocrine cell counts, which could also contribute to diarrhoea. Serotonin type 3 (5HT3) antagonists are effective at reduction of symptoms in diarrhoea-predominant irritable bowel syndrome. However, these findings might not necessarily be causally linked, and intervention studies are needed to establish whether inhibition of inflammation induces any clinical benefit. 5-hydroxytryptamine has an important role in the peristaltic reflex, because it is released by pressure or stroking from enteroendocrine cells and then it acts on primary intrinsic afferent neurones to initiate ascending excitation and descending inhibition.82 A 5HT3 antagonist, alosetron, delays transit, relaxes the colon, and improves symptoms of diarrhoea-predominant irritable bowel syndrome.83 Furthermore, the partial serotonin type 4 (5HT4) agonist tegaserod accelerates small bowel and right colonic transit, softens stools, and modestly improves symptoms of constipation-predominant irritable bowel syndrome.84 Houghton and colleagues85 reported that some patients with diarrhoea-predominant irritable bowel syndrome had exaggerated release of 5-hydroxytryptamine after a meal, which lends support to use of 5HT3 antagonists; however, these data need verification. Raised concentrations of serotonin-containing entero-endocrine cells have been reported in patients with irritable bowel syndrome after infection with campylobacter and possibly other organisms,86 which could explain the increased postprandial release of 5-hydroxytryptamine and bowel symptoms in these patients. Concentrations of these cells are reduced in idiopathic slow-transit constipation in some studies87 but not all.88 Success of 5HT3 antagonists in treatment of diarrhoea-predominant irritable bowel syndrome suggests that increased 5HT-containing enteroendocrine cells might be important in causing symptoms, though this possibility has still to be established by double-blind, randomised, placebo-controlled studies linking clinical response to enteroendocrine cell numbers. "from Volume 360, Number 9332 17 August 2002 Seminar Irritable bowel syndrome: a little understood organic bowel disease? Nicholas J Talley, Robin Spiller Lancet 2002; 360: 555-64


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## trbell (Nov 1, 2000)

that's odd from Lancet. It was part of the campaign against lotronex if memory serves.Did you get any help from chris on HT for other disorders you can share with us?tom


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## trbell (Nov 1, 2000)

by the way. thanks for posting. that's the best explanation of seen about the way zelnorm works. I'll have to check with my doctor.tom


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## bonniei (Jan 25, 2001)

He wasn't aware of any research with Crohn's or Celiac.Here is the link I had found Link" TARGET=_blank>[url="http://www.infotrieve.com/newmedline/detail.asp?NameID=10882886&Session=&searchQuery=Crohn%27s+and+hypnotherapy&count=1"][url="http://www.infotrieve.com/newmedline/detai...therapy&count=1"]http://www.infotrieve.com/newmedline/detai...therapy&count=1]Link</A> about Crohn's and Hypno[/url]


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## trbell (Nov 1, 2000)

this is the citation in pubmed which is free for the aabstract:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10882886&dopt=Abstract.chris is more likely to have information on its use in treatment as he's a practitioner and not a web researcher.tom


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## trbell (Nov 1, 2000)

kind of a fun older article on hypnosis and the immune system.tom


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## eric (Jul 8, 1999)

No wonder no one gets anywhere, when they jump from one subject to another, even before any one subject is understood better.First kelly asked this question in the UNC chat forum.She stated the gut sends 9 times more messages to the brain, and Dr Ringel told her "it maybe an overstatement that the gut influences the brain 9 times more then vise versa. Even though 90 percnt of the serotonin is found in the gut. The brain controls gut activity and sensation in various ways, including sensation, muscle activity and also emotional and behavioral reactions to gut activity. The influence of the brain is powerful, but divided between sevaral different influences."The brain is the Boss."How do you remember the way to your friend's house? Why do your eyes blink without you ever thinking about it? Where do dreams come from? Your brain is in charge of these things and a whole lot more. In fact, your brain is the boss of your body. It runs the show by controlling just about everything you do. It's faster and more powerful than any computer you've ever used.It's large and in charge - so large that it fills the upper half of your head. It looks like a soft, wrinkly, gray sponge, and it's almost as heavy as a carton of orange juice! By the time you're grown up, it will weigh about 3 pounds 1.4 kilograms. Read on to learn more about some important parts of your brain. http://kidshealth.org/kid/body/brain_SW.html The HPA axis is part of the iummune system.hypothalamic-pituitary-adrenocortical HPA axis.Biological links between the immune system and the central nervous system exist at several levelsThe Immune System and the Nervous System http://www.immunecentral.com/immune-system/iss27.cfm Serotonin is also connected to the hpa axis from the gut.All the systems are connected.Next, Tom, its a study and nothing to do with Lancets feeling for lotronex.Also, its the brain and the phycology and physiology HT works on I think you meant the mind there and it doesn't bybass the brain, it bypasses the concious brain down to the subconcious.The subconcious runs the autonomic nervous sytem!!!!!"HOW AND WHY HYPNOSIS WORKSThomas Yarnell, Ph.D.Licensed Clinical PsychologistHypnosis Specialist Modern hypnosis has been used for hundreds of years to build self-confidence, change habits, lose weight with weight loss programs, stop smoking, improve memory, end behavior problems in children and eliminate anxiety, fear and phobias. The question is, WHAT IS HYPNOSIS? Hypnosis is a state of mind characterized by relaxed brain waves and a state of hyper-suggestibility. Hypnosis and hypnotic suggestions have played a major role in healing for thousands of years. According to the World Health Organization, 90% of the general population can be hypnotized. Hypnosis is a perfectly normal state that just about everyone has experienced. What we call "highway hypnosis" is a natural hypnotic state. You drive somewhere and don't remember driving or even remember seeing the usual landmarks. You are on automatic pilot. The natural hypnotic state also exists when you become so involved in a book, TV show or some other activity that everything else is blocked out. Someone can talk to you and you don't even see or hear them. Whenever you concentrate that strongly, you automatically slip into the natural hypnotic state. The hypnotic state, by itself, is only useful for the relaxation it produces. The real importance of hypnosis to the healing and emotional change process is that while you are in the hypnotic state, your mind is open and receptive to suggestions. Positive and healing suggestions are able to sink deeply into your mind much more quickly and strongly than when you are in a normal, awake state of mind. I say positive suggestions because all research has demonstrated that while in the hypnotic state, you cannot be made to do anything against your moral values. All of our habitual and behavior controlling thoughts reside in what is called our subconscious mind. It's called that because it is deeper than our conscious mind. It's below our level of consciousness. We are unaware of the thoughts and feelings that reside there. Did you ever forget you had a dental appointment or some other appointment that you really didn't want to keep? Your subconscious mind is where that thought or memory that you had to go to the dentist at 2 PM went when you forgot you had the appointment. Once it was too late to go, your conscious mind relaxed and the memory came back. Imagine that there is a trap door between your conscious mind and your subconscious mind. Normally, the trap door is closed until your brain waves slow down to a relaxed, alpha brain wave level. This happens when you are asleep. The door opens for short periods of time and ideas, images and thoughts come out of your subconscious mind. We call what comes out in your sleep, "dreams". When you are in a state of hypnosis, the door also opens so helpful suggestions can be directed into your subconscious mind or forgotten memories can be retrieved. The hypnotic induction that hypnotists use is simply a way to focus your attention and concentration so you will go into that natural, normal hypnotic state. Once in the state of hypnosis, the trap door opens and suggestions to help you can be given. The list of ways hypnosis has been used to help children, adolescents and adults is practically endless but does include: weight loss, stopping smoking, building self-confidence and self-esteem, improving academic performance at every age level, improving test taking ability from children through high school, college, medical and law school as well as the National Teacher Certification Exam, pain management, eliminating anxiety, fear and phobias, stress management, insomnia and other sleep problems and helping to heal physical problems. 2. To really work well, suggestions must be reinforced by repetition. Most of the habits, feelings and emotions we want to change are deeply implanted in our subconscious mind and will not just "go away" with one set of suggestions. Most of the time, the hypnotic suggestions need to be repeated on a regular basis until you notice a change. This is one reason that most specialists in hypnosis give clients cassette tapes of their sessions so they can listen to them every day. It's also the reason why hypnosis tapes you buy can work so well. You get to listen to them every day or often enough that the suggestions become permanently a part of you. There is no way to predict how long it will take to see change. It will depend partly on your motivation and commitment. The Three Keys to the successful use of hypnosis for self improvement and personal growth are self motivation, repetition and believable suggestions. 1. The motivation to change must come from within you. If you are trying to change because someone else wants you to "lose weight" or "stop smoking", the chances are greately reduced that the hypnosis will work. For example, I've worked with many people for weight loss or to quit smoking who came to me because their physician or spouse wanted them to change. These people do not respond as well to the hypnosis as those who really want to change. Those who came because they wanted to quit smoking or lose weight responded quickly and easily. Before you start to use hypnosis for your self improvement, you should get it clear in your own mind why you want to change. This clear intention to change will help the hypnotic suggestions to take hold and manifest themselves in your everyday life. 3. The third key to the successful use of hypnosis for personal change is believable suggestions. If you are to accept a suggestion, your mind must first accept it as a real possibility. Telling a chocoholic that chocolate will be disgusting to them and will make them sick is too big a stretch for the imagination. If a suggestion like this even took hold, it would only last a short time because it would be so unbelievable to a real chocolate lover. In cases like this, one of the successful weight loss suggestions I use is that the next time the individual eats chocolate, it will not taste quite as good as the time before. This is far more acceptable and believable to most people. Then, with enough repetition over a period of time, chocolate loses much of it's positive taste and control over that person. One final note is that HYPNOSIS IS NOT DANGEROUS. There are almost no risks when used by trained professionals. You cannot be made to do anything that is against your moral values. An amateur or stage hypnotist might give you suggestions that might embarrass you, might not work or that might make you feel uncomfortable or self-conscious at the time. To avoid this, stick with professionally trained hypnosis specialists. The one risk I know about involves falling asleep. If you are tired or if you become too relaxed, you may move from the state of hypnosis to the normal sleep state. This is fine if you were going to go to sleep right after the trance but if you have other plans after listening to a hypnosis tape, you may want to set an alarm clock just in case you fall asleep. I've even had students fall asleep because they became too relaxed. In relation to this, never listen to a hypnosis tape while driving. It is very dangerous for you and everyone else on the road. Don't even listen to it if you are a passanger as the relaxation suggestions could make the driver fall asleep. Over the years, self improvement and personal growth using hypnosis has helped millions of people change their lives permanently because it is a safe and powerful tool for changing your thoughts, feelings and habits. Copyright C 2001 by Thomas D. Yarnell, Ph.D., Clinical Psychologist. All rights reserved This material may be copied for educational purposes as long as full credit is given to Dr. Yarnell.If Chris george would have taken the time to read the entire thread, *I have never ever in my life used the word cure with Hypnotherapy or in IBS* , if he would have read the thread he would have seen it was bonnie, who used those words and I corrected it. Although he seems to be on a mission in regards to me and Mike and I am sure this won't be his last comments. However, he has no idea who I am and what I know and who teaches me or what I am involved in.Nor do I get all my information off the web as implied, but a good portion of it through Dr Palsson the worlds second leading expert on HT and IBS. As well as Information from Dr Whorwell's research the leading expert and Mike, nor do I attempt to hypnotize anyone which would be just plain wrong.breathrough research in IBS 1997By using sophisticated imaging techniques that allow us to visualize the activity of the living human brain see ï¿½Looking Into the Living Human Brainï¿½, researchers at the UCLA Neuroenteric Disease Section have recently identified for the first time the regions within the brain that are involved in the perception and modulation of visceral sensations, including visceral pain. In addition, by comparing brain responses to an acute intestinal stimulus between healthy control subjects, patients suffering from IBS, and patients with ulcerative colitis, they were able to identify specific alterations in how the brains of IBS patients process and respond to acute colonic pain. These research results have recently been published in Gastroenterology. This is the first study which has been able to identify an objective biological marker that is only seen in IBS patients and that is located within brain regions, which are likely to be involved in the alterations in perception and autonomic responses that underlie the most common IBS symptoms. These findings are the first step in a better understanding of how these symptoms develop and how we can treat them by identifying specific targets for pharmacological therapy. The most prominent brain region found to be activated in response to intestinal stimulation in healthy subjects was a specific area within the anterior cingulate cortex which forms part of the limbic system. The limbic system, which has also been referred to as the ï¿½visceral cortexï¿½ plays a prominent role in a wide range of functionsï¿½from maintaining homeostasis, to autonomic control of the digestive system, to pain perception to the generation of feelings and emotions, and to memory of past emotional states. The specific area within the anterior cingulate cortex identified in the brain imaging studies plays a prominent role in several aspects relevant to IBS symptoms: 1. It is the ï¿½executive areaï¿½ in the regulation of colonic motility and water absorption which in turn determines the frequency and consistency of bowel movements. 2. It is part of the medial pain system which determines the affective component i.e. the degree of suffering or unpleasantness associated with pain perception. Specific regions with the medial pain system play an important role in suppressing the perception of pain by releasing endorphin molecules the bodyï¿½s own painkillers, while other regions participate in the memory formation of past painful experiences. 3. The brain region identified by the UCLA researchers plays a prominent role in the regulation of maternal behaviors and is crucial for mediating communication between newborns and their mother. The results of this study have wide ranging implications for all patients suffering from IBS. The findings for the first time have established IBS as a biological disorder, which can no longer be labeled psychological or ï¿½not realï¿½ by the healthcare system. The current results are the basis for future research efforts delineating the networks and receptors within the brain that are responsible for such IBS symptoms as abdominal pain and discomfort, sleep disturbance, and altered bowel habits. A range of brain imaging studies are currently underway at UCLA which aim at unraveling these mechanisms. Brain regions and receptor systems identified by functional brain imaging studies are likely to become targets for new drug developments in the near future. http://ibs.med.ucla.edu/Newsletters/Spring97Break.htm Pain in the brainDuring the last three years, we have been investigating how the human brain processes pain-related signals it receives from the bodyï¿½s internal organs. More recently, we have been examining what differences, if any, occur in the way the human brain processes these signals ï¿½ both in healthy subjects and in patients suffering from irritable bowel syndrome. Several pieces of evidence suggest that women are more prone to certain chronic pain conditions than men. In the United States, IBS is about twice as common in women than in men, and many other chronic pain conditions such as irritable bladder syndrome and fibromyalgia are also significantly more common in women. Despite these clinical findings, the biological basis underlying these gender differences remains unclear. Using positron emission tomography PET and corroborative functional magnetic resonance imaging fMRI, in combination with a protocol to stimulate the colon, investigators at the UCLA/CURE Neuroenteric Disease Program generated the first data to measure regional cerebral activity of intestinal pain in humans. They have also found a disease-specific pattern of alteration of that activity among patients suffering from the most common chronic gastrointestinal condition in the United States, IBS. For a more detailed account of that work, please see the Los Angeles Times ï¿½Scienceï¿½ sectionï¿½s feature article, 5 September 1996, or the January 1997 issue of Gastroenterology. To perform these studies, they employ a balloon catheter that is connected to a programmable pump which delivers precise distension pressures to the colon over fixed periods of time. The catheter is placed in the rectosigmoid colon approximately one hour before the brain imaging sessions. PET scans are then obtained at baseline and during inflation of the balloon to pre-specified distension pressures. Using this technique, the UCLA investigators discovered a failure in patients with IBS to activate a portion of the brain which is called the anterior cingulate cortex. This brain region has several properties which are pertinent to the symptoms of IBS. It has a high number of opiate receptors, suggesting that it plays a crucial role in the bodyï¿½s ability to inhibit pain by releasing endorphins. It has been identified as the brain region that determines the degree of suffering and unpleasantness associated with pain and it plays an important role in regulating the autonomic nervous systemï¿½s response to pain, i.e. in the regulation of heart rate and gastrointestinal motility and secretion. The balance between so-called parasympathetic and sympathetic nerve influences on the digestive system plays an important role in the etiology of constipation and diarrhea. By combining this kind of brain imaging protocol with continuous monitoring of autonomic measures skin conductance, pulse rate, heartbeat-to-heartbeat variability, measures of perception stimulus intensity, stimulus unpleasantness, anxiety level and timed sampling of hormones in the blood serum levels of estrogen, progesterone, norepinephrine, cortisol, ACTH, they have available a powerful method for establishing in detail the central and peripheral nervous systemsï¿½ responses to pain stimuli and how those responses differ between the sexes. The results of their most recent experiments so far involving 220 PET scans obtained from 36 subjects equally divided between males and females indicate that during both actual and anticipated colonic distention, significant differences between the regional cerebral blood flow patterns in the brains of men and women occur. The sex differences are even more dramatic among patients with IBS. Areas that differ most significantly include the anterior left insula, a brain region with close connections to the anterior cingulate cortex and the prefrontal cortex. These three brain regions form a network that is involved in pain processing, and in memory retrieval of past pain experiences and associated emotional and autonomic responses. Thus, the same networks in the brain that process an actual painful stimulus are involved in the formation of complete memories of such events. This may be of importance in view of the common association of IBS with post traumatic stress syndrome PTSD, a syndrome that develops after an extremely stressful situation during which an individualï¿½s life was threatened such as war combat exposure, motor vehicle accident or rape. Commonly, affected patients develop a flashback of the traumatic event, triggered by a sound or picture. This flashback is associated with all the emotional, sensory and autonomic responses that were part of the brainï¿½s response to the traumatic stimulus in the first place. Even though the majority of IBS patients do not have PTSD, it may be that certain life events, food intake or sensations from the gut can trigger memories of past abdominal pain and discomfort, which may have occurred as far back as childhood. Based on our findings it is intriguing to speculate that men and women differ in the degree to which they retrieve such memories in preparation for an anticipated pain from their gut. http://ibs.med.ucla.edu/Newsletters/Fall97Brain.htm This is also very important in IBS and is also a part of foods as triggers."it may be that certain life events, food intake or sensations from the gut can trigger memories of past abdominal pain and discomfort, which may have occurred as far back as childhood."The pain area of the ACC is not functioning right in IBS Patients and its regardless of d or c or d and c, although that may make for variations in the scans.And Tom's recent post in the news section to this fits into this also and its convergence seen in Fibro CFS and IBS is the HPA axis."Hart et al 2003 reviewed studies that examine cognitive functioning in patients with chronic pain with an emphasis on the role of emotional distress and the mechanisms of stress-related effects. They found an association between psychological distress and cognitive impairment in patients with chronic pain, especially pain-related negative emotions and variables that mediate suffering such as interference with activities and increased somatic vigilance. Further, they report on recent evidence that psychological distress is related to cognitive impairment independent of the effects of pain intensity. In examining possible underlying neurophysiologic substrates, they noted that the Anterior Cingulate Cortex ACC plays an important role in pain processing and affective-motivational experience, and mediates the impact of pain-related emotional distress on cognitive functioning through allocation of attentional resources. In addition, maladaptive physiologic stress responses and dysregulation of the hypothalamic-pituitary-adrenocortical HPA axis can produce negative effects on hippocampal function and memory. They postulated that the underlying mechanism for cognitive impairment may be the vigilant anticipation of unpredictable pain symptoms, especially in individuals high in trait neuroticism, which presents a significant stressor that repeatedly activates both the HPA axis and ACC areas, thereby disrupting cognitive efficiency." http://www.ibsgroup.org/ubb/ultimatebb.php...=1;t=033898;p=4 Neuropathophysiology of irritable bowel syndrome.Wood JD. *NOTE AND EXPERT ON FOOD ALLERGIES* Departments of Physiology and Cell Biology and Internal Medicine, Ohio State University College of Medicine and Public Health, Columbus, Ohio, USA. wood.13###osu.eduWidespread symptoms associated with the irritable bowel syndrome IBS are abnormal defecation and abdominal pain, both of which can be exacerbated by psychogenic stress. Disordered defecation may present as diarrhea or constipation. A subgroup of IBS patients alternate from one to the other over time. Urgency to stool often accompanies the diarrheal-state, and patients with the constipation-predominant form of IBS report straining and the feeling of incomplete evacuation. Basic scientific research aims for improved understanding of the physiology and pathophysiology of the digestive systems from which the arrays of IBS symptoms emerge. The key systems for the defecation-related symptoms are the intestinal secretory glands, the musculature, and the nervous system that controls and integrates their activity. Abdominal pain and discomfort arising from these systems adds the dimension of sensory neurophysiology. This review details current concepts of the underlying pathophysiology in terms of the physiology of intestinal secretion, motility, nervous control, sensing function, immuno-neural communication, and the brain-gut axis.Publication Types: Review Review, Tutorial PMID: 12184133 Am J Med. 1999 Nov 8;107 5A:12S-19S. Related Articles, Links Emerging disease model for functional gastrointestinal disorders.Mayer EA.Division of Digestive Diseases, University of California Los Angeles School of Medicine, USA.In response to perceived or experienced change that is considered threatening to the individual, the central nervous system mounts a stereotypic response that decreases the sensitivity to pain, modulates the autonomic nervous system outflow, and activates the hypothalamic-pituitary-adrenal HPA axis. This response of the "emotional motor system" may or may not be associated with the conscious experience of feelings of fear or anxiety. Alterations in these response systems either up- or downregulation may produce symptoms, such as viscero-somatic hypersensitivity, altered bowel habits, or increased anxiety.Publication Types: Review Review, Tutorial PMID: 10588168Eur J Surg Suppl. 1998;583:29-31. Related Articles, Links Intestinal and extraintestinal symptoms in functional gastrointestinal disorders.Mayer EA, Fass R, Fullerton S.UCLA/CURE Neuroenteric Disease Program, UCLA School of Medicine, Los Angeles, CA 90073, USA. emayer###ucla.eduFunctional gastrointestinal disorders such as irritable bowel syndrome or functional dyspepsia have traditionally been regarded as syndromes limited to the digestive system. However, both clinical experience and published evidence show that patients with such disorders also report a series of other symptoms of physical distress, such as fibromyalgia and irritable bladder and alterations in vital functions, such as sleep, libido, appetite and energy level. Some of these extraintestinal symptoms can be explained in the context of an evolving comprehensive disease model which views functional gastrointestinal disorders as manifestations of alterations in the interactions between the nervous system, the viscera and the musculoskeletal system. Alterations in central circuits concerned with arousal, attention and fear, cognitions about bodily symptoms and possible alterations in the hypothalamic pituitary adrenal HPA axis may all contribute to the wide range of symptoms reported by affected patients.PMID: 10027669


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## trbell (Nov 1, 2000)

quote: "If Chris george would have taken the time to read the entire thread, I have never ever in my life used the word cure with Hypnotherapy or in IBS , if he would have read the thread he would have seen it was bonnie, who used those words and I corrected it. Although he seems to be on a mission in regards to me and Mike and I am sure this won't be his last comments. However, he has no idea who I am and what I know and who teaches me or what I am involved in."perhaps that's because you never say who you are or what your credentials are except as expert on IBS. As I've said before it's fin for ou to post as an IBS sufferer who's read a lot and is knowledgeable and a nice guy but it's in the best interests of the people who come here for help to know what your credentials are. chrisgeorge is a practising hypnotherapist who I think has written to Palsson and Whorwell as well.As I've said before the standards for medical experts are higher than for others and this is for the good of people who read these posts.tom


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## eric (Jul 8, 1999)

FYI againPathophysiologyAltered Serotonin Signaling?The pathogenesis of IBS remains obscure, and in particular, an explanation for alternating diarrhea and constipation has been elusive. In arguably one of the most important papers presented during this year's meeting, Moses and colleagues 21 studied potential deregulation of the gut's serotonin transporter in IBS. It is known that serotonin 5-hydroxytryptamine or 5HT is released from enteroendocrine or enterochromaffin cells in response to either chemical or mechanical stimulation of the gut mucosa. Serotonin in turn initiates peristalsis, and then the serotonin released is taken up in health by a highly selective serotonin transporter SERT. One potential mechanism that could explain altered bowel function in IBS is an abnormality in the serotonin transporter itself. The study authors evaluated this hypothesis in patients with IBS with constipation and IBS with diarrhea compared with patients with ulcerative colitis and healthy controls. They were able to convincing show on blinded review that SERT immunoreactivity was less intense in patients with IBS with constipation and patients with ulcerative colitis. If these findings are indeed correct, they represent a landmark observation. The findings suggest that patients with constipation and IBS may have a reduced capacity to reuptake serotonin, leading to excess free serotonin and then desensitization of these receptors, thus reducing motor function. In contrast, in the setting of diarrhea, serotonin uptake was normal. If the underlying abnormality in serotonin transporter function alternated, then this would in turn explain alternating constipation and diarrhea. These data strongly suggest that IBS is a "real" gut disease and a potential diagnostic disease marker. They also suggest that it is valid to subdivide IBS into constipation and diarrhea symptom subgroups. This study also provides additional rationale for the use of serotonin-modulating agents in IBS and provides a new target for drug modulation. Confirmation of these very exciting initial findings in larger patient samples is awaited with great interest.Ask The Expert.Image of a cadeusus. .General Medical Questions.Q: I have suffered from irritable-bowel syndrome for many years. I get diarrhea. The doctors I've seen have offered little help. Recently, my daughter suggested I try an over-the-counter medicine called "5-Hydroxy-tryptophan," made by a company called Natrol Inc. My daughter says it is a mild antidepressant. It seems to have helped quite a bit, but it also seems to slow me down and make me feel tired. Can you give me any information on this? What is it, exactly, and are there any serious side effects? The only other medicine I take is Synthroid....The Trusted Source..Harold J. DeMonaco, M.S.Harold J. DeMonaco, M.S., is senior analyst, Innovative Diagnostics and Therapeutics, and the chair of the Human Research Committee at the Massachusetts General Hospital. He is author of over 20 publications in the pharmacy and medical literature and routinely reviews manuscript submissions for eight medical journals...June 19, 2001.A:Irritable bowel syndrome is now recognized as a disorder of serotonin activity. Serotonin is a neurotransmitter in the brain that regulates sleep, mood depression, anxiety, aggression, appetite, temperature, sexual behavior and pain sensation. Serotonin also acts as a neurotransmitter in the gastrointestinal tract.Excessive serotonin activity in the gastrointestinal system enteric nervous system is thought to cause the diarrhea of irritable-bowel syndrome. The enteric nervous system detects bowel distension expansion on the basis of pressure-sensitive cells in the bowel lumen opening. Once activated, these pressure-sensitive cells promote the release of serotonin, which in turn promotes both secretory function and peristaltic function the contractions of the intestines that force the contents outward. At least four serotonergic receptors have been identified to be participants in the secretory and peristaltic response.Patients with diarrhea-predominant IBS may have higher levels of serotonin after eating than do people without the disorder. This recognition led to the development of the first drug used specifically to treat diarrheal symptoms of IBS, alosetron also known as Lotronex. Alosetron blocked the specific serotonin receptors responsible for recognizing bowel distention. In doing so, it blocked the effects of serotonin and reduced both bowel secretions and peristalsis. Constipation was the most common side effect seen. Note: Alosetron was removed from the market by the manufacturer after repeated reports of a dangerous condition known as ischemic colitis became known. Tegaserod Zelmac is another drug under development and under review by the U.S. Food and Drug Administration for approval. Tegaserod is indicated for the treatment of constipation-predominant IBS and works to increase enteric nervous system serotonin activity.So, increasing serotonin activity in the enteric nervous system produces increased bowel secretions and peristalsis and potentially diarrhea, whereas depressing serotonin activity produces reduced secretions and reduce peristalsis and potentially constipation. Increasing serotonin activity in the brain would increase awareness and, in higher doses, produce anxiety, insomnia and restlessness. So I would have expected exactly the opposite effects of those that you experienced.I am unable to identify any possible drug interactions between 5-HTP and Synthroid levothyroxine but the symptoms described suggest a check with your doctor may be in order. Persistent feelings of tiredness and constipation may be signs of an underactive thyroid hypothyroidism.June 19, 2001 From Havard Intellihealth * The enteric nervous system detects bowel distension expansion on the basis of pressure-sensitive cells in the bowel lumen opening. Once activated, these pressure-sensitive cells promote the release of serotonin, which in turn promotes both secretory function and peristaltic function the contractions of the intestines that force the contents outward.* "It is well established that patients with IBS as a group have an increased sensitivity to balloon distension in the rectum and colon.6 There is also evidence that some patients with IBS, particularly those with postprandial symptoms, have an increased gastrocolonic response" http://www.ibsgroup.org/other/NTalley-DDWeek2000.html "postprandial (adjective) - 1. following a meal" gastrocolonic response is when the stomach send signals to the lower digestive system that food is on the way from the act of eating and the amount of calories in a meal and the lower digestive system, the large colon dumps its contents. And in IBS this process is altered and the lower colon has an exaggerated responce.enterochromaffin cells in the gut are pressure sensitive and store 70 percent of the serotonin in the gut, when activated in d predominate IBS they intiatie the *peristaltic Reflex* which ois why this is very important even though Mike No lo would like to downplay this in IBS. Serotonin is also majorally involved in pain signals coming from from the gut. As well as other properties it has in regards to the signaling potentials it has from the gut to the brain and back. hence why some emotions may start in the gut as gut feelings.Also Normals 15 minutes after eating in the lower colon







In IBSers 15 minutes after eating in the lower colon


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## eric (Jul 8, 1999)

I have a diclaimer on my signature Tom and I have never said I was an expert on IBS or hypnotherapy. I also have on there I am a thirty year IBS sufferer. I am not out to pull the wool over anyones eyes with IBS regarless of what you or anyone thinks and has sugested numerous times, in fact I am posting to this thread for that very reason so people get all the information and make thier own choices. However, your right I am missing soemthing there that I will add right now.


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## trbell (Nov 1, 2000)

If you read what you said to Chris you'll see I think that it was an attack on him and his credentials? That's why i posted what I did. From what I've seen of his posts and his background, I think he should be welcomed here.tom


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## bonniei (Jan 25, 2001)

You people are way behind on science. Note the words in bold in the following abstract. Wake up, smell the coffee. Hypnotherapy for crohn's disease. A promising complementary/alternative therapy. Author: Abela MB Source: , 2(2): 127-131 2000 Service Fee: $12.00 ; Copyright Royalties: Abstract: Crohn's disease is a nonspecific chronic syndrome of unknown origin for which, to date, no conventional (i.e., medical or surgical) cure exists. However, recent clinical case studies and anecdotal reports have shown that the use of *different forms of hypnotherapy for the treatment of Crohn's have actually resulted in cures*. This report reviews and compares the effectiveness of hypnotherapy in the treatment of Crohn's disease vis-a-vis current medical and surgical therapies, in addition to reviewing evidence of the modulation of immune function parameters by hypnosis, while providing support for current etiological hypotheses of Crohn's disease as an autoimmune disorder.


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## bonniei (Jan 25, 2001)

Re:the change of topics. eric I think you have your own agenda which is to bring your research into the pic. The first one who went off topic was you by posting the link on food intolerance tests. I must say I am miffed my topic never got discussed- which is Brostoff and what I said he says in his book. Specially about fungal type dysbiosis and gut permeability. Not this endless tiring research on hypnosis we have seen many times before. You wanted to engage in a debate with Mike, eric and you have wriggled your way in. Well if anyone has a serious comment on my topic I would be glad to hear it. I am done with my thread.


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## trbell (Nov 1, 2000)

I'll believe it when I see 10 studies like for IBS. tom


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## eric (Jul 8, 1999)

Bonnie, depends on the source of the article and quite frankly I would say that one is extremely questionable. Crohn's is an organic disease and should be treated as such. IF HT is used for it it should only be complementary. Those patients could have gone into remission on there own.HT can hel;p digestion of course so it maybe a adjunct therapy to a lot of problems esecailly stress related ones. Chrohn's also has a mind gut connection to it.Tom, he was trying to put words in my mouth I never said and cast doubt on my integrity. I know why.


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## bonniei (Jan 25, 2001)

The source is Integr. Med.. 2000 Mar 21;2(2):127-131 for the Crohn's article.


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## eric (Jul 8, 1999)

I read the source Bonnie, I also was not the one who broght up HT on this thread.I was pointing out how inaccurate Mike's food connections were and that study he has shown us for years nowto convince people of the loss of oral tolerence and inflammation and d in IBS and foods causing it. The bottom line they don't know what causes it, from that study and some of them already had inflammation from an enteric infection and some of them didn't even have d? Also is a very very small minority and he like's people to believe its a huge amount of d IBS sufferers. Why don't you ask him those questions, what role does serotonin have in IBS, what is the gastro colonic responce in IBS and why is it altered? What other r4easons are there for foods to cause problems in IBS, regarless of loss of oral tolerence? Why do more women then men get it? Why do hormones effect it if its a loss of oral tolerence problem or how does it effect sleep or why does it wax and wane or why does even the weather effect it? Why is there rectal sensitivity, because foods don't cause that, and many other important questions that should be asked. Foods are triggers that for sure, but there are some basic's IBSers should learn first. As for Kel's previous statements I don't have food advise for IBS I have a whole page on my site for it. http://www.ibshealth.com/ibsfoodsinfo.htm


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## eric (Jul 8, 1999)

Bonnie, " eric I think you have your own agenda which is to bring your research into the pic"Its not my research its top experts in IBS research.Who is Dr Gershon?Who is DR Wood?I keep giving you their credentials and who there are? Its information on IBS from leading experts in the field, not my personal view or MY research. My agenda is for you to see all the research not just immune which is seriously one sided, that's the point.


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## chrisgeorge (Feb 28, 2003)

WOW! Go away for an hour or two, and all hell breaks out!Just for clarification, I have never taken Mike and his tapes to task.In fact I have a copy and they're quite good.I have on several other forums (and on other BB's) questioned the credentials of Eric.I'm a firm believer, if you're going to talk about a subject atleast have the practical experience or credentials to back it up. Thanks for letting me clarify that.Chris


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## trbell (Nov 1, 2000)

"Tom, he was trying to put words in my mouth I never said and cast doubt on my integrity. I know why."I'm sure if he put words in your mouth he'll clarify this. I think also though that you are the one wo puts his integrity on the line when you talk as if you were an expert or authority on hypnosis it needs to be backed up with some educational credntials and that's what he may have been referring to.tom


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## kel1059 (Feb 28, 2003)

Eric,Here is a part of the problem in a nutshell. I have tried your methods to the best of my abilities over an extended period of time --close to 7 or 8 years--and I got no better.Therefore I had no choice but to try a different method. My new method has given me an extreme amount of success, but I have a ways to go.I believe that us long-time IBS sufferers will sometimes need to peel this problem of IBS like an onion. (i.e. modulating/or strengthening the immune system, correcting any dysbiosis, reducing yeast/fungus if symptoms point to it, avoiding sucrose or other addictive foods if present in the diet, discovering and avoiding all food hypersensitivities, and balancing out the body.)My focus has been on the actual gut for quite some time. I needed to forget the brain for a while because it has not helped -----BUT (!!!) in the future, I will return to the brain aspect of it and use that method to put the finishing touches on my problems.However, in the meantime, I must continue to be vigilant on diet because food causes absolutely horrible symptoms --especially dairy, wheat, corn, cheese, yeast, beef....I also need to place a strong emphasis on dysbiosis. There seems to be some microorganisms in my gut that need to be constantly kept in check by various means such as, garlic, herbs, antifungals, colonic flushes, and even bentonite seems to be doing a nice job pulling something out.I have been on several serotonin acting drugs and they do not help with my gut or GI symptoms. However, I am still curious about Zelnorm and even naltrexone (endorphin-opioid system [although i don't have any pain any longer]). I will leave no stone unturned.However, as you know, Ibsacol (an immunomodulator) has given me my only solid relief that I have ever experienced. I do not know if it will hold up but right now it appears that my problem seems to be centered around prostaglandins and leukotrienes because of the relief from Ibsacol.I believe that the abstract that you provided from Dr Spiller has been very informative ...also the one you provided from the mayo clinic also helped me see that there is some type of "immune reaction" associated with yeast/fungus in a subgroup of people.


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## bonniei (Jan 25, 2001)

I don't ask Mike any tough questions because he doesn't give me a hard time. I have had a long history with you eric. When I was talking about serotonin type drugs you made entire threads about how people should say what they were taking drugs for. When I talk about fructose intolerance, you are ready to put old studies dismissing it. You think research is all that counts? Experience counts even more. With all the research they have been doing for hundreds of years it is only now that they are coming up with drugs that help. I have been on my own trying out what works long before I came to the BB. Eliminating fructose works so please don't dismiss it. It is very irritating. Seotonin is not the whole picture. It has helped with D but not gas. So let us try to find solutions without you making every discussion a debate between you and Mike.


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## trbell (Nov 1, 2000)

Bonniei, This is your thread and I can understand your getting impatient with all the weird turns it's taken. I hope you don't mind another suggestion from me, but what is it that you want solutions for specifically? Yell at me here if you want.tom


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## bonniei (Jan 25, 2001)

Just an example of a thread which eric made just to draw attention to what I was doing long ago when he wasn't so much into serotonin http://www.ibsgroup.org/cgi-local/ubbcgi/u...c;f=45;t=000487 I am trying to understand if gluten sensitivity leads to altered gut permeability because bread gives me gas and I have deficiency of B12 and I am trying to figure out if I should cut out gluten completely out of my diet


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## trbell (Nov 1, 2000)

why not try it for awhile? I don't think it can hurt.tom


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## bonniei (Jan 25, 2001)

Well I am a vegetarian at home- no veggie, no fruits, no grain. Not only will I will have to become a meat eater, I will become constipated with no fiber. It is a drastic change. In any case I wanted to hear Mike's opinion on the topic of my thread which never took off because eric came in with his food intolerance link and it took the weird turn it did.


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## trbell (Nov 1, 2000)

funny how that happens. I hate to make another suggestion but why not ask Mike on another thread? He doesn't visit very often these days but will answer eventually.tom


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## bonniei (Jan 25, 2001)

MikeNL, what is your opinion on gut permeability and can it affect the absorption of B12 and can gluten sensitivity affect gut permeability?


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## trbell (Nov 1, 2000)

on a new thread I think. everybody has stopped reading this thread ong ago except the diehards and he'll never see the question here.tom


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## kel1059 (Feb 28, 2003)

Mike NL posted some links on page 1 of this thread that discuss vit B12 problems. http://www.canceralt.net/Bowel%20I%20Alter...l%20Ecology.htm I think this is it. it says that dysbiosis (which flux dismisses) can cause a b12 deficiency. excerpt from Dr majid ali's article: _LAPs confer many important host defenses upon the bowel discussed later in this section. TAPs are equally versatile in their functions and produce a very large number of noxious substances in the bowel. Among these are ammonia; phenols; tryptophan metabolites; vaso-constrictive amines such as histamine, tyramine, agmatine and cadaverine; certain steroid metabolites; and many toxins - most notably mycotoxins derived from fungi (yeasts). This area has received rather limited investigative attention, and it is almost certain that future research will uncover a host of as yet undetected bacterial and fungal toxins and metabolic villains_ The entire article by this pathologist is extremely fascinating. However, i do not think that dysbiosis is going to explain all our problems and it may not even explain any problems for some people.(however, i bet eric has a serious case of dysbiosis from all those antibiotics he took over the years) (i just found an article that conclusively states that the fungus likes to hide between the intestinal villi and also in the crypts. I will fetch it if anyone wants to view it.)


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## flux (Dec 13, 1998)

> quote:However, we are talking about what the "INITIATING" mechanism is. ....and the hypothalumus does not -out of the blue- just decide to create a fever.


The hypothalmus regulates temperature. So in a sense, it is always creating a fever.









> quote:When it comes to typical and atypical allergy, intolerances, and hypersensitivities --- the brain is not the director. it is the target.


The brain is the target? Are you trying to say that food is out to get your brain? I can't imagine those M & M guys beating up one's brain. Aunt Jeminma. The Quaker oat guy. Mrs. Paul's. These food folk are nice people


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## kel1059 (Feb 28, 2003)

> quote: "but in order to fully understand it which is super complicated you have to know a lot about the mechanisms behind it all" Eric its statments like this that bug me. fully understand and super complicated don't go together. If it was fully understood it wouldn't be super complicated. You see what I mean? If it was fully understood then everyone would agree and there would be much more percise debate going on. Where's my buddy Flux? Over on the Autism Board spreading his good cheer around? ( a joke, I really don't even know if there is a Autism board )


I found this post from the archives (2 years ago) Hilarious!!! hey flux, are you still harrassing those people?###############################################3back to business.....Bonniei,I think my last post with the link to a pathologist's essay on dysbiosis is my attempt to get your very nice thread back on target.(p.s. i like your comment on enzymes and faulty catabolism...... I have had those same thoughts myself concerning my situation. when i was very sick or even presently, it is during the catabolic and eliminative cycles. there are 3 cycles that operate during the day. The anabolic cycle is when I feel normal.)


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## ohnometo (Sep 20, 2001)

MikeSounds like your 4th of July was fun







I had a good vacation from work and I painted my porch and my kitchen . Now I had to come back to work just to rest !!!







There isnt much I can say about this post because I dont want my stress level to get up to high because I will get really sick..







I sit on fire ants one time in Myrtle Beach at my MIL house...I dont think I have ever moved that fast before....No apple pie over the Holiday...As American As Apple Pie


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## bonniei (Jan 25, 2001)

MikeNl, I have addressed a thread just to you. The others are not invited







And I suppose today will be the day that MikeNL doesn't show up.


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## ohnometo (Sep 20, 2001)

EricHere is your story http://www.ibsgroup.org/ubb/ultimatebb.php...c;f=17;t=000002 Your IBS started from maybe drinking some water that was bad .So a real physical condition would have been your trigger for IBS correct ? So the hypnosis helped with the pain ?


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## Mike NoLomotil (Jun 6, 2000)

BONNIE AND DONNA!Hi. Saw the other thread and wrote something quick with a quick explanation why I have to run after a quickie here.OhNOU2: delving into the history of symptom onset which might link to the possibility of some pathogenesis which might be tangible may be an unwlecome point. Steel thyself!Onwards as daylight is burning...._________________________ï¿½So, Mike. are you saying you'd be happier if the hypno forum were opened up to include all kinds of hypnotherapy? if there were a food intolerance forum should it be restricted to the LEAP program or include other programs?ï¿½___________________________Wish I had more time as you pose interesting questions. But I gotta hurry. See Bonnies thread asking about gut permability for my cop out for today....people waiting! But quickly:No, happy or unhappy would not characterize what I am expressing as my happiness is not dependent upon what transpires in discusson forums, so that is not actually an issue. To clarify, I try at times to understand, or is it convey?, when HT is discussed that it should be discussed in a fashion no different than any other therapeutic modality. There are few if any panaceas. It seems from the literature and from hypnotherapists I have met who perform various forms of medically-directed HT, that there are variables in outcomes between, in the coarsest sense, HT by audio program vs. HT administered in face-time, and that the protocols within each delivery system vary and make a difference as well. Also like any lifestyle modification the outcomes are also dependent upon adherence to the protocols and on the affective behaviors of the patient (valueing). It is not reasonable simply to apply all HT outcomes to all HT protocols any more than it is to apply all dietary treatment outcomes to all dietary protocols. I just think this generalizing happens sometimes and to the patients unfamiliar with the subject this can result in the formation of false conclusions.Also it is important to reinforce consantly that my core premise in any patient care IBS inclusive is that multi-modality treatment should be the game plan, and it should made as patient-specific as possible as this maximizes the therapeutic outcomes. This should be the goal of any treatment program for any condition.Interesting questions as far as ï¿½branded programs goesï¿½ . The diet forum I know, since I go there from time to time, covers a lot more territory than just the LEAP protocols. Oligoantigenic dieting for GI problems is a broad subject if one looks at from all perspectives and all mechanisms known, and the more discussion brings those multiple mechanisms to the fore the better it is for the patients trying to understand the subject. I suspect it is healthy if the HT Forum has input from various sources of HT protocols as well. This may very well be the case. I do not know for certain how often this occurs as I am not active in the forum and only pop in an observe occasionally to see who is there from the ï¿½provider sideï¿½ of the equation.But if patients want to talk about modalities other than HT I assume they will do so in an area where the topic is monitored for discussion by people who do work in that area of care. Another good point, from a post by Bonnie, which IS the point about proinflammatory and proalgesic mediators in the symptoms of IBS:_____________________________ï¿½Inflammation is associated with production of mediators including prostaglandins, bradykinins, nerve growth factors, adenosine, and 5-hydroxytryptamine. These mediators induce visceral hypersensitivity, exaggerated motor responses, and increased intestinal secretions81 (figure 2), which could contribute to episodic diarrhoea.ï¿½_____________________________Donï¿½t misunderstand the word ï¿½includingï¿½ to imply ï¿½exclusiveï¿½, rather it would be accurately phrased as ï¿½including but not limited ï¿½ï¿½the following mediators. And indeed PGE2 was the very first to be isolated many years ago in elevated concentratuions in the stool of diarrheic IBS victims. It causes smooth muscles contraction and increased secretionï¿½.diarrheaï¿½. It also is implicated in patients where dysmenorrhea is a comorbidity as it causes increased contraction of uterine smooth muscle as well..ouch. There are a number of tutorials out there to read which cover the wide range of various mediator types and their influences upon specific organs and tissues and which have been implicated in symptom generation in IBS victims.____________________ï¿½was pointing out how inaccurate Mike's food connections were and that study he has shown us for years now to convince people of the loss of oral tolerence and inflammation and d in IBS and foods causing it.ï¿½____________________Just gotta love this guy! The inaccuracy is in your claims of such, not ï¿½Mikeï¿½s connectionsï¿½ as they are not MY connections they are the ï¿½connectionsï¿½ of researchers and clinicians who have actually done specific work which quantifies the connections of which I speak. So if you wish to pretend such work, spanning 25 or more years, does not exist please feel free to persist with this scotomic mantra of detachment. ï¿½One studyï¿½ indeed. Apparently refers to all that has been persoanlly read on the subject, and all other material is ignored so it does not exist. One may wish to noter, for exzmple, the extensive bibliographies of some studies, which also must be acquaired an read so as to master the peripheral material to the matter investigated, pro and con. Try to Reread what I wrote again until you can see Allll the words. Meanwhile, Like I said, there are literally hundreds of realted referecnes on the topic if one chose to do oneï¿½s homework. You need to read a few books too as they have related content and it of course is drawn from a substantial bibliography anyone is free to, and compelled to, refer to and make an effort to read.Try at least these to start and maybe one day one will see the difference between belief systems and reality:IBS: A DOCTORS PLAN FOR CHRONIC DIGESTIVE TROUBLESBy Gerard Guillory, M.D.; Vanessa Ameen, M.D.; Paul Donovan, M.D.; Jack Martin, Ph.D. http://www.amazon.com/exec/obidos/ASIN/088...3369143-6824157 ï¿½FOOD ALLERGIES AND FOOD INTOLERANCE: THE COMPLETE GUIDE TO THEIR IDENTIFICTION AND TREATMENTï¿½, Professor Jonathan Brostoff , M.D.. Allergy, Immunology and Environmental Medicine, Kingsï¿½ College, London http://www.amazon.com/exec/obidos/ASIN/089...6487508-3420903 FOOD ALLERGY AND INTOLERANCE, Professor Jonathan Brostoff, MD, Stephen Challacombe, MD (NEW 2002) http://www.amazon.com/exec/obidos/ASIN/070...product-details ________________ï¿½My agenda is for you to see all the research not just immune which is seriously one sided, that's the point..ï¿½_______________The Pot frantically denounces The Kettle for being black.







the beach beckons!







MNL


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## Mike NoLomotil (Jun 6, 2000)

Oh I forgot this is also paert of, and at the root of, the issues when they turn into debates..one example: _______________________BMC Gastroenterol. 2001;1(1):11. Epub 2001 Oct 26 Do Published Guidelines for Evaluation of Irritable Bowel Syndrome Reflect Practice?Yawn BP, Lydick E, Locke GR, Wollan PC, Bertram SL, Kurland MJ.Department of Research, Olmsted Medical Center, Rochester, Minnesota, USA. BACKGROUND: The only US guidelines listed in the National Guideline Warehouse for the diagnosis of Irritable Bowel Syndrome (IBS) are the expert opinion guidelines published by The American Gastroenterology Association. Although the listed target audience of these guidelines includes family physicians and general internists, the care recommended in the guidelines has not been compared to actual primary care practice. This study was designed to compare expert opinion guidelines with the actual primary care provided and to assess outcomes in the 3 years following the IBS diagnosis. METHODS: This is a retrospective medical record review study using a random sample of incident IBS cases from all Olmsted County, Minnesota providers diagnosed between January 1, 1993 and December 31, 1995. Data was collected on all care and testing provided to the subjects as well as 3-year outcomes related to the IBS diagnosis. RESULTS: Of the 149 IBS patients, 99 were women and the mean age was 47.6 years. No patient had all of the diagnostic tests recommended in the guidelines. 42% had the basic blood tests of CBC and a chemistry panel. Sedimentation rate (2%) and serum thyroxine level (3%) were uncommon. Colon imaging studies were done in 41% including 74% of those over the age of 50. In the 3 years following the diagnosis, only one person had a change in diagnosis and no diagnoses of gastro-intestinal malignancies were made in the cohort. CONCLUSIONS: Primary care practice based diagnostic evaluations for IBS differ significantly from the specialty expert opinion-based guidelines. Implementation of the specialty guidelines in primary care practice would increase utilizationwith apparent limited improvement in diagnostic outcomes. _______________________Curious.







MNL


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## ohnometo (Sep 20, 2001)

Really not trying to step on anyone's toes ...I am just trying to figure things out..There are real physical conditions that can trigger IBS beside the brain and gut theory... I know that is a very important part in IBS...The big brain and little brain...


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## kel1059 (Feb 28, 2003)

I agree! I do not think that a single remedy or treatment is going to do much for the majority of moderate to severe sufferers.That is why I believe in my multimodal approach which incorporates the "peel the onion" method.Since i have not had decent stool formation and low peristalsis for a number of years I think it is very important to try and get the colon as detoxified and clean as possible. I believe that a clean colon will help the body function better. If stool just sits around all day, it will end up causing problems.I also think that taking probiotics over a very long period of time will be very beneficial.I think that if the symptom set indicates that there could be fungal overgrowth or hypersensitivity then corrective action should be taken.I take antiparasitic, antifungal, antibacterial herbs and garlic. This has given me quite a bit of symptom reduction in terms of gas.Removing all simple sugar and fruit has given me extreme relief from cramping and gas.A zero grain (no wheat, corn, oats...), no dairy, no beef, chicken, pork, dairy (especially cheese), no yeasty or fungus type of foods has also given me substantial relief.However, only Ibsacol seems capable of putting the finishing touches on allowing me to have stool formation (peristalsis is still sluggish).The question remains....will i ever conquer this nightmare??? Will Ibsacol be the missing link or the key to the whole thing? ...or will my hypersensitive immune system find a way to thwart the Ibsacol? Am I doomed?I think that once I get things stable for a considerable period of time like 3 to 6 months, I will try the hypnosis tapes again. This time I will purchase the tapes that are recommended by MNL. Eric's tapes did not seem to do anything for me; however, that does not mean they are not effective. It is just that my problems are much more deeply rooted in organic causes and were much too complicated. Hypnosis can not overcome a bad case of dysbiosis. It is like eric using hypnosis to overcome his amoeba infection --it does not work. It is also very ineffective against IgE type allergies.


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## eric (Jul 8, 1999)

To be fair kel, the tapes might not have worked for you , because of your diet and all the things you have taken out of your diet as well as all the things your taking and do to upset the balance. For sure your worrying about every possible thing on the planet that is or could be contributing to your symptoms and basically diagnosing yourself with them all.Nor do you go by my methods, you said fats don't bother you, but the other day you ate avacdo which is high in fat and had an attack, go figure? You don't know what my methods are even.IBS is a real physical condition, both the brain and the gut can trigger it. Which is why effective treatments are targeted at both systems.Its also majorally important to have healthy bacteria in the colon to protect your immune system.Intestinal Bacteria:Friend and Foe in the FloraYou may think of bacteria as the creatures that you rid yourself of with antibiotics, or rid your bathroom of with Lysolï¿½. Actually, these small organisms exist within your gastrointestinal GI tract, and you may want to keep some of them around. Researchers are gaining new insight into the bacteria that exist in the intestine, otherwise known as the enteric microflora, and how it can contribute to inflammation in IBD, or may help to alleviate it."...It has long been recognized that the anatomic sites of highest bacterial concentration distal ileum and colon are the sites most frequently affected by inflammation in patients with IBD," note Massimo Campieri, M.D., and Paolo Gionchetti, M.D. Policlinico S. Orsola, Bologna, Italy in an editorial in the May 1999 issue of Gastroenterology. "...A dramatic increase in bacterial concentration is present across the ileal cecal valve with the total number of microorganisms increasing by approximately a million-fold."The Enemy, or Enemies, WithinScientists vary on how bacteria may influence inflammation in IBD. Some believe that the disease is due to infection from a single pathogen, or disease-causing organism, such as Mycobacterium paratuberculosis. Saleh Naser, M.D., and colleagues University of Central Florida, Orlando reported a study at the 99th General Meeting of the American Society for Microbiology, in which they found this organism in seven of 20 tissue specimens of patients with Crohn's disease.Others believe that, while there is no conclusive evidence that M. paratuberculosis causes Crohn's, it may play some role in the pathogenesis the process that causes disease of IBD. Kensuke Suenaga, M.D., and colleagues Kochi Medical School, Japan, et al. have shown that M. paratuberculosis also exists in the intestines of healthy people. In the June 1999 issue of Digestive Diseases and Sciences, this group reports finding increased antibodies to M. paratuberculosis in patients with Crohn's, and concludes that people with Crohn's may have a unique immune response to this normally occurring organism.Other theories point to the involvement of many species of bacteria. "There is now overwhelming evidence from animal models that resident luminal intestinal bacteria influence experimental intestinal and systemic inflammation," comments R. Balfour Sartor, M.D. (University of North Carolina, Chapel Hill), in Research and Clinical Forums, Vol. 20, Issue 1. Bacteria have been shown to induce a type of colitis in animal models that relapses, and involves complications such as arthritis, liver disease, and anemia. Mice who are made genetically susceptible to IBD, but are raised in a germ-free (sterile) environment, do not develop the disease.Studies in humans also point to bacteria as a culprit, specifically, a report by Gert R. D'Haens, M.D., Ph.D., and colleagues University Hospital Gasthuisberg, Leuven, Belgium in the February 1998 issue of Gastroenterology. Patients underwent surgery to remove diseased segments of their intestine, and the healthy segments were connected, in a process known as ileoanal anastomosis. For several months, patients had a loop ileostomy, in which a hole is made in the ileum to divert stool before it gets to the site of the anastomosis, to prevent stool from infecting the site of surgery. When the ileum was again exposed to the contents of the intestine, patients relapsed within eight days. Since these contents were not different from those of patients without Crohn's disease who underwent ileostomies, the authors comment, "This strengthens the hypothesis that patients with Crohn's disease develop an abnormal immune reaction in response to probably common bacteria or dietary agents."Dr. Sartor reports on studies that aim to determine which species of bacteria trigger inflammation in people with IBD. The results indicate that different species of bacteria cause disease in different animal models. For example, in animals containing the HLA-B27 gene, which has been associated with colitis and arthritis, Bacterioides vulgatus induced inflammation. This was not the case in IL-10 knockout miceï¿½mice who develop IBD because of a lack of IL-10, a protective protein in the immune system.These results indicate the importance of genetic and environmental factors acting along with bacteria to develop IBD. Dr. Sartor hypothesizes that, in healthy people, the bacteria in the intestine attempt to stimulate inflammation, but are prevented by a protective intestinal lining, and an immune response that suppresses inflammation. In people with IBD, however, genetic factors may be causing the intestinal lining or the immune response to function poorly. The disease process is helped along by environmental factors, such as diet, smoking, NSAID use, or stress.The Good GuysResearch also is pointing to a role for some bacteria in preventing intestinal inflammation. Karen L. Madsen, M.D. and colleagues University of Alberta, Edmonton, Canada report on a study of Lactobacillus in the May 1999 issue of Gastroenterology. This organism also is known as "probiotic," for its role in restoring balance in the enteric microflora, as opposed to antibiotic, which involves destroying bacteria.Dr. Madsen's group found that IL-10 knockout mice had an increase in bacteria invading through the intestinal lining. However, they also had decreased levels of Lactobacillus bacteria, and when these levels were restored, the levels of other bacteria were reduced and colitis was prevented."These studies provide a very provocative message," comment Drs. Campieri and Gionchetti in their above-mentioned editorial on Dr. Madsen's study. "The onset of inflammation may be associated with an imbalance in the intestinal microflora with relative predominance of 'aggressive' bacteria and insufficient concentration of 'protective' species. Furthermore, reconditioning of the flora through either direct supplementation with protective bacteria or by indirect stimulation exerts a protective role in intestinal inflammatory disease."Drs. Campieri and Gionchetti report on their own investigation of a probiotic preparation VSL#3 to maintain remission in patients who had been treated with antibiotics for pouchitis. Seventeen of 20 patients treated with VSL#3 were still in remission at nine months. Of 20 patients who received placebo, all relapsed within four months.Some researchers prefer the concept of probiotics to antibiotics in the treatment of IBD. "Alteration of bowel flora with antibiotics seems too simplistic and crude to achieve sustained therapeutic efficacy in IBD, whereas manipulation of bowel flora with probiotics is conceptually more appealing," comment Fergus Shanahan, M.D., and colleagues National University of Ireland, Cork in the December, 1998 issue of Gastroenterology.Another appealing theory is that of prebiotics, food substances, such as carbohydrates, which promote the growth of certain bacteria. Researchers are investigating the use of prebiotics in intestinal inflammation as well. In fact, Dr. Madsen's group found that lactulose, a nondigestible carbohydrate, also prevented inflammation.However, more study is necessary before we know how probiotics or prebiotics may help people with IBD. "There is presently a paucity of rigorously controlled and well-designed studies of probiotic therapies for gastrointestinal disorders," comments Dr. Shanahan's group.New interest in the importance and ability of probiotics may change this situation. S. Bengmark, M.D. Lund University, Sweden, emphasizes the importance of restoring probiotic bacteria. "The condition and function of the GI tract are essential to our well being," Dr. Bengmark writes in an article in the January 1998 issue of Gut. "After the respiratory tract, the GI tract constitutes the largest body surface area, described to be somewhere between 250 and 400m2, or comparable in size to a tennis court. During a normal lifetime 60 tons of food pass through this canal, which is important for well being, but also constitutes an enormous threat to he integrity of the digestive tract and the whole body. It is not surprising, therefore, that this organ is often affected by inflammatory diseases and cancer."Dr. Bengmark explains that prehistoric food contained several thousand times more bacteria, mainly probiotic, but today's diet contains many threats to gut flora. "...The desire of the food industry to prolong shelf life promoted alternative production methods such as the use of enzymes instead of live bacteria. Combined with extensive hygiene measures practiced during delivery and in child care, children in Western societies may have difficulty developing a satisfactory protective indigenous gut flora." Medical treatments such as antibiotics and radiation also affect the gut's natural environment.For better or for worse, the bacteria in your intestine play an important role in gastrointestinal health. "A better understanding of the bacterial species which selectively drive the inflammatory response and the genetic and environmental modifying factors will allow us to develop more specific therapies which can fundamentally alter the natural history of these chronic, insidiously relapsing diseases," concludes Dr. Sartor.ï¿½SARA M. SILBERMANMedical Reporter & EditorDate Posted: July 23, 1999


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## trbell (Nov 1, 2000)

kel, you might want to find a hypnotherapist or biofeedback person who knows IBS. One of the problems with cds is that one size doesn't fit all and your problems sound pretty individual.tom


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## kel1059 (Feb 28, 2003)

Eric, Believe me when I tell you that fat causes ZERO problem. In fact, i need to cut back on my olive oil intake. I was getting too many calories that way, and it may have been causing problems via other means. .....such as malabsorbtion of my doctor prescribed omega 3 fatty acids and gamma -LA.I can drink a cup of olive oil and experience ZERO problems. In fact, I will do a liver cleanse once in a while which calls for 1/2 a cup of olive oil to be chugged followed by lemon juice. (you would not believe what comes out the next morning.... LIME GREEN CHOLESTEROL BALLS.... i'm not kidding (they float and they are unmistakeable), my friend did it and hers were huge and numerous (she has high cholesterol--I have low cholesterol-- she had quadruple the amount that I had)Concerning the AVOCADO, believe me it is NOT the fat!!!!!! It is either a fungus or a protien / glyco protein or something that I am extremely allergic to. I ended up getting severely fogged up which proves it is allergic. When i am under a really bad attack my joints even ache.Nice abstract that you posted on the probiotics. i love reading that type of information.


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## kel1059 (Feb 28, 2003)

eric,concerning my diet, I believe that it is still far healthier than the average person's diet.I eat hormone free, grass fed meat such as ostrich and venison from new zealand. I am about to order EMU which is one of the healthiest meats known to man. occasionally I will eat pheasant.I eat whole legumes that I prepare myself from dried beans/legumes.I eat pumpkin and squash. I used to eat a lot of dark green vegetables but after undergoing the antifungal treatment, I actually became more sensitive to fungus so I had to give up the veggies. The reason i became more sensitive was due to the fact that I was finally feeling normal, but re-introduction of fungus caused a severe rebound effect.I am hoping that as my immune system stabilizes, I will gradually be able to re-incorporate the vegetables. however, dairy, wheat, and cheese will probably never be eaten safely again.I also consume approx 2 ounces of wheatgrass juice per week and am experimenting with Garden of Life's --Perfect Food. however, I need to be careful because the ingredients list several things that have caused reactions in the past like sunflower and pumpkin seeds.I am more fit than most teenagers, and if it was not for the IBS and the associated nervous symptoms -- I would have perfect health. I believe i am just about recovered from my devastating collapse that peaked 2 years ago.Incidentally, probiotics gave me some relief back then, but yogurt (homemade) gave me extreme relief until i became allergic to it. (I think one of your studies says that yogurt helps to relax a person via increased tryptophan synthesis)


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## kel1059 (Feb 28, 2003)

> quote:because of your diet and all the things you have taken out of your diet as well as all the things your taking and do to upset the balance.


You have got to be kidding!!!What balance???? I have not had balance to my system since I was a teenager. every time i removed a food such as wheat or corn I helped to restore balance. When i was eating wheat my gut was locked up in a severe spasm for a minimum of 3 hours every single night or afternoon. Do you call that balance?When i was eating dairy you couldn't use a firehose to unblock the congestion. You call that balance?When i was eating sugar and other simple sugars my moods and temper were all over the place. I has chronic insomnia and fatigue and energy shifts all day long. You call that balance?Unbelievable!!!actually last fall I was not engaged in any treatments at all except I was on a no sugar, no fruit diet, and my carbs were low. This was the only time that I experienced a reduction in the brain fog, reduction in the gas and cramps. But I still had no stool formation and no peristalsis, and i still was pretty desperate. My problems are not the same as your problems.Actually my problems are about 5% mind-gut /stress related. In all honesty, I have minimal stress. Today i just played around on the computer for most of the day and talked to a few friends. The other 95% of my IBS is a mixture of intolerances, fungal hypersensitivity, intestinal dysbiosis, and immune dysfunction.therefore, it is no wonder i wasted my money on the tapes. The tapes do not work for people who suffer from my type of IBS. However, i may give them another try in the future to solve the remaining 5% of my problem. Plus it was an okay experience but it was a pain in the rear having to be so consistant and devote the time...I am really getting into the accupressure. i am refining my technique. I am using one of the homedics hand massagers to hit all the key nerve points along the spine. Each one is 1 inch to the left and right of each vertebrae.i am getting very curious about a lot of the alternative allergy cures like NAET (which I experienced 3 years ago), kinesiology, energy medicine, homeopathy, EDS, synchrometers....I am very open to this idea of blocked energy pathways. I want to investigate it all.


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## eric (Jul 8, 1999)

Kel, you worry all the time, IBS is caused by fungus , yeast food allergy, bactieria, everything but what they really know about in regards to what is causing your problems, *worry is a form of anxiety and that stresses the body and digestive tract and you are a major worrier* . Not to mention all stress and the type of stress in IBS is not conciously perceieved so you would not conciously know it anyway.I also don't get what is so wrong and why certain people view using relaxation techniques in IBS as some bad thing its not and it can't hurt you and it can help IBS tremedously.Now if its not for you okay, but it doesn't mean it doesn't help the majority of IBS patients, this is already extremely well known.Our widespread inability to relax is rarely acknowledged. Few of us are comfortable admitting that we have a tremendous amount of difficulty in being able to relax. Come Monday morning, when asked about your weekend, you reflexively spout out that is was ï¿½great.ï¿½ It is equally as common for us to list our relaxation activities (i.e., we were at the beach house, out on the boat, etc., etc.) as though these activities clearly imply that we truly enjoyed them and we were readily able to relax. However, relaxation is usually about a state of ï¿½beingï¿½ and not about a state of ï¿½doing.ï¿½ Therefore, no list of relaxation activities guarantees ï¿½beingï¿½ in a state of relaxation. Most people view being able to relax as simply mind over matter. Should someone tell you that they were unable to relax, you might listen sympathetically but also might feel that the person was just not exercising enough control over himself or herself. Often, we see the inability to relax as a sort of weakness on the part of the person. In addition, many people also believe that relaxation is a natural state. You just take time off, do things you like to do, and relax. If there is a barrier to relaxation, it is believed that it is linked to stress ï¿½ too much work, too little money, too little time, and too many responsibilities. Many believe that if they had both more time and more money, then relaxation would be sure to follow. News Flash: All of the above beliefs are false ï¿½ relaxation is an unnatural state!To understand this you need to look at human brain development and observe some basic elements in nature. One major feature here is the instinctual drive for survival. Nature gives all animals some protection against its natural predators. But, in order to survive, surveillance is required. The bird that decides to take a nap at the base of the feeder might be easy prey for the local cat. The chipmunk that doesnï¿½t keep a close lookout will fall prey to a hawk. The unpleasant reality is that in nature, most everyone is trying to eat everyone else. ï¿½Eat or be eatenï¿½ is one of the primary laws out there. Although human beings are capable of rational thought, our brains developed in an evolutionary way. Part of early brain development (often called the reptilian brain) is where primitive impulsive and archaic behaviors reside. We can often override these primitive impulses, but they remain intact and emerge episodically through life. Therefore, our natural state is to maintain our sense of alertness in order to protect ourselves. Relaxation implies that we let down this antenna system. It means turning off the radar so that we will not be attuned to incoming missiles. The natural state is to maintain round the clock radar. Our built in radar system does not come with an on ï¿½ off switch. It is hard wired and always working. Hence, when we try to relax, we are often frustrated. You may have a planned day off and you want to relax. Although you have created the ï¿½rightï¿½ environment, you sit there trying to relax while your radar system fills your head with all kinds of stuff. The next day, rather than feel refreshed, you feel depleted. Remembering that relaxation is an unnatural state, recognize the bind you are in and relieve yourself of the pressure and the guilt you may feel as a result. Rather than help you to relax, pressure and guilt only serve as barriers. Many of you feel that you are supposed to be relaxed and try to drive yourself into a state of relaxation. Pressuring yourself to relax will guarantee your inability to relax. Relaxation only comes when allowed; it cannot occur when forced. Similarly, guilt is both unwarranted and non-productive. So, how do you relax? Can anything be done to achieve a relaxed state? The answer is a conditional ï¿½yesï¿½. It can be done. However, your expectations need to be realistic. Although you can learn to relax, you probably will not be able to do it ï¿½on commandï¿½ and ï¿½at will.ï¿½ Some days it will go well. Other days, for a variety of reasons, it will not.The key to relaxation is to find ways to temporarily fool the reptilian brain into going on vacation. If it remains at its sentry post, then you will be too aroused and defended to achieve a state of relaxation. Next, there are a lot of individual differences in what will work. Below are just a few of the more common methods to achieve a state of relaxation. None are universal. You will need to experiment to see what works for you. And, even then, it may not work consistently. Bottom line: you must pick and choose techniques that are suited to your needs, temperament and lifestyle.1) Music: ï¿½ For many people, music is effective. It bypasses the sensor and can draw you in, in a meaningful and pleasurable way. Most all cultures have rituals based in music that have evolved over many centuries. The key here is to focus on what music evokes in you. The idea is to feel something. Numbness is not equivalent to relaxation. If any activities are making you feel numb, then you are narcotizing yourself, not relaxing. 2) Meditation: ï¿½ Meditation has been a staple for relaxation for quite some time. This technique is about focusing your attention. The problem with it is that its results are subtle; it takes a good deal of time and effort, and is easy to abandon. Meditation is not for everyone. But, it is worth a try. Herbert Bensonï¿½s ï¿½Relaxation Responseï¿½ may be a suitable beginning guide as is ï¿½The Relaxation and Stress Reduction Workbookï¿½ (New Harbinger Publications). 3) Religion: ï¿½ Religion, if it provides you with a sense of sanctuary, often achieves a relaxed state. The key here is your sense of safety and security. If you feel you achieve this feeling, then religion may be one of your avenues to relaxation. 4) Move Your Butt: ï¿½ Exercise, if not compulsively driven, can help relieve some of the physical tension that builds up in the course of a day. Walking, jogging, running, bicycling, swimming, or playing tennis relaxes muscles and relieves tension. Give yoga a try ï¿½ itï¿½s a soothing way to exercise. Note: some find the relaxation in the aftermath of the exercise rather than during the exercise. 5) Touch: ï¿½ Touch is the only universal relaxer. It bypasses all of the defenses and is actually vital to survival. If you are not getting enough touch, then achieving a relaxed state will be very difficult. But there are some caveats here. The main one is that there are two kinds of touch. One is a ï¿½giving touchï¿½ in which you feel someone is giving something to you. The other is a ï¿½taking touchï¿½ in which you feel someone is taking something from you. The ï¿½giving touchï¿½ is essential and productive one. The ï¿½taking touchï¿½ has nothing to do with the spirit of touch. Do not be a party to ï¿½taking touchï¿½. It will only get you father away from where you need to be. ï¿½Giving touchï¿½ leads to genuine intimacy and relaxation. Sensual and erotic touch is a legitimate part of ï¿½giving touchï¿½. ï¿½Taking touchï¿½ turns the people into objects. The intimacy is counterfeit and will only re-energize the sensor. Most everyone can instinctively tell the difference between the two. 6) Relax Your Muscles: Learn about progressive muscle relaxation, s-t-r-e-t-c-h your muscles on a regular basis, or treat yourself to a massage, all great ways to relax muscles and enhance feelings of relaxation. 7) Get Practical: Learn about the benefits of deep breathing, visualization techniques, or picture yourself relaxed through guided imagery. Cut down on caffeine (a potent central nervous system stimulant), get plenty of rest (sleep deprivation compromises your immune system, reduces your ability to cope with daily stressors, clouds your cognitive functioning, makes you sound stupid, and increases irritability. Use alcohol in moderation, when the ï¿½highï¿½ wears off, youï¿½ll feel drained ï¿½ not relaxed. 8) Get Smart: Learn to say ï¿½noï¿½ to excessive demands on your time and energy that increase your stress level, deal with and express your anger/rage, learn to manage your time effectively, and rejuvenate yourself through a hobby ï¿½ all wayï¿½s for you to cognitively and socially nurture yourself.9) Get Connected: Develop a social network. An influx of new research suggests that emotional support helps protect people against the ill effects of stress. Consistent contact with supportive people, community organizations, and/or satisfying causes, all act as a built-in buffer to stress. Therefore, make your world larger than your spouse, lover, family and/or your immediate circle of friends. Carve out time for each and nurture these attachments and they will nurture you. 10) Too Bad If They Canï¿½t Take a Joke: Have a good laugh! Laughter deepens your breathing, lowers your blood pressure and releases endorphins, stimulating the pleasure center of the brain. At the same time, studies show, laughter seems to decrease the production of stress hormones from the adrenal glands. http://www.ec-online.net/Knowledge/Article...tionresist.html


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## bonniei (Jan 25, 2001)

Very interesting article, eric


> quote:But, in order to survive, surveillance is required. The bird that decides to take a nap at the base of the feeder might be easy prey for the local cat. The chipmunk that doesnï¿½t keep a close lookout will fall prey to a hawk. The unpleasant reality is that in nature, most everyone is trying to eat everyone else. ï¿½Eat or be eatenï¿½ is one of the primary laws out there.


I think you are saying we are in a constant state of surveillance. For e.g. constantly on the lookout for slights, imagined or real. Eat or be eaten. i think we feel it is better to be wary and while it may have its benefits, we pay a high price in not being able to relax. The vestiges of our reptilian, chipmunkian memories are hard to overcome indeed.


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## kel1059 (Feb 28, 2003)

> quote:Eventually he published some 80 papers. His main research interests were allergens, particularly those of mites and fungi. His interest in moulds may have been kindled by his wife's intense allergy to some of them, plus a severe episode, in one house, of dry rot! His interest in fungi led him into a critical appraisal of the ill defined condition ascribed by the popular media to "chronic intestinal candida" (or simply, but incorrectly, "candida"). To this he devoted a considerable research effort in his last decade, contributing a definitive review to the second edition (2002) of Brostoff and Challacombe's Food Allergy and Intolerance. While accepting the clinical reality of the condition, he pleaded strongly for the abandonment of its popular simplistic name in favour of the more cautious "fungal-type dysbiosis." Ironically, he was on the verge of publishing his findings on ergosterol (which provide the first real evidence for intestinal fungal growth in the condition) when death intervened.


 http://bmj.com/cgi/content/full/326/7384/339/c/DC1 This is some info from dr keith eaton who wrote the chapter on fungal dysbiosis in brostoff's book.


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## eric (Jul 8, 1999)

Bonnie, the reptilian brain centers are evolved from long ago to run the bodies systems, such as digestion and the autonomic systems.Now read this and think about the fight or flight and a perceived threat very carefully, *which is not concious to the person* . When you preceive a threat the brain rleases stress hormones to the gut, which in turn release histimine, which in turn causes the nmuscles of the gut to contract.Read this carefully with what I just said above in mind. Because this has to do with the immune system.Worry is a fear!!!! Worry where a bathroom is is a fear, or whill I have a good day or be in pain.All fear responces that trigger fight or flight. Fight or flight is tied directly to the immune system.Part 1DISCOVER Vol. 24 No. 3 (March 2003)Table of ContentsLearning Series: The Brain and Emotions - part 1FearRecent research shows that when something bad happens to you, part of your brain begins thinking independently, storing its own memories so it can save you next time. That worked fine a million years agoBy Steven JohnsonPhotograph by Elinor CarucciGraphics by Don FoleyYou are driving at night down a quiet suburban street, listening to Van Morrison's ''Brown Eyed Girl'' on the stereo. As you cross an intersection, your peripheral vision picks up the flash of headlights descending on the right side of the car. In the split second before you hear the sound of metal grinding into metal, your body tenses, blood flows to your extremities, adrenaline surges, and time slows down. At impact you find yourself noticing surreal detailsï¿½the bright orange jacket of a startled pedestrian, the low-hung branches of a dogwood tree at the side of the road. After a split second that seems like 10 minutes, your car lurches to a halt against the curb.The physical event of one car colliding with another has run its course, but its emotional impact continues. The adrenaline and other stress hormones released in your body have brought you to a state of almost superhuman alertness; you feel more awake than you've felt in your entire life. You can review the details of the crash as though you were replaying a DVD of the event, all the details immaculately preserved. For weeks, as memory fades, details continue to haunt you. Driving through an intersection causes you to flinch, anticipating another crash; the flash of headlights makes your gut tighten. For months, driving at night seems far more dangerous than driving during the day. Even a year later, the sight of drooping dogwood flowers triggers a sense of dread. Hearing ''Brown Eyed Girl'' brings the whole sequence back to consciousness with astonishing clarity.Anyone who has been through a traumatic event will recognize this scenario immediatelyï¿½ the sudden physical response of fear and its often debilitating persistence in memory. The feeling of fear, like all emotions, is something that happens to the body and the mind. Few memories are as easily triggered and as hard to shake as those in which we are confronted with an immediate threat. For people who have undergone serious trauma, including war veterans and rape survivors, memories of fear can sometimes play a dominant role in shaping personality, a condition we now call post-traumatic stress disorder.Unraveling the mystery of how the mind experiences fearï¿½ perhaps the most primal and enduring of all the emotionsï¿½ turns out to be one of the most interesting and instructive quests in the annals of recent neuroscience. We have learned that fear plays tricks with our memory and our perception of reality; we have also learned that the fear systems in the brain have their own perceptual channels and their own dedicated circuitry for storing traumatic memories. As scientists have mapped the path of fear through the brain, they have begun to explore ways to lessen its hold on the psyche, to prevent that car accident from keeping us off the road months later.It seems intuitive to us that we would remember vividly the details of a frightening event like a car accident. But here is a question with a surprising answer: Would we remember our fear if we had no long-term memory?An experiment performed nearly 100 years ago by Swiss psychologist ï¿½douard Claparï¿½de provides a clue: Claparï¿½de was treating a woman suffering from a debilitating form of amnesia that left her incapable of forming new memories. She had suffered localized brain damage that preserved her basic mechanical and reasoning skills, along with most of her older memories. But beyond the duration of a few minutes, the recent past was lost to herï¿½ a condition brilliantly captured in the movie Memento, in which a man suffering similar memory loss solves a mystery by furiously scrawling new information on the backs of Polaroids before his memories fade to black.Claparï¿½de's patient would have seemed straight out of a slapstick farce had her condition not been so tragic. Each day the doctor would greet her and run through a series of introductions. If he then left for 15 minutes, she would forget who he was. They'd do the introductions all over again. One day, Claparï¿½de decided to vary the routine. He introduced himself to the woman as usual, but when he reached to shake her hand for the first time, he concealed a pin in his palm.It wasn't friendly, but Claparï¿½de was onto something. When he arrived the next day, his patient greeted him with the usual blank welcomeï¿½ no memory of yesterday's pinprick, no memory of yesterday at allï¿½ until Claparï¿½de extended his hand. Without being able to explain why, the woman refused to shake. She was incapable of forming new memories, yet she had nevertheless remembered somethingï¿½ a subconscious sense of danger, a remembrance of past trauma. She failed utterly to recognize the face and the voice she'd encountered every day for months. But somehow, buried in her mind, she remembered a threat.Click on the image to enlarge. (23k)The amygdala, which directs signal traffic in the brain when danger lurks, receives quick and dirty information directly from the thalamus in a route that neuroscientist Joseph LeDoux dubs the low road. This shortcut allows the brain to start responding to a threat within a few thousandths of a second. The amygdala also receives information via a high road from the visual cortex. Although the high road encodes much more detailed and specific information, the extra step takes at least twice as longï¿½ and could mean the difference between life and death. LeDoux says the disconnection between the two routes may underlie some disorders: "While in terms of survival it may be better to mistake a stick for a snake, people who have pathological fears may be treating sticks as snakes much of the time."ï¿½ Jocelyn SelimAbout 25 years ago, a young postdoctoral student at weill Medical College of Cornell University in Manhattan named Joseph LeDoux was casting about for a research focus. Cognitive science, with an emphasis on computer modeling, was the hot new field. But LeDoux was interested in emotions, and "there wasn't a lot going on there,'' he remembers, sitting in his office at New York University, where he is a professor of neural science. ''So I read around and came across studies on fear conditioning." Claparï¿½de's pin turns out to be a somewhat diabolical twist on the classic behaviorist experiment of fear conditioning: Put a rat in a cage, play a tone, and simultaneously deliver a shock to the animal. After a few rounds of tone and shock, the rat starts to fear the tone even if it's not accompanied by the shock. The fear reactionï¿½ noticeable because the rat freezes in placeï¿½ has been observed in species as diverse as pigeons, rabbits, baboons, and humans. It is called a conditioned response. The rat has an unconditioned innate fear of shocks, but it can be conditioned to be afraid of tones if the two are associated with each other. In Claparï¿½de's version of the experiment, the pin was the shock. His outstretched hand was the tone. After only one exposure to the shock and the tone, the amnesiac patient acquired a conditioned fear response to shaking hands with her doctor.Conditioned fear is easy: Fruit flies, marine snails, even lizards can be trained to display defensive behavior in response to threatening stimuli, along the lines of the tone and shock experiments. Conditioned fear turns out to be one of the most essential techniques that natural selection stumbled across to increase the survival odds of organisms in an unpredictable environment. But until a few decades ago, we had almost no idea how that learning actually took place. The ubiquity of conditioned fear in the animal kingdom, combined with the amnesiac's ability to remember potential threats, made it clear that learning to be afraid involved different mechanisms than, say, learning how to ride a bicycle or memorizing the capitals of all 50 states. But what was the mechanism? That's what LeDoux set out to determine. There had been almost no research into how the fear response actually came into being. ''In fact,'' LeDoux says with a smile, ''my first grant on this topic in the early 1980s was turned down," because scientists reviewing his application believed it was impossible to scientifically study emotions.LeDoux forged ahead anyway. ''I started from the outside,'' he says. ''I had the sound that produced the fear response. I wanted to know: How does that sound go through the brain and create the response?'' Like most brain researchers in the age before advanced imaging technology, LeDoux's approach was surgical subtraction. Take a healthy rat and begin extracting specific parts of his brain. If you remove a region and the rat can still learn to associate the tone with the shock, then the region you've removed isn't relevant to fear conditioning. But if the rat stops learning, you know you've got something relevant.Click on the image to enlarge. 85kANATOMY OF FEARWithin seconds of perceiving a threat, the primitive amygdala sounds a general alarm. The adrenal system promptly floods the body with adrenaline and stress hormones. Nonessential physiological processes switch off. Digestion stops, skin chills, and blood is diverted into muscles in preparation for a burst of emergency action. Breathing quickens, the heart races, and blood pressure skyrockets, infusing the body with oxygen while the liver releases glucose for quick fuel. The entire body is suddenly in a state of high alert, ready for fight or flight.ï¿½ J. S.''Because the auditory pathways are fairly well worked out in mammals, I could use that as a starting point. I started with the top of the auditory pathway, which is the auditory cortex. I took that out, and the animals learned fine. Then I went down one station to the auditory thalamus, took that out, and they couldn't learn at all. So that meant that the sound had to go through the system to the level of the thalamus but didn't go through the cortex. So where was it going?'' The question was puzzling because the traditional understanding of the brain's activity emphasized the role of the cortex over most other regions. The cortex was where the sensory informationï¿½ in this case, the sound of the toneï¿½ was integrated into conscious awareness, alongside other sensory data transmitted from other parts of the brain. The auditory thalamus was supposed to be just a relay station from the ear to the primary destination, the auditory cortex. So there was something strangely inverted about LeDoux's result. You could eliminate the primary destination altogether without affecting the learning, but if you took out the relay station, the learning stopped.LeDoux's assumption was that the auditory thalamus harbored a link to another part of the brain, in addition to its link to the cortex. Using a tracer dye to follow pathways out from the auditory thalamus, LeDoux discovered a connection to the amygdala, an almond-shaped region in the forebrain long associated with emotional states. When he removed the amygdala, the rats failed to learn. Perusing the literature, he found earlier experiments that demonstrated a crucial part of the amygdala known as the central nucleus contained links to the key brain stem areas that control the autonomic functions involved in the fear response, like acceleration of breathing and heart rate. ''I didn't start out looking for the amygdala,'' LeDoux says. ''The research led me to it.''The key insight that emerged is that the experience of danger follows two pathways in the brain: one conscious and rational, the other unconscious and innate. These were quickly dubbed the high road and the low road. Say you're walking though a forest, and out of the corner of your eye you detect a slithering shape to your left, accompanied by a rattling sound. Before you even have time to formulate the word snake, your body has frozen in its tracks; your heart rate has accelerated; the sweat glands on your palms have dilated. In your brain, the information flow looks something like this: Your eyes and ears transmit basic sensory information to the auditory and visual thalamus, where the information is then transmitted along two paths. One stream of data heads towards the cortex, where it will be integrated with other real-time sensory data, along with more elaborate associations like the word rattlesnake, or your childhood memories of a pet python, or the snake scene from Raiders of the Lost Ark. At the same time, the slithering is also transmittedï¿½ in less rich detailï¿½ to the amygdala itself, which blasts out an alarm to the brain stem, alerting the body that a potential threat is nearby. The key difference between the two paths is data transmission time. It might take a few seconds to establish the presence of the snake and formulate a response via the high road, but the low road kicks the body into a freezing response within a fraction of a second. And you don't have to learn the elaborate bodily choreography involved, the way you might learn a complicated yoga position. Your body knows how to execute the freezing response without any training at all. In fact, it knows the response so well that it is nearly impossible to keep it from happening.As a survival mechanism, LeDoux's low road made perfect sense. But other questions remained: How did the amygdala know to be afraid of a snake in the first place? How could Claparï¿½de's patient learn to be afraid if she lacked memory?We're accustomed to describing someone as having a good or a bad memory, as though memory were a single attribute that covers the entire range of storing and recalling information. We now know that the brain's memory systems are far more diverse than this. There are systems devoted to explicit or declarative memories, like your childhood recollection of that pet python, and systems devoted to procedural memories that usually involve physical movement, like learning how to ride a bicycle. And then there are emotional memories. If you watch the activity in someone's brain using a modern fMRI scanner, you see a different profile depending on which kind of memory the subject is conjuring up.In ordinary cases of fear conditioningï¿½ encountering that snake in the grassï¿½ a declarative memory will occur more or less simultaneously with an emotional memory. You'll feel the freezing response kick in, and moments later you'll remember seeing that scene from Raiders of the Lost Ark. The latter feels like our traditional idea of memory; there's a mental picture from the past experience that comes into consciousness, as though you were sifting through pages of a photo album. The transition to a freezing response doesn't feel like a memory in that conventional sense of the term, but for all intents and purposes it is one. It is recalled information from past experience that alters your state of mind. The transition to a freezing response happens too fast for it to be a conscious, deliberate memory, but it's a form of memory nonetheless.In brain anatomy terms, the declarative memory of Indiana Jones in the snake pit is laid down by the hippocampus, a long, curved ridge located next to the amygdala. The emotional memory of a threat, on the other hand, is mediated by the amygdala itself. This explains the mystery of the remembered pinprick: Claparï¿½de's patient lacked the ability to form declarative memories, but she had a functioning amygdala that kept the memory alive, albeit unconsciously. If you had a past encounter with a snake and you felt actively threatened, a trace of that memory would have been stored by the amygdala as well as by the hippocampus. Some brain scientists believe that our fear systems are prepared to learn about threatsï¿½ snakes, spiders, or heightsï¿½ that have been major obstacles to survival over the millions of years it has taken the modern brain to evolve, which explains why it is easier to develop phobias about snakes than about threats that are statistically much more likely to kill you, such as electricity.Some scientists believe the amygdala doesn't have its own discrete storage system for emotionally charged memories but rather marks memories created by other brain systems as being somehow emotionally significant. In 2001 James McGaugh of the University of California at Irvine conducted a telling variation on the classic fear-conditioning experiment. He took a rat and subjected it to the traditional foot shock if the animal took a step. After administering the shock, McGaugh injected cyclic AMPï¿½ a cellular messenger that strengthens neuronal synapses, leading to stronger memoryï¿½ into the animal's cortex. Two days later, the rats were tested to see how well they were conditioned; those that received the injections turned out to have enhanced memories of the shock. ''So we know the cortex is involved in the memory that's based on fear in that situation,'' McGaugh says. ''Now, if we make a lesion of the amygdala, the stimulation of the cortex doesn't do anything. In other words, you have to have a working amygdala for the cortex to do its job.''McGaugh concludes, ''That experiment tells me that fear is not learned in the amygdala. Amygdala projections are coming up to brain regions where information is being stored, and they're saying: 'You know this memory you're storing? Well, it turns out to be a very important one, so make it a little stronger, please.' It provides selectivity in our lives. You don't need to know where you parked the car three weeks ago, unless it was broken into that day.'' You can think of it as the brain's way of underlining.Neuroscientists have determined that the memory of a fear stimulus triggers dramatic changes in the vital signs of rats. In a series of conditioned-response experiments, rats are first exposed to a painful shock accompanied by a tone. Whenever the tone is repeated, the rats immediately stop dead in their tracks. Blood pressure shoots up within three seconds, and heart rate peaks within five seconds. After 20 seconds, increased levels of stress hormones like corticosterone flood the body, and highly oxygenated and fuel-charged blood is pumped into the muscles to prime them for action.The trouble with emotional memories is that they can be fiendishly difficult to eradicate. The brain seems to be wired to prevent the deliberate overriding of fear responses. Although there are extensive neural pathways from the amygdala to the neocortex, the paths running the reverse direction are sparse. Our brains seem to have been designed to allow the fear system to take control in threatening situations and prevent our conscious awareness from reigning.This may have been an optimal design for predator-rich environments in which survival was a minute-by-minute question, but it is not a good adaptation for modern environments in which the stressors can be job performance reviews. The amygdala may be looking out for your best interests by preserving a memory of that nighttime car accident, but if the result is an inability to drive after dark, the fear circuitry has gone too far. Because the low-road memories are so tenacious, one question neuroscience is now wrestling with is how to subdue the amygdala when those memories hurt the organism.As a New Yorker who works in downtown Manhattan, LeDoux has been thinking a lot about these issues since September 11, 2001. Many local residents experienced a conditioned fear response that day, making it hard for them to work in tall buildings or visit the downtown area. LeDoux suspects those traumatic memories will persist in the brains of New Yorkers. The treatment possibilities are not about eliminating the memories so much as retraining the amygdala to respond differently when those memories are triggered.''The contrast,'' LeDoux says, sitting in his university office above Washington Square Park, with Ground Zero lurking not far to the south, ''is between taking action and being stuck, frozen in fear, headed toward despondency, unable to control your life. There's an interesting experiment along these lines: You have a rat that goes into a chamber. A tone goes off, and he gets a shock, and he freezes with the fear response. The next day he goes into chamber B, the tone goes off, and he freezes. But if he takes a step, the tone stops. Eventually he learns that he has to crawl across the chamber to eliminate the tone completely. So by taking that action, he's able to prevent fear from existing in his life.''In order for the rat to do this,'' LeDoux continues, standing up to sketch out his ideas on a cluttered white board, ''he's got to throw a switch in the amygdala. Normally, the fear response goes from the lateral nucleus to the central nucleus and then out of the amygdala. In order for the rat to take a step, the stimulus has to go not to the central nucleus but to the basal nucleus, and then out to the parts of the brain that are involved in active behavior.'' In other words, the amygdala wants to associate the memory with the freezing response, but it can be trained to associate it with something less debilitating. When you hear an airplane rumbling overhead, you can freeze, or you can take a step. And with every step you reroute the path of fear through the amygdala.Our new understanding of fear has also led to cunning pharmacological treatments for post-traumatic stress disorder. McGaugh talks about two recent studies that involved giving beta-blockers to people who had recently suffered a traumatic event, studies that built on McGaugh's own research: ''Say you have a traumatic experience. The memory of that experience will pop into your brain the next day, whether you want it to or not. And when that memory pops into your brain, you're going to have that whole autonomic response that you had originally. It's going to come back again. So it's not only that you remember that you were mugged, but you also get very emotionally excited about it when the memory happens.'' That emotional excitement triggers the memory-enhancing cycle all over again, making the traumatic memory even stronger, like a spinning tire deepening the muck hole it's stuck in with each jab on the accelerator. By preventing the autonomic reaction, beta-blockers keep the memory from forming deeper grooves in the brain, making post-traumatic stress symptoms less severe, ''which I think is a really interesting development,'' McGaugh says with a hearty laugh. ''Forty-five years of my life I've spent studying rats and out pops something useful!"Because the fear response can play a direct role in life-and-death struggles, it's not surprising to find that the brain contains elaborate machinery dedicated to its routines. The fact that the amygdala's basic architecture reappears in so many species is testimony to its evolutionary importance: Natural selection generally doesn't tinker with components that have proved essential to basic survival. Of course, the persistence of the low road in a world where predators are largely nonexistent may no longer be adaptive, but that's the trade-off of human culture. Evolution made our brains so smart that we ended up building environments that made some of our mental resources obsolete. No matter how calculating and erudite the neocortex becomes, it can't simply switch off the amygdala. In that sense, you can see the battles between these different regions as a re-enactment of Freud's clash between man's civilized superego and his primal id.There is great elegance in the way this system has evolved, with its complex mix of instinct and learning. Like all emotions, the fear circuitry steers the organism toward desirable statesï¿½ away from predators or other threatsï¿½ without knowing that much in advance about the world that the organism will actually inhabit. We are not slaves to our emotions, but they are hardly at our beck and call either. They propel us in directions that our rational minds don't always understandï¿½ fear most of all. The amygdala, like the heart in Pascal's famous phrase, has reasons of which reason knows nothing. www.discover.com/search/index.html"Within seconds of perceiving a threat, the primitive amygdala sounds a general alarm. The adrenal system promptly floods the body with adrenaline and stress hormones. Nonessential physiological processes switch off. Digestion stops, skin chills, and blood is diverted into muscles in preparation for a burst of emergency action. Breathing quickens, the heart races, and blood pressure skyrockets, infusing the body with oxygen while the liver releases glucose for quick fuel. The entire body is suddenly in a state of high alert, ready for fight or flight.ï¿½ J. S."Within seconds, and it developed that way because if you had to stop and conciously think about the threat you may lose valuable time in escape and would probably get eaten in the process.So understanding the gut problems are a big part but understand the brain in IBS is just as big a part, not to mention all pain is processed in the brain and the brain is not functioning the way it should be in IBS, from the signals from the gut and this is known, no matter what is the root cause of IBS.


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## bonniei (Jan 25, 2001)

Interesting###kel's and eric's articles.


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## kel1059 (Feb 28, 2003)

> quote: Now read this and think about the fight or flight and a perceived threat very carefully, which is not concious to the person . When you preceive a threat the brain rleases stress hormones to the gut, which in turn release histimine, which in turn causes the nmuscles of the gut to contract.


i never get cramps any longer. after i made dietary changes and took care of some other issues the odor, gas, cramps, and bloat disappeared. however, they did start to creep back in a few times when i re-incorporated sugars back into my diet, and when I went off my antibacterial/fungal herbal concoction. (also when i started on fruit again)well i guess this proves my point that I don't have stress, and that sugars and foods were the driving force. in fact, i kind of miss my stress. I think things are a little too easy around here. in fact, I am bored.


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## kel1059 (Feb 28, 2003)

the link below is one of the better ones that i have read on leaky gut. the doctor lists over 150 references to back up his claim. Flux denies the existence of this condition except in certain very rare conditions. Unbelievable!!! http://www.mdheal.org/leakygut.htm After reading the information, I do not think any of us should ever believe our very foolish doctors again when they say, "IBS is not dangerous".It very well can be depending on what the cause of your IBS is.


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## bonniei (Jan 25, 2001)

Thanks for the link, kel. What I like through a rief glance at it is they have solutions for Leaky Gut.Just a word of caution all the references may not be in reputable journals.Anyway, I have got a few chores to do now but will read that link more when I have time


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## Kathleen M. (Nov 16, 1999)

In some ways "Leaky Gut" seems to be the current "Hypoglycemia" .Basically many people who would have gotten diagnosed with "hypoglycemia" in the 1980's would now get "leaky gut" diagnosis based on the same symptoms.There are SOME people who ALL medical and scientific people agree have leaky gut or hypoglycemia, but it certainly isn't every other person that feels a bit tired once in a while, or ever has any vague symptomst of something.One of the ways "fad" diagnosis take off is that there is some small basis in reality, but they are applied to symptom sets without the proper diagnostic tools being used to determine if people really have them. Most Alt. Med types that make these diagnosis do not do the same types of testing that someone would get at a fully equiped research hospital. Generally if one makes a diagnosis and are firm that this is the problem, recommend a bunch of lifestyle modifications and herbs most people feel better after a while because they were taken seriously and given a certain course of action. That can cure many people even when the "what was wrong" and the "what they are given to cure them" have no basis in objective scientific reality.Look in PubMed under Leaky Gut and there are papers listed about problems in those with Crohn's and their first degree relatives. But Crohn's is not IBS, and I don't know what kinds of symptoms the relatives actually have and if they in any way match what most of the "leaky gut" proponants feel it causes.K.


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## Kathleen M. (Nov 16, 1999)

> quote:CONCLUSIONS: Fecal calprotectin, intestinal permeability, and positive Rome I criteria provide a safe and noninvasive means of helping differentiate between patients with organic and nonorganic intestinal disease.


"Intestinal Permeability" AKA Leaky Gut was a marker for INFLAMATORY Bowel Disease and not seen in the IBSers. in this studyGastroenterology. 2002 Aug;123(2):450-60. ï¿½ Use of surrogate markers of inflammation and Rome criteria to distinguish organic from nonorganic intestinal disease.Tibble JA, Sigthorsson G, Foster R, Forgacs I, Bjarnason I.Department of Medicine, Guy's, Kings, St. Thomas' Medical School, London, England. jeremy.tibble###virgin.netSo basically if you really have a leaky gut, you probably do not have IBS.K.


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## Kathleen M. (Nov 16, 1999)

> quote: Intestinal permeability, although ideally suited for diagnostic screening for small bowel Crohn's disease, appears to give reliable predictive data for imminent relapse of small bowel Crohn's disease and it can be used to assess responses to treatmen


: World J Gastroenterol. 2001 Aug;7(4):460-5. Non-invasive investigation of inflammatory bowel disease.Tibble JA, Bjarnason I.


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## Kathleen M. (Nov 16, 1999)

Now in the year following a particular GI infection where people get Post infectious IBS there can be gut permeability issues that contribute. But how dangerous this is for all aspects of your health....added to most people with this sort of IBS get over it after a couple of years...it doesn't typically cause a unending health deteriorating year after year decade after decade sort of thing.


> quote: CONCLUSION: Increased EC, T lymphocytes, and gut permeability are acute changes following Campylobacter enteritis which can persist for more than a year and may contribute to PD-IBS.


Gut. 2000 Dec;47(6):804-11. Increased rectal mucosal enteroendocrine cells, T lymphocytes, and increased gut permeability following acute Campylobacter enteritis and in post-dysenteric irritable bowel syndrome.Spiller RC, Jenkins D, Thornley JP, Hebden JM, Wright T, Skinner M, Neal KR.


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## Kathleen M. (Nov 16, 1999)

Here is the Crohn's paper with the relatives in it thing.Proc Soc Exp Biol Med. 1997 Apr;214(4):318-27. Intestinal epithelial barrier dysfunction in Crohn's disease.Ma TY.Department of Medicine, DVA Medical Center, Long Beach, California 90822, USA.Despite extensive research, the etiology of Crohn's disease remains unknown. Accumulating evidence suggests the possibility that a primary defect of intestinal barrier function may be present in Crohn's disease. In this review, the possible role of intestinal barrier defect in Crohn's disease is discussed. It has been recognized for some time that Crohn's patients have a defective intestinal epithelial barrier function manifested by an increase in intestinal permeability. Recent studies indicate that a subgroup of healthy first-degree relatives of Crohn's patients (a population at high risk for developing Crohn's disease) also have increased intestinal permeability. Additionally, this subgroup of patients have evidence of increased exposure to foreign antigens, suggesting a possible link between increase in intestinal permeability and increase in antigenic penetration. Furthermore, exacerbation of Crohn's disease is produced by agents that disrupt intestinal epithelial barrier function, while remission of active disease is induced by decreasing intestinal antigenic load. A "leaky gut" hypothesis is advanced which proposes that a preexisting disorder of intestinal permeability is responsible for the intestinal inflammation of Crohn's disease.The vast majority of people with IBS do not go on to develop Crohn's, but mild Crohn's is sometimes misdiagnosed until you go in during a flare up.K.


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## kel1059 (Feb 28, 2003)

Here is my theory. I believe that since crohn's disease has a very strong genetic link (probably several gene expressions must be present), then the overwhelming majority of the population does not aquire it.However, I think that the environmental factors that trigger the crohn's in westernized populations is the same set of factors that trigger the immune activity that I am experiencing.Possibly i have some of these gene expressions but not enough of them to develop full blown crohn's. My nephew just came down with it --he is 13, and my dad's sister has it.It almost seems like there should be another "disease category" for people who have immune activity but not runaway inflammation.I am without question receiving astounding benefits from ibsacol. this product states that the mechanism of action is the immune system. It claims to alter prostaglandin ratios and to inhibit the release of leukotrienes among other things. ...and sure enough my asthma is down.It did nothing for my IgE allergies though. My doc put me on quercetin and Nettle and i was stunned when it worked. I did not think that would help.


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## kel1059 (Feb 28, 2003)

> quote: Recent studies indicate that a subgroup of healthy first-degree relatives of Crohn's patients (a population at high risk for developing Crohn's disease) also have increased intestinal permeability


This explains a lot!!!I have 2 relatives!!! ...and yet the odds of getting this disease is extremely low. i think it is 1 in 4000 or 1 in 10,000???? I know that it is increasing, but I think that UC (colon) is holding steady. i was reading up on it last april when my nephew came down with it.My sister even wondered if there was a link to my condition. Well, i am glad because members of my family think i am faking it when i refuse their food or tell them that i can't eat bread.I think that this intestinal barrier problem is not so much a situation of it exists or it does not exist but instead a problem of varying degrees. It probably also depends on the genetics of the person. I think this whole idea of intestinal permeability is rather fascinating. thanks


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## bonniei (Jan 25, 2001)

Just go away for an hour and there is so much interesting info. If I stay glued to my computer nothing happens







Thanks for the leads K! I will try to read up these papers


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## kel1059 (Feb 28, 2003)

I think it would be nice if there was some type of established criteria to further categorize patients so that they would know what the best treatment protocol is.I think that people should know whether or not they would be more likely to obtain better results with immune modulation or CBT as far as treating their IBS.So long as the focus is on mind-gut or on serotonin then the immune system is not being given its proper due.


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## trbell (Nov 1, 2000)

you may have missed the research that suggests hypnosis acts through the immune system and the kind of protocols and decision trees are what practitioners go through in deciding appropriate treatment and the good ones discuss it with you.tom


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## bonniei (Jan 25, 2001)

It seems that gut permeability is a matter of degree. Wonder if the altered gut permeability in Crohn's allows for the absorption of macromolecules.


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## bonniei (Jan 25, 2001)

I just read a couple of papers on Crohn's and Leaky Gut and it seems Leaky gut and Crohn's might be a chicken and egg problem. Which came first?I would also like to say after I took Ibuprofen with alcohol for a week I definitely feel more acidity and the walls of my GI tract seem sore. I hope it is not due to Leaky Gut. NSAIDs are supposed to cause altered gut permeability by kel's article(I think it was kel's).


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## kel1059 (Feb 28, 2003)

It is good to know that a doctor as esteemed as brostoff is taking these issues seriously.Ibs will never be pinned on one, two, or three causes but it is still important to identify as many as possible.


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## kel1059 (Feb 28, 2003)

Some people are going to look awfully embarrassed as soon as the major research centers around the world start to conclusively prove that people are reacting to toxins from fungal byproducts like acetylaldehyde.They have already shown that this is happening to people who suffer from chronic sinusitis. Now it is only a matter of time before these rocket scientists can put 2 and 2 together to show how the same thing is happening in the guts of certain people.


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## flux (Dec 13, 1998)

> quote:They have already shown that this is happening to people who suffer from chronic sinusitis.


No, it doesn't even appear that they are attempting to do this.


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## kel1059 (Feb 28, 2003)

You are simply viewing the research from a warped point of view just to defend your incorrect opinion.It is very obvious that certain people -due to various reasons- experience odd or extreme reactions to various triggers like mold spores.


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