# Is IBS a Baterial Infection? from IFFGD



## eric (Jul 8, 1999)

Is IBS a Bacterial Infection? By: William E. Whitehead, Ph.D., Professor of Medicine and Co-Director, University of North Carolina Center for Functional GI and Motility Disorders ï¿½ 2001 IFFGD This article can be viewed at http://www.aboutibs.org/IFFGD_IBS%20%26%20...0Infection.html The whole study can be viewed here. http://www-east.elsevier.com/ajg/issues/9512/ajg3368fla.htm ------------------ http://www.ibshealth.com/ www.ibsaudioprogram.com [This message has been edited by Jeffrey Roberts (edited 01-23-2001).]


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## Krissy (Jul 6, 2000)

interesting Eric,thankyou...Krissy


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## JeanG (Oct 20, 1999)

Thanks for the article Eric. I hadn't realized that the participants in the study were already people whom the docs suspected of bacterial overgrowth. It needs a lot more reseaarch.JeanG


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## partypooper (Mar 22, 2000)

One interesting thing about this article was that the doc says that bacterial overgrowth is a seperate problem from IBS, and that GIs should be testing their patients for this specifc problem before arriving at the IBS diagnosis.I have been too many, many docs (including head of the GI dept at Mayo Scottsdale, Hopkins etc) and none of them have ever even mentioned "bacterial overgrowth in the small intestine" as a possible diagnosis for me, much less set up this hydrogen breath test. I don't get the impression that most GIs even knew that this was a cause for chronic diarrhea before this study. Have other BB members had a differnt experience?


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## trbell (Nov 1, 2000)

i talked at length to my gi specialist at a secondary care center about this particular study. this is actually fairly old information and the technique is several years old. the test itself is not as reliable as the article suggests, but it's still a possibility.tom


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## eric (Jul 8, 1999)

I just want to add that DR Whitehead is a top Doctor at the UNC and is very involed in IBS research. ------------------ http://www.ibshealth.com/ www.ibsaudioprogram.com


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## Rose (Mar 25, 1999)

I read the article also. I don't claim to be the brightest bulb on the face of the earth







, so I wonder if Eric or somebody could clarify something for me or rather re-inforce what I "think" I read. I "sounded" to me that constipation predominent patients were not included in this study, is that right? From what I think I read the criteria they were looking for was pain, bloating and "D", is that correct?? Also Flagyl was one of the four recommended antibiotics. I was on a 10 day round of Flagyl a while back and my IBS was "worse" while on it and for a while afterward. Does that mean it is safe for me to assume, my IBS is not bacteria-induced??------------------"Remember To Stop and Smell the Roses"Rose (C-type)


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## eric (Jul 8, 1999)

Rose, I would say its pretty safe to assume your IBS is not caused by a bacterial problem, but is more a funtional problem.------------------ http://www.ibshealth.com/ www.ibsaudioprogram.com


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## Guest (Jan 24, 2001)

Good Information Everyone! Thanks!


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## Mike NoLomotil (Jun 6, 2000)

I would suggest that the best point made was already quoted...that bacterial overgrowth is a separate problem from so-called "IBS". And what makes an etiology of bacterial-overgrowth unique from other etiologies mistakenly lumped together under this syndrome?The fact is, once all the etiologies of the similar, overlapping but differing symptom sets that lumped under the "syndrome" of IBS are one by one isolated there will be no more IBS it is not a single disease entity nor will it/they prove to be idiopathic. If aproached like many European immunologists. allergists, and gastroenterologists who do not "see" some idiopathic syndrome, they see and seek the casual basis for distinct symptom sets and isolate the mechanisms. This perspective is at times elusive but from the scope and breadth of information being uncovered in a discoordinated fashion worldwide this is how it shapes up.MNL_______________ www.leapallergy.com


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## eric (Jul 8, 1999)

Mike you keep saying different symptoms sets etc. For the most part it seems that there is one major problem, causing a multitude of symptoms for IBS. Alot of top doctors are working to isolate it into a single entity.------------------ http://www.ibshealth.com/ www.ibsaudioprogram.com


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## Jackie (Sep 15, 2004)

Just wondering - why does Eric assume that Rose's problems are not due to infection because Flagyl made her symptoms worse ???Jackie


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## eric (Jul 8, 1999)

Jackie, from two years of reading Rose's posts. Although, I don't want to be miscontrued here, I said it was pretty safe for her to assume this, but if she feels it neseccary to have these tests done she should.------------------ http://www.ibshealth.com/ www.ibsaudioprogram.com


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## Mike NoLomotil (Jun 6, 2000)

Eric,I only say it because I have seen it to be true. In your case, you keep using this word "top doctors" as if there is only one investigatinal rout being followed by only one group of doctors who have a corner on the market of understanding the gastrointestinal tract and related systems. The doctors I know yo associate with are highly respected and competent and there is much interest in their work. But it is a big medical-world, and there is no exclusivity in these investigations.This is not the case, but your question is illustrative and is symptomatic of the problem with our approach to so called IBS in the USA. Some of the "top docs" in the USA prefer to let the causal approach take a back seat to the functional approach. This is one perspective. European investigators, also "top docs" in their fields, prefer a causal approach as it leads to prophylaxis not interventional solutions. keep the horse in the barn rather than studyin his actions once he is let loose, and looking fior ways to trip him up. Part of it is cultural and part of it is based upon what drives medicine and research here versus in Europe. Some other "top doctors" are investigating the gut as a digestive organ regulated by the neuro-endocrine system. This drives the investigations in a crtain direction. These fellows, actually quite competent and respected by their peers, working on so-called IBS strictly from a causal aproach...in fact they do not look at the symptoms and perceive IBS...they perceive an explainable dysfunction whsoe organci basis can and will be identitified and they set out to do so. They do so by approaching the dysfunctional bowel disorders (which are differentiated etiologies but as yet indeterminate with overlapping but distinct symptom sets into "IBS" as if it were a diagnosis per se) from a totally different perspective.These investigators approach the GIT as the bodies largest immune organ (which it is). It is an interface with the outer environment, and is designed to not only process nutrients for assimilation and eliminate wastes but to protect the body from internal trauma. These are groups led by immunologists, allergists, and gastroeneteroligists across the big water (esp. in the Scandinavian countries)and some here as well as you know hwo are revealing an altered picture of the immune functions as earlier understood...sort of. The problem which causes us to be debating at the moment is that the two groups have findings which are not being integrated. If they were closely compared (and we will get there over the next several years I beleive) they would quickly clarify some of the observed phenomena related to altered neurologic activity by providing an origin for same in a large population of so-called IBS patients. But they do no do that yet. Unfortunately this is just a fact. The odd part is you personally are hanging with one group and I am hanging with the other, that's all, each performing work from different perspectives. There are top doctors as you say who are investigating the correct shcok organ...small bowel...not the large bowel and related structure which is and are effected organ systems afterthe fact.These doctors are unravelling what actually happens IN VIVO to patients with the GI symptoms we call "idiopathc". The chemicals of concern which medite and upregulate ultimatley the integrated GIT andCNS function, along with other organs systems, are being spewed from their reserovoirs in the gut mucosa and microvasculature, and mobilized from the cirulating immune system. In general from mast cells of the small bowel mucosa, polymorphonuclear cells, even platelts in response to aberrant immunologic reactions that begin in the small bowel mucosa and then propagated in the microvasculature...in the absence of detectable IgE by RAST or even SPT but confirmed by DBPCOC...as we say, Not-allergy-something -else. This elicits the up to now hypothetical "leaky gut" (this can be easily deostrated with technques developed in Sweden), eaosinophilic migration to the interstitium, and macromolecule migration out into the cascular bed...there are even signs of this triggering the compement cascade as well. Some have found the lamina propria to be rich in Cd1[x] receptors in the reactive patients but not in normal controls. And it goes on and on. These "top" European doctors started isolating jejunem a few years ago with a special method and then challenging it directly in patients with NON ALLERGIC functional bowel symptoms to see why the nervous systems motor and ncociception is uprated, why smooth muscle depolarozation potentials are reduced making the bowel smooth muscle twitchy, why serotonergic-mediated rsponses are upregulated and even why central (CNS) activity is exsaggerated in specific symptom sets. It can all (even the symptoms sets linked to infection) be traced back to immunolgoic mediators themselves (stored or synthesized) as well as hormonal alterations that result. It remains for time and some impetus yet to occur to link the groups together. I am aware of some top docs who possess the desire and are seeking the means of fulfilling this integration of knowledge, and involved in the active process of acauiring the means. I beleive in the next 3 to 5 years this will occur...as there are things I have seen with my eyes with the tiop docs I associate with from the altrnative perspective which lead me to believe it will be accomplishded within this time.Just try to keep in mind that this is not a single-entity form of dysfunction...there is ample evidence that it is multicausal and multimechenism, and each will be sorted out progressively until there is no such thing as so called IBS left...only specific non-idiopathic processes which were once considered idiopathic.I have seen it too many times before observing and particpating actively over the last 30 years to belive it otherwise. Soem of the things that wer considered idioptahic "syndromes" 30 years ago are todays Merck Manual headings.have a DFDMNL________________ www.leapallergy.com


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## eric (Jul 8, 1999)

The doctors I know are looking at the nervous system and digestive system with a microscope. They are some of the top doctors in the world, not just the USA. I am sure the doctors you know, know of them, or at least I hope they do. I do know there are many people looking at this from different angles though. I just thing you add to new people's confusion when you say some of the things you say about it being many conditions causing many symptoms when in fact the observations point more to a main factor causing many symptoms.------------------ http://www.ibshealth.com/ www.ibsaudioprogram.com


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## Mike NoLomotil (Jun 6, 2000)

Hi Eric,Sorry to have to disagree with you but there is no confusion whatsoever being added by pointing out the fact that there are multicausal factors involved in so-called IBS. To illustrate my point you may quote Jonathon Brostoff ("...IBS is probably a general term for a variety of conditions. These look similar, in terms of symptoms, but can be caused in a number of different ways....". Then you can quote Douglass Drossman ("...not only can IBS symptoms be varied and multiple, but they may also coexist with or be initiated by other organic disorders...").Where the "camps" part ways is here, as illustrated by Drossman: "...From a biopsychosocial perspective deciding wheter a symptom is functional or organic is not as important as determining which factors need further attention" [Drossman & Ringel] vs. Brostoff:"IBS is little more than an umbrella term for various bowel distrubances of unknown origin. In some cases there may be a srious underlying problem or a very simple underlying problem thay can be easily cured.".The apparent upregulation of sensory and motor innervation of the gut and CNS, as well as the altered contractility of gut smooth muscle and the sources of such, have been examined in vivo repeatedly and with progressive clarity from as far back as 1987 by Sjolund (Scandinavian Journal of Gastroenterology) found that fasting d-predominant IBS patients had elevated plasma motilin levels and pancreatic polypeptide, and a spike in PP postprandiallly, while in c-types gastrin, motilin, and PP were decreased across the board. These findings were most recently reconfirmed by Simrena and Bjornsson as published in the January 2001 issue of GUT...also noting that c-predominant patients had lower levels of corticotrpoin releasing factor than d-types but both were eleveted relative to normal controls. In between those years are numerous publications from groups in both Scandinavia and Japan studying the resultant upregualtion of gut motility from aberrant gut peptide levels which RESULT IN altered smooth muscle contractility and lowered threshold stimuli as well the the resultant alteration in serotonergic and opiode receptors. Just about anybody can see that element which is an altered mechanism as a symptom not a cause.The question that has remained is what is the etiology....which can be and has been traced by in vivo study of the shock organ reaction that has not been reported in the US as it is not being looked at from that perspective...small bowel muscosal response and microvascular response immunologiclly.The various mediators (histamine,serotinin, cytokines, leukotrienes and other mediators) which upregulate the gut motor and sensory functions (the end-point being detectable by researchers studying serotonergic receptor function) has been traced to an aberrant 3 step process originating in the small bowel mucosa and microvasculature. For over 5 years various groups from Sweden (primarily the Univerisity Hospitals/Med schools in Upsala and Goteberg, Sweden; Dept. of Medicine, Sahlgren Hospital, University of Goteborg; University Hospital, Uppsala; Allergy Center, Sahlgrenska University Hospital, Goteborg) centered around the procedures first developed by Bengtsson back in 1994 I think (have to pull all the references but that would be a time waster..they are all tere in the Scandinavian Allergy and Immunology Journals) have evolved a clearer picture of origin of the immune mediator triggered reactions in several IBS symtpom-sets....1. small bowel mast cell NOT IgE mediated2. microvasculature granulocytic and lymphocytic reaction3. elevated mast cell counts in the upper large bowel (cecum only: entry to the large boel from the small bowel, indicating mast cell recruitment and concentration in the site of a chronic insult)...and reported the specific measurements of mast cell mediator release, eosinophilic mediator release (indicating a chronic not acute reaction in the small bowel), basophilic responses, and that this is precipitated by aberrant reaction to various meats, veggies, fruit, dairy etc. confirmed by DBPCOC and the reactions confirmed by isolating the jejunun and using direct-challenge and collecting and analyzing the washings for the specific mediators. Their published findings over the last 6 years correlate with the in vitro test results elicited in the same symptom sets from the patented MRT method (granulocytic end-point responses)developed by Signets immunologists and clinicians.If one looks at the mediators released from mast cells and granulocytes, and the ensuing immuniologic pathways, one finds the chemical basis for the upregulation seen "functionally" by US investigators.This is further confirmed as a primary etiology of thus symptoms that appear functional but are actually organic in origin by seperate work done in the UK and Italy starting in 1992 (Stefanini, University of Bologna) whose efforst to confirm the mucosal response in IBS (prior to Bengtssons work confirming it in vivo) by using the outcome-oriented method of oral comolyn sodium adminsutration to d-predominant IBS patients. It was interesting as they found not only overlapping IgE and non IgE mediated mucosal involvement, but the SPT + patients responded to oral CS (1500 mg/day) at a rate of 67%, not surprising as SPT sugested IgE involvement in the group, but 41% of the NON IgE implicated group responded to cromolyn sodium showing mast cell involvement in IgE negative patients. This has been confirmed in later separate trials.I could go on, as the references of work being done in "loci" of other University centers around the world that is not being centrally coordinated is notable.To suggest that pointing it out is creating confusion is to suggest that the investigators work committed to the causal approach and their finidings of an etiology for the so called "idiopathic syndrome" of IBS should be ignored and not put forth. Sorry, that would be a gross disservice to people sufering from IBS who can be relieved in large part by methods which identify the ingested substances which trigger these quantified small bowel and systemic immune responses thus eliminating the reaction. The mediators released locally and which then have systemic effects that are known including CNS upregulation and/or triggering other mechanisms which can lead to alterations in gut peptide levels which will then upregulate local neurologic, smooth muscle, and central neurologic function would remain within their granules intracellularly or not be synthesized. Take a look at what altering motilin levels does, what altering CRF levels does, and all mast cell and granulocyte mediators...there are about 100 to study the effects of. Then a clearer picture can be integrated of this multi-mechanism "syndrome". The mechanism of effect(s) may be a common PATHWAY but the causal mechanism is not synonymous with the reaction-pathway mechanism(s).As I said, for whatever reason (and there are many not the least of which is the lack of complete cross-connecton between the US medical community and the European medical community, as well as the "causal vs non-causal approach to IBS")this problem exists. Not only will I not cease to point out the facts under any circumstances, I will be further encouraged to redouble my efforts do so whenever met with an effort to dissuade me from doing so.It is my responsibility to do this as a healthcare professional committed to working with patients with symptoms precipitatd by these aberrant immunologic responses. Not only that, I am also working with people aggressively seeking private funding to further this work. We seek to construct the first tangible cross-linking of work between those HERE in the USA focused on these phenomena and those in the United Kingdom, Sweden and Italy by the end of 2001. They have to be and will be linked up if we have to continue to beg borrow and steal (well, not steal) funding to get the in vitro technology linked to the in vivo investigations of small bowel reactivity at the same time. Then the various PROPHYLACTIC modalities can be linked to provide the best possible prophylactic protocol for PREVENTION, not intervention post-reaction, in this specific population.I was lucky enough to have been "trained" by some of the best pulmonologists an the country back in the 1980's, whom I did research in pulmonary medicine with, in how "cells" of researchers working from different perpsectives can obtain part of the puzzle in an idiopathic problem, and thus form partial conclusions, and watched how they would go about pursuing their goals with singular determination, then disseminating it to the betterment of the overall advancement of the disgnostic and therapeutic arts.This is no different than countless problems that came before, whose solutions evolved the same way...one group here sees one perspective and forms one conclusion the promulgates that. Another over here sees another perspective and promulgates that. The inertia of resting-state in the current knowledge for a time prevents integration and progress as the mainstream core firmly holds onto that which we do not know. Until enough dust is raised or some catalyst is applied which pulls it all together.We used to do cardiac output for decades by the tried-and-true Fick Method. Indirect, cumbersome, fraught with error, non-acute care applicable. Some guy one day (actually 2 named Swan and Ganz) dreamt up a ctaheter which was then used to apply a method to measure it in vivo based upon thermal dilution principles. When it was first proposed it was heresy. When it was first done it was lunacy. The first prototpye catheters and instruments were troublesome due to computer technology limitations. The usefullnes of the findings was held up to ridicule...and new applications were heralded with scorn (wedge pressure? Fools!).At the Cleveland Clinic we set up one of the first prototype shock units incorprorating this controversial technology...and the only reason we got away with it and were not derided for endangering people with this unproven invasive method was because it WAS the Cleveland Clinic).Within 5 years using Swan-Ganz catheters and thermodilution cardiac output computers became a standard modality in ICUs all over the USA and you were considered an idiot and a flat-earther who was behind the times and disservicing your ventilator patients if you did not shove one in the pulmonary artery of everybody.So I am accustomed to the "not invented here" syndrome and do not fall for it at my advanced age, and based upon my own remission after 30+ years and that of many, many others.And frankly I do not think that the Bengtssons, Knutssons, Halgrens, Brostoffs, Fells, Stefaninis, Sandbergs et als which have spent decades zeroing in on the underlying causes are any less credible than any other competent practitioners. Some guys start at the tailpipe and other start at the carburetor.When they meet at the combustion chamber the circle will be complete. And not until then. I think we should catalyze that proces, Eric, not try to inhibit it.Now if only I could learn to type more accurately...not in the cards.I suspect you will not see my perspective which is of course your prerogative. Have a DFD Anyway!







MNL__________________ www.leapallergy.com [This message has been edited by Mike NoLomotil (edited 01-26-2001).]


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## eric (Jul 8, 1999)

Mike, I think I will stick to Havard, UCLA, International foundation for Gastroentestinal Diorders, UNC Center for Functional GI and Motility Disorders at Chapel Hill North Carolina, Johns Hopkins, and the Mayo clinic and not a food allergy theory thanks.------------------ http://www.ibshealth.com/ www.ibsaudioprogram.com


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## Mike NoLomotil (Jun 6, 2000)

ERIC:I am not sure I comprehend your behavior, but professionally I think it is unfortunate that for some reason you think this must be perceived and argued as some "either-or" or "black-and-white" issue. Everybody understands upregulation of the integrated system based upon 5HT upregulation. The search in some medical universities is not for drug interventions based on that knowledge but for "why" so as to achiev prophylaxis.If the patients small bowel mucosal immune cells dump their mediators (histamine, serotonin, and a 100 more perhaps) and granulocytic mediators appear from the microvasculature of the small bowel in response to food challenge in non-allergi cpatients, and it is quantified by direct measurement, and it is known these chemical are the specific ones which do upregulate 5-HT receptors it is hard to ignore. Since 95% of the serotonin is stored in the bowel in mast cells and EC cells and they can be evoked in Swedeis jejumum...it is entirely possible that American jejunums may be the same and this may be an etiology of the 5HT upregulation seen. I am sure you have a reason to feel like it is a mutually exclusive process....I just do not see what it is...this "I'll stick to"...nobody told you not to "stick to" anyone. I suggest that just maybe somebody found a physiologic reason for what is observed in the can and myenteric plexus and integration of that knowledge will advance the science. Since applying the observations to people with dietary manipulation works pretty good I suspect that they will stick to that too.MNL_____________ www.leapallergy.com


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## Mike NoLomotil (Jun 6, 2000)

PSNo one said it was food allergy....I keep explaning it is not food allergy.MNL


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## eric (Jul 8, 1999)

Mike, sorry food intolerances and chemical reactions. I know a small percentage have food allergies. I know people have trigger foods and some of this is based on chemical reations. I also know many people with IBS have a high percentage of food phobias. I think its good people see dieticians if it helps to figure this all out and find a healthy diet and aviod trigger foods or foods you maybe allergic too.My personal concern however is more that it is easy to confuse new poeple before they get the basics in IBS and make an informed decision on what is going on with funtional disorders. ------------------ http://www.ibshealth.com/ www.ibsaudioprogram.com


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## Mike NoLomotil (Jun 6, 2000)

I could not agree more about "food phobic patients". Too manyy people are removing foods from their diets unnecessarily, as they are the wrong foods, potentiating the continuation of their symptosm becasue they do not understand the physiology involved. Therefore they use the wrong methods to identifiy grosss reactions, and even with the best methods have extreme difficulty identifying the dose dose-related and delayed reactions. The majority of IBS victims do not know with accuracy the foods and chemcials which exacerbate their conditions.The answer to this is Education in the physiology of food sensitivity and then when a person understands the phsysiology the different and correct method that need to be followed makes sense. But not to withold the information as it is not easy to assimilate. Teach better. Learn better.This is the entire reason I became affilitated with the practitoners I work with. Prophylaxis saved my life, and that of many others I knew and have had the privilege of seeing return to normal lives since. Their goal is first and foremost prophylaxis. This is not the same goal as most other research. Most research done here in this country, and the words of Richard Locke, MD of the Mayo Clinic crystallize it best, spoken in closing about the studies focused on ICC networks and 5HT receptors, at a symposium sponsored by Novartis is: "They (their findings) also offer new targets for drug development".If you want to develop the most effective pharmaceutical interventions one must focus on the neural pathways involved in mediating gut function (or any other system...I worked from that angle for 20 years with prominent pulmonologists on that side of the investigational fence for chronic cardiolpulmonary disease drugs with funding from pharmaceutical firms and the like, so I understand the system). However, my IBS was not resolved in 30 years by pharmaceutical intervention...nor have I yet met the person whose IBS was resolved by pharmaceutrical intervention. The symptoms can be attenuated as they can be via CBT and hypnotherapy. As well as patient specific dietary therpy. Combining the three therapeutic modalities, developed to their nth degree, will produce the best outcomes in the long run.So my affiliation is simply with those who do not seek pharmacotherapy interventions, or psychogenic attenuation of neruologic response and stimuli and perception, but prophylaxis. Keep the horse in the barn rather than trying to tie his legs or alter our perception of his behavior once out. It is simply a causal approach as opposed to a symptomatic approach to the syndrome. So it is by nature and focus that one investiagtional goal will lead to expansion of knowledge in that area, and the other in the other aspect. But both must be done for the circle to be closed eventually.And this results in different approaches clincially such a symptomatic diagnosis and treatment (ROME) versus causal diagnosis and treatment (insult-response elicitation identification and avoidance). So in the course of events the causal investigators are uncovering things in their medical university research that can perhaps provide an uplink to the upregulation of 5-HT[x] and other neural mechanisms up to and including aberrant CNS activity...the chemicals which produce this result can be captured as they are released in the small bowel. circulation, and (ultimately) the CSF and the stimulus which elicited their release controlled.Putting the two camps together somehow will bring us all to the end of the journey that too many millions must suffer. So you have been improved from the top-down via attentuation and intervention and I from the bowwom up by prophylaxis. Neither physisology can be overlooked as each are as real as the pains in our guts.Also, after 20+ years of experience teaching, I can assure you that integrating the facts, any physiology, can be confusing. But if your mission is to help, you must provide the information and try to convey it to those who need it to make judgements on their health. One cannot flinch from providing the facts to those who need them, again and again if necessary, until the knowledge is assimilated. If we are here to help then we must teach, and be able to convey the fact that the condition is not A or B or C....but A and B and C.Have a good weekend...and may the Giants barbecue the Blackbirds.MNL___________ www.leapallergy.com


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## moldie (Sep 25, 1999)

Interesting discussion. I had to think back as to what was meant by the Giants and the Ravens reference, but then I remebered they did at the Superbowl! My first thoughts were Giants (the big guys) of which scienctific camp or Ravens (the dark/bad guys) of which type of research? I too think that much of medical research has largely become pharmaceutically motivated today, and while drugs can be of importance in many conditions, sometimes the rush to judgement about their benefits does not always include their drawbacks which on occasion can be devastating. I would recommend less lethal ways of managing IBS first; like dietary measures and hypnosis, but of course that is not always very profitable for doctors or drug companies. In fact, if one does have either an acute or chronic case of intestinal infection, it can be very serious. I don't think it would be prudent to treat those who have very little bowel symptoms with any anti-microbial drugs as indicated in the study though. If, however, the condition is seriously affecting the function of the patient and the species is identified, then I think that treatment with antimicrobials shown to be effective against the particular infection should be used; but not without caution in finding the correct dosage/frequency/and length of time for the therapy along with proper follow-up of the patient.I, too, hope that the camps can get together, and the focus of the research should be on the total positive outcomes for patients rather than money. Okay, Call me a dreamer.







Whether allergens, stress, or infections exacerbate/ecite our sensitive neuro systems, if we can find ways to alleviate the symptoms, all the better for us! My thoughts are that many of us that have IBS were wired for it from birth, but things along the way that happen to us can make our IBS worse/unmanageable. I also think that it is quite possible that infections can trigger symptoms much like IBS, and in fact perhaps after they are healed, our systems are then wired to react much like someone who was born with IBS activity (and then, maybe even considered then to have "IBS" thereafter). Was IBS passed on to us from generation to generation by poorly developed/defective/pooling of GI genes (not to be confused with GI joes), or was there a virus or an infection passed on or aquired? It is all very complicated and I think it will be a long time coming before we come to an agreement, much less a real cure. What might happen is that the promise of unlocking our DNA could lead to some positive developments in the way diseases/conditions are treated in the future.


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