eric and mike - puzzled
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To add my two cents eric is really miffed that Mike does not talk about serotonin often enough and Mike gets real indignant when eric talks only about mast cells from an immunologic perspective when there are t-cell lymphocytes(I'll have to refer back to that thread to get it right) or some such thing which are part of the equation. They both believe in an integrated approach to deal with IBS. It is just a case of one saying the glass is half full and the other saying it is half empty is what I have understood
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. Beyond that I haven't had time to study it. Not sure I'd follow it if I did. And I have no idea where real science fits into all these impressive studies and books.
To add my two cents eric is really miffed that Mike does not talk about serotonin often enough and Mike gets real indignant when eric talks only about mast cells from an immunologic perspective when there are t-cell lymphocytes(I'll have to refer back to that thread to get it right) or some such thing which are part of the equation. They both believe in an integrated approach to deal with IBS. It is just a case of one saying the glass is half full and the other saying it is half empty is what I have understood
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. Beyond that I haven't had time to study it. Not sure I'd follow it if I did. And I have no idea where real science fits into all these impressive studies and books.
Don't look now tom, but they're doing it again! I turned it off awhile ago. If they want to go back and forth, let them have at it. I do look at it as a teaching tool. The fact is all doctors don't have the "real science" in all their medical books. There's a lot of political finagling that goes on behind the scenes and funding goes where funding will. There are also different methods of testing, and basis for criteria of acceptance. Beyond that, what works for one, does not always work for another for various reasons, including both psychological and biological conditions of individuals. Personally, I'm especially glad mnl is here, because now I don't have to work so hard. Both eric and mnl provide useful information to bb members here. Yes, it can be long-winded and technical, but that is the nature of science. Sometimes, we almost need an interpreter.
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Don't look now tom, but they're doing it again! I turned it off awhile ago. If they want to go back and forth, let them have at it. I do look at it as a teaching tool. The fact is all doctors don't have the "real science" in all their medical books. There's a lot of political finagling that goes on behind the scenes and funding goes where funding will. There are also different methods of testing, and basis for criteria of acceptance. Beyond that, what works for one, does not always work for another for various reasons, including both psychological and biological conditions of individuals. Personally, I'm especially glad mnl is here, because now I don't have to work so hard. Both eric and mnl provide useful information to bb members here. Yes, it can be long-winded and technical, but that is the nature of science. Sometimes, we almost need an interpreter.
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This may be too simplistic for ya, but I have one question:If IBS is the result of food allergies (of course excluding exceptions to every rule), then, how come clinical hypnotherapy has such a high success rate WITHOUT modification or change or elimination of foods in the diet; and in most cases, how can once offending foods be reintroduced after successful completion of the hypnotherapy sessions, if IBS is secondary to food allergies, etc.???? How come??? I NEVER enter into these discussions, but sometimes the complex can be succint in its simplicity! That's all I'll be sayin'~ Peace~
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This may be too simplistic for ya, but I have one question:If IBS is the result of food allergies (of course excluding exceptions to every rule), then, how come clinical hypnotherapy has such a high success rate WITHOUT modification or change or elimination of foods in the diet; and in most cases, how can once offending foods be reintroduced after successful completion of the hypnotherapy sessions, if IBS is secondary to food allergies, etc.???? How come??? I NEVER enter into these discussions, but sometimes the complex can be succint in its simplicity! That's all I'll be sayin'~ Peace~
I also never get in to these "debates". Frankly all the VERY long posts go right over my head! I've tried to read them, but I barely understand half of it. I realize that is how science is, but most here aren't scientists, which for me at least makes most of those long posts worthless to me.I don't doubt that everyone involved is trying to help people. Otherwise no one would be here. I think it's kinda silly to be fighting over which method is the right method. There have been things that have worked great for me, and I've been surprised to see that they don't work on others. One of course is Calcium. I saw good results with calcium. I've also been able to use Immodium with good results for over 3 1/2 years. Others can't. Cutting out certain foods help me. Relaxing helps me. Not being stressed helps me. I think a good combo of what being fought about here has helped. So what I'm getting at is that there probably isn't going to be ONE answer. IBS is different for everyone. I don't think there is ONE cause to it, ONE reason for it. And I don't believe ONE thing will cure it, control it, or help it. Sharing your information is what this board needs. Although I wish it could be straight forward and in simple terms. I'm a Mom of a very active 4 year old. I simple don't even have the time to read those long article posts, if I could even understand them! But that doesn't mean I don't appreciate the people who do care and want to make a difference in someone who needs help. I think some should think about that, and get back to what were all here for. To help eachother.Jennifer
I also never get in to these "debates". Frankly all the VERY long posts go right over my head! I've tried to read them, but I barely understand half of it. I realize that is how science is, but most here aren't scientists, which for me at least makes most of those long posts worthless to me.I don't doubt that everyone involved is trying to help people. Otherwise no one would be here. I think it's kinda silly to be fighting over which method is the right method. There have been things that have worked great for me, and I've been surprised to see that they don't work on others. One of course is Calcium. I saw good results with calcium. I've also been able to use Immodium with good results for over 3 1/2 years. Others can't. Cutting out certain foods help me. Relaxing helps me. Not being stressed helps me. I think a good combo of what being fought about here has helped. So what I'm getting at is that there probably isn't going to be ONE answer. IBS is different for everyone. I don't think there is ONE cause to it, ONE reason for it. And I don't believe ONE thing will cure it, control it, or help it. Sharing your information is what this board needs. Although I wish it could be straight forward and in simple terms. I'm a Mom of a very active 4 year old. I simple don't even have the time to read those long article posts, if I could even understand them! But that doesn't mean I don't appreciate the people who do care and want to make a difference in someone who needs help. I think some should think about that, and get back to what were all here for. To help eachother.Jennifer
Amen to that, Jennifer. It either goes over my head or I don't have time to read it. I would hate to offend either M or E, however, as both have been supportive, helpful, etc on numerous occasions.Mybe there should be an extra forum. It could be called"Testosterone anonymous"!Or, to put it in a nicer way, how about "Great minds don't always think alike"!liz
Amen to that, Jennifer. It either goes over my head or I don't have time to read it. I would hate to offend either M or E, however, as both have been supportive, helpful, etc on numerous occasions.Mybe there should be an extra forum. It could be called"Testosterone anonymous"!Or, to put it in a nicer way, how about "Great minds don't always think alike"!liz
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Note...before comment one may wish to take quick look at this thread as well, as anexample of the basis from which I speak: http://www.ibsgroup.org/ubb/ultimatebb.php...ic&f=1&t=025795 Comment: ____________________________________"Look at the dates of these studies. Also some weren't controlled and in others a lot of information is missing. If these patients were diagnosed with IBS is wasn't under the Rome criteria as they did not have that then and used a different criteria. " _____________________________________Lord is it futile to explain in detail "here is an example of HOW FAR BACK the work goes...EARLY findings" etc. ...THEY ARE SUPPOSED TO be OLD! that was the point Oy! dude!I have hundreds of abstracts running from the 1970s to 2001...and have cherry-picked about 40 pages of them if anyone wants them but you cannot POSt 40 pages of abstracts or whole books.So the people that WANTED to learn and read them and assimilate them ASKED for them by email and received them, and those who did show interest or request them of course did not receive them. Rhetoric again. _______________________________________"Also on any food studies I would like to see a follow up after a couple years. That would be interesting to me" ________________________________________If you were up on all the material you would already know about it an your interest would have been satisfied. Broaden your study and reading material and you will see.This cracks me up too,again, as one commences to railing against old abtsrtacts and then posts old ones himself. LOL Enough rhetoric already.One needs to comprehend the full implication of each of the elements in the "model" (Figure 1) in the article I referenced. It appears one dioes not, otherwise one would see that the perpetuation of what one says I write (which I do not) and what one says I ignore (which I do not) is merely rhetoric again. If the practitioners I work with, the researchers who study the phenomena referenced, and myself did not comprehend the role of the CNS and ENS and IRS in the activation and regulation of the IRS and its relationship to symptom provocation in IBS then I could not possibley state over and over unequivicolly that the Diagram (with the addition of role of circualting immunocyte reactivity) was representative of the integration of each aspect of current understanding of IBS.I can only repeat myself so many times. Scotomas often are not self-resolving, which is clearly the case.So lets see if there is a question posted by anyone to which one can respond and be read accurately.Yes here is one: _____________________________________"If IBS is the result of food allergies (of course excluding exceptions to every rule), then, how come clinical hypnotherapy has such a high success rate WITHOUT modification or change or elimination of foods in the diet; and in most cases, how can once offending foods be reintroduced after successful completion of the hypnotherapy sessions, if IBS is secondary to food allergies, etc.???? How come??? " ________________________________________Actually this is several questions. And I will try try try keep it SIMPLE and by doing so I suspect someone will come back and suggest I left ou A and B and C. If so I will anser that too at that time. SIMPLE and SHORT are not synonymous. In fact they are ofetn mutually exclusive. This is one such instance. Sorry. First we have to keep in mind that IBS is not said by anyone especially me to be CAUSED by FOOD ALLERGY.Food ALLERGY is a reaction of the immune system (primarily the "fixed" cells found in the mucosa and skin) called mast cells which is virtully immediate onset, not dose dependent, and a specific antigen-antibody reaction mediates it. That is the person has become sensitized to a food the same way they became sensitiized to, say, an inhalant. The body formed a specific immunoglobulin to the food. The body should not do this, only to pathogens or parasites. It is a case of mistaken identity. It is a specific malfunction as the immune system has mechanisms which begin in the small bowel to identify safe stuff like foods from pathogens. In the case of allergy this mistaken formation of an immunoglobulin occurs. These circulate around. When the person ingests the food, this triggeres a specific type of immunologic response which is supposed to be protective. Mediators are released from the mast cells (and basophils if they have any around), which set of a chain of events which results in the immediate onset of sympotms of food allergy up to and including shock. Then there is a late-phase reaction hours later.In the general population this ocurs about 2%-5% frequency....depends whose estimate you use. Actual food ALLERGY by the classic definition of allergists occurs with a higher frequency it appears among IBS victims. One investigation suggests about 8%. This does not cause IBS it causes food allergy as a COMORBIDITY seen in IBS. So it has been thought, but recent events now call old definitions to question as you will see.Most dietary evaluation methods used in evaluating the effect of food on IBS symptoms are structured such that they only find reactions which are sudden onset and not dose related. This means they find any food allergy if it exists (something easy to do with dietary monitoring or one of the common blood tests like RAST or ELISA) AND it can find pseudoallergy (FALSE allergy which is cuased by a direct chemical reaction with specific structures found in some foods...like lectins for example) or direct toxic reactions from certain chemicals in foods, natural and added (peptides or histamine for example).If you take those several sudden-onset and non-dose dependent food provoking mechanisms you will find comorbid food allergy and false-allergy and no more. This is the least important type of interraction in IBS between what you put into the intestine and the provocation of symptoms. And it is the easiest to isolate, treat by avoidance or immunomodulation, AND the most difficult to attenuate with HT since it is a very powerful form of immune response which even the mechanisms built into the CNS designed to attenuate immunologic reactions would have difficulty attenuating....as it intrinsically does not WANT to block this particualr mechansism (actually there are several but I have only shown one) BECAUSE this is essential to protecting the body from infection.In fact some of the mediators released are designed to decrease the permeability of the blood-brain barrier to permit the movement of mediators into the cereborspinal fluid which will accentuate the CNS response in these reactions...to amplify the responses.One can to a degree alter perspective to the chronic suffering from ALLERGY via CBT, and one can alter, and increase, the attenuating responses...or reduce the reflex rsponses of anxiety and stress-related repsonses which further amplify an allergic reaction, but the degree to which this works in actaul ALLERGY is limited since you must overcome massive angtigen-antibody interraction.Now, so far the only subpopulations of IBS which have been studied enough vis a vis reactivity to food and additives to make defibitive statements as to the OTHER mechanisms involved are the 1/3 that are D-types and the 1/3 that ar cyclic d&c. C-types can and do show both comorbid allergy and comorbid intolerance but other mechanisms at work in these victims which overly attenuate lower bowel motility are of greater significance, since if there is exposure these patients do not respond with the classic "evacuation" chain of events. So whenever I talk, or quote, or describe, you may have noticed I alwsy speak in the contet of the 70% or so who are NOT C-types. There are distinctly differing mechanisms much less well understood by anyone so far.Now if you have a copy of the diagram (Figure 1 in this article in front of you printed out it will be easier to exxplain...without it most people who have not read alot on the usbject cannot follow along...)http://www.blackwell-synergy.com/servlet/userag ent?func=synergy&synergyAction=showFullText&doi=10.1046/j.1365-2036.2001.00951.x[/URL]Now to fionish the diagram draw a line between the "IgG" box and the OTHER NON IGE Mediated" box. The draw a line down from there directly to RELEASE OF MEDIATORS without going THROUGH the MAST CELL BOX.Now you have all the known mechanisms represented.The IgE box represents the food ALLERGY part, and the other (2) represent the myriad different types of direct immunologic and non-immunologic reactions that are triggered all by themseleves without any help from the ENS or the CNS in response to something in a food, or a food additive. There are, say, 7-8 other mechanisms.For example, see where it shows MUCOSAL ANTIGEN PROCESSING...this is the reactions that occur by lymphocytes in the wall of the small bowel. They criculate in and out of the lymphatics and blood stream so as to be always available locally in the gut wall in case of invasion.For years such researchers as Bengtsson and others in Sweden have been able to show that both the mast cells in the small bowel AND circulating immunocytes, such as the lymphocytes, react in IBS patients to certain foods and release the mediators which produce the d-type cascade of symptom onset.They take a bunch of patients who meet the ROME criteria for IBS and then remove all those who have comorbid food ALLERGY as confirmed by various conventional means of isolating circulating antibodies to foods. Get rid of the comorbid ALLERGY people so there is no confusion. They check for food provocation with double blind oral challenge to see which foods provoke symptoms.Since we are not talking ALLERGIES now we are tlaking about OTHER MECHANISMS (see diagram). What sets these apart from allergy cliniclly is that the reaction is DOSE DEPENDENT (it may take a goodly portion of the food to cause a response or a combination of two provoking foods together or consumptions over several meals to accumulate the dose which brings on symptoms) AND the onset of symptoms is DELAYED....from a few hours up to as much as 72 hours. So the oral challenge process is very time consuming if you try to find all the foods. So they chosoe a few of the most common that the persons are eating and just check those.Once they isolate which foods provoke symptoms for each patient they take them off those foods for a few days to make sure any provocation is removed.Then they take those people in slide a tube down their esophagus, stomach and isolate a section of the small bowel with a tube which 2 inflatable cuffs. Yout then have isolated section of small bowel so you can do a true blind challenge and you can capture evidence of what occurs in a true lind challenge (the patient has no way of knowing if anything, much less what, is instilled into the tube at any time...could be saline or could be a slurry containing the food challenge.Now to cut to the chase you always find the mediators in the washings which show that the gut immunocytes are either degranulating (mast cells) or circulating immunocytes are apoptosizing (losing cell wall integrity) and releasing their dozens of different and very powerful mediators into the small bowel mucosa and wall where the blood vessels, nerves, smooth muscle are that they are known to act directly upon.While all this has been going on the past few years, confirming not only what others have shown indirectly over the years with oral challenges to IBS patients and elimination diets and mast cell stabilizers, another investigator got the bright idea (Tornbloom) to talk a few IBS patients into letting him take full thickness biopsies of the small intestine to see if there are signs of inflammatory staging and/or long term reaction within the tissue.So he stuck in his thumb and pulled out the accumulations of t-cells that the other guys were finding their mediators in the washings provoked by specific foods. Which of course when you stopped instilling them the mediators went away because the reactions stopped and so did the symptoms. All the while this has been going on others have been studying the blood reactions of white cells in vitro and finding that the circulating cell reactions can be duplicatd OUTSIDE the body out of reach of the ENS and the CNS. This was first discovered, crudely, back in 1956.Anyway, the most recent step which confirms the accuracy of that diagram is that specific markers of immunoligic activation of t-cells (certain lymphocytes)in the small bwel wall were found when Bengtsson not only stsudied the washing BUT hje klast year started taking biopsies in these patients (ROME Criteria, non allergic, food provoked symptoms) and found, well, here is a direct quote on the findings from September 2001, which are being readied for publication sometime this year...."....we can show an allergy-like inflammation during challenges with parameters like Il-4, IFN-gamma, CD3, CD4, CD8 and IgE."If one understands a little about allergology and immunology one understands the significance of these markers. Simply put....the mediators noted IL-4 and IFN are T-cell mediators..,lymphocytes are breaking down in the small bowel of the subjects and releasing their intracellular inflammtory mediators and different types of foods provoked it. CD[3] [4] [8] are hard to explain simply...these are like receivers of information that differntiate different kinds of lymphocytes which perform different roles in inflammatory reactions...they interract with another substance called Major Histocompatability Complexes (I & II) which are supposed to make sure the right antigen (provoking agent of an immune response) gets presented to the right kind of t-cell for the right reaction. While Tornbloom showed the lymphocytes accumulating in the bowel walls of the IBS patients, Bengstsson found that there are several different classes involved in the inflammatory reaction by finding multiple class markers.Further, the really surprising thing is the presence of local IgE...remember the patients with CIRCULATING IgE indicating allergy were ELIMINATED. So this, and some earleir findings of IgE in the small bowel of food reactive but no allergenic subjects, shows one thing...an allergy-like mechanism (think IgE-mast cells) IS involved in even those where the classic allergy markers disaqualify them from beigna llegedly allergic, and IgE and the other mechanisms all occur absent input from the ENS or CNS...this is not reqired nr even a part of this type of reactivity...except after the reaction has begun and the ENS and CNS are provoked by the mediators.The cart, in this case, comes before the horse.Now from the diagram and from other study you know that the CNS and ENS are fully integrated with the imune system, and certain stressors on the CNS, or even certain kinds of other stimuli direct to certain aprts of the brain, can and do result in efferent (down-travelling) signals which can activate the fixed immune cells (mast cells) ABSENT any immediate immunolgic provocation. You can see that it can happen the opposite as well. BOTH can and do occur, so the question becomes in a given subject what is the combination? THIS is why the info has to be integrated so that future studies preferably would take into account the direct-immunilogic ally mediated reactions to diet provocation that occur in these patients. SO FAR that is not being done.So understanding this diagram and this grossly simplified example/explanation answers the question.CBT, for example, Grossly Simplified, is very effective in some and ineffective in others depending upon which portion of the "system" predominates as a source of symptoms.This therapy alters reaction to symptoms, perception of the consequences, and reaction to those consequeces etc....pure behavioral modification which first helps the victim gain better control over her responses to symptom onset and respond with less symptom-amplifying stress to the situations created by the syndrome. Therefore CBT alone will reduce the patients symptoms, even in the face of ongoing provocation, proportionate to the degree to which the patients RESPONSE TO the initial symptom has AMPLIFIED the symptoms....in some people this is SIGNIFICANT since their underlying symptoms may have been initially relatively mild but over time the way they react to the symptoms, and what they did to the persons life, and how the person adjusted or maladjusted, as you can see from the diagram showing the interraction of STRESS with the CNS and then in both directions the IRS and the ENS, may have ben significant.The same goes for HT, though at a more fundamental level. In simple terms, as you can see, the CNS can provoke the IRS to activate as can Immunologic (allergic) mechanisms as well as OTHER (non IgE mechanisms). Each can happen, and does absolutely, independently.Once can attenuate the IRS response, first by attenuating both the persons emotional reaction to a develping symtom, pain or cramping or chills, etc, AND especially in the case of NON IGE or IGG subclass meduated reactions, one can attenuate the reaction itslef. Not just after the fact BUT one can raise the threshold of reactivity. One may even bea ble to modulate the, for example, messengers like MHC within the IRS via certain specific cells located in the brain which perform that function. This is also an intriguing line of investigation.Anyway, In some cases where a pateint has no comorbid food allergy, and the provoking dose of a given food via one of the non allergic mechanisms is fairly high, the threshold of response can be raised through HT sufficiently that the reaction is attenuated enough that it eventually becomes subclinical (so weak as to not be noticed). This is one mechanism. Another is by altering perception of the symptom, and reducing the stresas and anxiety responses to symptoms and to the psychosocial consequences one interrupts the REFLEX LOOP you can see exists after provocation.Now if it were only certain cells or mechanisms involved, (for example only the "mucosal" immune system) it would theoretically be possible to produce extreme attenuation of the IRS response to non-pathogens. In a patient where this is the case it could occur.The trouble is, since there are mechanisms involved which are not "hard wired" to the CNS, the degree of success varies widely. In general, 80+% of patients will experience at least a moderate degree of symptom reduction. Do not forget that no studies measure successful outcome as 100% remission or nothing. Each has a different threshold of their definition of success which has to be taken into account, along with the selection process.Anyway, to repeat, one can not only break the reflex arc to locally provoked IRS responses which are independent of the CNS and ENS, but one can reduce or eliminate the CNS-locus of IRS activation, which varies in contribution to symptoms from person to person, AND one can raise the threshold of non IgE mediated reactions to some degree as well. Like KM is fond of saying "Your mileage may vary".Hence some people will actually regain some oral tolerance...in some cases total tolerance to some foods...as a result of HT. This is not a mystery to anyone including the immunologists who study the "middle 3 boxes" in this diagram...and the missing line we drew in to rpesent the cellular responses. hell, as simply stated, you can regain all oral tolerance if you simply either stabilize the cell walls of the immunocytes against all stimuli via immunomodulation, or eliminate all sources of provocation from each source.Conversely, the reason that studies on DIETARY manipulation alone prodcue similar results consitently over the years to any other single mode therapy is just that...70, 80, 90% experiencing a reduction in symptoms from modest to extreme in like fashion to HT is again because the response is going to be proportionate to the degree of comorbid allergy removed, and the degree of contribution of IRS activation by mechanisms other than IgE/IgG in eliciting a small bowel centered inflammatory response.This is why many patients who undergo dietary therapy alone, but who do have measurable signs of exaggerated stress and anxiety, simply "lose" that behavior after the provoking fods are removed even though CBT or HT was not used along with dietary therapy.The direct chemical effects of mediators upon the CNS and ENS are removed and this reduces the activation of those parts of the brain-gut axis which respond directly to certain mediators among the over 100 that may be involved.Also, when you remove the fear of loss of bowel control, pain, bloating chills dizziness etc. the causal basis of ther anxiety in some folks is removed and they respond accordingly (they may have no great degree of patterned-in learned response to stress).So hopefully you can see why any single-mode therapy for IBS will be very successful for some, moderately for others, and not at all for others...hence the cinsistency in the outcomes between the single modalities. Like a car with plugged injectors and a bad chip in the EEC, if you fix one you will get response to the degree that one contributes to the malfunction...in the case of the injectors the EEC has the capacity to make adjustments to partially compensate and reduce the symptoms.THAT IS WHY THE MODALITIES HAVE TO BE COMBINED in an integrated fashion to get the BEST outcomes. This is my mantra, nothing more or less, and so it shall remain regardless of assertions to the contrary.
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If everyone could put aside their predjudices and agendas, and instead opened themselves up to the clinical experience and finidings of others working from a diffenret anghle and openly integrated the best of both. ALL IBS patients would enjoy an opportunity to achieve the highest chance at the greatest degree of remission possible for themselves. This would require the renunciation of human behavior, however...an unlikely event.Until we do that, there will always be a degree of compromise in the outcomes, and varying degrees of success, with any modality or treatment program.If that whole thing still cannot be comprehended as to what the message is, I must say I know of know simpler way of answering the question(s) and still include enough information to be meaningful and accurate. A few other articles which explore the areas discussed here, in the Diagram I referred you to and that article, and many others beyond these few more...one must seek a very broad specturm of study to visualize the exquisite integration of the CNS, ENS, and INS...then to understand their various roles in conditions like IBS.....just a very few examples of what I mean... ___________________________________Nord Med 1996 Apr;111(4):109-12, 118 Related Articles, Books, LinkOut [Sick of food? Knowledge and hypothesis on food intolerance][Article in Norwegian]Jacobsen MB, Vatn MH.Medisinsk avd A, Rikshospitalet, Oslo.Food intolerance is frequently reported by patients and represent a diagnostic and therapeutic challenge. We review the nomenclature and report on symptoms, diagnostic tests and treatment. The nomenclature presented is based on the primary events such as toxic reactions, allergy or an undefined mechanism, including psychosomatic, although these subgroups may involve common pathogenetic mechanism. Double blind placebo controlled food challenge is the golden standard in the diagnostic workup and the importance of elimination diets--individually tailored to each patients requirements in cooperation with a nutritionist--is stressed. Through strict adherence to diagnostic and therapeutical guidelines, therapy may resolve food induced symptoms. Based on preliminary findings of signal transduction, we propose that symptoms in some patients may depend on an allergy type IV reaction. (** a 1-3 day delayed-onset reaction involving macrophages and effector T-cells)This working hypothesis forms the basis for further accumulation of knowledge of food intolerance reactions.Publication Types: � Review � Review, Tutorial ____________________________: Baillieres Best Pract Res Clin Gastroenterol 1999 Oct;13(3):429-36 Related Articles, Books, LinkOut Putative inflammatory and immunological mechanisms in functional bowel disorders.Collins SM, Vallance B, Barbara G, Borgaonkar MIntestinal Diseases Research Unit, McMaster University Medical Center, Hamilton, Ontario, Canada.The observations that irritable bowel syndrome (IBS) may be precipitated by an acute enteric infection, or occurs commonly in patients in remission from inflammatory bowel disease (IBD) has prompted consideration of inflammation as a putative basis for symptom generation in IBS. In this regard, IBS may follow a pattern of pathogenesis that is similar to asthma--which was once considered a psychosomatic disease. This review examines the basic scientific evidence of a functional interface between the immune and sensory-motor systems of the gut and discusses how this may be relevant to a subgroup of IBS patients. In addition, review will examine the implications of this for the diagnosis and treatment of IBS.Publication Types: � Review � Review, tutorial __________________________________Page 1051 of the hard copy of the 2000 Merck manual: "RECENTLY FOOD INTOLERANCE WAS FOUND TO BE RESPONSIBLE FOR SYMPTOMS OF SOME PATIENTS WITH THE IRRITABLE BOWEL SYNDROME, CONFIRMED BY DOUBLE-BLIND FOOD CHALLENGE. AN INCREASE IN RECTAL PROSTAGLANDIN LEVELS WAS NOTED WHEN A REACTION OCCURRED. PRELIMINARY INFORMATION SUGGESTS THE SAME PHENOMENON MAY TAKE PLACE IN PATIENTS WITH CHRONIC ULCERATIVE COLITIS." ____________________________________: Lancet 2000 Jul 29;356(9227):400-1 Related Articles, Books, LinkOut Relation between food provocation and systemic immune activation in patients with food intolerance.Jacobsen MB, Aukrust P, Kittang E, Muller F, Ueland T, Bratlie J, Bjerkeli V, Vatn MH.We found that food provocation in food intolerant patients was characterised by a general and systemic immune activation accompanied by an increase in systemic symptoms. Our findings might be important for the understanding of the mechanisms involved in the pathogenesis of food intolerance. ____________________________________HISTOPATHOLOGICAL FINDINGS IN JEJUNUM OF PATIENTS WITH SEVERE IRRITABLE BOWEL SYNDROMETornbloom H, Lindberg, G, Nyberg B, Veress BUniversity if Lund, Malmo, SwedenDIGESTIVE DISEASE WEEK, MAY 21-24, 2000, SAN DIEGO CALIFORNIA(6) patients with documented severe IBS which met all ROME criteria and normal antroduodenal manometry (thus not misdiagnosed cases of idiopathic intestinal pseudo-obstruction) where laparoscopized to the level of the jejunum. In all (6) when jejunal biopsies were obtained inflammatory infiltration of lymphocytes was found in the myenteric plexus (the network of nerve fibers and neuroganglie found between the longitudinal and circular layers of smooth muscle of the intestine). The lymphocytes were situated in periganglionic and intraganglionic locations. (4) patients showed hypertrophy of the longitudinal muscle layer, and (5) patients showed abnormailities of the interstitial Cells of Cajal **[**Synapse like contacts between ICC and nerve endings are characteristic, ICC make contact with smooth muscle cells by means of close appositions or gap junctions. ICC are crucial in generation of slow waves and in neural transmission in the gut.] ____________________________Am J Physiol Gastrointest Liver Physiol 2001 Mar;280(3):G315-8 Related Articles, Books, LinkOut Stress and the Gastrointestinal Tract IV. Modulation of intestinal inflammation by stress: basic mechanisms and clinical relevance.Collins SM.McMaster University Medical Centre, Hamilton, Ontario L8N 3Z5, Canada. scollins###fhs.mcmaster.caThe stress response in a healthy organism is generally viewed as a warning and thus a protective reaction to a threat. However, the response may be deleterious if it is linked to an inflammatory stimulus or if it proceeds an inflammatory event. Prior stress enhances the response to an inflammatory stimulus by a mechanism that is independent of the release of hypothalamic corticotropin-releasing factor (CRF) or arginine vasopressin. Putative mechanisms include an increase in intestinal permeability as well as the release of the proinflammatory neuropeptide substance P. Stress may also reactivate previous inflammation when applied in conjunction with a small luminal stimulus. This reactivation involves increased permeability and requires the presence of T lymphocytes.Inflammatory mediators activate hypothalamic pathways, and a negative feedback loop, mediated by CRF release, has been proposed because animals with impaired hypothalamic CRF responses are more susceptible to inflammatory stimuli. Together, these experimental observations provide insights into the expression of inflammatory disorders in humans, including inflammatory bowel disease and postinfective irritable bowel syndrome.Publication Types: � Review � Review, Tutorial _____________________________: Glia 2001 Nov;36(2):180-90 Related Articles, Books, LinkOut Immune function of astrocytes.Dong Y, Benveniste EN.Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0005, USA.Astrocytes are the major glial cell within the central nervous system (CNS) and have a number of important physiological properties related to CNS homeostasis. The aspect of astrocyte biology addressed in this review article is the astrocyte as an immunocompetent cell within the brain. The capacity of astrocytes to express class II major histocompatibility complex (MHC) antigens and costimulatory molecules (B7 and CD40) that are critical for antigen presentation and T-cell activation are discussed. The functional role of astrocytes as immune effector cells and how this may influence aspects of inflammation and immune reactivity within the brain follows, emphasizing the involvement of astrocytes in promoting Th2 responses. The ability of astrocytes to produce a wide array of chemokines and cytokines is discussed, with an emphasis on the immunological properties of these mediators. The significance of astrocytic antigen presentation and chemokine/cytokine production to neurological diseases with an immunological component is described. Copyright 2001 Wiley-Liss, Inc.Publication Types: � Review � Review, Academic ___________________________________Psychosom Med 2001 Nov-Dec;63(6):959-65 Related Articles, Books, LinkOut Phobic anxiety changes the function of brain-gut axis in irritable bowel syndrome.Blomhoff S, Spetalen S, Jacobsen MB, Malt UF.Department of Psychosomatic and Behavioral Medicine, National Hospital, Oslo, Norway. svein.blomhoff###riskshospitalet.noOBJECTIVE: Disease severity in the irritable bowel syndrome (IBS) is highly influenced by psychiatric comorbidity. The mechanism of this influence is generally unknown, even if the brain-gut axis seems to be involved. Recent research has indicated that IBS patients have aberrant perception of visceral stimuli in the CNS. We compared IBS patients with and without comorbid phobic anxiety to see if the comorbid disorder influenced brain information processing of auditory stimuli, and looked for possible consequences with respect to visceral sensitivity thresholds and disease severity. METHODS: Eleven female patients with IBS with comorbid phobic anxiety disorder were compared with 22 age-matched female IBS patients without such comorbidity. The groups were compared with respect to event-related potentials (ERP), auditory-presented words with emotional contents, barostat-assessed visceral sensitivity thresholds, and symptom levels the last week before assessment. RESULTS: The comorbid group had a significantly enhanced first negative ERP wave (N1) to all stimuli, indicating increased use of brain attentional resources. It also had increased visceral threshold for the sensation of gas, and reduced gas-stool and gas-discomfort tolerances compared with the noncomorbid group. Enhanced N1 amplitude at the frontal electrode and reduced gas-stools tolerance significantly predicted subjective gas complaints, explaining 47% of the symptom variation. CONCLUSIONS: The study suggests an association between information processing in the frontal brain and visceral sensitivity characteristics in IBS patients, and indicates that subjective disease-related symptomatology is predicted by brain perceptual characteristics. The findings indicate that an interaction between IBS-related and anxiety-related hyperreactivity in the frontal brain may constitute a psychophysiological mechanism for the contribution of psychiatric comorbidity to severity and duration of the irritable bowel syndrome.PMID: 11719635 [PubMed - in process] ____________________________________The beat goes on.....Eat well. Think well. Be well.MNL
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Note...before comment one may wish to take quick look at this thread as well, as anexample of the basis from which I speak: http://www.ibsgroup.org/ubb/ultimatebb.php...ic&f=1&t=025795 Comment: ____________________________________"Look at the dates of these studies. Also some weren't controlled and in others a lot of information is missing. If these patients were diagnosed with IBS is wasn't under the Rome criteria as they did not have that then and used a different criteria. " _____________________________________Lord is it futile to explain in detail "here is an example of HOW FAR BACK the work goes...EARLY findings" etc. ...THEY ARE SUPPOSED TO be OLD! that was the point Oy! dude!I have hundreds of abstracts running from the 1970s to 2001...and have cherry-picked about 40 pages of them if anyone wants them but you cannot POSt 40 pages of abstracts or whole books.So the people that WANTED to learn and read them and assimilate them ASKED for them by email and received them, and those who did show interest or request them of course did not receive them. Rhetoric again. _______________________________________"Also on any food studies I would like to see a follow up after a couple years. That would be interesting to me" ________________________________________If you were up on all the material you would already know about it an your interest would have been satisfied. Broaden your study and reading material and you will see.This cracks me up too,again, as one commences to railing against old abtsrtacts and then posts old ones himself. LOL Enough rhetoric already.One needs to comprehend the full implication of each of the elements in the "model" (Figure 1) in the article I referenced. It appears one dioes not, otherwise one would see that the perpetuation of what one says I write (which I do not) and what one says I ignore (which I do not) is merely rhetoric again. If the practitioners I work with, the researchers who study the phenomena referenced, and myself did not comprehend the role of the CNS and ENS and IRS in the activation and regulation of the IRS and its relationship to symptom provocation in IBS then I could not possibley state over and over unequivicolly that the Diagram (with the addition of role of circualting immunocyte reactivity) was representative of the integration of each aspect of current understanding of IBS.I can only repeat myself so many times. Scotomas often are not self-resolving, which is clearly the case.So lets see if there is a question posted by anyone to which one can respond and be read accurately.Yes here is one: _____________________________________"If IBS is the result of food allergies (of course excluding exceptions to every rule), then, how come clinical hypnotherapy has such a high success rate WITHOUT modification or change or elimination of foods in the diet; and in most cases, how can once offending foods be reintroduced after successful completion of the hypnotherapy sessions, if IBS is secondary to food allergies, etc.???? How come??? " ________________________________________Actually this is several questions. And I will try try try keep it SIMPLE and by doing so I suspect someone will come back and suggest I left ou A and B and C. If so I will anser that too at that time. SIMPLE and SHORT are not synonymous. In fact they are ofetn mutually exclusive. This is one such instance. Sorry. First we have to keep in mind that IBS is not said by anyone especially me to be CAUSED by FOOD ALLERGY.Food ALLERGY is a reaction of the immune system (primarily the "fixed" cells found in the mucosa and skin) called mast cells which is virtully immediate onset, not dose dependent, and a specific antigen-antibody reaction mediates it. That is the person has become sensitized to a food the same way they became sensitiized to, say, an inhalant. The body formed a specific immunoglobulin to the food. The body should not do this, only to pathogens or parasites. It is a case of mistaken identity. It is a specific malfunction as the immune system has mechanisms which begin in the small bowel to identify safe stuff like foods from pathogens. In the case of allergy this mistaken formation of an immunoglobulin occurs. These circulate around. When the person ingests the food, this triggeres a specific type of immunologic response which is supposed to be protective. Mediators are released from the mast cells (and basophils if they have any around), which set of a chain of events which results in the immediate onset of sympotms of food allergy up to and including shock. Then there is a late-phase reaction hours later.In the general population this ocurs about 2%-5% frequency....depends whose estimate you use. Actual food ALLERGY by the classic definition of allergists occurs with a higher frequency it appears among IBS victims. One investigation suggests about 8%. This does not cause IBS it causes food allergy as a COMORBIDITY seen in IBS. So it has been thought, but recent events now call old definitions to question as you will see.Most dietary evaluation methods used in evaluating the effect of food on IBS symptoms are structured such that they only find reactions which are sudden onset and not dose related. This means they find any food allergy if it exists (something easy to do with dietary monitoring or one of the common blood tests like RAST or ELISA) AND it can find pseudoallergy (FALSE allergy which is cuased by a direct chemical reaction with specific structures found in some foods...like lectins for example) or direct toxic reactions from certain chemicals in foods, natural and added (peptides or histamine for example).If you take those several sudden-onset and non-dose dependent food provoking mechanisms you will find comorbid food allergy and false-allergy and no more. This is the least important type of interraction in IBS between what you put into the intestine and the provocation of symptoms. And it is the easiest to isolate, treat by avoidance or immunomodulation, AND the most difficult to attenuate with HT since it is a very powerful form of immune response which even the mechanisms built into the CNS designed to attenuate immunologic reactions would have difficulty attenuating....as it intrinsically does not WANT to block this particualr mechansism (actually there are several but I have only shown one) BECAUSE this is essential to protecting the body from infection.In fact some of the mediators released are designed to decrease the permeability of the blood-brain barrier to permit the movement of mediators into the cereborspinal fluid which will accentuate the CNS response in these reactions...to amplify the responses.One can to a degree alter perspective to the chronic suffering from ALLERGY via CBT, and one can alter, and increase, the attenuating responses...or reduce the reflex rsponses of anxiety and stress-related repsonses which further amplify an allergic reaction, but the degree to which this works in actaul ALLERGY is limited since you must overcome massive angtigen-antibody interraction.Now, so far the only subpopulations of IBS which have been studied enough vis a vis reactivity to food and additives to make defibitive statements as to the OTHER mechanisms involved are the 1/3 that are D-types and the 1/3 that ar cyclic d&c. C-types can and do show both comorbid allergy and comorbid intolerance but other mechanisms at work in these victims which overly attenuate lower bowel motility are of greater significance, since if there is exposure these patients do not respond with the classic "evacuation" chain of events. So whenever I talk, or quote, or describe, you may have noticed I alwsy speak in the contet of the 70% or so who are NOT C-types. There are distinctly differing mechanisms much less well understood by anyone so far.Now if you have a copy of the diagram (Figure 1 in this article in front of you printed out it will be easier to exxplain...without it most people who have not read alot on the usbject cannot follow along...)http://www.blackwell-synergy.com/servlet/userag ent?func=synergy&synergyAction=showFullText&doi=10.1046/j.1365-2036.2001.00951.x[/URL]Now to fionish the diagram draw a line between the "IgG" box and the OTHER NON IGE Mediated" box. The draw a line down from there directly to RELEASE OF MEDIATORS without going THROUGH the MAST CELL BOX.Now you have all the known mechanisms represented.The IgE box represents the food ALLERGY part, and the other (2) represent the myriad different types of direct immunologic and non-immunologic reactions that are triggered all by themseleves without any help from the ENS or the CNS in response to something in a food, or a food additive. There are, say, 7-8 other mechanisms.For example, see where it shows MUCOSAL ANTIGEN PROCESSING...this is the reactions that occur by lymphocytes in the wall of the small bowel. They criculate in and out of the lymphatics and blood stream so as to be always available locally in the gut wall in case of invasion.For years such researchers as Bengtsson and others in Sweden have been able to show that both the mast cells in the small bowel AND circulating immunocytes, such as the lymphocytes, react in IBS patients to certain foods and release the mediators which produce the d-type cascade of symptom onset.They take a bunch of patients who meet the ROME criteria for IBS and then remove all those who have comorbid food ALLERGY as confirmed by various conventional means of isolating circulating antibodies to foods. Get rid of the comorbid ALLERGY people so there is no confusion. They check for food provocation with double blind oral challenge to see which foods provoke symptoms.Since we are not talking ALLERGIES now we are tlaking about OTHER MECHANISMS (see diagram). What sets these apart from allergy cliniclly is that the reaction is DOSE DEPENDENT (it may take a goodly portion of the food to cause a response or a combination of two provoking foods together or consumptions over several meals to accumulate the dose which brings on symptoms) AND the onset of symptoms is DELAYED....from a few hours up to as much as 72 hours. So the oral challenge process is very time consuming if you try to find all the foods. So they chosoe a few of the most common that the persons are eating and just check those.Once they isolate which foods provoke symptoms for each patient they take them off those foods for a few days to make sure any provocation is removed.Then they take those people in slide a tube down their esophagus, stomach and isolate a section of the small bowel with a tube which 2 inflatable cuffs. Yout then have isolated section of small bowel so you can do a true blind challenge and you can capture evidence of what occurs in a true lind challenge (the patient has no way of knowing if anything, much less what, is instilled into the tube at any time...could be saline or could be a slurry containing the food challenge.Now to cut to the chase you always find the mediators in the washings which show that the gut immunocytes are either degranulating (mast cells) or circulating immunocytes are apoptosizing (losing cell wall integrity) and releasing their dozens of different and very powerful mediators into the small bowel mucosa and wall where the blood vessels, nerves, smooth muscle are that they are known to act directly upon.While all this has been going on the past few years, confirming not only what others have shown indirectly over the years with oral challenges to IBS patients and elimination diets and mast cell stabilizers, another investigator got the bright idea (Tornbloom) to talk a few IBS patients into letting him take full thickness biopsies of the small intestine to see if there are signs of inflammatory staging and/or long term reaction within the tissue.So he stuck in his thumb and pulled out the accumulations of t-cells that the other guys were finding their mediators in the washings provoked by specific foods. Which of course when you stopped instilling them the mediators went away because the reactions stopped and so did the symptoms. All the while this has been going on others have been studying the blood reactions of white cells in vitro and finding that the circulating cell reactions can be duplicatd OUTSIDE the body out of reach of the ENS and the CNS. This was first discovered, crudely, back in 1956.Anyway, the most recent step which confirms the accuracy of that diagram is that specific markers of immunoligic activation of t-cells (certain lymphocytes)in the small bwel wall were found when Bengtsson not only stsudied the washing BUT hje klast year started taking biopsies in these patients (ROME Criteria, non allergic, food provoked symptoms) and found, well, here is a direct quote on the findings from September 2001, which are being readied for publication sometime this year...."....we can show an allergy-like inflammation during challenges with parameters like Il-4, IFN-gamma, CD3, CD4, CD8 and IgE."If one understands a little about allergology and immunology one understands the significance of these markers. Simply put....the mediators noted IL-4 and IFN are T-cell mediators..,lymphocytes are breaking down in the small bowel of the subjects and releasing their intracellular inflammtory mediators and different types of foods provoked it. CD[3] [4] [8] are hard to explain simply...these are like receivers of information that differntiate different kinds of lymphocytes which perform different roles in inflammatory reactions...they interract with another substance called Major Histocompatability Complexes (I & II) which are supposed to make sure the right antigen (provoking agent of an immune response) gets presented to the right kind of t-cell for the right reaction. While Tornbloom showed the lymphocytes accumulating in the bowel walls of the IBS patients, Bengstsson found that there are several different classes involved in the inflammatory reaction by finding multiple class markers.Further, the really surprising thing is the presence of local IgE...remember the patients with CIRCULATING IgE indicating allergy were ELIMINATED. So this, and some earleir findings of IgE in the small bowel of food reactive but no allergenic subjects, shows one thing...an allergy-like mechanism (think IgE-mast cells) IS involved in even those where the classic allergy markers disaqualify them from beigna llegedly allergic, and IgE and the other mechanisms all occur absent input from the ENS or CNS...this is not reqired nr even a part of this type of reactivity...except after the reaction has begun and the ENS and CNS are provoked by the mediators.The cart, in this case, comes before the horse.Now from the diagram and from other study you know that the CNS and ENS are fully integrated with the imune system, and certain stressors on the CNS, or even certain kinds of other stimuli direct to certain aprts of the brain, can and do result in efferent (down-travelling) signals which can activate the fixed immune cells (mast cells) ABSENT any immediate immunolgic provocation. You can see that it can happen the opposite as well. BOTH can and do occur, so the question becomes in a given subject what is the combination? THIS is why the info has to be integrated so that future studies preferably would take into account the direct-immunilogic ally mediated reactions to diet provocation that occur in these patients. SO FAR that is not being done.So understanding this diagram and this grossly simplified example/explanation answers the question.CBT, for example, Grossly Simplified, is very effective in some and ineffective in others depending upon which portion of the "system" predominates as a source of symptoms.This therapy alters reaction to symptoms, perception of the consequences, and reaction to those consequeces etc....pure behavioral modification which first helps the victim gain better control over her responses to symptom onset and respond with less symptom-amplifying stress to the situations created by the syndrome. Therefore CBT alone will reduce the patients symptoms, even in the face of ongoing provocation, proportionate to the degree to which the patients RESPONSE TO the initial symptom has AMPLIFIED the symptoms....in some people this is SIGNIFICANT since their underlying symptoms may have been initially relatively mild but over time the way they react to the symptoms, and what they did to the persons life, and how the person adjusted or maladjusted, as you can see from the diagram showing the interraction of STRESS with the CNS and then in both directions the IRS and the ENS, may have ben significant.The same goes for HT, though at a more fundamental level. In simple terms, as you can see, the CNS can provoke the IRS to activate as can Immunologic (allergic) mechanisms as well as OTHER (non IgE mechanisms). Each can happen, and does absolutely, independently.Once can attenuate the IRS response, first by attenuating both the persons emotional reaction to a develping symtom, pain or cramping or chills, etc, AND especially in the case of NON IGE or IGG subclass meduated reactions, one can attenuate the reaction itslef. Not just after the fact BUT one can raise the threshold of reactivity. One may even bea ble to modulate the, for example, messengers like MHC within the IRS via certain specific cells located in the brain which perform that function. This is also an intriguing line of investigation.Anyway, In some cases where a pateint has no comorbid food allergy, and the provoking dose of a given food via one of the non allergic mechanisms is fairly high, the threshold of response can be raised through HT sufficiently that the reaction is attenuated enough that it eventually becomes subclinical (so weak as to not be noticed). This is one mechanism. Another is by altering perception of the symptom, and reducing the stresas and anxiety responses to symptoms and to the psychosocial consequences one interrupts the REFLEX LOOP you can see exists after provocation.Now if it were only certain cells or mechanisms involved, (for example only the "mucosal" immune system) it would theoretically be possible to produce extreme attenuation of the IRS response to non-pathogens. In a patient where this is the case it could occur.The trouble is, since there are mechanisms involved which are not "hard wired" to the CNS, the degree of success varies widely. In general, 80+% of patients will experience at least a moderate degree of symptom reduction. Do not forget that no studies measure successful outcome as 100% remission or nothing. Each has a different threshold of their definition of success which has to be taken into account, along with the selection process.Anyway, to repeat, one can not only break the reflex arc to locally provoked IRS responses which are independent of the CNS and ENS, but one can reduce or eliminate the CNS-locus of IRS activation, which varies in contribution to symptoms from person to person, AND one can raise the threshold of non IgE mediated reactions to some degree as well. Like KM is fond of saying "Your mileage may vary".Hence some people will actually regain some oral tolerance...in some cases total tolerance to some foods...as a result of HT. This is not a mystery to anyone including the immunologists who study the "middle 3 boxes" in this diagram...and the missing line we drew in to rpesent the cellular responses. hell, as simply stated, you can regain all oral tolerance if you simply either stabilize the cell walls of the immunocytes against all stimuli via immunomodulation, or eliminate all sources of provocation from each source.Conversely, the reason that studies on DIETARY manipulation alone prodcue similar results consitently over the years to any other single mode therapy is just that...70, 80, 90% experiencing a reduction in symptoms from modest to extreme in like fashion to HT is again because the response is going to be proportionate to the degree of comorbid allergy removed, and the degree of contribution of IRS activation by mechanisms other than IgE/IgG in eliciting a small bowel centered inflammatory response.This is why many patients who undergo dietary therapy alone, but who do have measurable signs of exaggerated stress and anxiety, simply "lose" that behavior after the provoking fods are removed even though CBT or HT was not used along with dietary therapy.The direct chemical effects of mediators upon the CNS and ENS are removed and this reduces the activation of those parts of the brain-gut axis which respond directly to certain mediators among the over 100 that may be involved.Also, when you remove the fear of loss of bowel control, pain, bloating chills dizziness etc. the causal basis of ther anxiety in some folks is removed and they respond accordingly (they may have no great degree of patterned-in learned response to stress).So hopefully you can see why any single-mode therapy for IBS will be very successful for some, moderately for others, and not at all for others...hence the cinsistency in the outcomes between the single modalities. Like a car with plugged injectors and a bad chip in the EEC, if you fix one you will get response to the degree that one contributes to the malfunction...in the case of the injectors the EEC has the capacity to make adjustments to partially compensate and reduce the symptoms.THAT IS WHY THE MODALITIES HAVE TO BE COMBINED in an integrated fashion to get the BEST outcomes. This is my mantra, nothing more or less, and so it shall remain regardless of assertions to the contrary.
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If everyone could put aside their predjudices and agendas, and instead opened themselves up to the clinical experience and finidings of others working from a diffenret anghle and openly integrated the best of both. ALL IBS patients would enjoy an opportunity to achieve the highest chance at the greatest degree of remission possible for themselves. This would require the renunciation of human behavior, however...an unlikely event.Until we do that, there will always be a degree of compromise in the outcomes, and varying degrees of success, with any modality or treatment program.If that whole thing still cannot be comprehended as to what the message is, I must say I know of know simpler way of answering the question(s) and still include enough information to be meaningful and accurate. A few other articles which explore the areas discussed here, in the Diagram I referred you to and that article, and many others beyond these few more...one must seek a very broad specturm of study to visualize the exquisite integration of the CNS, ENS, and INS...then to understand their various roles in conditions like IBS.....just a very few examples of what I mean... ___________________________________Nord Med 1996 Apr;111(4):109-12, 118 Related Articles, Books, LinkOut [Sick of food? Knowledge and hypothesis on food intolerance][Article in Norwegian]Jacobsen MB, Vatn MH.Medisinsk avd A, Rikshospitalet, Oslo.Food intolerance is frequently reported by patients and represent a diagnostic and therapeutic challenge. We review the nomenclature and report on symptoms, diagnostic tests and treatment. The nomenclature presented is based on the primary events such as toxic reactions, allergy or an undefined mechanism, including psychosomatic, although these subgroups may involve common pathogenetic mechanism. Double blind placebo controlled food challenge is the golden standard in the diagnostic workup and the importance of elimination diets--individually tailored to each patients requirements in cooperation with a nutritionist--is stressed. Through strict adherence to diagnostic and therapeutical guidelines, therapy may resolve food induced symptoms. Based on preliminary findings of signal transduction, we propose that symptoms in some patients may depend on an allergy type IV reaction. (** a 1-3 day delayed-onset reaction involving macrophages and effector T-cells)This working hypothesis forms the basis for further accumulation of knowledge of food intolerance reactions.Publication Types: � Review � Review, Tutorial ____________________________: Baillieres Best Pract Res Clin Gastroenterol 1999 Oct;13(3):429-36 Related Articles, Books, LinkOut Putative inflammatory and immunological mechanisms in functional bowel disorders.Collins SM, Vallance B, Barbara G, Borgaonkar MIntestinal Diseases Research Unit, McMaster University Medical Center, Hamilton, Ontario, Canada.The observations that irritable bowel syndrome (IBS) may be precipitated by an acute enteric infection, or occurs commonly in patients in remission from inflammatory bowel disease (IBD) has prompted consideration of inflammation as a putative basis for symptom generation in IBS. In this regard, IBS may follow a pattern of pathogenesis that is similar to asthma--which was once considered a psychosomatic disease. This review examines the basic scientific evidence of a functional interface between the immune and sensory-motor systems of the gut and discusses how this may be relevant to a subgroup of IBS patients. In addition, review will examine the implications of this for the diagnosis and treatment of IBS.Publication Types: � Review � Review, tutorial __________________________________Page 1051 of the hard copy of the 2000 Merck manual: "RECENTLY FOOD INTOLERANCE WAS FOUND TO BE RESPONSIBLE FOR SYMPTOMS OF SOME PATIENTS WITH THE IRRITABLE BOWEL SYNDROME, CONFIRMED BY DOUBLE-BLIND FOOD CHALLENGE. AN INCREASE IN RECTAL PROSTAGLANDIN LEVELS WAS NOTED WHEN A REACTION OCCURRED. PRELIMINARY INFORMATION SUGGESTS THE SAME PHENOMENON MAY TAKE PLACE IN PATIENTS WITH CHRONIC ULCERATIVE COLITIS." ____________________________________: Lancet 2000 Jul 29;356(9227):400-1 Related Articles, Books, LinkOut Relation between food provocation and systemic immune activation in patients with food intolerance.Jacobsen MB, Aukrust P, Kittang E, Muller F, Ueland T, Bratlie J, Bjerkeli V, Vatn MH.We found that food provocation in food intolerant patients was characterised by a general and systemic immune activation accompanied by an increase in systemic symptoms. Our findings might be important for the understanding of the mechanisms involved in the pathogenesis of food intolerance. ____________________________________HISTOPATHOLOGICAL FINDINGS IN JEJUNUM OF PATIENTS WITH SEVERE IRRITABLE BOWEL SYNDROMETornbloom H, Lindberg, G, Nyberg B, Veress BUniversity if Lund, Malmo, SwedenDIGESTIVE DISEASE WEEK, MAY 21-24, 2000, SAN DIEGO CALIFORNIA(6) patients with documented severe IBS which met all ROME criteria and normal antroduodenal manometry (thus not misdiagnosed cases of idiopathic intestinal pseudo-obstruction) where laparoscopized to the level of the jejunum. In all (6) when jejunal biopsies were obtained inflammatory infiltration of lymphocytes was found in the myenteric plexus (the network of nerve fibers and neuroganglie found between the longitudinal and circular layers of smooth muscle of the intestine). The lymphocytes were situated in periganglionic and intraganglionic locations. (4) patients showed hypertrophy of the longitudinal muscle layer, and (5) patients showed abnormailities of the interstitial Cells of Cajal **[**Synapse like contacts between ICC and nerve endings are characteristic, ICC make contact with smooth muscle cells by means of close appositions or gap junctions. ICC are crucial in generation of slow waves and in neural transmission in the gut.] ____________________________Am J Physiol Gastrointest Liver Physiol 2001 Mar;280(3):G315-8 Related Articles, Books, LinkOut Stress and the Gastrointestinal Tract IV. Modulation of intestinal inflammation by stress: basic mechanisms and clinical relevance.Collins SM.McMaster University Medical Centre, Hamilton, Ontario L8N 3Z5, Canada. scollins###fhs.mcmaster.caThe stress response in a healthy organism is generally viewed as a warning and thus a protective reaction to a threat. However, the response may be deleterious if it is linked to an inflammatory stimulus or if it proceeds an inflammatory event. Prior stress enhances the response to an inflammatory stimulus by a mechanism that is independent of the release of hypothalamic corticotropin-releasing factor (CRF) or arginine vasopressin. Putative mechanisms include an increase in intestinal permeability as well as the release of the proinflammatory neuropeptide substance P. Stress may also reactivate previous inflammation when applied in conjunction with a small luminal stimulus. This reactivation involves increased permeability and requires the presence of T lymphocytes.Inflammatory mediators activate hypothalamic pathways, and a negative feedback loop, mediated by CRF release, has been proposed because animals with impaired hypothalamic CRF responses are more susceptible to inflammatory stimuli. Together, these experimental observations provide insights into the expression of inflammatory disorders in humans, including inflammatory bowel disease and postinfective irritable bowel syndrome.Publication Types: � Review � Review, Tutorial _____________________________: Glia 2001 Nov;36(2):180-90 Related Articles, Books, LinkOut Immune function of astrocytes.Dong Y, Benveniste EN.Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0005, USA.Astrocytes are the major glial cell within the central nervous system (CNS) and have a number of important physiological properties related to CNS homeostasis. The aspect of astrocyte biology addressed in this review article is the astrocyte as an immunocompetent cell within the brain. The capacity of astrocytes to express class II major histocompatibility complex (MHC) antigens and costimulatory molecules (B7 and CD40) that are critical for antigen presentation and T-cell activation are discussed. The functional role of astrocytes as immune effector cells and how this may influence aspects of inflammation and immune reactivity within the brain follows, emphasizing the involvement of astrocytes in promoting Th2 responses. The ability of astrocytes to produce a wide array of chemokines and cytokines is discussed, with an emphasis on the immunological properties of these mediators. The significance of astrocytic antigen presentation and chemokine/cytokine production to neurological diseases with an immunological component is described. Copyright 2001 Wiley-Liss, Inc.Publication Types: � Review � Review, Academic ___________________________________Psychosom Med 2001 Nov-Dec;63(6):959-65 Related Articles, Books, LinkOut Phobic anxiety changes the function of brain-gut axis in irritable bowel syndrome.Blomhoff S, Spetalen S, Jacobsen MB, Malt UF.Department of Psychosomatic and Behavioral Medicine, National Hospital, Oslo, Norway. svein.blomhoff###riskshospitalet.noOBJECTIVE: Disease severity in the irritable bowel syndrome (IBS) is highly influenced by psychiatric comorbidity. The mechanism of this influence is generally unknown, even if the brain-gut axis seems to be involved. Recent research has indicated that IBS patients have aberrant perception of visceral stimuli in the CNS. We compared IBS patients with and without comorbid phobic anxiety to see if the comorbid disorder influenced brain information processing of auditory stimuli, and looked for possible consequences with respect to visceral sensitivity thresholds and disease severity. METHODS: Eleven female patients with IBS with comorbid phobic anxiety disorder were compared with 22 age-matched female IBS patients without such comorbidity. The groups were compared with respect to event-related potentials (ERP), auditory-presented words with emotional contents, barostat-assessed visceral sensitivity thresholds, and symptom levels the last week before assessment. RESULTS: The comorbid group had a significantly enhanced first negative ERP wave (N1) to all stimuli, indicating increased use of brain attentional resources. It also had increased visceral threshold for the sensation of gas, and reduced gas-stool and gas-discomfort tolerances compared with the noncomorbid group. Enhanced N1 amplitude at the frontal electrode and reduced gas-stools tolerance significantly predicted subjective gas complaints, explaining 47% of the symptom variation. CONCLUSIONS: The study suggests an association between information processing in the frontal brain and visceral sensitivity characteristics in IBS patients, and indicates that subjective disease-related symptomatology is predicted by brain perceptual characteristics. The findings indicate that an interaction between IBS-related and anxiety-related hyperreactivity in the frontal brain may constitute a psychophysiological mechanism for the contribution of psychiatric comorbidity to severity and duration of the irritable bowel syndrome.PMID: 11719635 [PubMed - in process] ____________________________________The beat goes on.....Eat well. Think well. Be well.MNL
How many of us have had a Blood antibody test? I had one which showed high levels of IgA and IgG. So I had my liver tested, normal. Again I had a blood test done for H. Pylori, high levels of IgA. This was thrown out as a positive because IgA is disreguarded as a marker for H. Pylori. I had this first test done years ago because of chronic Thrush infections and was thought to have a immune system problem. this test is used on HIV infections to see how the immune system is holding up. I don't think it is normaly given to IBS patients but it would be interesting to see if alot of us have higher than normal levels of circulating antibodies. It seems that MNL theory of IBS would indicate higher levels of circulating antibodies. Maybe Eric's would also? I recall reading somwhere that higher levels of these proteins ( they are called proteins also )were found in IBS sufferers.
How many of us have had a Blood antibody test? I had one which showed high levels of IgA and IgG. So I had my liver tested, normal. Again I had a blood test done for H. Pylori, high levels of IgA. This was thrown out as a positive because IgA is disreguarded as a marker for H. Pylori. I had this first test done years ago because of chronic Thrush infections and was thought to have a immune system problem. this test is used on HIV infections to see how the immune system is holding up. I don't think it is normaly given to IBS patients but it would be interesting to see if alot of us have higher than normal levels of circulating antibodies. It seems that MNL theory of IBS would indicate higher levels of circulating antibodies. Maybe Eric's would also? I recall reading somwhere that higher levels of these proteins ( they are called proteins also )were found in IBS sufferers.
LOL Lizbec!! I think your right, maybe they need a board to hash it out all the time. It would sure save my fingers a lot of ache from all the long scrolling I have to do in all these threads!
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I sure wouldn't want to offend either, I think they are both great guys who want to help. But yes, they need their own board for these fights.
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Jennifer
LOL Lizbec!! I think your right, maybe they need a board to hash it out all the time. It would sure save my fingers a lot of ache from all the long scrolling I have to do in all these threads!
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I sure wouldn't want to offend either, I think they are both great guys who want to help. But yes, they need their own board for these fights.
![]()
Jennifer
Joined
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1,992 Posts
BQ and others -- somewhere about halfway down Volume I of Mike's three novels, I thought I saw the phrase "To cut to the chase..."What happened?My mother (or someone like that), always said if you can't say something right the first time, don't try again.
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