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You both have lost me. I'm not loner sure what the two of you disagree about. Food, the immune system, and the hypnosis/serotonin system all seem related to some kinds ibs and other disorders but they all seem to do the same thing in different ways?I'm not sure what you disagree with each other about.tom
 

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Real science has discovered that the immune system of the gut is instrumental in removing ingested substances are generally regarded as toxic (e.g, bacteria cause gastroenteritis). It it performs this removal process at least in part by mast cells degranulating and releasing histamine which causes diarrhea.Real science has also discovered that the brain is wired to the immune system portion of the gut and it appears that the brain can utilize this mechanism to rid of the gut of material when it is sees fit, that is in times of stress.Thus a potential mechanism for bringing about IBS symptoms is through the brain misusing the gut's immune system.I believe that Mike believes that food plays a major role in inciting the gut's immune system and the immune system magnifies this by responding inappropriately to food.Real science has yet to establish this claimed connection. Part of this is because it is difficult to test experimentally. This is because symptoms fluctuate and because of possible "placebo" responses. Double-blinded trials are ideal, but it is not easy to feed someone without their knowing what it is..The other reason is probably because for the most part there is nothing to discover. That is, it may be for a very few people diagnosed with IBS there is something involved with food but for the vast majority it is not the case (as Mike wants us to believe).The gut normally has responses to what is put in it. In IBS, these responses appear to be abnormally exaggerated, leaving one to believe incorrectly that what is put in is the culprit rather its simply being the temperamental nature of the "IBS gut".
 

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Real science has discovered that the immune system of the gut is instrumental in removing ingested substances are generally regarded as toxic (e.g, bacteria cause gastroenteritis). It it performs this removal process at least in part by mast cells degranulating and releasing histamine which causes diarrhea.Real science has also discovered that the brain is wired to the immune system portion of the gut and it appears that the brain can utilize this mechanism to rid of the gut of material when it is sees fit, that is in times of stress.Thus a potential mechanism for bringing about IBS symptoms is through the brain misusing the gut's immune system.I believe that Mike believes that food plays a major role in inciting the gut's immune system and the immune system magnifies this by responding inappropriately to food.Real science has yet to establish this claimed connection. Part of this is because it is difficult to test experimentally. This is because symptoms fluctuate and because of possible "placebo" responses. Double-blinded trials are ideal, but it is not easy to feed someone without their knowing what it is..The other reason is probably because for the most part there is nothing to discover. That is, it may be for a very few people diagnosed with IBS there is something involved with food but for the vast majority it is not the case (as Mike wants us to believe).The gut normally has responses to what is put in it. In IBS, these responses appear to be abnormally exaggerated, leaving one to believe incorrectly that what is put in is the culprit rather its simply being the temperamental nature of the "IBS gut".
 

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I beleive that both Mike and Eric have a lot to offer many of us here but, I do not see the point of these public disagreements elsewhere on this board as it serves no purpose in helping anyone.At the end of the day we should all be united in helping each other as much as we can with good factual advice or just listening to others and offering support whoever we are and wherever we come from.Please keep this stuff to yourselves guys if you don't mind me saying and have a private argument. I offer this in peace and hope that neither of you are not offended, that is not my intention.
 

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I beleive that both Mike and Eric have a lot to offer many of us here but, I do not see the point of these public disagreements elsewhere on this board as it serves no purpose in helping anyone.At the end of the day we should all be united in helping each other as much as we can with good factual advice or just listening to others and offering support whoever we are and wherever we come from.Please keep this stuff to yourselves guys if you don't mind me saying and have a private argument. I offer this in peace and hope that neither of you are not offended, that is not my intention.
 

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jb2 - I absolutely agree!! And the arguments/disagreements are expressed in such a long-winded way - It takes ages to wade through and I end up more confused - please, no more of these mystifying debates!!liz
 

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jb2 - I absolutely agree!! And the arguments/disagreements are expressed in such a long-winded way - It takes ages to wade through and I end up more confused - please, no more of these mystifying debates!!liz
 

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Comment: _____________________________________"I believe that Mike believes that food plays a major role in inciting the gut's immune system and the immune system magnifies this by responding inappropriately to food." _____________________________________On the contrary I merely have studied the findings of real scientists, of which I am not one, which confirm the validity of the integrative model of the roles of the CNS, ENS and IRS in IBS.Belief denotes an act of faith. There is no faith involved in the extensive work along these lines. there is ample hard evidence, clinically an investigatory, that not only can the IRS be activated in ISb by the CNS and ENS but immunologically and non-immunologically as well independent of CNS and ENS factors...the IRS can and does serve in IBS patientrs as the origin of the upregulation of the CNS and ENS.The question remains as to how to isolate whether there are specific subpopulations which are characterized by one system being primary, or does the primary mechanism vary within each patient from time to time depending upon the provoking stimulus.At least science is far enough along now to know that all (3) are ionvolved!! This is a big step.There is a diagram, Figure 1, in the following article which anyone can "click on" then print out and look at. It illustrates the interrdependency of these systems in the process of elicitng IBS symptoms. http://www.blackwell-synergy.com/servlet/u...36.2001.00951.x The part that is missing is the activation of the IRS circulating cells (lymphocytes, granulocyte classes, macrophages and platelets) in IBS which has been confirmed by "real scientists" who isolate and challenge the small bowel with various dietary componenets then assess inflammatory response, and those who study circulating immunocyte response in vitro...absent input from the CNS and ENS. By capturing IRS activators which function independent of the input of the CNS and ENS, one shows that the "third leg of the stool" is active and this of course explains why the response of the non-mast cell immunocytes can be duplicated in vitro.If you take the diagram and draw a line between the 2 boxes that connect the NON IgE mechanisms in the way the author separated them (IgG[x] subclasses vs OTHER Non IgE mechanisms) and then extaned that line down to the MEDIATOR RELEASE box, the picture is then complete for the sum total of what is known so far about the interraction between the IRS ENS and CNS in IBS.If one chooses to ignore part of the information and only look at that which suits that person then of course they will only see and acknowledge part of the integrated dynamics.Thankfully the investigation into the key role of proinflammtory activation in IBS is not being conducted solely by one group and from one perspective. Since some European scientists have been wise enough to study the small bowel immune response diretly, they have been able to confirm what has already been known since 1979: that certain dietary components, which vary from patient to patient, will provoke a proinflammtory reaction within the sructures of the small bowel IN THE ABSENCE of specific circulating antibodies to that food, and thus precipitate the symptoms of diarrheaic type and cyclic type symptom sets of so-called IBS.The mechanisms are well documented in numeraous places, and if one makes a serious study of the literature on the subject absent selective thinking then one would be aware of these mechanisms. No one in that portion of the scientific community which works with non-allergenic food intolerances is so uneducated and naive and simple-minded as to base their conclusions on mere cause-effect observations. If the literature were actually studied such a silly statement would not have been made.To not do so by a non-healthcare provider is a matter of personal choice which bears no ill consequence to anybody accept those who may attribute some credibility to that prsons' denouncements, and then manage their treatment program accordingly. In a healthcare providers case, to ignore and not intergate that understanding into the recommended care and clinical management of patients would be to fall short of a professional obligation to excellence and ethics.Some folks read the published material, books, studies and tutorials provided by doctors and scientists who have both studied this area and cared for patients in this manner successfully. Some do not. So posts like this thread contains reflects the opinion of those who chose not to, or are unable to. The rendering of that opinion does not render the information false. True and false ar characteristics of speech not of tangible things. In this case we are talking about tangible phsyiologic events, therefore no true or false can exist, only the fact that they do occur regardless of opinion or assertion to the contrary by the ill-informed.When one constructs a patient care program accordingly for patients wherein the reactions do occur, the program is successful as measured by outcomes proportionate to the degree of patient compliance. ________________________________"I do not see the point of these public disagreements elsewhere on this board as it serves no purpose in helping anyone." ________________________________I respect your view, yet disagree. On the contrary if there is information pertinent to the welfare of the sick, and the information is not shared, then it is to the detriment of the sick. Based upon what the sick ofetn experience by way of available education as to the causal basis to their condition this may be the only venue by which they can see certain expanded, integrative and contrary views and understandings expressed.In the process of discovery in advancements in medicine, since this process involves humans, it also involves human nature and all that this entails. Therefore here and elsewhere (right up to the entertaining shouting matches and denouncements in Q&A sessions at medical conferences which become "lively") this is bound to occur as part of the process of moving from the ill-defined "syndrome" phase or "idiopathic" phase of some condition into the eventual place where the "disease" and "cause" become fully understood.Since that process always occurs, here or elsewhere, in an environment where any other persons involvement is voluntary, if the discussion displeases you "change the channel", in this case exit the discussion, and don't read it.Everyone does that every day, as there are some things which interest some and some things which do not. Sometimes a sense of fascination sets in...like at a car wreck. On the one hand it offends a persons psyche yet they feel compelled to observe and observe and observe. So it must perform some function and hold some form of interest for the person whose attention lingers over the incident, no?
________________________________ "At the end of the day we should all be united in helping each other as much as we can with good factual advice or just listening to others and offering support whoever we are and wherever we come from." _________________________________We are, regardless of the fact that the practitioners some of us work with posess differign views and follow differnt treatment methods. Each person acts in what he or she belives (I hope) is in the best interests of the patients here.This is all part of that process, yet still we may not all agree as to what parts of the process we each think are useful and which are not. That is because we all value different things. Use that which you value and discard that you do not. A natural reaction. Conversely one persons poison may be anothers' revelation of understanding. __________________________________"Please keep this stuff to yourselves guys if you don't mind me saying and have a private argument." ___________________________________One persons argument is anothers tutorial. If you do not like it do not read it and you won't then be bothered. Sometimes we all look at things and say "See? At least I don't do that!!". So whose voice is that self-talking when we think that and then express it... _________________________________"I offer this in peace and hope that neither of you are not offended, that is not my intention. " ___________________________________
I know.
I am not.
____________________________________"The other reason is probably because for the most part there is nothing to discover. That is, it may be for a very few people diagnosed with IBS there is something involved with food but for the vast majority it is not the case (as Mike wants us to believe)." _____________________________________Mike does not suggest "beleif" as this is an act of faith. there is no faith-based component to whatI have learned from the doctors and dieticians I work with.The majority of patients who suffer d-predominanat and cyclic symptoms sets can and do suffer provocation of onset of symptosm by dietary compnenets. Done properly this can be duplicated in vivo and in vitro and their dieta djusted accordinlgy to reduce or eliminate sympotms. There are at least (8) known immunologic and non-immunologic mechanisms, which are also non-ENS and CNS mechanisms, by which this can occur. The markers of many have been recovered directly from the GI tract.Irrespective of which of the Immunologic, Non Immunologic, CNS or ENS mechanisms which can and do influence the activation of the IRS; regardless of which can be isolated as a primary "arming mechanism" in a given subject (rendering the other mechanisms secondary or amplificatory), it has been shown over and over again since at least 1955 (with the best work beginning in 1979 or so) that in AT LEAST the 2/3 of IBS patients a partial, dose-dependent loss of oral tolerance to harmless food components and/or chemical additives occurs as compared to asymptomatic people. Thus the introduction of certain provoking foods, beyond those which cause pseudoallegry or direct chemotoxicity, provokes symptoms reliably. This is absent any comorbid food allergy. It is a fact that the identification and removal of thise specific substsnces from the diet reduces or eliminates the patients symptoms. Fact.In spite of the fact that scientists have not only been isolating the markers of neurologic activity in IBS but the markers of immunologic and alternative-pathway IRS activation in the small bowel of IBS victims the most recent 25 years or so, right up to recovering proof of, for example, specific lymphocytic activation in response to dietary components as well as local IgE in the small bowel specific to the dietary components that provoke the symptoms, lay people and practitioners alike continue to perpetuate the myth that this is illusory. Its kind of funny since the very chemicals which upregulate the ENS and CNS are released into the gut parenchyma and systemic circulatiion in these reactions...yet when they are isolated they are simply ignored as they do not fit "the model" perhaps someone invented elsewhere.Not an unusual practice when syndromes are studied from differeing perspectives that the owner of the one perspective should not acknowledge the validity of those whose work comes from an alternative perspective. Eventually the collective medical community gets past it and integrates all the knowledge. It is not there yet and that is reflected in what trickles down to and through non-healthcare professionals. ___________________________________"The gut normally has responses to what is put in it. In IBS, these responses appear to be abnormally exaggerated, leaving one to believe incorrectly that what is put in is the culprit rather its simply being the temperamental nature of the "IBS gut". " ____________________________________Sadly for the reader of this disinformation, the first statement is of course correct as it is the grosseest possible generality. The books I recommend would elucidate this process in detail.The second "action-response-conclusion" thinking indeed could be said of both investigatory ad diagnostic approaches....symptom based and causal alike. One observes a specific neurologic "event" and, not having quantified whether there is the prior presence of some chemical mediator (endogenous or exogenous) which would account for the neuolgic event, presumes and postulates the mechanism at work. Someone reads the posulate and infers fact. The inferred fact is implicated in reptition and thus becomes fact by acclimation. I see that in the IBS "research" done by many in the United States all the time, and then how it is explained here in foruims like this to patients hungry for information.In the case of food elements provoking the local inflammatory response in the small bowel at least the first step is accomplished that the scientists studying the allergologic and immunologic aspects of the syndrome have been espousing since it was first documented lo these many years. That is at least finally everyone acknowledges that (at keast in these 2 populations) some weird inflammatory reaction (which is not a measurable food "allergy" reaction by conventional means) does occur, and an array of inflammtory mediators are released in the small bowel which can upregualte sensory and motor function.Just 18 months ago most the majority of "IBS investigators" and GI docs in the USA were denouncing such mechanisms as non existent ("there is NO inflammtory response involved in IBS" was the dogma). That claim was posted loudly and often in IBS self help communities as well, including here, as recemtly as 6 months ago in spite of the fact it has been known to be incorrect for 20 years.Now, since it has also been well known physiologically since, say, 1979, that prostaglandins produced in proinflammatory reations in the gut and other forms of tissue and serotonin released in the same fashion upregulate bowel functiona and cause diarrhea....all of a sudden the persons who made these proclamation of folly have begun debating "ownership" of this weird IRS activation...CNS/Stress...ENS/Stress....Immunologic mechanisms. what an incredible laugh, and so typical of what I have had the dubious privilege of watching time and time again over the last 30 years.
To cut to the chase, It is just a stupid argument since it is self evident from an integrative view that the systems are fully interractive, codependent, and can be armed by specific mechanisms which can be sourced to each of the systems in question depending upon the patient and circumstance. AND it is obvious that there are subpopulatons where each is going to be found to be true vis a vis what is the primary arming mechanism after which the IRS can be provoked.Since, however, so far at LEAST IgE (mast cells, basophils) and T-lymphocyte arming mechanisms which are "immunologic" (and the circulating immuncoytes themselves ecrutied to the lamina propria) have been isolated along with the non-immunologic mechanisms, to suggest that the IRS activation by dietary components is not an etiologic mechanism of the proven loss of oral tolerance, rather it is somethng I have personally cooked up and deluded myself and others into beleiving (along with thousands of patients who have benefittted from this misbelief), well, said kindly this is simply an obsolete theory as it has been disproved. Get over it.When the scientists findings who have done this most recent work is added to the mix sometime in the coming year, along with a new medical text on Food Allergy and Intolerance written by experts in that field of medicine is published this year, these errors hopefully can be overcome and another step at integrating all the knowledge can be accomplished.Ohh yeah...I referenced the 1970's as a time of evolving understanding of proinflammatory mediators role in gut motility...a couple oldies from that time which illustrates what I mean by early steps towards understanding: ____________________"Lancet 1978 Apr 29;1(8070):906-8Prostaglandin-synthesis inhibitors in prophylaxis of food intolerance. Buisseret PD, Youlten LF, Heinzelmann DI, Lessof MH Prophylactic doses of aspirin, indomethacin, or ibuprofen prevented symptoms of food intolerance in five out of six patients who on several occasions had had acute gastrointestinal symptoms after the ingestion of specific foodstuffs. Blood and stool prostaglandin E2 and F2alpha concentrations during unprotected challenge were consistent with the idea that these symptoms were mediated through prostaglandin release. Prostaglandin-synthetase inhibitors may benefit some patients with specific food intolerance who are unable or unwilling to avoid the offending food. ___________________________: World J Surg 1979 Sep 20;3(5):565-78Prostaglandins and serotonin: nonpeptide diarrheogenic hormones.Jaffe BM.Prostaglandins and serotonin are vasoactive compounds with profound effects on the gastrointestinal tract. Both cause inhibition of gastric acid secretion (although serotonin stimulates gastric pepsin secretion), stimulation of intestinal motility, and conversion of small intestinal mucosa from absorption to secretion of water and electrolytes. Their effects on pancreatic and biliary function are still not clear. Although prostaglandins appear to elicit their effects primarily by a paracrine mode of action, and serotonin is primarily a neurotransmitter (neurocrine), it is clear that even under normal conditions both can function as humoral agents. For example, we have shown that serotonin plays a physiologic role as a humoral inhibitor of gastric acid secretion. However, the effects of these agents become more pronounced in patients with humorally mediated diarrheogenic syndromes. Serotonin (and related indoles, particularly 5-hydroxytryptophan) has been firmly implicated as a cause of diarrhea in patients with carcinoid syndrome; our recent studies suggest that the diagnosis can be more effectively made by measuring circulating immunoreactive serotonin concentrations than urinary excretion of 5-HIAA; that some circulating serotonin escapes hepatic inactivation and, thus, large intestinal tumors can cause carcinoid syndrome in the absence of hepatic metastases; and that large amounts of serotonin are produced by some noncarcinoid diarrheogenic tumors, including medullary carcinomas of the thyroid and tumors associated with the WDHA syndrome. A large number of tumors of probable neural crest origin, including medullary thyroid carcinoma, carcinoids, and tumors associated with the WDHA syndrome, secrete large amounts of prostaglandins, particularly PGE2. The clinical response of at least some of the patients harboring these tumors to inhibitors of prostaglandin synthesis (particularly indomethacin) suggests that prostaglandins play a role in the etiology of these diarrheogenic syndromes.Publication Types: � Review _______________________________________Adv Prostaglandin Thromboxane Res 1980;8:1627-31 An approach to evaluation of local intestinal PG production and clinical assessment of its inhibition by indomethacin in chronic diarrhea. Bukhave K, Rask-Madsen J No abstract ON LINE..Summary of Findings:The connection between gut motility and prostaglandin release was studied. PGE2 levels in the jejunal secretions IBS patients were elevated in 10 of 17 (59%) with cyclic IBS (D & C) and in "gluten enteropathy". Six IBS patients treated with indomethacin (INDOCIN: non-steroidal analgesic anti-inflammatory which works by inhibiting prostaglandins, which are inflammatory and pain mediators of various types) had a 50% reduction in stool volume and frequency. And withdrawal of the indocin caused the symptoms to return.Due to the absence of indicators of Type I inflammatory-allergic response, the authors state the findings suggested localized or gut-wall reactions . ___________________________Later they went on to study cromolyn sodium instead as an imunomdulator and got results in up to 95% of the subjects stduied depending upon dose and selection criterion.Anyway, just a couple of early examples of specific mediator assay and relationships in non-alergenic gut reactivity and symptom provocation. there's about 100 pages more abstracts on the subject since.The gut does not have a temperemental "nature" in IBS. The upregulation of the local and central structures, muscular and neurologic, along the "brain-gut axis" have biochemical basis, the total of which is yet to be fully elucidated, but it can be seen thus far that, like many other syndromes, it is not going to turn out to be some idiopathic mystery as was once believed not so long ago.Eat well. Think well. Be well.MNL
 

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Comment: _____________________________________"I believe that Mike believes that food plays a major role in inciting the gut's immune system and the immune system magnifies this by responding inappropriately to food." _____________________________________On the contrary I merely have studied the findings of real scientists, of which I am not one, which confirm the validity of the integrative model of the roles of the CNS, ENS and IRS in IBS.Belief denotes an act of faith. There is no faith involved in the extensive work along these lines. there is ample hard evidence, clinically an investigatory, that not only can the IRS be activated in ISb by the CNS and ENS but immunologically and non-immunologically as well independent of CNS and ENS factors...the IRS can and does serve in IBS patientrs as the origin of the upregulation of the CNS and ENS.The question remains as to how to isolate whether there are specific subpopulations which are characterized by one system being primary, or does the primary mechanism vary within each patient from time to time depending upon the provoking stimulus.At least science is far enough along now to know that all (3) are ionvolved!! This is a big step.There is a diagram, Figure 1, in the following article which anyone can "click on" then print out and look at. It illustrates the interrdependency of these systems in the process of elicitng IBS symptoms. http://www.blackwell-synergy.com/servlet/u...36.2001.00951.x The part that is missing is the activation of the IRS circulating cells (lymphocytes, granulocyte classes, macrophages and platelets) in IBS which has been confirmed by "real scientists" who isolate and challenge the small bowel with various dietary componenets then assess inflammatory response, and those who study circulating immunocyte response in vitro...absent input from the CNS and ENS. By capturing IRS activators which function independent of the input of the CNS and ENS, one shows that the "third leg of the stool" is active and this of course explains why the response of the non-mast cell immunocytes can be duplicated in vitro.If you take the diagram and draw a line between the 2 boxes that connect the NON IgE mechanisms in the way the author separated them (IgG[x] subclasses vs OTHER Non IgE mechanisms) and then extaned that line down to the MEDIATOR RELEASE box, the picture is then complete for the sum total of what is known so far about the interraction between the IRS ENS and CNS in IBS.If one chooses to ignore part of the information and only look at that which suits that person then of course they will only see and acknowledge part of the integrated dynamics.Thankfully the investigation into the key role of proinflammtory activation in IBS is not being conducted solely by one group and from one perspective. Since some European scientists have been wise enough to study the small bowel immune response diretly, they have been able to confirm what has already been known since 1979: that certain dietary components, which vary from patient to patient, will provoke a proinflammtory reaction within the sructures of the small bowel IN THE ABSENCE of specific circulating antibodies to that food, and thus precipitate the symptoms of diarrheaic type and cyclic type symptom sets of so-called IBS.The mechanisms are well documented in numeraous places, and if one makes a serious study of the literature on the subject absent selective thinking then one would be aware of these mechanisms. No one in that portion of the scientific community which works with non-allergenic food intolerances is so uneducated and naive and simple-minded as to base their conclusions on mere cause-effect observations. If the literature were actually studied such a silly statement would not have been made.To not do so by a non-healthcare provider is a matter of personal choice which bears no ill consequence to anybody accept those who may attribute some credibility to that prsons' denouncements, and then manage their treatment program accordingly. In a healthcare providers case, to ignore and not intergate that understanding into the recommended care and clinical management of patients would be to fall short of a professional obligation to excellence and ethics.Some folks read the published material, books, studies and tutorials provided by doctors and scientists who have both studied this area and cared for patients in this manner successfully. Some do not. So posts like this thread contains reflects the opinion of those who chose not to, or are unable to. The rendering of that opinion does not render the information false. True and false ar characteristics of speech not of tangible things. In this case we are talking about tangible phsyiologic events, therefore no true or false can exist, only the fact that they do occur regardless of opinion or assertion to the contrary by the ill-informed.When one constructs a patient care program accordingly for patients wherein the reactions do occur, the program is successful as measured by outcomes proportionate to the degree of patient compliance. ________________________________"I do not see the point of these public disagreements elsewhere on this board as it serves no purpose in helping anyone." ________________________________I respect your view, yet disagree. On the contrary if there is information pertinent to the welfare of the sick, and the information is not shared, then it is to the detriment of the sick. Based upon what the sick ofetn experience by way of available education as to the causal basis to their condition this may be the only venue by which they can see certain expanded, integrative and contrary views and understandings expressed.In the process of discovery in advancements in medicine, since this process involves humans, it also involves human nature and all that this entails. Therefore here and elsewhere (right up to the entertaining shouting matches and denouncements in Q&A sessions at medical conferences which become "lively") this is bound to occur as part of the process of moving from the ill-defined "syndrome" phase or "idiopathic" phase of some condition into the eventual place where the "disease" and "cause" become fully understood.Since that process always occurs, here or elsewhere, in an environment where any other persons involvement is voluntary, if the discussion displeases you "change the channel", in this case exit the discussion, and don't read it.Everyone does that every day, as there are some things which interest some and some things which do not. Sometimes a sense of fascination sets in...like at a car wreck. On the one hand it offends a persons psyche yet they feel compelled to observe and observe and observe. So it must perform some function and hold some form of interest for the person whose attention lingers over the incident, no?
________________________________ "At the end of the day we should all be united in helping each other as much as we can with good factual advice or just listening to others and offering support whoever we are and wherever we come from." _________________________________We are, regardless of the fact that the practitioners some of us work with posess differign views and follow differnt treatment methods. Each person acts in what he or she belives (I hope) is in the best interests of the patients here.This is all part of that process, yet still we may not all agree as to what parts of the process we each think are useful and which are not. That is because we all value different things. Use that which you value and discard that you do not. A natural reaction. Conversely one persons poison may be anothers' revelation of understanding. __________________________________"Please keep this stuff to yourselves guys if you don't mind me saying and have a private argument." ___________________________________One persons argument is anothers tutorial. If you do not like it do not read it and you won't then be bothered. Sometimes we all look at things and say "See? At least I don't do that!!". So whose voice is that self-talking when we think that and then express it... _________________________________"I offer this in peace and hope that neither of you are not offended, that is not my intention. " ___________________________________
I know.
I am not.
____________________________________"The other reason is probably because for the most part there is nothing to discover. That is, it may be for a very few people diagnosed with IBS there is something involved with food but for the vast majority it is not the case (as Mike wants us to believe)." _____________________________________Mike does not suggest "beleif" as this is an act of faith. there is no faith-based component to whatI have learned from the doctors and dieticians I work with.The majority of patients who suffer d-predominanat and cyclic symptoms sets can and do suffer provocation of onset of symptosm by dietary compnenets. Done properly this can be duplicated in vivo and in vitro and their dieta djusted accordinlgy to reduce or eliminate sympotms. There are at least (8) known immunologic and non-immunologic mechanisms, which are also non-ENS and CNS mechanisms, by which this can occur. The markers of many have been recovered directly from the GI tract.Irrespective of which of the Immunologic, Non Immunologic, CNS or ENS mechanisms which can and do influence the activation of the IRS; regardless of which can be isolated as a primary "arming mechanism" in a given subject (rendering the other mechanisms secondary or amplificatory), it has been shown over and over again since at least 1955 (with the best work beginning in 1979 or so) that in AT LEAST the 2/3 of IBS patients a partial, dose-dependent loss of oral tolerance to harmless food components and/or chemical additives occurs as compared to asymptomatic people. Thus the introduction of certain provoking foods, beyond those which cause pseudoallegry or direct chemotoxicity, provokes symptoms reliably. This is absent any comorbid food allergy. It is a fact that the identification and removal of thise specific substsnces from the diet reduces or eliminates the patients symptoms. Fact.In spite of the fact that scientists have not only been isolating the markers of neurologic activity in IBS but the markers of immunologic and alternative-pathway IRS activation in the small bowel of IBS victims the most recent 25 years or so, right up to recovering proof of, for example, specific lymphocytic activation in response to dietary components as well as local IgE in the small bowel specific to the dietary components that provoke the symptoms, lay people and practitioners alike continue to perpetuate the myth that this is illusory. Its kind of funny since the very chemicals which upregulate the ENS and CNS are released into the gut parenchyma and systemic circulatiion in these reactions...yet when they are isolated they are simply ignored as they do not fit "the model" perhaps someone invented elsewhere.Not an unusual practice when syndromes are studied from differeing perspectives that the owner of the one perspective should not acknowledge the validity of those whose work comes from an alternative perspective. Eventually the collective medical community gets past it and integrates all the knowledge. It is not there yet and that is reflected in what trickles down to and through non-healthcare professionals. ___________________________________"The gut normally has responses to what is put in it. In IBS, these responses appear to be abnormally exaggerated, leaving one to believe incorrectly that what is put in is the culprit rather its simply being the temperamental nature of the "IBS gut". " ____________________________________Sadly for the reader of this disinformation, the first statement is of course correct as it is the grosseest possible generality. The books I recommend would elucidate this process in detail.The second "action-response-conclusion" thinking indeed could be said of both investigatory ad diagnostic approaches....symptom based and causal alike. One observes a specific neurologic "event" and, not having quantified whether there is the prior presence of some chemical mediator (endogenous or exogenous) which would account for the neuolgic event, presumes and postulates the mechanism at work. Someone reads the posulate and infers fact. The inferred fact is implicated in reptition and thus becomes fact by acclimation. I see that in the IBS "research" done by many in the United States all the time, and then how it is explained here in foruims like this to patients hungry for information.In the case of food elements provoking the local inflammatory response in the small bowel at least the first step is accomplished that the scientists studying the allergologic and immunologic aspects of the syndrome have been espousing since it was first documented lo these many years. That is at least finally everyone acknowledges that (at keast in these 2 populations) some weird inflammatory reaction (which is not a measurable food "allergy" reaction by conventional means) does occur, and an array of inflammtory mediators are released in the small bowel which can upregualte sensory and motor function.Just 18 months ago most the majority of "IBS investigators" and GI docs in the USA were denouncing such mechanisms as non existent ("there is NO inflammtory response involved in IBS" was the dogma). That claim was posted loudly and often in IBS self help communities as well, including here, as recemtly as 6 months ago in spite of the fact it has been known to be incorrect for 20 years.Now, since it has also been well known physiologically since, say, 1979, that prostaglandins produced in proinflammatory reations in the gut and other forms of tissue and serotonin released in the same fashion upregulate bowel functiona and cause diarrhea....all of a sudden the persons who made these proclamation of folly have begun debating "ownership" of this weird IRS activation...CNS/Stress...ENS/Stress....Immunologic mechanisms. what an incredible laugh, and so typical of what I have had the dubious privilege of watching time and time again over the last 30 years.
To cut to the chase, It is just a stupid argument since it is self evident from an integrative view that the systems are fully interractive, codependent, and can be armed by specific mechanisms which can be sourced to each of the systems in question depending upon the patient and circumstance. AND it is obvious that there are subpopulatons where each is going to be found to be true vis a vis what is the primary arming mechanism after which the IRS can be provoked.Since, however, so far at LEAST IgE (mast cells, basophils) and T-lymphocyte arming mechanisms which are "immunologic" (and the circulating immuncoytes themselves ecrutied to the lamina propria) have been isolated along with the non-immunologic mechanisms, to suggest that the IRS activation by dietary components is not an etiologic mechanism of the proven loss of oral tolerance, rather it is somethng I have personally cooked up and deluded myself and others into beleiving (along with thousands of patients who have benefittted from this misbelief), well, said kindly this is simply an obsolete theory as it has been disproved. Get over it.When the scientists findings who have done this most recent work is added to the mix sometime in the coming year, along with a new medical text on Food Allergy and Intolerance written by experts in that field of medicine is published this year, these errors hopefully can be overcome and another step at integrating all the knowledge can be accomplished.Ohh yeah...I referenced the 1970's as a time of evolving understanding of proinflammatory mediators role in gut motility...a couple oldies from that time which illustrates what I mean by early steps towards understanding: ____________________"Lancet 1978 Apr 29;1(8070):906-8Prostaglandin-synthesis inhibitors in prophylaxis of food intolerance. Buisseret PD, Youlten LF, Heinzelmann DI, Lessof MH Prophylactic doses of aspirin, indomethacin, or ibuprofen prevented symptoms of food intolerance in five out of six patients who on several occasions had had acute gastrointestinal symptoms after the ingestion of specific foodstuffs. Blood and stool prostaglandin E2 and F2alpha concentrations during unprotected challenge were consistent with the idea that these symptoms were mediated through prostaglandin release. Prostaglandin-synthetase inhibitors may benefit some patients with specific food intolerance who are unable or unwilling to avoid the offending food. ___________________________: World J Surg 1979 Sep 20;3(5):565-78Prostaglandins and serotonin: nonpeptide diarrheogenic hormones.Jaffe BM.Prostaglandins and serotonin are vasoactive compounds with profound effects on the gastrointestinal tract. Both cause inhibition of gastric acid secretion (although serotonin stimulates gastric pepsin secretion), stimulation of intestinal motility, and conversion of small intestinal mucosa from absorption to secretion of water and electrolytes. Their effects on pancreatic and biliary function are still not clear. Although prostaglandins appear to elicit their effects primarily by a paracrine mode of action, and serotonin is primarily a neurotransmitter (neurocrine), it is clear that even under normal conditions both can function as humoral agents. For example, we have shown that serotonin plays a physiologic role as a humoral inhibitor of gastric acid secretion. However, the effects of these agents become more pronounced in patients with humorally mediated diarrheogenic syndromes. Serotonin (and related indoles, particularly 5-hydroxytryptophan) has been firmly implicated as a cause of diarrhea in patients with carcinoid syndrome; our recent studies suggest that the diagnosis can be more effectively made by measuring circulating immunoreactive serotonin concentrations than urinary excretion of 5-HIAA; that some circulating serotonin escapes hepatic inactivation and, thus, large intestinal tumors can cause carcinoid syndrome in the absence of hepatic metastases; and that large amounts of serotonin are produced by some noncarcinoid diarrheogenic tumors, including medullary carcinomas of the thyroid and tumors associated with the WDHA syndrome. A large number of tumors of probable neural crest origin, including medullary thyroid carcinoma, carcinoids, and tumors associated with the WDHA syndrome, secrete large amounts of prostaglandins, particularly PGE2. The clinical response of at least some of the patients harboring these tumors to inhibitors of prostaglandin synthesis (particularly indomethacin) suggests that prostaglandins play a role in the etiology of these diarrheogenic syndromes.Publication Types: � Review _______________________________________Adv Prostaglandin Thromboxane Res 1980;8:1627-31 An approach to evaluation of local intestinal PG production and clinical assessment of its inhibition by indomethacin in chronic diarrhea. Bukhave K, Rask-Madsen J No abstract ON LINE..Summary of Findings:The connection between gut motility and prostaglandin release was studied. PGE2 levels in the jejunal secretions IBS patients were elevated in 10 of 17 (59%) with cyclic IBS (D & C) and in "gluten enteropathy". Six IBS patients treated with indomethacin (INDOCIN: non-steroidal analgesic anti-inflammatory which works by inhibiting prostaglandins, which are inflammatory and pain mediators of various types) had a 50% reduction in stool volume and frequency. And withdrawal of the indocin caused the symptoms to return.Due to the absence of indicators of Type I inflammatory-allergic response, the authors state the findings suggested localized or gut-wall reactions . ___________________________Later they went on to study cromolyn sodium instead as an imunomdulator and got results in up to 95% of the subjects stduied depending upon dose and selection criterion.Anyway, just a couple of early examples of specific mediator assay and relationships in non-alergenic gut reactivity and symptom provocation. there's about 100 pages more abstracts on the subject since.The gut does not have a temperemental "nature" in IBS. The upregulation of the local and central structures, muscular and neurologic, along the "brain-gut axis" have biochemical basis, the total of which is yet to be fully elucidated, but it can be seen thus far that, like many other syndromes, it is not going to turn out to be some idiopathic mystery as was once believed not so long ago.Eat well. Think well. Be well.MNL
 

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Tom, Thanks for asking the question.
BQ
 

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Tom, Thanks for asking the question.
BQ
 

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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. Also on any food studies I would like to see a follow up after a couple years. That would be interesting to me.Also the active top IBS investigators aren't real scientists, last time I check there were three top immunology scientists studying the exact mechanisms were talking about. Not to mention the top scientist on the ENS or gut brain and others in all fields."At least science is far enough along now to know that all (3) are ionvolved!! This is a big step." Your right about this, but it is believed from the most cuurent research from top IBS researchers that the Brain-Immune reaction is one of the most important players in D symptoms via this reaction.As Flux said perhaps for a very few food maybe in part the culprit for this."Thankfully the investigation into the key role of proinflammtory activation in IBS is not being conducted solely by one group and from one perspective." This has never been the case. Studying IBD, IBS and other conditions gives input into the real science behind these conditions and there are many active IBS researchers from all fields and in different parts of the world, working in conjunction on the problem and there is a internationally known and respected immunologist working on IBS among others.We post this and Mike just seems to ignore it. I think in part because it does not help the focus on food but many other mechanisms in immunology and IBS.The scientist also know there is a really high percentage of food phobia in IBS. I don't think I have ever heard Mike say that? Or that IBS is cyclic and can disappear for years and come back regardless of a persons change in diet. Or that there is a very high placebo rate in IBS which also plays into some of this.If in part all this was the case when you isolated and removed the foods, should the person not be "cured". Or is there more to IBS? They can give Rats a kind of IBS and about 30 percent of IBSers have IBS from gastroenterists or some other shock to the digestive system. If you don't eat an offending food at all and were to inflate a ballon rectally and inflate it you would have pain from a different mechanism and certain parts of your brain lite up.You have to read the science abstracts very carefully for wording as well, such as the ones above. they are very careful what they say most times."Later they went on to study cromolyn sodium instead as an imunomdulator and got results in up to 95% of the subjects stduied depending upon dose and selection criterion." This study had flaws in it.You would think these studies presented here would be interrgrated it into the current IBS research and information since there from the 70 and 80's, and I am sure they are in some ways. They also understand way more now about serotonin and its crucial role in IBS and that its being dysregulated. Perhaps one of the most important chemicals in IBS, athough there are other players, serotonin is responcible for Peristaltic Reflex and others mechanisms and symptoms. You don't here him talk about this much if at all and all of this is connected to IBS and the importantance of other cells like the enterochromaffin cells, are crucial in symptoms. Soon as the bowel expands before food hits the gut serotonin is being released dysregulated and causing symptoms.As for the immunology aspect. If you are stressed or have an attack, caused by anything, hot weather, a food, stress etc.. And you have d, the sensations of having to go, are registered and processed in the brain and this starts an alter immunological responce via the brain which releases a chemical that trips the whole HPA access and releases histamine that gives you d.What I am posting here is a couple years old and they have studied this in much more depth now and have a much better understanding of its is a major player in IBS.IBS is a prolonged stressor. http://www.med.ucla.edu/ndp/Newsletters/Wi...teredStress.htm Food is a trigger and we all now that. I personally have nothing against Mike or leap,maybe some of the information he posts sometimes, but if people want to try that route, so be it and hopefully they feel better.
 

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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. Also on any food studies I would like to see a follow up after a couple years. That would be interesting to me.Also the active top IBS investigators aren't real scientists, last time I check there were three top immunology scientists studying the exact mechanisms were talking about. Not to mention the top scientist on the ENS or gut brain and others in all fields."At least science is far enough along now to know that all (3) are ionvolved!! This is a big step." Your right about this, but it is believed from the most cuurent research from top IBS researchers that the Brain-Immune reaction is one of the most important players in D symptoms via this reaction.As Flux said perhaps for a very few food maybe in part the culprit for this."Thankfully the investigation into the key role of proinflammtory activation in IBS is not being conducted solely by one group and from one perspective." This has never been the case. Studying IBD, IBS and other conditions gives input into the real science behind these conditions and there are many active IBS researchers from all fields and in different parts of the world, working in conjunction on the problem and there is a internationally known and respected immunologist working on IBS among others.We post this and Mike just seems to ignore it. I think in part because it does not help the focus on food but many other mechanisms in immunology and IBS.The scientist also know there is a really high percentage of food phobia in IBS. I don't think I have ever heard Mike say that? Or that IBS is cyclic and can disappear for years and come back regardless of a persons change in diet. Or that there is a very high placebo rate in IBS which also plays into some of this.If in part all this was the case when you isolated and removed the foods, should the person not be "cured". Or is there more to IBS? They can give Rats a kind of IBS and about 30 percent of IBSers have IBS from gastroenterists or some other shock to the digestive system. If you don't eat an offending food at all and were to inflate a ballon rectally and inflate it you would have pain from a different mechanism and certain parts of your brain lite up.You have to read the science abstracts very carefully for wording as well, such as the ones above. they are very careful what they say most times."Later they went on to study cromolyn sodium instead as an imunomdulator and got results in up to 95% of the subjects stduied depending upon dose and selection criterion." This study had flaws in it.You would think these studies presented here would be interrgrated it into the current IBS research and information since there from the 70 and 80's, and I am sure they are in some ways. They also understand way more now about serotonin and its crucial role in IBS and that its being dysregulated. Perhaps one of the most important chemicals in IBS, athough there are other players, serotonin is responcible for Peristaltic Reflex and others mechanisms and symptoms. You don't here him talk about this much if at all and all of this is connected to IBS and the importantance of other cells like the enterochromaffin cells, are crucial in symptoms. Soon as the bowel expands before food hits the gut serotonin is being released dysregulated and causing symptoms.As for the immunology aspect. If you are stressed or have an attack, caused by anything, hot weather, a food, stress etc.. And you have d, the sensations of having to go, are registered and processed in the brain and this starts an alter immunological responce via the brain which releases a chemical that trips the whole HPA access and releases histamine that gives you d.What I am posting here is a couple years old and they have studied this in much more depth now and have a much better understanding of its is a major player in IBS.IBS is a prolonged stressor. http://www.med.ucla.edu/ndp/Newsletters/Wi...teredStress.htm Food is a trigger and we all now that. I personally have nothing against Mike or leap,maybe some of the information he posts sometimes, but if people want to try that route, so be it and hopefully they feel better.
 

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I want to add something and that is some people really have food allergies and intolerences. Also some studies are still being looked at in regards to food senstitivitiesHere are somethings newer then what Mike has posted. Am J Gastroenterol 1998 Nov;93(11):2184-90 Related Articles, Books, LinkOut Are adverse food reactions linked to irritable bowel syndrome? Niec AM, Frankum B, Talley NJ. Department of Medicine, University of Sydney, Nepean Hospital, Penrith, NSW, Australia. OBJECTIVE: We undertook to determine whether adverse food reactions play a role in irritable bowel syndrome (IBS). METHODS: A systematic review of the literature using Medline (1980-1996), targeting IBS and adverse food reactions, was performed. All clinical trials whereby dietary exclusion was followed by food challenge were selected. Each study was reviewed using a structured format to examine methodological issues and study outcomes. RESULTS: Of the seven studies included, the positive response to an elimination diet ranged from 15% to 71%; double-blind placebo-controlled challenges identified problem foods in 6% to 58% of cases. Milk, wheat, and eggs were most frequently identified to cause symptom exacerbation; of the foods identified the most common trait was a high salicylate content. Foods high in amines were also identified. Studies of diarrhea-predominant IBS identified a higher percentage of adverse food reactions. However, all studies had major limitations in their trial designs, including inadequate patient selection, appropriateness of--and duration of--exclusion diets, and methods of food challenge. CONCLUSION: Whether adverse reactions to foods are a key factor in exacerbating IBS symptoms or whether dietary manipulation is a valid treatment option is unclear. Carefully designed controlled clinical trials are now needed to specifically test the potential role of adverse food reactions in diarrhea-predominant IBS. Publication Types: Meta-Analysis PMID: 9820394 [PubMed - indexed for MEDLINE] Notice they say exassberation of symptoms.
 

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I want to add something and that is some people really have food allergies and intolerences. Also some studies are still being looked at in regards to food senstitivitiesHere are somethings newer then what Mike has posted. Am J Gastroenterol 1998 Nov;93(11):2184-90 Related Articles, Books, LinkOut Are adverse food reactions linked to irritable bowel syndrome? Niec AM, Frankum B, Talley NJ. Department of Medicine, University of Sydney, Nepean Hospital, Penrith, NSW, Australia. OBJECTIVE: We undertook to determine whether adverse food reactions play a role in irritable bowel syndrome (IBS). METHODS: A systematic review of the literature using Medline (1980-1996), targeting IBS and adverse food reactions, was performed. All clinical trials whereby dietary exclusion was followed by food challenge were selected. Each study was reviewed using a structured format to examine methodological issues and study outcomes. RESULTS: Of the seven studies included, the positive response to an elimination diet ranged from 15% to 71%; double-blind placebo-controlled challenges identified problem foods in 6% to 58% of cases. Milk, wheat, and eggs were most frequently identified to cause symptom exacerbation; of the foods identified the most common trait was a high salicylate content. Foods high in amines were also identified. Studies of diarrhea-predominant IBS identified a higher percentage of adverse food reactions. However, all studies had major limitations in their trial designs, including inadequate patient selection, appropriateness of--and duration of--exclusion diets, and methods of food challenge. CONCLUSION: Whether adverse reactions to foods are a key factor in exacerbating IBS symptoms or whether dietary manipulation is a valid treatment option is unclear. Carefully designed controlled clinical trials are now needed to specifically test the potential role of adverse food reactions in diarrhea-predominant IBS. Publication Types: Meta-Analysis PMID: 9820394 [PubMed - indexed for MEDLINE] Notice they say exassberation of symptoms.
 

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I'm tryin boys, I really am; LOL. I'll have to read it all again... LOL I still don't get it.. LOLBQ
 

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I'm tryin boys, I really am; LOL. I'll have to read it all again... LOL I still don't get it.. LOLBQ
 
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