"From the presentations" at this conference one can conclude that an entire body of evidence spanning 25-30 years be immediately disregarded?You do raise interesting questions, but if one is to disregard prior evidence and clinical outcomes one must be experincing a revolution in the disgnostics of "IBS".To state flatly that this phenomenon has nothing to do with IBS, means that one must ignore a lot of information which is plain to the naked eye. For example, that when d-type IBS patients are placed on an elimination diet and achieve symptom remission rates of 60%-90%, one must now state that this is an “artifcat”? Or one must consider it artifact when the same patients are returned to their prior diet the symptoms of IBS reappear, but are then suppressed in from 60% to 97% by the use of immunomodulation such as sodium chromoglycate, (response depending upon dose administered)? What is this then to be indicative of ? No immunocyte provocation by specific dietary components? The evidence even sufficient to compel the Merck Manual of diagnosis to suggest that there is a population of IBS patients whose symptoms are provoked by food intolerance is a misinterpretation of data? Puzzling.We had better not only "distance" any Disease Management Programs which incoroprate treatment of food sensitivity, but all them IBS diet books and protocols, and immunomodulating substances which block food provoked immunocyte reactions along with stress provoked reactions, and articles and instructions vis a vis dietary symptom provocation as well, since it must ALL be unrelated to the population of IBS sufferers. At this years DDW conference, as in all prior conferences, while all the abstracts are not released yet but the topics are, it is my impression so far that as of yet NO one has integrated the investigative assessments of ENS and CNS activity quantification with the in vivo investigation of endogenous mediators which can be and are provoked to release via dietary provocation to the proximal small bowel, and their role in upregulation of the ENS and CNS in the same patients at the same time selected by the same criteria…nor assessed the plasma or cerebrospinal fluid for proinflammtory mediators whciah are recovered from the small bowel during jejunal isolation in patients with IBS symptoms provoked by direct blind challnge to the isolated jejunum.Until that is done, no one cannot quantify whether the upregulation observable of the brain-gut axis, endocrine function, and immunologic function, is provoked consistently by the same mechanisms, or which precipitating event results in which aberrant observed function in each of the subsystems. It is not possible to form a conclusion, only a postulate since the patient groups studied are separate and the multiple symptom generating mechanisms are not studied at the same time in the same people using all the parameters that can be assessed.Now, what I must assume here is that either an entire body of evidence that IBS symptoms can be and are provoked by specific dietary components in a population of IBS patients best defined as diarrheic predominant is now to be dismissed as irrelevant, or mass-artifact, as well as the clinical outcomes of patients who achieve remission by dietary therapy, OR there must be a change in what IBS is defined as. It must be one or the other.In the first case, since Rome II Criteria IBS patients can be shown to suffer food or chemical induced immunocyte activation in the small bowel by direct jejunal isolation and provocation, and the specific mediators which would then upregulate the local ENSW and smooth muscle as well as the CNS when released systemically can be recovered following provocation by either jejunal washing or biopsy, and said reactivity can also be demonstrated in vitro, AND if food sensitivity then has nothing to do with IBS, the then ROME Symptom based Diagnostic criteria are unable to differentiate whatever one now wishes to define as IBS from what one wished to define as "food sensitivity". Therefore they must be changing the diagnostic criterion and I did not see the related abstracts yet, or even the topics. I will be sure to get the CD ROM and study it carefully and consider whatever was presented, which is sufficient to erase an entire body of evidence.Now, if the Rome criteria are unable to discriminate IBS from food sensitivity induced symptoms, since food sensitivity can be proved and used therapeutically in d-predominant subpopulations, it has limited value as a diagnostic tool if any.Perhaps, as at recent AAAAOA conference, there has been a shift away from symptom based diagnosis and a recognition of the fact that not only mast cell activation by dietary provocation in the gut absent circulating antibodies but T Cell activation and other cell mediated reactions to dietary components produce symptoms that are clinically identified or associated with so called IBS and the phenomenon not only should be acknowledged but addressed therepeutically.It is interesting, the juxtaposition, that at a conference where the focus is from the allergo-immunologic perspective people return with a sudden interest in non IgE mediated food sensitivity and its role in symptom generation, but someone returning from the DDW meeting would express the exact opposite view...attendees at one conference react as if the light bulb blinks on, and after another conference someone says, blinks the light blinks off. Illustrative of the sheer confusion over what is so called IBS and what is it not.Yet there we are...with years of patients diagnosed with IBS (presenting with IBS symptoms and no signs of organic disease) responding to dietary therapy and immunomodulaton with symptomologic relief. One is left to wonder how many people have to sail off into the east then return from the west before everyone recognizes that perhaps the earth is not flat....and as a result that there are multiple ways to get to a given destination...as in 'IBS" there are multiple mechanisms of symptom generation which can and do originate in multiple systems.Conversely, one may wish to even suggest that the food sensitivity observed in IBS is a secondary consequence of an endogenous event in the CNS...in which case it does not mean it does not exist it means that a certain mechanism, non IgE mediated, is primary.But to flatly state that food sensitivity has nothing to do with IBS based upon the evidence and based upon how IBS is currently defined is at best a puzzling view....If that be the case, then, there are HUGE NUMBERS of people not only in the population at large but who are members of this community and others who are NOT IBS sufferers...rather they suffer from lost oral tolerance, food sensitivity or whatever one wished to call it.In either case, the semantics are less important than the selection and then the therapeutic outcomes.Everyone, physicians, dieticians, investigators, moderators ad infinitum is absolutely entitled to belief and to pick and choose that evidenciary material which supports their personal beleiefs.. But objectivity dictates that belief and fact are often 2 different things....or perhaps it is an issue of semantics…one cannot tell.In any case the question is moot since a large population of patients who have been told they have IBS can be shown to suffer from various forms of symptom-provoking reactions (immunologic and non immunologic) to foods and additives which would normally be benign. And that population, properly treated with dietary manipulation, can achieve high rates of symptomatic relief without the need for ongoing pharmacotherapy, or with significant reduction in their dependence on pharmacotherapy. A Disease Management Program (LEAP) which clearly is effective for those patients exists, whether one finds it here or not, or at their doctors office or not yet. As long as patients continue to achieve high rates of positive outcomes I doubt that it will go away regardless of whether those who do not follow it believe or do not believe that the people for whom it works have IBS or not. Whether or not they belong within the so called "IBS" population is moot if they have IBS symptoms, have been told they have IBS, follow the protocol, and get relief. There is nothing within that to debate…especially when the effects persist for months and years.Some things are better left to speak for themselves after a point.Eat well. Think Well. Be well.MNL
