The rub in such questions always comes back to "what is IBS" since it is a syndrome not a casual diagnosis.If, for example, you have patients with chronic or cyclic "d" whose symptoms can be provoked by particluar foods by double blind placebo controlled oral challenge, or the truest blind oral challenge of direct instillation into the small bowel, and who are negative for all normal food allergy markers by RAST and even SPT, the King Of False Positives, and then you are able to quantify both mast cell response in the small bowel and cellular immune response by captuing physically the inflammatory mediators that have been released as the result of an immunologic response to the provoking foods, AND the symptoms disappear when the foods are removed becasue the reactions no longer take place and/or they can be reversed with known chemical immunomodulators which stabilize mast cells, lymphocytes and granulocytes...should all these patients be diagnosed as having so-called "IBS" or should a name be assigned to the physiologic condition they are suffering which defines it separately from those, say, who have chronic constipation? Especially since the endocrine hormone profiles between the two seem to also be different as a consequence?Right now there are proponents of both schools of thought: one says all three subpopulations should just be lumped together under the umbrella diagnosis of IBS empirically, and another schoool of thought is that when a physiologic mechanism which accounts for the symptom set can be isolated that the population which is subject to that mechanism be identified uniquely as the clear markers of a causal basis have been isolated.LIKE COPD is now known to be, in simple terms, various degrees of comorbidity of asthma, chronic bronchitis, and emphysema. So a patient with with chronic bronchitis ha chronic bronchitis, one of the comorbid diseases of COPD. This seems supremely logical.So from that point of view the questions of "is this IBS or is it something else" is by nature rhetorical and unanswerable since it hase to answered framed to point of reference of which practitoner you are asking the question to.Eat well. Think well. Be well.MNL__________________wwwleapallergy.comPSThat is not a hypothetical mechanism described, it has been isolated, demonstrated, and repeated any number of times over the years. It is only recently that (primarily) Swedish investigators have actually begun going right into the small bowel of pts. who would be identified as "IBS" and capturing the actual proinflammatory neuralactivating immunomediators being released upon food provocation. It is easier (less potentially traumatic) to isolate the colon for direct examination than it is the duodenum or jejunum but it can be and is now done.[This message has been edited by Mike NoLomotil (edited 09-25-2001).]