LML: ___________________________________"Mike ... since I'm not in the 70% D category, andI can eat most anything if I keep the amounts small, much of your information doesn't seem to apply to me specifically. And since IBS is a "syndrome" rather than a disease, I wouldn't expect all of anyone's ideas to apply to all sufferers. " ____________________________________Oh yeah you be so 100% right. This is why I qualify carefully the subjects addressed and the different symptom sets and subpopulations that presently are all lumped-together under the Syndrome Sign of "IBS". There are, it is becoming more obvious all the time, some isolatable etiologies for specific symptoms and sets of symptoms that, when finally fully understood, are going to reveal "disease". From that point forward those people will then be called (Disease or Etiology A), and the total populaton counted as inscrutable-etiology, thus "IBS", will be reduced. Not everyone on all sides agrees that this is how it is, but from watching the evolution historically of other syndromes (from literature and during my own life) eventually this is where it all ends up when the core of people without agendas on either side of the issue size it all up and publish their manifestos.It is far easier to asses the patients who suffer the symptom sets which are d-dominated or cyclic-dominated from a causal viewpoint simply because the body has developed good and sound reasons and many mechanisms which are designed to INTENTIONALLY evacuate the GI tract. Alot is known about those mechanisms, and they all involve an integrated group of systems which act in consort, each can be primary at any given time but they always act in consort. That would the the digestive system, the enteric nervous system, the immune system, the central nervous system, the endocrine system, the exocrine system, and even other portions of the peripheral nervous system.It is not that difficult to study neural function, endocrine function, immune function etc and observe events. The events observable and quantifiable in the 70% "majority" are going to be understood in full sooner, simply because some of the mechanisms are simply already known. One has to isolate what provokes the responses, where is the origin of the response at different times and in repsosne to different provocations, then eventually piece them together as to the "why" information.This is one reason that there are more, and more effective, modalities right now for the people who evacuate than the people who retain, so to speak.Just ONE little indicator of where how the study of the symptoms experienced by IBS-C types has to diverge from the rest is revealed here **: ____________________________Gut 2001 Jan;48(1) An exaggerated sensory component of the gastrocolonic response in patients with irritable bowel syndrome.Simren M, Abrahamsson H, Bjornsson ESDepartment of Internal Medicine, Sahlgrenska University Hospital, Goteborg, Sweden.[Record supplied by publisher]BACKGROUND/AIMS: Visceral hypersensitivity is a feature of the irritable bowel syndrome (IBS). Postprandial symptoms are common in these patients. The effects of nutrients on colonic perception in IBS are incompletely understood. SUBJECTS: We studied 13 healthy subjects and 16 patients with IBS-eight had diarrhoea predominant (IBS-D) and eight constipation predominant (IBS-C) IBS. METHODS: Colonic perception thresholds to balloon distension and viscerosomatic referral pattern were assessed before and after duodenal infusion of lipid or saline, respectively. At the end of the infusions, plasma levels of gastrointestinal peptides were determined. RESULTS: Lipids lowered the thresholds for first sensation, gas, discomfort, and pain in the IBS group but only for gas in the control group. The percent reduction in thresholds for gas and pain after lipids was greater in the IBS and IBS-D groups but not in the IBS-C group compared with controls. IBS patients had an increased area of referred discomfort and pain after lipids compared with before infusion whereas the referral area remained unchanged in controls. No group differences in colonic tone or compliance were observed. In both groups higher levels of cholecystokinin, pancreatic polypeptide, peptide YY, vasoactive intestinal polypeptide, and neuropeptide Y were seen after lipids. **Motilin levels were higher in patients and differences in the subgroups were observed. **Levels of corticotrophin releasing factor were lower in the constipated group than in the diarrhoea group. CONCLUSIONS: Postprandial symptoms in IBS patients may be explained in part by a nutrient dependent exaggerated sensory component of the gastrocolonic response.PMID: 11115818 ____________________________So there is a chemical (CRF) red flag (on of them)which in this case distinctly separates the two groups chosen to be studied. While it may not be found to be some silver-bullet that is the main point of divergency, it points out that one trail is marked with bread-crumbs and one trail is marked with Reeses Pieces.Which of course is not meant to suggest that C-types are actually victims of alien abduction or some genetic relationship to E.T. (but do think about phoning home occassionally, ok?), only that there are reasons to explore which will explain way, for example since I work with the IRS investigators, even some C-types do show a (lesser overall)occurrence of dietary related PROVOCATION of symptoms, esp. pain or the bloating sensations, but quite the opposite of an evacuatory response which normally accompanies the types of IRS activation seen in the other subpopulations and the mediators which account for it can be isolated in the majority (d side)....in fact quite the opposite occurs vis a vis reduced motility in the lower colon.So if for no other reason than that it has been clear that something more, or differnt, is afoot which will distinguish these souls...CRF is merely one indicator (beyond symptoms) that this is the case.The way things work though is that in a way the C-types are going to be of a lower-order in the research pecking order if for no other reason that (at least in the USA) they represent a smaller market so when funding the search for solutions all sources of $$$ have a tendency to be driven to solving the problem experienced by the biggest market first.It kind of sux that this is the way it is, as in a perfect world "all would be equal" in the eyes of the medical world. Not that way, but thankfully there ARE enough victims(millions) that work DOES get funded and DOES go on regarding THAT distinct subpopulation too.Eat well. Think well. be well.MNL
