# IBS gas & more caused by Bacteria



## Talissa (Apr 10, 2004)

Hi all,This may not apply to everyone here, but just a ï¿½subsetï¿½, esp if you have postinfectious IBS~Can we talk gas? For the average person, passing gas occasionally is a normal part of digestion. It happens. But for people with IBS, frequent flatulence, pain & cramping from gas are a sign of bacterial fermentation. Fermentation caused by imbalanced gut flora--ï¿½dysbiosis.ï¿½When this happens in the small intestine, itï¿½s called ï¿½small bowel bacterial overgrowthï¿½ and when it happens in the lg intestine, itï¿½s called ï¿½colonic fermentation.ï¿½Theyï¿½ve tried to treat colonic fermentation w/ the probiotic strain L. Plantarum, with mixed results or negative results in studies.Well, yeh, L. Plantarum is aerobic, it needs oxygen. Most of the colon has no oxygen, and for a bacteria to survive it needs to be anaerobic--one of the Bifidobacterium strains. Lactobacillus (L) strains work in the sm. bowel.So if someone has bacterial overgrowth/dysbiosis in both intestines, just taking L. strains wonï¿½t work.This is an interesting study:ï¿½IBS may follow gastroenteritis and be associated with an abnormal gut flora and with food intolerance. Our study was designed to assess whether these factors were associated with colonic malfermentation. ï¿½FINDINGS: The maximum rate of gas excretion was significantly greater in patients than in controls INTERPRETATION: Colonic-gas production, particularly of hydrogen, is greater in patients with IBS than in controls, and both symptoms and gas production are reduced by an exclusion diet. This reduction may be associated with alterations in the activity of hydrogen-consuming bacteria. Fermentation may be an important factor in the pathogenesis of IBS. http://www.ncbi.nlm.nih.gov/entrez/query.f...6&dopt=Abstract The following article delves into dysbiosis & food intolerance & the gassy byproduct:FOOD INTOLERANCE AND THE IRRITABLE BOWEL SYNDROME John Hunter Addenbrookes Hospital, Cambridge, UK ï¿½Despite the link with food, no evidence of classical food allergy exists, and research has concentrated on elucidating the mechanisms of food intolerance. IBS has been shown in prospective studies to arise following gastroenteritis and antibiotic therapy, and the bacterial flora of the colon in IBS is unstable, with overgrowth of facultative anaerobes and a reduction in the number of lactic acid bacteria. Because of this, we studied colonic fermentation in IBS patients and normal controls. Subjects spent 24 hours in a purpose-built calorimeter through which air was drawn at a constant rate, allowing repeated sampling of gases released on the breath and in rectal flatus. The maximum rate of gas excretion was significantly greater in patients than controls and hydrogen production was higher. In patients an exclusion diet produced a considerable fall in maximal gas excretion. Further studies have shown that gas production is also less after antibiotics and enteral feeds, and that symptoms improve in parallel with reductions in gas production. Production of fermentation gases in patients unresponsive to exclusion diets was not different from controls. IBS is not a homogenous condition, and other mechanisms may also be responsible for the production of gastrointestinal symptoms. These include anxiety and air-swallowing, menstrual disturbances, and constipation. A history of IBS arising after gastroenteritis or repeated courses of antibiotics is a strong indication for the trial of an exclusion diet, however, in as many as 50% of IBS patients symptoms are caused by abnormal fermentation of specific food residues as a result of damage to the colonic microflora. References: 1. Alun Jones V, Mclaughlin P, Shorthouse M et al. Food intolerance: a major factor in the pathogenesis of irritable bowel syndrome. Lancet 1982;2(8308):1115-1117 2. Nanda R, James R, Smith H et al. Food intolerance and the irritable bowel syndrome. Gut 1989;30:1099 1104 3. Parker TJ, Naylor SJ, Riordan AM et al. Management of patients with food intolerance in irritable bowel syndrome: the development and use of an exclusion diet. J Hum Nutrit Diet 1995; 8:159-66 4. Balsari A, Ceccarelli A, Dubini F et al. The fecal microbial population in the irritable bowel syndrome. Microbiology 1982;5:185-94 5. King TS, Elia M, Hunter JO. Abnormal colonic fermentation in irritable bowel syndrome. Lancet 1998;352:1187-1189. 6. Garcia Rodriquez LA, Ruigomez A. Increased risk of irritable bowel syndrome after bacterial gastroenteritis:a cohort study.BMJ 1999;318:565-66 http://64.233.161.104/search?q=cache:S8bDr...vergrowth%22&hl =en&start=10[/URL]Besides antibiotics, NSAIDs, chronic alcohol use, etc., can also cause imbalanced micro-flora.________________________________The study in my signature found that ALL the IBS symptoms are from imbalanced gut flora(ï¿½microbiataï¿½)________________________________I wrote all of this out because, unless youï¿½re lucky, your MD wonï¿½t talk about it much, if at all. Iï¿½ve found this knowledge a godsend in getting myself better & felt the need to pass it on. It still isnï¿½t easy for most of us to overcome, but I really feel itï¿½s a start.For some with mild imbalances, itï¿½s easier to fix, others (like me) may have to work at it longer, plus deal with abnormal intestinal wall inflammation caused by the imbalanced gut flora.Iï¿½m at about 95% & gaining. Was once crippled by IBS-D.DISCLAIMER: I know nothing, but hope this is helpful. And I want everyone to know we ainï¿½t nuts, itï¿½s our guts!Please keep trying & donï¿½t give up, Talissa


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## Emmab2003 (Apr 22, 2004)

This is interesting. I had thought my symtoms developed either after eating a weird piece of fish, or after a winter tummy virus three years ago. My doctor checked for H Pylori, and said my problem could be bacterial, but the next time I asked her about it she insisted I had severe GERD and needed the tube down the throat. I had not been complaining of severe GERD symptoms, but rather this noisy gassy tummy that is at the most annoying.I'm still wondering what diet to try....


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## eric (Jul 8, 1999)

I wish you really understood PI IBS.also do you think abnormal motility and transit of food in the colon fermenting could be a factor in why some IBSers bacterial flora maybe altered? Or diet, or alcohol consumtion, or possible meds like nasids or even stress? Or people who believe IBS is a chronic specific bacterial infection with no proof and the research not backing it up?Irritable Bowel Syndrome: An Overview By: Lin Chang, M.D., CNS: Center for Neurovisceral Sciences & Womenï¿½s Health; CURE: Digestive Diseases Research Center, Division of Digestive Diseases, UCLA School of Medicine Irritable bowel syndrome (IBS) is a chronic functional bowel disorder characterized by abdominal pain or discomfort and alterations in bowel habits. The clinical diagnosis of IBS is based on identifying symptom criteria with a ï¿½positive diagnosisï¿½ and excluding organic disease with minimal diagnostic evaluation. Although there are many expensive and sophisticated tests available for the evaluation of IBS symptoms, these are generally not needed for patients with typical symptoms and no features suggestive of organic diseases. This article provides a comprehensive overview of the prevalence, symptoms, diagnosis, and treatment options for IBS. "Post Infectious IBS"Symptoms suggestive of IBS occur in approximately 7-30% of patients following acute gi infections, *often persisting for years following complete resolution of the infection.* A large cohort study indentified a self reported history of accuete Gastroenteritis(intestinal infection) as a major risk factor for the development of IBS. *Reported risk factors for the development of post infectious IBS include female sex, duration of the acute diarrheal illness, and the presence of sustainied psychosocial stressors around the time of infection.* *Post infectious IBS is not restricted to a particular organism and has been documented with a variety of bacterial infections (salmonella, campylobacter and e.coli) as well as parasitic infection.* However, the role of accute viral gastroenteritis in this condition is unknown.In Post infectious IBS, low grade GI inflammation, or immune activation, maybe a basis for altered motility, and/or nerve and mucosal(lining of the bowl) function of the gut in IBS. Recent studies have also shown that in a subset of of unselected IBS patients (no documented history of a preceeding gut infection), there is evidence of increased inflammatory cells in the colon mucosa. It remains to be determined if altered gut immune function is a general characteristic of IBS patients. The implication of stressful life events in the development of post infectious IBS suggests a convergence of central (brain) and (peripheral (gut) mechanisms in the clinical presentation of this syndrome. http://www.aboutibs.org/Publications/currentParticipate.html Mast cells are one of the inflammed cells they found and they are linked to chronic stressors and the fight or flight and fighting infection. Chronic stress can reinflame the cells when the intial inflammation has resolved.The cells can be degradulated with out a pathogen through stress.Stress and the Gastrointestinal TractIV. Modulation of intestinal inflammation by stress: basic mechanisms and clinical relevance "" it is only recently that the role of stress in modulating intestinal inflammatory processes has received the attention of investigators. The feasibility of considering stress as a modulator of inflammatory processes in the gut arises from the following developments: 1) the understanding that corticosteroids elaborated through activation of the hypothalamic-pituitary-adrenal (HPA) axis by stress are anti-inflammatory and that attenuated HPA responses to stress may predispose to inflammation (22); 2) the recognition that many immune and inflammatory cells recognize and respond to neuropeptides (24); and 3) *the knowledge that stress may render an organism susceptible to an inflammatory stimulus by altering intestinal physiology, such as the permeability of the epithelium (10). * " " http://ajpgi.physiology.org/cgi/content/full/280/3/G315 "dysbiosis & food intolerance"These are not IBS and you need to really learn this before you promote it!!!I think I mentioned before being proactive and reactive.You are only being reactive to leaky gut and food intolernce and not proactive first in trying to understand the research on IBS, before you draw major conclusions like these.The underlying disorder of Irritable Bowel Syndrome is Not caused by leaky gut or by food intolerences and in PI IBS, the symptoms are linked to an increased of cells after the resolution of infection. people with PI IBS, might be treated in the early stages with steriods and they are investigating that, if they can change PI IBS, before it LEADS to full blown clinical presentation of IBS.


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## eric (Jul 8, 1999)

FYI"Curr Gastroenterol Rep. 2004 Jun;6(3):247-53. *Chronic and acute life stress, especially during childhood, has been recognized as central to the initiation of the disorder and the induction of acute symptoms. * Related Articles, Links Across the developmental continuum of irritable bowel syndrome: clinical and pathophysiologic considerations.Besedovsky A, Li BU.Division of Gastroenterology, Hepatology, and Nutrition, Children's Memorial Hospital, 2300 Children's Plaza, #57, Chicago, IL 60614-3394, USA. bli###northwestern.eduIrritable bowel syndrome is a common functional gastrointestinal disorder that affects children and adults. The lack of consensus diagnostic criteria and pathophysiologic understanding has hampered clinical progress in diagnosing and treating this disorder. The recent development of the Rome diagnostic criteria, mapping of brain-gut pathways using neuroimaging, and serotonergic pharmacology have greatly advanced the field. Chronic and acute life stress, especially during childhood, has been recognized as central to the initiation of the disorder and the induction of acute symptoms. We propose a developmental continuum whereby the clinical presentation of irritable bowel syndrome changes with age from irritability during infancy, to diarrhea in toddlers, to recurring abdominal pain during school age, and to pain and altered bowel habits during later adolescence and adulthood.PMID: 15128493


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## kel1059 (Feb 28, 2003)

i used to have so much gas but now everything is normal. i suspected that i had dysbiosis and i was correct. my experience is that this problem can be very difficult to address. this is probably one of many reasons why it is being ignored by medical doctors. (another reason is that they are taught to treat symptoms through pharmacological supression -- symptom supression)just because something is hard to address does not mean it should be ignored.


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## flux (Dec 13, 1998)

Where's the gas?


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## bonniei (Jan 25, 2001)

> quote:Because of this, we studied colonic fermentation in IBS patients and normal controls. Subjects spent 24 hours in a purpose-built calorimeter through which air was drawn at a constant rate, allowing repeated sampling of gases released on the breath and in rectal flatus. The maximum rate of gas excretion was significantly greater in patients than controls and hydrogen production was higher.


Look at this thread for a discussion of the reference for this quote. http://www.ibsgroup.org/ubb/ultimatebb.php...t=000515#000000


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## kel1059 (Feb 28, 2003)

maurice,do you still believe this to be true?quote maurice -----"Extreme flatulence due to altered gut flora IS an infection!"http://groups.google.com/groups?hl=en&lr=&...hl%3Den%26lr%3D %26ie%3DUTF-8%26selm%3D3317f25b.2714525%2540nntp.ix.netcom.com%26rnum%3D1[/URL]


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## eric (Jul 8, 1999)

Funny Kel, you ignore all the IBS research, then say doctors ignore the research. Yet, you don't even understand the research and have disconnected from it altoghether and still don't have a clue to dysbiosis or IBS to begin with?You don't seem to understand intestinal permeability is a functional disorder also?So enema abuse has nothing to do with your case and c?Killing bacteria in your gut for years has nothing to do with it either? That you may have altered flora? That's no surprize really. And Homepathy was your cure for dysbiosis?Okay we get it.but you still have not answered this?What kind of Dysbiosis do you have? Putrefaction Dysbiosis? Lack of fiber Dysbiosis? Fermentation Dysbiosis ? Diet Dysbiosis? Medication Dysbiosis? Stress Dysbiosis? Also Leaky gut is not a disease!!! You don't even understand what you think you have?leaky gut is a functional disorder!If the system is not functioning properly!also Leaky gut is caused by inflammation, that is not seen in IBS, the way people here THINK it is and are portraying it, its not overt inflammation, it is specific cells!!! They do not see it, until they peel back the layers of the digestive system and then it is macroscopic, specific cells, in some IBSers. Second, there is good reason to believe there is abnormal flora, BECAUSE of altered transit in some IBSers for one. The sigmoid colon can contract abnormally anywhere along its length in IBS, this traps foods that ferment which can alter bacterial flora. But there can be many reasons for abnormal flora anyway, diet, meds, enviroment, alcohol and others.


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## Talissa (Apr 10, 2004)

> quote:Normal gut physiology is molded by the interaction between the intestinal microbiota and the host's gastrointestinal tissues, including motility, absorption and secretion, and intestinal permeability.


(see link in signature) From above, in english, normal gut flora balance regulates motility, absorption of bile, nutrients, water, etc, and intestinal permeability. The latter is a HUGE factor for those of us with permeability(leaky gut).


> quote:Small but powerful players in tipping the balance towards digestive health or disease are the microorganisms that inhabit the gastrointestinal tract. These microbes can affect intestinal health in some surprising ways.Recent studies have shed light on how the ï¿½goodï¿½ bacteria found in the gut are beneficial. A type of cell found in the gut, the ï¿½Panethï¿½ cell, appears to have a significant role in fighting disease. Researchers showed that the Paneth cells in mice produced a molecule, called Ang4, which is important in preferentially attacking harmful, invading microbes. Interestingly, the resident ï¿½goodï¿½ bacteria in the gut were responsible for directing the Paneth cells to make Ang4. Another research team showed that the ï¿½goodï¿½ bacteria, again working through Paneth cells, had an important role in developing the capillary networks found in the small intestine. In the absence of bacteria, these networks--which are important for absorption of nutrientsï¿½do not form properly. ...The significance of appropriate interactions between intestinal cells and bacteria in creating a healthy intestinal immunity was also demonstrated by this research. With this knowledge, researchers have a better perspective on what goes awry in some intestinal diseases.


 http://www.niddk.nih.gov/federal/advances/2004/ddn.pdf And Medscape has already attested to imbalanced gut flora being found in IBS patients. Same goes for abnormal permeability in some of us.________________Er, I am SO not going to re-post everything like you do--things on the HYPNOTHERAPY thread & gut flora thread, in my case.I'm just putting the info out there, & folks can decide for themselves. Better yet, they can research these things themselves & make informed decisions.Talissa


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## Talissa (Apr 10, 2004)

> quote:Where's the gas?


You really do crack me up sometimes, thanx!But if you don't have gas, do what I do & go to the local Shell station


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## jwade (Jan 19, 2004)

Hi Talissa. I am glad to hear that you are improving. Would you mind sharing with me what you have done to get to 95%. I almost can't imagine being there. I am hopeful though. Thanks


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## kel1059 (Feb 28, 2003)

eric, i will be the first to admit that i am a bit baffled as to exactly what has happened to cause my remission (recovery???). i tried almost everything and everything failed. somehow or another i put the right combination together and here i am -- finally able to eat almost anything i want, go to the bathroom like everyone else, not worry about odor or gas, not feel nauseous, and several other striking improvements.i know that dysbiosis played a role probably a very big role.i know that dr dahlman's program is very good and he helped me out quite a bit. his human strain probiotics seemed to really help.i also know --just as garywest knows-- that homeopathy does indeed work. it is counterintuitive therefore i expect most people to be cynical or skeptical but i am free at last.







i just hope it lasts. still nervous about this nightmare returning.


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## bonniei (Jan 25, 2001)

> quote:From above, in english, normal gut flora balance regulates motility, absorption of bile, nutrients, water, etc, and intestinal permeability. The latter is a HUGE factor for those of us with permeability(leaky gut).


But is still unclear whether a causal relationship exists, or whether the altered flora is a consequence of the gut dysfunction. And again most of these studies were done on mice including in the link in your signature.


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## eric (Jul 8, 1999)

This is a problem you don't understand here. First you don't understand inflammation in IBS period.Second you don't understand the control of these systems by the enteric nervous system and the brain and also neurotransmitters or there roles, you are so focused on IBS and bacteria. Its called tunnel vision. "Normal gut physiology is molded by the interaction between the intestinal microbiota and the host's gastrointestinal tissues, including motility, absorption and secretion, and intestinal permeability. "Molded is a word and there is nothing new to the above. They play important roles, but with out the chemical and electrical impluses controlling the gut, the gut would not work and hence all the bacteria would be dead, not to mention a lot of them are not pathogens and help the system, so probiotics are a good thing to try for IBS symptoms."Normal gut physiology is molded by the interaction between the intestinal microbiota and the host's gastrointestinal tissues, including motility, absorption and secretion, and intestinal permeability. "This left out a big part in IBS, its called sensations and the communication from gut to brain and back!!!There are many things that can disturbe what your talking about here you just don't understand well or bacteria flora either which is different in people, due to many reasons, including there environemnt which protects them from pathogens in their house and community.and Diet, meds, alcohol, stress, lack of fiber, ect..If your are going to keep calling IBS a chronic bacterial infection get some real research and more then one, because there is none other then PI IBS and that resolves and leaves people with IBS. They already know quite a bit about this and IBS, but you have not caught up yet to the research yet.Even the researchers studying gut flora in IBS do not believe it will be a cure, but a management treatment. Not to mention people who just get better regardless of the treatment or any treatment, some just get better for no reason they know of yet, it can also wax and wane for years at a time for some IBSers.Also if you promote leaky gut understand what that really is also (a functional disorder) an all the things that can cause it and the symptoms. And not just off any site promoting it on the web either. Even with your remission and feeling better, it can be explained through the real research. on IBS is a couple different ways, other then what you might think or in someways you are thinking.Also, you are leaving so much research and things they know alreay out of the picture, you missing the the bigger picture. This is extremely important!I think I mentioned this before when I said be proactive not reactive. Be proactive and go do the research first. Your being reactive to your own beliefs and some things your reading and don't fully have a grasp on, without all the actual IBS research which has come a long long way. in englishIBS is not leaky gut!!!!!"intestinal permeability"Is not a disease and again is a consequence!!!IBSers have high stress levels and that can effect "intestinal permeability" this is a fact and known, but you leave it out. Your putting the cart before the horse here.They can also have very altered diets, that is a factor, they maybe on meds that effect it like nasids that is a factor and they maybe not getting enough fiber that is a factor in intestinal permeability. You just are not getting this, reardless of all that is being posted on it and about it. " Better yet, they can research these things themselves & make informed decisions."I wish you would research it better before you post it. That would help.try to understandIBSthe role of neurotransmitters in all thisinfection or inflammation in IBS.understand that inflammation cannot be the marker for pain in IBS, but may contribute to it in some IBSers. "Common names for this condition include spastic colon, nervous colon, nervous stomach, mucous colitis and spastic colitis. Physicians often refer to this condition by the initials IBS. The typical symptoms of IBS include crampy abdominal pain, bloating, distention and abnormal bowel habits. There may be diarrhea, constipation or a combination of both. It is common for IBS to affect teenagers and young adults. Symptoms may even date back to early childhood. Occasionally the syndrome can start in middle age. The symptoms can wax and wane and return in periods of stress throughout a personï¿½s lifetime. What is the role of stress and what is visceral hypersensitivity? Stress is a major factor that plays a significant role in many patients who have IBS. Some people react to stress by getting tension headaches. People with IBS often get tension and pain in the abdomen in response to stress, anxiety and depression. People who are prone to IBS are affected by many stimuli to various levels of the nervous system. An overly sensitive neurological sensory system is a major component that contributes to IBS - this is often referred to as visceral hypersensitivity. This system is susceptible to the effect of stress. What is abnormal in people with IBS? Patients with IBS have an abnormal electrical system of their colon with a higher electrical cycling activity and are set up to be more contractile under various stimuli. Intense prolonged, spastic contractions of the colon occur in IBS. When two parts of the colon go into contraction, the colon in between becomes stretched out like a balloon. As a result the abdomen will feel bloated or distended. The sensory or pain nerve fibers get stimulated when there is a stretching of the colon wall. The brain perceives this as pain. The brain actually communicates with the gut through a complex series of nerves that is called the Brain-Gut connection. These connections are abnormal in IBS and the location can be in either the brain or the gut. Stress, depression and various chemical imbalances can affect the Brain-Gut connection. The nerves and muscles of the intestine that are abnormal in IBS may be affected directly by specific food that is eaten. Some researchers feel that a viral infection is responsible for a long-lasting disturbance of the Brain-Gut system. It is also possible that this disturbance is inherited or occurs as the fetus develops in the uterus. With abnormal nerves and heightened responses to digestive hormones, IBS patients have abnormally strong and prolonged contractions of their intestines compared to people without IBS. These strong contractions of the colon help explain why people with IBS often have an urge to have a bowel movement 15 to 30 minutes after eating. The bowel movement is often diarrhea because the muscular contractions are spastic and move the waste material quickly from the right side of the colon to the left side and does not allow for the time required to absorb the water and form the stool. When colon spasms relaxes in one area, the stool can rush into another segment and with a sudden contraction it will come out as diarrhea. If the colon remains in spasm for too long, the stool that is staying in one area can get dried out because the colon is a very effective sponge to wick out or absorb water. This can results in small hard stools, which can alternate with diarrhea. There may be different levels of the Brain-Gut connection that are affected and result in a similar set of symptoms in people labeled with IBS. A combination of the abnormal Brain-Gut system, visceral hypersensitivity and hyperactive intestines appear to be responsible for IBS. Why is IBS called a syndrome and not a disease? IBS is called a syndrome rather than a disease because it is comprised of a group of symptoms and there are no specific blood tests, endoscopic findings or biopsy results that are diagnostic for IBS. A syndrome may feel like a disease but you cannot die from IBS like you can from a disease. The symptoms of IBS can be so oppressive that it can severely impact oneï¿½s life. How is IBS diagnosed? Abdominal pain or discomfort is the hallmark symptom of IBS. In order to make a clinical diagnosis of the IBS there should be a change of bowel habits and all other medical conditions that could produce these gastrointestinal symptoms need to be excluded. Other symptoms that occur with irritable bowel syndrome many include relief of pain with defecation, bloating, passage of mucus and an incomplete sense of evacuation. In this case one may feel never completely empty and it may be necessary to return to the toilet multiple times. There may also be a sense of urgency and need to strain. Other symptoms unrelated to the digestive system occur frequently and include anxiety, depression, back pain, urinary frequency and discomfort with sexual intercourse. " http://www.aliperti.net/irritablebowel.html


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## calid (Aug 4, 2003)

Haven't you guys learned a thing yet? Eric is ALWAYS right and he is the only one who knows anything about IBS. No one in the world knows more than him so you'd better listen to him only. To heck with what your own body says, be sure and throw out all the new studies and don't listen to any doctors with different views than him. ONLY LISTEN TO ERIC


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## Talissa (Apr 10, 2004)

Jwade,Everyone's different, but here goes--I started getting better after taking a natural antibacterial called "ParaGone" by Renewlife & followed with iFlora(was Flora Source), a multi-strain probiotic. With digestive enzymes & a food journal, I was able to pinpoint fructose as major trigger for D attacks.Got it down to three Ds ea am, formed by hi dosing Metamucil.Recently have been able to eat any foods w/o getting attacks after starting DA-IBS. Also bms became normal looking again. Am currently waiting on more iFlora & also started ibsacol 3 days ago to try to deal with the inflammation aspect.ibsacol is fatty acid esters, known for anti-inflammatory effects.My hope is ibsacol will get me off the fiber.I also do yoga daily, and now that I'm better, I teach pilates 4 xs/week____________Er,Serotonin is malfunctioning--the transporters, the mast cells. Serotonin, made from tryptophan by the body, is the best EXAMPLE of nutrients not being properly assimilated in IBS.You fix it at the source, the flora & the intestinal wall, things normalize. I know, because it's what's been happening with me. My motility was through the roof, and I had severe social anxiety. By balancing the flora, I've balanced the other problems. Other folks are 100% or close too & kind enough to stick around & put up with you, others have left. Life's too short, who can blame them.If the researchers not trying to make drug $ are studying this, so should we! Power to the People







I'm not arguing anymore. I've got company coming next week, a novel to write<wink>, and a dirty house!Best to all, T-


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## Kathleen M. (Nov 16, 1999)

I think the difficulty comes from "caused by".There are some papers, unfortunately one is quite old and I am sure there are better ways to quantify colonic flora bacteria now, that show some differences in the bacteria of IBSers (and other GI disorders) and "healthy normals" that were used in the study.Lower levels of some of the probiotic bacteria and fewer people with IBS than usual are methane producers.But is it the "CAUSE" or one of the effects....a coorelation does not prove causation, ever, for any reason.And the record of treating IBS with probiotics is quite spotty. Sometimes in some trials it sometimes helps some people, in others there isn't any difference between it and the placebo group...so it is hard to know.Altering bacterial flora is unlikely to be the cure for everyone, but there does seem to be a subset it helps, but that doesn't prove that you first got the bad bacteria (or from what I can glean from what little record there is you lose some of the good ones) and then they caused (or the reduction in some species) caused the IBS.For example. In a healthy normal person if you go through a bowel prep for a colonoscopy you have a higher chance of losing the methane producing bacteria than you would otherwise (they can be spontaneously lost). So how much of that may be that IBSers are more likely to have certain medical proceedures than usual???And the % without methanogens was not hugely different (something like 35% with rather than 50% with seen in the normal population) Now with Crohn's disease almost everyone with it had lost the methane producers so there seems to be something different going on there (but Ulc. Col. patients were about the same as IBSers).It is a complicated thing.Now I had big gas production (high normal to just above the normal range in fart frequency) before, during, and after my bad bout with IBS.Probiotics did reduce that (although it wasn't really causing any other symptoms at the time) after the bad IBS. But stuff I took earlier didn't help much (but then given the regulation of supplements maybe they didn't have anything or the right things in them to start with).Yep, there are some with IBS who have issues that probiotic bacteria do help with. But that and the finding that some IBSers have differences in the flora do not prove "causation".As for Serotoniin issues being a result of Tryptophan mal-absorption due to bacteria mucking up absorption...I think that is a MAJOR stretch.Some people the problem seems to be co-related with too MUCH serotonin in the blood after meals if memory serves.And I can't remember if that is an amino acid we only get from the diet....let me check...some we can make, others are absorbed.But I would assume if you are to the point you are not absorbing amino acids you would have other problems that are related to NOT having IBS, but having a different disease.OK Google came through. It is essential, and strict vegetarians may not get enough of it in the diet because it is not found much in plant protiens. But not all vegans get IBS, and plently of I NEED my MEAT types get IBS. And like I said, at least in some cases it seems to be too much rather than too little.K.


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## Talissa (Apr 10, 2004)

double post--sorry


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## Talissa (Apr 10, 2004)

KM--Tryptophan is an essential amino acid, meaning we need to get it from our diets. So are the 5 amino acids needed for serotonin transport. You're cool, & I'd like to agree to disagree.But one point, how serotonin malfunctions is diff in those who end up with "C" & in those with "D".And I LOVE meat--just had to throw that in. We're omnivores, we need to eat our meat...or we can't get any pudding(pink floyd)See ya! T-


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## Kathleen M. (Nov 16, 1999)

Yep, serotonin is a very complicated issue.It isn't just how much you have (so how much tryptophan etc you absorb from your food).Most of it is about the who is releasing it when, where and how, and who (which nerves) are receiving it when where and how.What receptors are hit, do you have the right ones in the right places, is the response to those receptors correct or not...very complicated...The whole "serotonin is just a matter of not absorbing tryptophan because you got bad bacteria" seems like a VERRRRRRRY shaky arguement and seems to ignore most of what is known about biology in humans IMHO.AND we still have the whole chicken egg conundrum. Are the minor differences seen in bacterial flora in IBS what comes first...or is a result of what happnens along the way (did your colonoscopy get rid of your methanogens???)K.


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## eric (Jul 8, 1999)

Tal, did you get a colonoscopy? Did they see Inflammation in your colon with a colonoscopy?Also for how long have you had IBS?


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## Talissa (Apr 10, 2004)

Er,You really can be a sh*t.I have had IBS-D for almost six years following an infection by Giardia & failed Flagyl treatment. The diagnosis followed a clear colonoscopy about 5 1/2 years ago._______________Er,Did you know that serotonin itself cannot pass through the blood-brain barrier, becasuse its precursor tryptophan must share its transport 'bus' with five other amino acids: leucine, isoleucine, valine, tyrosine and phenylalanine. All are NUTRIENTS we absorb through the small intestine.Did you know that when neurons convert tryptophan into serotonin, they first use a vitamin B-3-dependent enzyme to convert tryptophan into 5-HTP. A vitamin B6-dependent enzyme is then used to convert 5-HTP into serotonin. MORE nutrients involved.Serotonin is the perfect proven example of nutrients failing to assimilate correctly due to changes in cells along the intestinal wall--due to abnormal inflammation--which has been shown to be caused by imbalanced intestinal flora, in ctn cases.


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## eric (Jul 8, 1999)

Did your colonoscopy show inflammation???" abnormal inflammation"You don't understand there is no overt inflammation in IBS!!! Your not understanding what kind of inflammation is seen in a subset of IBSers."overt colonic inflammation precludes a diagnosis of IBS."!!!!!!!!!!!!!!You are also leaving out there is an increase in enterochromaffin cells that store the majority of serotonin in the gut and mast cells after the infection has subsided. The reason why serotonin is dysregulating has not been established.Your also not understanding that in PI IBS there is infection/Inflammation and then that totally resolves. What can reactivate it is chronic stressors. The inflammation seen is specific cells, I think I have mentioned this a lot now. And again I am saying the HPA axis is involved in fighting infection and in the bodies fight or flight responce." *An increase in inflammatory mediators alone is insufficient to explain the pathogenesis of IBS. * From post-infective IBS, we know that the most people who have gastroenteritis and accompanying inflammation do not develop IBS. As discussed earlier, several factors may be important in interacting with the gut insult and in predicting those who develop symptoms - one interesting factor here is the role of stress. Psychological stress is known to affect gut function in normal healthy humans, and in people with IBS stress may trigger or exacerbate symptoms. More recently there is evidence of a link between stress and inflammatory responses. Exposure to stress in both animals and humans has been shown to result in the release of mast cell mediators in the colon (18,19) and in a recent study stress was capable reactivating previous inflammation in rats (15). An important challenge for future work will be to clarify the interaction between inflammation, stress and IBS symptoms." http://www.med.unc.edu/wrkunits/2depts/med...rymediators.htm ROMEIrritable Bowel Syndrome: How far do you go in the Workup?"For example, there is a subgroup of patients, called "post-infectious IBS" who appear to respond to an enteric infection such as campylobactor jejuni with an increased inflammatory cell response (22). *This is associated with activating enterochromaffin cells to produce 5HT, and CD3 cells to produce cytokines, which in turn leads to enhanced motility and lowered visceral sensation thresholds "* *"But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it.* *All patients with active celiac disease have microscopic inflammation, but a large proportion do not have abdominal pain, and patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds* (24). In individuals with these disorders, there may be central nervous system counter-regulatory measures responding to the peripheral pain/inflammatory processes that increase pain thresholds. *With regard to IBS, the gut-related effects of microscopic inflammation may be only one component of a dysfunctional brain-gut system. * In addition, and often in response to stress, there may be a failure to activate descending pain inhibitory systems that enable the clinical experience of pain and other symptoms that typify this disorder (25). In one prospective study of post-infectious IBS, it was *found that those who retained their symptoms 3-months after an enteric infection had not only increased mucosal cellularity, but also had increased psychosocial distress at the time of the infection.* *Furthermore, lowered visceral sensation thresholds and increased motility were present after the infection regardless of whether or not the patients retained their symptoms * (26). *Therefore, the microscopic inflammation and its physiological effects on motility and sensation contribute to, but are not always sufficient for the clinical expression of IBS pain. * At least for post-infectious IBS this provides some evidence that psychological distress alters brain pain regulatory pathways to amplify incoming visceral signals leading to the full clinical expression of this syndrome" http://www.romecriteria.org/reading1.html Inflammatory Mediators in Irritable Bowel Syndrome"Mast Cells and IBS The mast cell has potential to be a key player in IBS. Although mast cells are most widely known for their role in allergic responses, these cells are normally present throughout the gut and are involved in a range of physiological and pathological activities including mucosal defense mechanisms and inflammation. Mast cells may release an array of inflammatory mediators that act on smooth muscle, nerves and immune cells, which may ultimately result in gastrointestinal dysfunction and symptoms. In addition, mast cells in the gut are located close to nerves providing a structural basis for communication between the gut and the nervous system. In 1993, Weston and colleagues reported increased mast cell numbers in the mucosa of IBS patients(10) - these changes were identified in tissue from the end of the small bowel (terminal ileum). Similarly we identified significant increases in mast cells in IBS patients compared to controls in the colon (specifically at the caecum) (11). There were also trends for increases in other regions of the colon (ascending and descending colon) but no differences could be seen at the rectum. The lack of changes in mast cell infiltration in the rectum has since been confirmed by others (9). Collectively these studies suggest that mast cells were increased in IBS patients - this may be part of a low-grade inflammatory response, although the components and nature of this response remain poorly understood. " http://www.med.unc.edu/wrkunits/2depts/med...rymediators.htm GastroenterologySeptember 2003 ï¿½ Volume 125 ï¿½ Number 3 Basic-alimentary tractStress-induced disruption of colonic epithelial barrier: Role of interferon- and myosin light chain kinase in mice http://www2.us.elsevierhealth.com/scripts/...16508503010576& Report on the 4th International Symposium on Functional Gastrointestinal DisordersMarch 30th - April 2nd, 2001 Milwaukee, Wisconsin"Mary Perdue from McMaster University, Ontario discussed the importance of the epithelial intestinal barrier to maintain immune tolerance to potentially harmful matter, such as bacteria, ingested when we eat or drink. (Everything that enters the human body must pass through an epithelial layer. Various types of epithelial tissues line not only the body cavities, blood vessels, and most organs, but also our outer surface-our skin. Within the intestines, epithelial tissue forms an intestinal barrier involved with absorption, secretion, sensation, contractility, and protection.) Studies in animal models show that psychological stress can disrupt this barrier, leading to the penetration of bacteria into the gut, inflammation, an immune system response (inflammatory cytokines), and ultimately sensitization of neural signals from the gut to the brain that can heighten the perception of pain." http://www.iffgd.org/symposium2001.html "From - Report on the 5th International Symposium onFunctional Gastrointestinal DisordersApril 4, 2003 to April 7, 2003 Milwaukee, Wisconsin By: Douglas A. Drossman, M.D., UNC Center for Functional GI and Motility Disorders at Chapel Hill, and William F. Norton, IFFGDBasic Principles -- Brain-Gut Moderators: Emeran Mayer MD; Robin Spiller MD. Panel: Robin Spiller MD; Jackie Wood PhD; George Chrousos MD; Yvette Tachï¿½ PhD; Lisa Goehler PhD; G.F. Gebhart PhD; Emeran Mayer MD. " *There are immune responses to infections. To defend itself from a foreign substance or invader, such as a bacterium or virus, the body mounts an immune response controlled by the brain.* There needs to be a balance between infection and the body's immune response; the immune system needs to turn on and turn off at the right times to destroy the invader but not to the degree that it may harm healthy tissue." " *One of the more exciting areas of recent research relates to the basic and translational aspects of the effects of stress on inflammation, cytokine and immune modulation, and pain. * (Cytokines are a type of protein released by cells of the immune system, which act through specific cell receptors to regulate immune responses.) This series of presentations address three important research areas in the field of functional GI disorders, which have recently attracted considerable attention: the role of immune activation in the gut and the interactions of the gut immune and nervous systems; the role of the central nervous system in the regulation (modulation) of pain perception (nociception); and the emerging field of animal models with relevance for functional GI disorder research. This section demonstrates the rapid progress seen in the last few years in better understanding of basic mechanisms, in particular the neuroimmune interactions underlying symptom generation in patients with "functional" GI disorders. " http://www.iffgd.org/symposium2003brain-gut.html "Robin Spiller, University Hospital, Nottingham, England began the session by noting the difficulty in separating disorders of structure ("organic") from disorders of function. He noted, "The difference is based on how high the power of your microscope is." This was elaborated upon in his presentation on Post-infectious Functional GI Disorders. It has been observed that IBS-like symptoms, that persist for 6 months to a year or longer, may appear after a bout with an acute infection in the gastrointestinal tract (e.g., food-poisoning). This is termed, "post-infectious IBS." A study by Gwee et al showed that the presence of unusual or amplified life stress at the time of onset of infection increased the chances of developing IBS symptoms. *Inflammation persisted in patients with IBS-like symptoms but did not in patients whose symptoms resolved. This suggests that the brain's management of certain stressful stimuli (i.e., psychologic distress) affects the brain-gut system's ability to inhibit inflammation. * It has frequently been observed that some individuals with more severe symptoms of IBS have coexisting psychologic distress. Stress has been thought to influence health-care seeking behavior, either by increasing motility, visceral hypersensitivity or inflammation, or by enhancing one's perception of gut symptoms, all of which lead to a greater need to seek care for them. The concept of post-infectious IBS suggests that in some circumstances stress (the biological process by which the body adapts in response to a stimuli) may influence symptoms. *An initial response to an infection in the gastrointestinal tract can involve the neurotransmitter, serotonin, which acts as a messenger (mediator) to cells involved with the immune response.* Immune cells -- mostly in the blood, but also in the lymphatic system -- enter the infected area and remove the invader. Additionally, the body adaptively removes the infection (e.g., via vomiting or diarrhea -- normal beneficial responses that help the body expel an infecting organism). Persistence of the underlying inflammatory response may lead to post-infectious disorders of function. A variety of neuroimmune responses can lead to intestinal over-responsiveness (sensitization) and other clinical effects. *These responses include direct toxicity to nerves that influence intestinal contractions, alteration in gut immune activation, abnormalities of serotonin metabolism, and persisting low-grade inflammation.* *IBS developing after infective gastroenteritis is associated with subtle increases in enteroendocrine and chronic inflammatory cells in the gut mucosa.* *The net effect may be to increase serotonin availability in the gut and enhance secretion and propulsive motility patterns.* Serotonin antagonists may be beneficial in such patients http://www.iffgd.org/symposium2003brain-gut.html


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## Kathleen M. (Nov 16, 1999)

What happens to people who cannot absorbe nutrients from the small intestine (which BTW are not seen in IBS) and BTW also it can't just be we do not absorb anything to do with serotonin production buy absorve EVERYTHING else 100% normally now can it







AnemiaBone LossInexplicable weight lossBunches of OTHER nutritional deficieny syndromes.All sorts of body parts falling out/off/not functioning.See the thing this most people with IBS are "perfectly healthy" other than having IBS (and if they have other diagnosable unrelated diseases which make sense they may not be "perfectly healthy...they may have heart diesease or acne or other things).WIDESPREAD rampant lack of nutrients is a BIG RED FLAG THAT IT IS *NOT IBS!!!!!!*Really it is...This line of reasoning that the ONLY cause of serotonin malfunction in IBS MUST BE WE DON'T ABSORB NUTRIENTS for the most part does nothing but degrade any credibility you may have built here.And it is sad to see...really it is.BTW. There is a fairly good very workable theory as to how post-infectious IBS occurs.Gut gets BugImmune system fights bugBug dies, AND there is collateral damage to the nerves in the gut wall (experimental work with inflamation in rodents and the continuation of symptoms in people with Inflamatory bowel disease in remission are used for this).Damaged nerves do not control the gut properly.ANDPost-infectious IBS is more likely to persist in people who for psycho-social reasons do not do well at the getting the brain to re-regulate the gut nerves thing.Post-infectious IBS had a tendancy to resolve itself in about the same amount of time that nerves recovering from injury tends to occur (strangely enough).Sigh.Why I bother, I do not know. Unlikely anyone will listen to someone with a deep understanding of biology...and all that will happen is I will get way too attacked over this.Sigh.K


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## Talissa (Apr 10, 2004)

KM-While I only took 3 biology courses in college, and studied nutritional science after graduating, I'm sure my knowledge of bio is much, much less than yours.I'm not going to attack you.My question is, why do so many people who get PI IBS or antibiotic associated D have IBS symptoms for 10, 15, 20 + years?Why did I go from having 14 D's per day to 3-7 times/day 7 days into taking the natural antibacterial?Re: nerve damage:"There is much growing and accumulated data on the development of IBS after acute gastroenteritis. This is called 'post-infective IBS'. The resulting IBS may be either diarrhoea-predominant or constipation-predominant IBS, which suggests that both chronic diarrhoea and chronic constipation may be bacterially derived. Because metronidazole and vancomycin markedly reduce diarrhoea and constipation-predominant IBS respectively during treatment and so it appears that these forms of IBS may be mediated by an ongoing, bowel flora infection rather than a persisting damage of gut nerves. After all, such antibiotics would scarcely have affect dead or dying nerves. *Hence, currently, the most likely cause of IBS would appear to be a chronic infection of the luminal bacteria which live within the bowel. Nonetheless, progressively nerve damage can develop with such an infection, and this can be seen in some patients with severe constipation.* http://www.cdd.com.au/html/expertise/diseaseinfo/ibs.html Since I have "D", I'm not going to sit around and hope nerves that aren't damage heal when I can & have been pro-active.But hey, that's just me.


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## kel1059 (Feb 28, 2003)

quote talissa----"Serotonin is the perfect proven example of nutrients failing to assimilate correctly due to changes in cells along the intestinal wall--due to abnormal inflammation--which has been shown to be caused by imbalanced intestinal flora, in ctn cases."i see nothing shockingly incorrect about this statement. to one extent or another there is probably a great deal of truth to it.the problem is when people twist talissa's meanings to be something that they are not.one way to twist her meaning is to exaggerate her comment into something it is not. i don't think that talissa is saying that IBSers have some type of extreme malabsorption problem which would point to some other diagnosis.if instead she is saying that there might be some minor changes in the brush border due to various factors (bacterial, etc) and these minor changes might impair absorption to some degree (not easily detected by medical tests) ---- then i say that she could be dead on correct.


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## Kathleen M. (Nov 16, 1999)

For some people the amount of gas the colonic bacteria produce becomes problematic.You reduce the gas, you reduce the symptoms. The nerves are still mucked up, but you change things so that things function better.This is why for some people limiting starches, or other foods that feed the bacteria in the colon that make gas relieves the diarrhea.AFAIK the people with IBD's who by definition have lots of inflamation in the colon all the time do not universally end up constipated. But many have IBS symptoms (pain bloating altered stool of both kinds) when the ulcers and all other visible and microscopic signs of inflamation are gone.Much of the antibiotics versions of treating IBS that I have read (Cedar-Sinai/Pimental) are also all about altering the gas.Reducing colonic bacteria (assuming you don't end up with something really pathogenic when you disrupt the flora with whatever antibacterial you took...there are things that will overgrow only when the normal flora is disrupted), changing what you feed them, or addig probiotic bacteria (which BY DEFINITION do not produce gas from carbohydrates) can alter the gas in beneficial ways.Doesn't mean the bacteria you have are necessarily any different than most people, just that the gut no longer handles normal levels of gas properly. Change the gas, change the symptoms.The last time I saw it checked out the majority of PI-IBS do get better over a two year period. Not all. Sometimes nerve damage doesn't repair. But there is a theory of all functional diseases I read that I like and that part of healing them can be getting the damaged part re-connected with the CNS/Brain so that other information that is needed for the damage to be regulated properly occurs. This may explain why so many of the functional disorders of all kinds respond so well to mind-body therapies that tend to have that re-integrating type of feel to them.K.


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## Kathleen M. (Nov 16, 1999)

PS.Most of what I see on the site about IBS indicates LARGE intestinal bacterial issues (Pimental focuses on small intestinal AND recommends avoiding all probiotic bacteria as they over-colonize the small intestine as well as so-called bad bacteria)Your nutrient absorbtion does not depend at all on the large intestine. Only small intestine. In the colon you basically only absorb water.Small bacterial overgrowth tends to be related to a lot of the "general malabsorption" stuff I talked about, except in Pimental's IBS cohort. Most of the other diseases that lead to SIBO they see the weight loss and other problems and they use repeated antibiotics to keep the small intestine clear.K.


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## Talissa (Apr 10, 2004)

This article from Medscape is from June 2002, co-authored by Er's buddy Drossman: _"Inflammation, Infection, and Irritable Bowel Syndrome: An Update"_ "...He presented data from clinical studies showing the development of IBS symptoms following acute gastroenteritis (ie, postinfectious [PI] IBS) and a higher than expected prevalence of IBS symptoms among patients with inflammatory bowel disease that was in remission. Additionally, *data from animal studies demonstrated that altered gut physiology can persist even after the infection and associated inflammation have resolved. Furthermore, studies of mucosal biopsies, from both human and animal models, have shown increased inflammatory cells and inflammatory mediators in patients with IBS* and in previously sensitized/stressed animals. Finally, some recent studies have shown proximity between nerve trunks and the inflammatory cells, suggesting a local neuroimmune interaction that may contribute to the *pathogenesis* of IBS. " http://www.medscape.com/viewarticle/434527?src=search The nerves are damaged? No, the inflamed intestinal cells are deregulating normal interaction.Sounds familiar doesn't it?Lowered benficial bacteria=opportunistic pathogen overpopulations=inflammation of intestinal wall cells"pathogenesis" of IBS=Pathogen origin of IBS


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## Talissa (Apr 10, 2004)

KM-I know both sm & lg intestines both can get pathogen overgrowths, as stated in my origin post.The small intestine absorbs nutrients and that is why it was germaine to the discussion of nutrients & serotonin.In fact if you want to get picky, while a few nutrients are absorbed(in a healthy intestine) byin the duodenum section, most are absorbed in the jejunum.And how are nutrients similar to serotonin, besides the nutrients of serotonin?Active transporters.In healthy bodies, most vitamins and some minerals have active transports in place for absorption and are taken into the body in very specific ways. These active transports act as shuttles, picking up the vitamin or mineral and taking it through the intestinal cell wall into the body, where it may be directly released or transferred to another transport molecule. What happens when there is abnormal inflammation along the cell wall?Malfunctions with the process.


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## Talissa (Apr 10, 2004)

"... Research studies have shown that the small intestinal tract barrier can become leaky under some conditions. That is, the cells loose their attachments to each other, resulting in a wall with holes between the cells instead of the cells forming a strong, connected and continuous surface. When this ï¿½leaky gutï¿½ happens, molecules can get inside the body that normally wouldnï¿½t be transported through the intestinal cell wall. *Furthermore, studies have shown that this leaky gut can also cause problems in the normal transport of nutrients.* *This is probably because most nutrients are taken into the body through the cells in the intestinal wall by the selective process of active transport, and they may need to go through the cells and not around them to get to the right transport systems in your body. * Therefore, with leaky gut, the things that shouldnï¿½t get in do, and those that should canï¿½t get where they need to be for adequate transport through the body. *The result is the body doesnï¿½t get the nutrition it needs. * Anything that irritates the lining of the gastrointestinal tract can cause leaky gut, *but a major contributor is inflammation * (e.g., food allergies)." http://www.whfoods.com/genpage.php?tname=faq&dbid=16


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## Kathleen M. (Nov 16, 1999)

Still...most people with IBS show NO evidence of nutritional absorption problemsReally they do not.All the tests that show nutritional absorption problems are typically 100% totally normal in IBSers.And even with what you posted there is still a problem with the nerves, and I doubt that is because people do not absorb serotonin precursors.Not sure how well accepted "leaky gut" is. I believe that theory is not anywhere close to fact, but is still a very disputed idea scientifically.But the majority of the treatments that fix IBS effect nervous system function, whether that is by over damage or by interactions.And we still haven't really got a good handle on just what any bacterial difference between IBSers and healthy normals really are or really mean (It seems to be most of the enumerations show a fair amount of overlap between them).Whatever...I am getting into a feelign of talking to a brick wall..so whatever you believe is absolutely true in your body and your universe, how much it relates to the world the rest of us live in...I dunnno,have a nice life.. I just get you want to argue for the sake of it, and not have a real discussion of ideas or listen to anything other than your own voice. I may be wrong, but my life is too short and full for this.K.


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## Kathleen M. (Nov 16, 1999)

Did look at the medline posting. One thing to remember before you use it as absolute proof.Abstracts from meetings tend to be preliminary and how much they after rigourous scientific review tend to be proven completely true is hard to guess ahead of time.Just so you know.K.


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## Kathleen M. (Nov 16, 1999)

PPS. Have you read the whole article you link to the abstract from.From the conclusions and on the whole "causality" issue.(I love having access to full journal articles on-line...just a word of warning, abstracts alone are often misleading even when done)"Although patienst with IBS appear to have quantitative differences in the intestinal microbiota when compared to normal individuals it is still unclear whether a causal relationship exists, or whether the altered flora is a consequence of the gut dysfunction." which was one of my main points after all.If I was confusing about nutrient absorption the question I was trying to pose is: How can every nutrient involved in serotonin be so badly absorbed when for some reason all other indicators of malabsorption (including pelegra and other diseases from malabsorption of serotoni n precursosr) appear to be absent?Either you malabsorb a lot of things, or you don't. Malabsorption has a lot of symptoms, all of which tend to be absent in IBSers. Yet, serotonin seems to have abnormalities all the same.Confusedly yours..Yeah...I know I'm not shutting up, but having a bit of fun this afternoon.


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## Kathleen M. (Nov 16, 1999)

PPPS.Is your sig talking about the mouse study. That is different than proving something happens causally in humans.AND.Everyone agrees the intestinal flora do something as germ-free mice do tend to have a lot of strange abnormalities.But we still come to chicken and egg. Did the bacteria go bad first causing the IBS, or did the IBS (or what caused it) alter the bacteria.We also do not have IMO enough data on the range of "normal" vs the range of "IBSers" where colonic flora is enumerated. This paper still goes back to that 1982 paper (only the abstract available on line) and I do not know how different the differences are. REally would have been nice to see some stats in the abstract. Everyone refers back to it, but I don't know how different the differences are. Were all people with IBS lower than all people with IBS, or was as I suspect that while the averages were different there may be some overlap, especially given the wide range of what is reported as normal for colonic flora. K.K.


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## Kathleen M. (Nov 16, 1999)

And I'm not saying that bacteria can play no role in the whole thing, but that there must be some connection in the whole package to the nervous system given the obvious role it plays in the whole thing.Changing bacteria for some people may help (they interact with what goes on) But you also must remember that there is a lot of overlap between nervous system and immune system. The nervous system can set off the mast cells in the gut separately from any other immune respones. after all "...and hyperactiviy of the enteric nervous system that induces mast cell activation" From the role of mast cells in common gastrointestinal disease Siddiqui and Milner Curr Allergy Asth Rep 2004.It is unlikely IMO that any thing digestive happens in complete isolation from "the second brain" the enteric nervous system. It is just too big and too complex to not play some role in things digestive (hard to believe it can be 100% normal and there be functional disease just becasue a few bacteria are lower than usual in the colonic flora...which is what the difference in IBSers is as far as we know)


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## Kathleen M. (Nov 16, 1999)

Looking into leaky gut. Something is up with intestinal permeabiltiy in people with crohns and their relatives, but as a general problem that afflicts all not quite well people (which is what most people mean when they say leaky gut...a problem that causes all malaise in humans.....It tends to come off as just the latest version of hypoglycemic. There is always some problem that does occur in a few people in a few specific conditions that gets transformed into the answer of all human ills (esp when MD's tell you that you are just fine).K.


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## kel1059 (Feb 28, 2003)

based on some of the concomitant mental health issues that many of the IBS people have i would say that talissa's thinking and abstracts should not be so readily dismissed.overall, i still feel that IBS is a rather complicated problem and i am not 100% positive that it is all due to dysbiosis. although i do think that this is an excellent place to start.this was my hunch (dysbiosis) and i am better. the troubling part of all this is that i have come across a few anomalies during my recovery that have me scratching my head.one such anomaly is that oddball treatments like acupuncture and gi gong can help. talissa has also spoken of interest and participation in such types of treatments (she referred to polarity therapy and yoga a few times). therefore i don't think that she is stating that the ENTIRE problem is a result of the things that she has posted in this thread. --but i can't speak fo her.something that i would like to mention is that a person i know underwent 18 acupuncture treatments and that has cured her of arthritis. i find this to be extremely interesting.i also know of a medical professional who used acupuncture to get rid of her IBS but it took 9 months of treatment. she is one of the people who recommended that i try homeopathy the other was my MD.i have been wondering for a long time now if treatments that correct the body's communication and energy pathways might be able to slowly unfold the mess that is going on inside of the body such as dysbiosis or a motility problem (motility problem due to dysbiosis or some other means????).anyway, those are some of my thoughts.


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## bonniei (Jan 25, 2001)

> quote:Although patienst with IBS appear to have quantitative differences in the intestinal microbiota when compared to normal individuals it is still unclear whether a causal relationship exists, or whether the altered flora is a consequence of the gut dysfunction.


And the fact that the studies were done on mice.These are points I have been making all along.


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## Kathleen M. (Nov 16, 1999)

The differences in GI flora was done in humans in 1982. I'd like to see a newer study with better techniques (and I probably need to find the article just to make sure what the "differences" really look like)Found this for the "IBS is Leaky Gut" hypothesis.Use of surrogate markers of inflamtiaon and Rome criteria to diestinguis organic from nonorganic instinal disease (basically is it IBS or IBD with minimal invasive testing).They lookd at fecal calprotecin, small intestinal permeability (which is big in crohns) and Rome I criteria oh and blood tests for inflamation (ESR, CRP, blood count). Tibble et all Aug 2002 Gastroenterology.All patients were also tested invasively to get a solid diagnosis one way or the other.The non-invasive tests were all pretty good at distinguighin between IBSers and People with inflamatory bowel disease. So at least the general view (and it was not 100% I think IP if I am reading the stats right was more likely to miss organic problems and had relatively few false positives.Because of issues with each test doing a combined thing (calprotectin, permeability and criteria) was found to be a safe and noninvasive means to differentiate between organic (IBD) and non-organic (IBS) disease.So the leaky gut thing is not really IBS, in fact evidence of a leaky small intestine should be a red flag that you have crohns in the small intestine (assuming I read this right)







K.PS. AGAIN...manipulating the bacterial flora may help some people some of the time (and for those that it works for...great for you!!!!! congrats!!!! you are a lucky person that has a fairly simple way to control things!!!!) by mechanisms that are not well understood. Clinical trials of probiotics have a mixed history. That manipulating the bacterial flora may resolve some symptoms for some people does not in any way prove causation.K.


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## Talissa (Apr 10, 2004)

Hi guys,Want to clarify that I believe altered gut flora is the reason that some people get PI IBS, and others who don't get IBS can fight off the infections in 3-7 days with no repercussions.I certainly don't think that by balancing the flora, IBS will go away. I think its key to not getting PI IBS for some, as well as a STEP in getting back to normal.You still have the inflammation, and in some, permeability.My guess is that only the IBSr's with some degree of inc'd permeability have impaired absorption and/or assimilation of nutrients.But many MDs make blanket statements that IBS includes a malabsorption problem. They just aren't the experts on Medscape.My goal is now to bring down the inflammation, and hopefully heal the wall. I will work forever at keeping the flora balanced with probiotics._______________________Also--All the drugs for IBS are first tested on mice. They test on mice because mice have digestive systems similar to ours.It's also a great way to establish that when the intestinal microflora is altered, it affects motility, absorption & secretion, and permeability.Have a good weekend!


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## StillHoping (Sep 16, 2002)

Eric?







Isn't the UNC conducting a clinical trial looking at the effect of probiotics in the treatment of IBS,chronic diarrhea & functional bloating?I think a Dr. Y. Ringel was or is going to head up the study.Wait a minute.I found the UNC newsletter.It says on page 23 of the "Ask The Expert" colum that "Until such studies are performed the use of probiotics in the treatment of IBS should remain speculative & experimental".Now this is in the Winter 2003/2004 newsletter.Do you have any info as to whether they did do this experiment and it's outcome?Thanks.


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## bonniei (Jan 25, 2001)

> quote:But many MDs make blanket statements that IBS includes a malabsorption problem


These IBS'ers with a malabsorption problem are either those with SIBO which seems to be a small percentage , despite Pimental's studies(I already posted the critique) and those who have lactose or fructose malabsorption. With Lactose malabsorption the problem seens to be the deficiency of lactase, an enzyme required to digest lactose. and fructose malabsorption which has to do with the problem with the GLUT5 transporter. These have nothing to do with inflammation or increased permeability. Further lactose and fructose malabsorbers don't all develop painful symptoms. It seems to be only those who have IBS who develop pain and disconfort.


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## kel1059 (Feb 28, 2003)

in my case it is not so cut and dried. i am still not so sure what took place. i had taken bottle after bottle after bottle of probiotics ever since 1990. yet i received very little benefit other than some weight gain and the consequent slight improvement that that brought.the only thing i did with dr dahlman was take extremely high amounts of his human strain probiotics for an extended period of time. the miracle recovery for me happened shortly after taking a homeopathic sulphur remedy (it caused a week long discharge from me, and my food allergies radically reversed at that point.) i wish i did not have to report this because it makes me lose credibility but that is exactly what happened. like madelienne ennis, "the results compel me to suspend disbelief".i wonder if taking the antibacterial/fungal herbs for 9 months was able to eradicate something in my intestines that helped allow for the recovery. maybe the digestive enzymes that he recommends helped something change for the better.my CDSA showed no bifidus and no healthy e coli. i think that that is a big clue. why would someone ignore something as glaring as this? jhouston has an even worse problem she also has no or low acidophilus growth. ********i am baffled. i took 90 TRILLION (not billion but trillion) VSL#3 bacteria from june until january yet problems remained. could there be such a big difference between the metagenics human strain bacteria and the overpriced VSL that just runs out of the system? i wonder. maybe the human strain bacteria really can "TURN ON" genes like the article that eric posted.i think there is another explanation but maybe not.


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## Kathleen M. (Nov 16, 1999)

www.med.unc.edu/medicine/fgidc/studies.htm lises what they are doing currently...and I do not see it. But there is one that I need to post over on the pain/gas/bloating...they are working on making a better way for doctors to assess bloating and you don't need to go to the center, and we've got people here who might be good for that.Let my check on Ringel on the UNC website. Looking at his bio they do not mention the study (it maybe at the getting the money stage??? that would mean they aren't recruiting, etc yet).K.


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## StillHoping (Sep 16, 2002)

Let my check on Ringel on the UNC website. Looking at his bio they do not mention the study (it maybe at the getting the money stage??? that would mean they aren't recruiting, etc yet).I saw it mentioned in the Winter 2003/2004 newsletter.It said for details regarding this study please go to the Center website:www.med.unc.edu/medicine/fgidc/research_subjects.htm.You can also contact the study principal investigator Dr. Y.Ringel at:919-843-3195 or the research coordinator Ms.Alesia Alio at 919-843-4838.


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## Kathleen M. (Nov 16, 1999)

I was talking about generalized malabsoption (the small intestine isn't working) Which is different than specific carbohydrate issues (missing the lactase enzyme).If you are not absorbing tryptophan and all the other amino acids and vitamines involved in serotonin that is more of a "what I assume they mean by leaky gut" not absorbing nutrients at all sort of thing.Carbohydrate issues are JUST you over feed the bacteria in the colon sort of thing. They do not cause unusal weight loss, anemia, broken bones, losing your hair, pellegra, or scurvy or anything like that.They just make you gassy, and do not occur in all people with IBS.In fact in some cases it appears that carb malabsoption in a normal person may not cause symptoms, but IBSers because they do not handle gas so well are the only carb people with problems (the carb malabsorp didn't cause the IBS, but made things worse one IBS occured).K.


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## bonniei (Jan 25, 2001)

I don't know if the last post was directed at me kmottus. I know that both you and Talissa were talking about generalized malabsorption problem. But when Talissa said Drs talk about it I was pretty sure they were talking about carbo malabsorption.


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## bonniei (Jan 25, 2001)

In fact carb *malabsorption which has nothing to do with inflammation or increased permeabiity* areCarbohydrates that may be incompletely absorbed leading to gas and cause of malabsorptionFructose- Slow intestinal transport-fruit , veggies, wheat, HFCSLactose-Low lactase activityTrehalose-Low Trehalase activity - mushroomsRaffinose, Stachose- Absence of alpha-galactisodase activity- Raffinose is a complex sugar found in many cruciferous vegetables (cabbage, Brussels sprouts, broccoli, cauliflower) and in beans. Beans also contain stachyose, another form of sugar that is digested poorly.Resistant starch-nturally resistant to amylase- potatoes and bananas, or in processed foods and starches, grains, pulsesRetrograde starch(like refrigerated wheat products-pasta)-Crystallization-amylase resistanceFiber- Absence of beta-glucosidase activity


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## bonniei (Jan 25, 2001)

And another malabsorption problem for IBS'ers is of bile acid.


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## Talissa (Apr 10, 2004)

kel,At the Crohns.net site, I just found today that you can order the Great Smokies' Comprehensive Digestive Stool Analysis for only $225.And they ship int'l!!That's a pretty good price comparatively speaking. I'm friends with a local MD here & I think I'm going to go ahead & get tested if he doesn't mind sending it in for me.I feel so good & can eat everything again(last night I had buttered popcorn--3 months ago it caused much pain & D the next am), but I'm really curious if I have truly balanced my intestinal flora.I'm tired of guessing!If anyone else is interested, here's the link to buy a test kit(cost also covers analysis results & suggested products/anti's to correct any imbalances found.): http://www.crohns.net/Merchant2/merchant.m...ategory_Code=CP


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## Kathleen M. (Nov 16, 1999)

WHat happens to you if you do not get enough tryptophan (assuming you are somehow not absorbing it specifically).Besides you don't have enough serotonin???? which I am not so sure you could JUST miss that (and serotonin isn't just too little anyway but there I go talking to walls again).Generally damage to the small intestinal lining cannot be so specific that it knocks just one thing out and not the whole shebang (the bacteria in your colon make the small intestine lose a specific receptor??? just for tryptophan?? without causing pellagra??)Pellegra is both lack of niacin and tryptophan both are missing in corn.Pellegra used to be common in the US south, but with better nutrition (eating more than corn bread and greens every meal) it is rarely seen anymore).Cutaneous lesions usually bilaterally symetric (this is all from Merck).Mucous membrane problems (bright scarlet tongue and oral membranes)GI...diarrhea often becomes bloody. Buringin of the mouth , discomfort and distension.CNS. Organic psychosis (must not make joke about those arguing they do not absorb tryptophan...accckkk.strangling noise...thunk...)Now this is both niacin and tryptophan...do not know about if you just miss tryptophan...most of the diets that cause this cause both (and I suspect if you can't abosorb one becasue your villi are shot you can't absorb the other, either).I'm having problems finding just that that seems trustworthy.One that just focuses on what happens if you don't have enough serotonin, but I don't know how good "diagnose-me.com" is. BUt none of what they say it helps have any GI symptoms with them.(FWIW 95% of the serotonin in your body is found in the gut nerves, and you don't need to get that into the brain)Lets see if I can find anything that has to do with the poor college students they fed diets missing one of the amino acids to find out which are essential. It is old enough the paper probably is not online, but maybe someone talks about which sick people got with what.I know they fed them a diet missing one amino acide until they either got sick or it was long enough they weren't gonna...but all I find is stuff in animals.Oh well...try later


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## Kathleen M. (Nov 16, 1999)

I was assuming what you were quoting was to refute my most IBSers are typically normal and do not miss out on nutrinets...so I wanted to clarify anything I said that might have been misinterpreted.K.


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## Kathleen M. (Nov 16, 1999)

I've heard conflicting things about the GSL testing.In any case much of what they test for are not things you can buy to supplement with (so how much it will help beyond doing hit and miss probiotics till you find the right one, I dunno).Also I do not know how sample handleing will effect the results. If stool sits at room temperature for awhile if nothing else the relative amounts of some of the organisms will change...and I don't know about making sure you still measure your anaerobes properly....I did grad school with people that studied methanogens and I know some of them are very hard to get out of critters and grow on petri dishes.I've met people on the board with various levels of happiness with this particular test...so your mileage may vary.Just thought You would want to know.But some people do seem to have results they like from this sort of testing.K.


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## kel1059 (Feb 28, 2003)

"Generally damage to the small intestinal lining cannot be so specific that it knocks just one thing out and not the whole shebang (the bacteria in your colon make the small intestine lose a specific receptor??? just for tryptophan?? without causing pellagra??)Pellegra is both lack of niacin and tryptophan both are missing in corn."maybe that could explain some of the emotional problems that many IBSers experience such as nervousness, iritability, anger, impulse control.i think you hit on something.


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## Kathleen M. (Nov 16, 1999)

But they would also tend to be anemic, have inexplicable weight loss and all the other stuff that goes along with not being able to absorb nutrients correctly.I don't think you can damage a villi so that It ONLY avoids serotonin-necessary things without missing stuff like B-12 (anemia) iron (anemia), etc.The emotional issues are about the same for IBSers as for any other disorder where people are in pain much of the time.Pain does not generally bring out the best in people, no matter what hurts.K.


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## Talissa (Apr 10, 2004)

KM--Your imput on the cdsa is interesting. I'll keep those things in mind, & I appreciate it.Thanks!


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## kel1059 (Feb 28, 2003)

"But they would also tend to be anemic, have inexplicable weight loss and all the other stuff that goes along with not being able to absorb nutrients correctly."yep that was me. i had low iron (i hope it is better now), and weight loss. of course that proves nothing because there could be dozens of other explanations for those to occur.my pain went away a long time ago after removing dozens of foods yet the brain was still suffering.once again, i am still baffled. the acupuncture example still intrigues me. the Holosync meditation experience still intrigues me. http://www.mercola.com/article/neuro_technologies.htm as much as i believe in the dysbiosis model i also think that possibly something else is going on that needs to be corrected. "blips" in the energy matrix as proposed by Dr sheldrake intrigues me to no end.reversal of energy flow as supposedly demonstrated by applied kinesiologists intrigues me further.


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## kel1059 (Feb 28, 2003)

---"with people that studied methanogens and I know some of them are very hard to get out of critters and grow on petri dishes."yes, i understand that only about 60 to 70% of the bacteria is identifiable by GSDLabs. that has always bothered me. t., i think the info you get from them is good but it is also limited. it does not tell the true story.i am very happy with the results of my test. it showed no bifidus or healthy e coli growth. the no bifidus growth is consistant with what dr dahlman says and with what you have posted. my peristalsis is normal now. FINALLY! i wonder if it is due to human strain bifidus??:?could have human strain bifidus turned on some gene?i am going to continue to watch the progress of people like arnie, jhouston, daisy, etc


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## Talissa (Apr 10, 2004)

Want to add in here--my first year with IBS I lost alot of weight and had muscle-wasting.It was awful. I was as skinny as Calista Flockhart(Ally McBeal), but without her healthy glow.When someone is too skinny, people have NO problem just coming out & saying--you look awful, you need to eat more. Like I had a choice. I ate, & it was killing me.I was also hyper-sensitive then & over-reactive, so the comments were very hurtful. Back then, my IBS was a secret. It was really hard.One thing after getting IBS & recovering(mostly), I'm much less judgemental of other people. You never know what's going on in their lives that may be affecting their behavior.


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## meribaibs (Jan 18, 2004)

I had my first consultation with Dr. Dalhman today. If anyone is interested, I can post my progress as well.


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## Talissa (Apr 10, 2004)

Meri--That would actually be great!! His program is very comprehensive & it also is centered around balanced flora & healing the intestinal wall, so it fits in here wellThanks alot, & we'll look forward to hearing about your slow but sure progress!T-


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## calid (Aug 4, 2003)

Meri: Great!!! The more the merrier! Please post on this thread though so we can keep it all together: Dr. Dahlman's Patient Thread


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## SpAsMaN* (May 11, 2002)

Lets party ladies!!!







I was just pushing testosterone in this thread







Oh .Kel.,do you think I should take your sulfur remedies?How long it take to feel something?It's a long shot but you are damn cured!


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## bonniei (Jan 25, 2001)

Weight loss can occur if you have fructose malabsorption and your major diet is foods containing fructose. I used to look like a ghost when I was loading up on 4-5 Seven-ups a day


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## meribaibs (Jan 18, 2004)

We'll see how it goes. I'm feeling confident.


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## SpAsMaN* (May 11, 2002)

Hi Meriba,I hope this feeling will be enough.IBS is so nasty. The few people that i know who have been cured,have passed a bad time before their "recovery".


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## meribaibs (Jan 18, 2004)

Thanks, Spasman, but it will take more than confidence to cure my gut, and I can't stomach placebos. I promise I will tell it like it is. Est-ce qu'on est d'accord?


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## bonniei (Jan 25, 2001)

Here is a study on nutrient absorption in diarrhea http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12311585 1: Glimpse. 1982 Jan;4(1):2-4. Related Articles, Links Utilization of nutrients during and after diarrhoea.[No authors listed]PIP: Review of studies examining the interaction between malnutrition and diarrheal infection with reference to several factors: appetite recovery after diarrhea, comparison of nutrient absorption by etiology, and feeding program during diarrhea. Diarrhea has been found to have the greatest impact on food intake in children--a 40% reduction compared to normal children. On the question of absorption efficiency of ingested food, it was suggested that transit time through the gut was not by itself a reliable indicator of malabsorption. Transient depression of enzymatic activity (with the exception of lactase) as a result of diarrheal infection was not found to greatly affect digestion. Rather, it was found that illness was of shorter duration in fed as compared to nonfed children. Food intake reduction was found to vary according to etiology, as did absorption of nutrients during both the acute and recovery stages. In general carbohydrate absorption was least affected during the acute stage and across all conditions. In diarrhea due to ETEC(enterotoxigenic Escherichia coli ), absorption of all nutrients was better in the acute stage; however, there was a marked increase in absorption between recovery stage 1 and recovery stage 2 (2 and 8 weeks after recovery, respectively). During the acute stage fat and caloric absorption was significantly less in rotavirus and shigella patients as compared to those suffering from ETEC. Rotavirus infection resulted in a longer period of malabsorption. In shigella, improvements in absorption of all nutrients improved considerably by recovery stage 1. It was concluded that feeding of children is to be encouraged because *substantial absorption takes place even during the acute stages of diarrhea. *PMID: 12311585 [PubMed - indexed for MEDLINE]


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## SpAsMaN* (May 11, 2002)

Bon anglais,bon francais,je suis impressionï¿½!Apparement Mtl n'est pas assez gros pour une guï¿½rison.C'est inadmissible!!!Connait-tu Dr. Pierre Poitras de l'hopital St-Luc?Il a ï¿½crit un article dans "le coeur au ventre"pour l'association des maladies gastrointestinales fonctionnelles.Il a ï¿½crit







es chercheurs ont trouvï¿½ des cellules particulieres inflammatoires en grande qtï¿½ comparï¿½ aux sujets "normaux".Non visible par les tests habituels.Je voudrais plus d'infos mais l'association n'ont pas acces aux recherches.Je pourrais dire nimporte quoi et les autre ni verrais que du feu.


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## bonniei (Jan 25, 2001)

J Am Diet Assoc. 1985 Dec;85(12):1591-9. Related Articles, Links This study suggests that the diet of people with IBS is poor not their absorption capacityNutritional status of gastroenterology outpatients: comparison of inflammatory bowel disease with functional disorders.Gee MI, Grace MG, Wensel RH, Sherbaniuk RW, Thomson AB.Dietary intakes of two groups of gastrointestinal patients, one group with inflammatory bowel disease (IBD)--Crohn's disease or chronic ulcerative colitis--and the other with functional disorders (FD)--irritable bowel syndrome, nonulcer dyspepsia, or gastroesophageal reflux disease, were assessed by means of 48-hour recalls. The relationships between dietary intake and anthropometric and biochemical measurements were examined. The IBD group had lower mean serum albumin and hemoglobin levels (p less than .05); however, FD patients had less adequate diets. The mean energy intake of women with FD was significantly lower than that of women with IBD (p less than .05) and was associated with inadequate or marginal intakes of many nutrients. Comparison of nutrient intakes between the IBD and FD groups revealed a significantly lower mean intake of folate, ascorbic acid, and vitamin A for women with FD than for women with IBD (p less than .05). In general, women had poorer diets and a higher prevalence of abnormal biochemical parameters than men. One notable feature of the dietary pattern of the women was that they consumed less meat than the general population consumed. Increasing meat consumption would improve the intake of many nutrients, including protein and iron. The results of this study suggest that more attention should be given to the adequacy of dietary intakes of gastrointestinal patients in general and of women in particular.PMID: 4067154 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.f...st_uids=4067154


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## meribaibs (Jan 18, 2004)

Spasman,L'ï¿½tude semble ï¿½tre la base du protocole utilisï¿½ par D. Dahlman. C'est sans preuve, mais je n'ai rien ï¿½ perdre que de l'argent. Au moins, j'aurais essayï¿½ quelque chose au-delï¿½ de la norme. Oui, on pourrais se dire n'importe quoi, mï¿½me lancer des insultes aux 'experts' sans objections! Voulez-vous des frites avec ï¿½a?


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## meribaibs (Jan 18, 2004)

Spas,Ton anglais est assez bon pour te faire comprendre et apprï¿½cier. C'est dï¿½jï¿½ trï¿½s beau. Moi, j'ai le vocabulaire d'un enfant de 11 ans. ï¿½a parrait quand j'ï¿½cris plus que deux phrases. Mais c'est pas grave---surtout pas ici!


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## eric (Jul 8, 1999)

God I hestitate to even post this, but regardless IBS is not leaky gut! "Leaky Gut (Increased Intestinal Permeability)Leaky gut is a disorder associated with an excessive increase in intestinal permeability. The greater-than-normal increase in intestinal permeability results in allowing partially digested foods, chemical toxins, and harmful organisms (bacteria, fungi and viruses) to permeate though the gaps in the lining of the intestinal barrier and enter the blood stream. This is believed to contribute to a growing number of health problems, probably through immune system activation. Leaky gut is believed to be a factor in causing some types of chronic inflammatory arthritis and certain skin conditions such as acne, psoriasis, and eczema. Chronic fatigue syndrome, fibromyalgia and food intolerance conditions may also looked upon as related to the leaky gut phenomena.By itself, leaky gut is a functional disorder, meaning that it is not a disease but an aberration of the gut barrier's normal function. Leaky gut is known to be caused by chronic alcohol intake and NSAID overuse, but also occurs from inflammatory and infectious bowel diseases such as Crohn's disease, ulcerative colitis, irritable bowel syndrome and dysentery.The notion of a leaky gut (correctly termed as increased intestinal permeability or intestinal hyper-permeability) is not new to the health sciences and has fallen in and out of favor during the past century as a credible health concern. However, recent breakthroughs in our understanding of the human immune system and the discovery of the gutï¿½s central role in the immune system appear to have paved the way for acceptance of leaky gut as an important clinical condition. Presently, leaky gut is thought to play a primary role in the evolution of certain diseases as well as causing existing diseases to become worse.How Common Is Leaky Gut?Virtually everyone will experience symptoms of leaky gut during his or her lifetime. Usually, the symptoms are short-lived and do not leave lasting effects.Unless the patient is specifically tested for intestinal permeability, leaky gut often goes unrecognized. Currently, estimates vary about how many people suffer health issues from leaky gut, ranging from less than 10 percent to more than 50 percent of males and females of all ages in the United States.As yet, there is no proven genetic basis for leaky gut. Leaky gut appears to be associated with low quality, highly processed foods heavy in food additives, drug usage and exposure to chemicals in the food chain.What Causes Leaky Gut?Leaky gut usually follows exposure to substances that damage the integrity of the protective intestinal mucosa. A number of factors may cause leaky gut, including: Some prescribed drugs Stressful lifestyle Overuse of antibiotics Overuse of NSAIDS (aspirin, ibuprofen, Tylenol) Overuse of stomach antacids A diet high in processed foods and refined sugars Frequent consumption of alcohol Exposure to environmental chemicals and toxins Intestinal infections How to Deal with Leaky Gut?Compelling research suggests that leaky gut arises in reaction to poor lifestyle habits. This is most relevant to those people who would rather take a pill, potion, or poultice instead of taking the time and effort to correct and improve their lifestyle habits. Simply put, using glutamine supplements, vitamin A and antioxidants to repair the harm caused by a meal consisting of beer, chips and preservative-laden hot dogs is not going to work.The time-tested three pillars of lifestyle improvement appear to be the best medicine at this time. These three pillars are eat healthy foods, stay fit and learn how to appropriately handle stress. In addition, one should:Limit alcohol intake Do not overuse NSAIDs and antacids Take dietary glutamine supplements as it appears to be vital for the normal intestinal wall maintenance Consume more fresh foods Avoid chemical or additive-laden foods and drinks Consult with a dietitian or licensed health care provider for further advice on managing leaky gut REFERENCESand GDSL has a test for it.







http://www.gsdl.com/assessments/ip/ and the test Kmottus posted is new and seems accurate.They also have this on there site.The Fight or Flight in Irritable Bowel SyndromeOveractivation Linked To Predominance of Diarrhea SymptomsAn intense, powerful "fight-or-flight" response comes in handy when you're running away from a hungry tiger, but it could be the source of misery for people with certain digestive disorders. The chronic gastrointestinal distress of Irritable Bowel Syndrome (IBS) has been linked to "miscommunication" between the gut and the brain. Although it's still unclear just exactly how a glitch in gut-brain interaction sparks specific symptoms, a recent study has uncovered one important potential mechanism in a subgroup of patients.In patients with IBS who regularly experience diarrhea, pain, and other symptoms soon after eating, an "overdominant" sympathetic nervous system - signaled in part by the heightened release of the stress hormone cortisol after eating - may play a key role in triggering their symptoms. Researchers evaluated a group of 24 patients with IBS and a group of healthy controls, measuring their salivary cortisol levels, their heart rates, and their heart rate variabilities at different times of the day. Compared to the controls and to IBS patients with constipation, IBS patients with chronic food-induced diarrhea "demonstrated a significant increase in cortisol" soon after eating - with levels nearly doubling. This subset of patients also showed a more dominant sympathetic nervous system response, as evidenced by their heart rate variability ratios.The sympathetic nervous system tends to mobilize the body's stimulatory "fight-or-flight" response. Normally it's kept in check by the dampening effects of the parasympathetic nervous system. In patients with IBS with diarrhea, however, this muting response (mediated by the vagus nerve) appears weaker - a condition called "vagal withdrawal." "Notably, this vagal withdrawal was significantly associated with patients' reports of gastrointestinal symptoms," the researchers pointed out. These included bloating, abdominal pain, indigestion, and heartburn.A heightened, stimulatory stress response, characterized by overactivation of both the HPA-axis and sympathetic nervous system, may be triggered by "abnormal ascending feedback from the gut," the researchers speculated. http://www.gsdl.com/news/connections/vol12/conn20010530.html This is something I keep saying here, the hpa axis is connected to cortisol, the fight or flight and to fighting infection, and to serotonin. There is no overt colon inflammation in IBS it is specific cells, mast cells for one which are very important in IBS and very important to the above info and more and more emerging evidence on their roles is emerging fast in IBS research.Which was was Tal, posted here but has not understood it yet."data from animal studies demonstrated that altered gut physiology can persist even after the infection and associated *inflammation have resolved.* Furthermore, studies of mucosal biopsies, from both human and animal models, have shown increased inflammatory cells and inflammatory mediators in patients with IBS."This is not the whole colon is inflammed, IBS is not inflammatory bowel disease, it is very specific cells conneted to fighting the intial infection in PI IBSers and they believe after the inflammation is resloved it can be reactivated from chronic stressors and stress mediators which are involved in fighting infection. But the point is the intial infection/inflammation is GONE!There is no visible inflammation in the colon of IBSers, it is not until they peel back the layers of the colon they notice cell abnormalities and specifc inflammed cells that can be seen with a microscope in some IBSers.It is not miscroscopic colitus either, which is another inflammtory bowel disease. And as a side note gastroenterologists and neurogastroenterologists study ALL these conditions and what they learn from one they can apply to others.the current theories on IBS can help to explain pain. Leaky gut cannot explain pain in IBSers.which is what I was posting here." An increase in inflammatory mediators alone is insufficient to explain the pathogenesis of IBS. From post-infective IBS, we know that the most people who have gastroenteritis and accompanying inflammation do not develop IBS. As discussed earlier, several factors may be important in interacting with the gut insult and in predicting those who develop symptoms - one interesting factor here is the role of stress. Psychological stress is known to affect gut function in normal healthy humans, and in people with IBS stress may trigger or exacerbate symptoms. More recently there is evidence of a link between stress and inflammatory responses. Exposure to stress in both animals and humans has been shown to result in the release of mast cell mediators in the colon (18,19) and in a recent study stress was capable reactivating previous inflammation in rats (15). An important challenge for future work will be to clarify the interaction between inflammation, stress and IBS symptoms." http://www.med.unc.edu/wrkunits/2depts/med...rymediators.htm ROMEIrritable Bowel Syndrome: How far do you go in the Workup?"For example, there is a subgroup of patients, called "post-infectious IBS" who appear to respond to an enteric infection such as campylobactor jejuni with an increased inflammatory cell response (22). This is associated with activating enterochromaffin cells to produce 5HT, and CD3 cells to produce cytokines, which in turn leads to enhanced motility and lowered visceral sensation thresholds " "But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it. All patients with active celiac disease have microscopic inflammation, but a large proportion do not have abdominal pain, and patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds (24). In individuals with these disorders, there may be central nervous system counter-regulatory measures responding to the peripheral pain/inflammatory processes that increase pain thresholds. With regard to IBS, the gut-related effects of microscopic inflammation may be only one component of a dysfunctional brain-gut system. In addition, and often in response to stress, there may be a failure to activate descending pain inhibitory systems that enable the clinical experience of pain and other symptoms that typify this disorder (25). In one prospective study of post-infectious IBS, it was found that those who retained their symptoms 3-months after an enteric infection had not only increased mucosal cellularity, but also had increased psychosocial distress at the time of the infection. Furthermore, lowered visceral sensation thresholds and increased motility were present after the infection regardless of whether or not the patients retained their symptoms (26). Therefore, the microscopic inflammation and its physiological effects on motility and sensation contribute to, but are not always sufficient for the clinical expression of IBS pain. At least for post-infectious IBS this provides some evidence that psychological distress alters brain pain regulatory pathways to amplify incoming visceral signals leading to the full clinical expression of this syndrome" http://www.romecriteria.org/reading1.html Inflammatory Mediators in Irritable Bowel Syndrome"Mast Cells and IBS The mast cell has potential to be a key player in IBS. Although mast cells are most widely known for their role in allergic responses, these cells are normally present throughout the gut and are involved in a range of physiological and pathological activities including mucosal defense mechanisms and inflammation. Mast cells may release an array of inflammatory mediators that act on smooth muscle, nerves and immune cells, which may ultimately result in gastrointestinal dysfunction and symptoms. In addition, mast cells in the gut are located close to nerves providing a structural basis for communication between the gut and the nervous system. In 1993, Weston and colleagues reported increased mast cell numbers in the mucosa of IBS patients(10) - these changes were identified in tissue from the end of the small bowel (terminal ileum). Similarly we identified significant increases in mast cells in IBS patients compared to controls in the colon (specifically at the caecum) (11). There were also trends for increases in other regions of the colon (ascending and descending colon) but no differences could be seen at the rectum. The lack of changes in mast cell infiltration in the rectum has since been confirmed by others (9). Collectively these studies suggest that mast cells were increased in IBS patients - this may be part of a low-grade inflammatory response, although the components and nature of this response remain poorly understood. " http://www.med.unc.edu/wrkunits/2depts/med...rymediators.htm GastroenterologySeptember 2003 ï¿½ Volume 125 ï¿½ Number 3 Basic-alimentary tractStress-induced disruption of colonic epithelial barrier: Role of interferon- and myosin light chain kinase in mice http://www2.us.elsevierhealth.com/scripts/...16508503010576& Report on the 4th International Symposium on Functional Gastrointestinal DisordersMarch 30th - April 2nd, 2001 Milwaukee, Wisconsin"Mary Perdue from McMaster University, Ontario discussed the importance of the epithelial intestinal barrier to maintain immune tolerance to potentially harmful matter, such as bacteria, ingested when we eat or drink. (Everything that enters the human body must pass through an epithelial layer. Various types of epithelial tissues line not only the body cavities, blood vessels, and most organs, but also our outer surface-our skin. Within the intestines, epithelial tissue forms an intestinal barrier involved with absorption, secretion, sensation, contractility, and protection.) Studies in animal models show that psychological stress can disrupt this barrier, leading to the penetration of bacteria into the gut, inflammation, an immune system response (inflammatory cytokines), and ultimately sensitization of neural signals from the gut to the brain that can heighten the perception of pain." http://www.iffgd.org/symposium2001.html "From - Report on the 5th International Symposium onFunctional Gastrointestinal DisordersApril 4, 2003 to April 7, 2003 Milwaukee, Wisconsin By: Douglas A. Drossman, M.D., UNC Center for Functional GI and Motility Disorders at Chapel Hill, and William F. Norton, IFFGDBasic Principles -- Brain-Gut Moderators: Emeran Mayer MD; Robin Spiller MD. Panel: Robin Spiller MD; Jackie Wood PhD; George Chrousos MD; Yvette Tachï¿½ PhD; Lisa Goehler PhD; G.F. Gebhart PhD; Emeran Mayer MD. " There are immune responses to infections. To defend itself from a foreign substance or invader, such as a bacterium or virus, the body mounts an immune response controlled by the brain. There needs to be a balance between infection and the body's immune response; the immune system needs to turn on and turn off at the right times to destroy the invader but not to the degree that it may harm healthy tissue." " One of the more exciting areas of recent research relates to the basic and translational aspects of the effects of stress on inflammation, cytokine and immune modulation, and pain. (Cytokines are a type of protein released by cells of the immune system, which act through specific cell receptors to regulate immune responses.) This series of presentations address three important research areas in the field of functional GI disorders, which have recently attracted considerable attention: the role of immune activation in the gut and the interactions of the gut immune and nervous systems; the role of the central nervous system in the regulation (modulation) of pain perception (nociception); and the emerging field of animal models with relevance for functional GI disorder research. This section demonstrates the rapid progress seen in the last few years in better understanding of basic mechanisms, in particular the neuroimmune interactions underlying symptom generation in patients with "functional" GI disorders. " http://www.iffgd.org/symposium2003brain-gut.html "Robin Spiller, University Hospital, Nottingham, England began the session by noting the difficulty in separating disorders of structure ("organic") from disorders of function. He noted, "The difference is based on how high the power of your microscope is." This was elaborated upon in his presentation on Post-infectious Functional GI Disorders. It has been observed that IBS-like symptoms, that persist for 6 months to a year or longer, may appear after a bout with an acute infection in the gastrointestinal tract (e.g., food-poisoning). This is termed, "post-infectious IBS." A study by Gwee et al showed that the presence of unusual or amplified life stress at the time of onset of infection increased the chances of developing IBS symptoms. Inflammation persisted in patients with IBS-like symptoms but did not in patients whose symptoms resolved. This suggests that the brain's management of certain stressful stimuli (i.e., psychologic distress) affects the brain-gut system's ability to inhibit inflammation. It has frequently been observed that some individuals with more severe symptoms of IBS have coexisting psychologic distress. Stress has been thought to influence health-care seeking behavior, either by increasing motility, visceral hypersensitivity or inflammation, or by enhancing one's perception of gut symptoms, all of which lead to a greater need to seek care for them. The concept of post-infectious IBS suggests that in some circumstances stress (the biological process by which the body adapts in response to a stimuli) may influence symptoms. An initial response to an infection in the gastrointestinal tract can involve the neurotransmitter, serotonin, which acts as a messenger (mediator) to cells involved with the immune response. Immune cells -- mostly in the blood, but also in the lymphatic system -- enter the infected area and remove the invader. Additionally, the body adaptively removes the infection (e.g., via vomiting or diarrhea -- normal beneficial responses that help the body expel an infecting organism). Persistence of the underlying inflammatory response may lead to post-infectious disorders of function. A variety of neuroimmune responses can lead to intestinal over-responsiveness (sensitization) and other clinical effects. These responses include direct toxicity to nerves that influence intestinal contractions, alteration in gut immune activation, abnormalities of serotonin metabolism, and persisting low-grade inflammation. IBS developing after infective gastroenteritis is associated with subtle increases in enteroendocrine and chronic inflammatory cells in the gut mucosa. The net effect may be to increase serotonin availability in the gut and enhance secretion and propulsive motility patterns. Serotonin antagonists may be beneficial in such patients http://www.iffgd.org/symposium2003brain-gut.html


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## I'll B Snookered (Apr 9, 2004)

Hey, Meribaibs and Spasman,No parlais francais on this or any other thread, or I will personally report these vile posts. Comprende.


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## Jhouston (Nov 9, 2003)

Tal and Kel, I looked at the site Tal posted re: GSDL stool tests. The sample test showed more than what I had on my tests. Didn't see an Microbiology Only test from GSDL. wondering if I had a short version? Kel, you are right about my test I had no growth for Lactobacillus or good E coli and 1+ for Bifid. Joann


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## Talissa (Apr 10, 2004)

Er,God I hate to say this but NO ONE IS SAYING IBS IS LEAKY GUT!!!!!Learn to read better.


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## Talissa (Apr 10, 2004)

INCREASED INTESTINAL PERMEABILITY IS ONLY IN A SUBSET OF IBS PATIENTS.___________________________SOME WITH IBS JUST HAVE SLIGHTY HIGHER INFLAMMATION WITH NO INC'D PERMEABILITY.___________________________THE LUCKY ONES HAVE THE NORMAL AMOUNT OF INFLAMMATION ALONG THE WALL & NO INC'D PERMEABILITY. (ie, after gallbladder removal)(they're probably the ones that take one or two supplements & go skipping happily away, all better now)


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## kel1059 (Feb 28, 2003)

> quote: God I hestitate to even post this, but regardless IBS is not leaky gut! "Leaky Gut (Increased Intestinal Permeability)Leaky gut is a disorder associated with an excessive increase in intestinal permeability. The greater-than-normal increase in intestinal permeability results in allowing partially digested foods, chemical toxins, and harmful organisms (bacteria, fungi and viruses) to permeate though the gaps in the lining of the intestinal barrier and enter the blood stream. This is believed to contribute to a growing number of health problems, probably through immune system activation.


gee eric i think i finally get it now -- "IBS is NOT leaky gut!" wow, thanks for clearing that up.imagine, all these years that i have been making an incorrect claim -- amazing!***********************************no wait --- as i now recall, i don't ever remember saying that it was.i do remember making a single isolated post about it one time. but i never claimed that it was IBS.


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## kel1059 (Feb 28, 2003)

quote eric:


> quote: God I hestitate to even post this, but regardless IBS is not leaky gut!


why would you "hate" to post information that could be a value to many people?does it interfere with your single-minded pursuit of "IBS is a brain-gut disorder and it can best be treated by buying hypnosis tapes" ?there are plenty of people here who have IBS and also suffer from very strange reactions after consuming certain foods.why would you want to prevent them from seeing relevant information?does this newly accepted information interfere with your once harebrained idea that these strange food reactions are due to the subconcious memory of past bad experiences when consuming the offending food?yes daisy and jhouston -- according to eric's FORMER thinking your strange food reactions (brain fog, dizziness, fatigue) are due to unconscious memories.anyway, it is good to see eric finally make the transition to correct information (no matter how much he HATES to post it).


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## Talissa (Apr 10, 2004)

Back to malabsorption..."Malabsorption can result from three major abnormalities in small intestinal function:_Firstly_, food may not be broken down into small enough molecules to be absorbed through the intestinal wall. _A second form_ occurs when there is a problem with the lining of the intestine that results in an inability to absorb nutrients into the cells of the intestine. (like with submucosa inflammation)_The third form_ occurs when food breakdown and absorption are normal, but there is a problem with transporting the absorbed nutrients into the appropriate circulatory systems. "----------------Re: bile salts, you guys probably already know this, but when I tried Caltrate with meals, it made things worse.Now I understand why. People w/ no gallbladder have too much bile salt in their intestines & even with normal absorption, they can't soak enough back up.For others of us with D, the problem is a bile salt insufficiency, to begin with--"Bile acid deficiency can result from: --bacterial overgrowth. When there are lots of bacteria in the small intestine, the bile acids are broken down (deconjugated), and cannot function to help fat absorption. " http://www.muschealth.com/ddc/organ/smalb.htm ____________________Another site that supports this view is:"Inadequate Bile Salt ConcentrationAnything that significantly decreases the intraluminal concentration of bile salts can result in fat malabsorption. This in part explains why children with liver disease often have diarrhea and growth failure. Inadequate luminal concentration of bile salts can also result from excessive losses in the stool. _This can occur in chronic Giardial infestations, bacterial contamination of the small intestine from a variety of causes_ , or terminal ileal resection or dysfunction such as occurs with inflammatory bowel disease." http://www.people.virginia.edu/~smb4v/case...se8/answer8.htm _______________This explains why some of us have trouble digesting fats when we have small bowel bacterial overgrowth!(this is like putting together a puzzle)


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## flux (Dec 13, 1998)

> quote:Back to malabsorption...


This, of course, has no relevance to IBS.


> quote:For others of us with D, the problem is a bile salt insufficiency


No, it is for others who have this, but *not* IBS.


> quote:This explains why some of us have trouble digesting fats when we have small bowel bacterial overgrowth!


But everybody here digests fats just fine.


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## Talissa (Apr 10, 2004)

"Irritable Bowel Tied to Fat and Fructose" http://www.healthfinder.gov/news/newsstory.asp?docID=515488 "IBS patients should avoid excess dietary fats and fried foods" http://www.positivehealth.com/permit/Artic...ealth/bowel.htm _______________________"Because digestion entails proper functioning of various systems, there are numerous conditions and diseases that can interfere with digestive health. According to the National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK), an arm of the National Institutes of Health (NIH), there are more than 60 digestive disorders -- ulcers, constipation and irritable bowel syndrome (IBS), to name a few."..."Lactobacillus acidophilus (L. acidophilus) is one of the most prominent strains of beneficial bacteria, a deficiency of which can result in the growth and proliferation of pathological organisms in the intestinal tract. *This can decrease digestion and absorption of nutrients, as well as increase production of gas, bloating and toxins.* The most common cause of L. acidophilus deficiency is the use of antibiotic drugs, although prescription drugs, stress, diarrhea and intestinal infections can also be factors." http://www.endonurse.com/articles/361feat3.html ________________We know:a. IBSr's are found to have imbalanced gut florab. Some with IBS have submucosa inflammation along the brush border of the intestinal wall.(Oh, we also know that the "syndrome" sucks)


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## eric (Jul 8, 1999)

Kel"why would you "hate" to post information that could be a value to many people?"Because it is misleading to IBSers and is not IBS and could cause them even more anxiety and worry, and no ones doctor has diagnosed them with this as IBS, at least not any right minded one another thing you don't understand.For one there in no inflammation in IBS except for what is stated from the experts and not understood by you or Tal."why would you want to prevent them from seeing relevant information?"relevant information is one thing, completely making it up as you go is another on this thread and relavant would be understanding intestinal permeability in the first place in the context of IBS. No overt inflammation in IBS and no digestion differences in normal as opposed to controls in IBS."does it interfere with your single-minded pursuit of "IBS is a brain-gut disorder and it can best be treated by buying hypnosis tapes" ?"extremely cheap shot as usaual and expected from you and your attitude. There are many treatments for IBS, it just so happens HT is one of highest staitistical success rates in research. But you wouldn't know that since you don't actually pay any attension to IBS research what so ever. Because you have tunnel vision to bacteria and leaky gut.Even leaky gut is a brain gut disorder, but you don't eeven understand that, because you have tunnel vision and it is the not my single minded pursuit, like yours on dysbosis, that IBS points increasingly more to brain gut dysregulation. But you ignore all facts, so its pointless with you.And yes the tapes have helped hundreds and hundreds of people with IBS and they would even help intestinal permeability since it can be caused by stress. At least the end of that article implied why the treatments suggested would help even IBSers."there are plenty of people here who have IBS and also suffer from very strange reactions after consuming certain foods."Yes and a lot of them don't know why in IBS. and you do not help explain it, an altered gastro colonic responce and a lot of eveidence oof receptor problems in the gut, controlling gut function. They may also have other comorbid issues. "does this newly accepted information interfere with your once harebrained idea that these strange food reactions are due to the subconcious memory of past bad experiences when consuming the offending food?"It is not newly accepted information, its actually very old information.""food reactions are due to the subconcious memory of past bad experiences when consuming the offending food?"although foods can be triggers for a lot of reasons, the above is a fact and it can happen. The brain stores all memories and if a food caused a bad reaction in the past the brain can remember it and launch and attack. But you wouldn't know that since you don't actually study any of that kind of information. Its all about leaky gut and a totol focus on luminal factors and almost nothing else."yes daisy and jhouston -- according to eric's FORMER thinking your strange food reactions (brain fog, dizziness, fatigue) are due to unconscious memories."Totally false and how Kel makes things up as she goes constantly. Are you really this slow on everything kel!Stress, neurotransmitters, hpa axis functioning (imuune), sleep abnormalities, and other reasons come together to cause those issues. There is much much more to the world of IBS then leaky gut, kel always leaves out. *Tal, name the functional disorders, what oher ones are there other then IBS?*


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## Talissa (Apr 10, 2004)

Eric, at the end of the day, when all of the information that we're learning presently (through amazing research) comes in, it is my firm belief that what PI IBS patients have is an organic disease that is treatable. Not a "functional disorder." But I can add 2 + 2 and don't need to wait on Medscape to tell me this.People are getting better, and not by shrugging their shoulders and saying well, it's a f*g functional disorder, nothing I can do but take drugs and hypnotize myself.___________My sources are good.The facts add up.You just need a brain that works to connect the dots.


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## eric (Jul 8, 1999)

You don't understand PI IBS yet, I think I have told you this about a hundreds times now.HT is one of the most effective treatments for IBS and recommend by the experts. Its a safe and natrual treatment, are you opposed to safe and natural treatments for IBS.Do you know HT is just a heightened state of focus. people get better for all kinds of reasons, some alternative treatments can help IBS and some standard medical care can help IBS."My sources are good.some of them yes, but you don't understand them and are also making things up as you go and also cherry picking only the information you want to believe and present and that is not being put into perspective of the big picture or the whole disorder, because you have tunnel vision on it all, not the rest of most of the articles your posting. IT does not add up, as you say.I have been studying the big picture of IBS longer then you have had it. There is so much you don't understand post about its quite a problem.I really hope you think you know what your doing, because you could be casuing a lot more worry and anxiety and doubt in people on inflammation and infection, without knowing what your doing, which could actually make people worse or seek the wrong treatments for IBS.I here from Kel, all the time get to the root cause, well leaky gut is not a root cause for one!!!!Tal, I will ask again, what are the other GI functional disorders, before we proceed any further can you name them?


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## Talissa (Apr 10, 2004)

Eric,You are an idiot.A fool who doesn't listen when the truth is staring him right in the face.You name 16 stains of probiotics in the body, and their functions.Then I'll answer your question.


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## Talissa (Apr 10, 2004)

What was I thinking? Medscape is already in the know:MEDSCAPE 2002" *The growing interest and the emerging evidence supporting the role of infection and inflammation in the pathogenesis of at least a subset of IBS patients * was also manifest in some key studies presented in the American Gastroenterological Association Research Forum on the "Medical Treatment of Functional GI Disorders."As discussed below, these studies explored possible new approaches in the treatment of IBS, *while focusing on modulating and reversing infections and/or inflammation. * http://www.medscape.com/viewarticle/434527 The experts at Medscape know this, with all of the reading you do there, why don't you know???Why don't you know? Pathogenesis of IBS=pathogen origin of IBS


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## Talissa (Apr 10, 2004)

Looks like Dr. Dahlman's on the cutting edge of treatment by reversing infection and/or inflammation.It's also what I've been doing.Seriously,Is this getting through to you?At all? Anything?_________________________Are you saying Medscape is WRONG????


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## Talissa (Apr 10, 2004)

Recap of some of the Medscape info relative to this threadï¿½s topic:ï¿½Based on recent reports of low-grade mucosal inflammation in subpopulations of patients meeting current diagnostic criteria for irritable bowel syndrome, therapeutic approaches shown to be effective in inflammatory bowel disease, such as probiotics, antibiotics, and antiinflammatory agents, have been suggested as possible therapies for certain patients with irritable bowel syndrome.ï¿½ http://www.medscape.com/viewarticle/457728_1 ï¿½The growing interest and the emerging evidence supporting the role of infection and inflammation in the pathogenesis of at least a subset of IBS patients was also manifest in some key studies presented in the American Gastroenterological Association Research Forum on the "Medical Treatment of Functional GI Disorders." As discussed below, these studies explored possible new approaches in the treatment of IBS, while focusing on modulating and reversing infections and/or inflammation. ï¿½ http://www.medscape.com/viewarticle/434527 ï¿½The results of studies that have thus far been conducted with probiotics are encouraging.ï¿½ http://www.medscape.com/viewarticle/434527 ï¿½Investigators have found that there are colonic mucosal abnormalities in PI-IBS.ï¿½ http://www.medscape.com/viewarticle/463521_3 ï¿½For both syndromes(IBS & IBD), histologic and functional alterations of the mucosal barrier have been recently reported.[11*, 12, 24, 25] ï¿½ Interestingly, gut permeability assessed by the lactulose/mannitol ratio is significantly elevated in PI-IBS patients.[15] ï¿½ http://www.medscape.com/viewarticle/457728_4 ï¿½Probiotics Significantly Reduce Symptoms of IBS, Ulcerative Colitisï¿½ http://www.medscape.com/viewarticle/455964?src=search


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## kel1059 (Feb 28, 2003)

quote eric...."Because it is misleading to IBSers and is not IBS and could cause them even more anxiety and worry, and no ones doctor has diagnosed them with this as IBS, at least not any right minded one another thing you don't understand."simply unbelievable. i don't know what else to say but simply unbelievable.


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## bonniei (Jan 25, 2001)

Talissa: regarding the digestion of fatFrom your health finder link in response to flux


> quote:"In the second study, researchers from the Mayo Clinic in Rochester, Minn., led by Dr. Yuri Saito, collected data on the diets of 221 adults, aged 20 to 50. Of these patients, 102 had gastrointestinal disorders and 119 were healthy.The research team found patients with IBS or dyspepsia reported eating more monounsaturated fats compared to healthy patients. These patients also ate fewer carbohydrates than their healthy counterparts.The Mayo investigators conclude that "future studies are needed to determine whether fat intake causes gastrointestinal symptoms."The Mayo investigators conclude that "future studies are needed to determine whether fat intake causes gastrointestinal symptoms."


So this just based on a survey that they conclude fat is a problem. Nowhere does it say that fat can't be digested.And fat causes a probllem not because it can't be digested but rather as far as it is known


> quote:"Physiologic concentrations of intestinal lipids exert an inhibitory control on intestinal gas transit, and this mechanism is up-regulated in patients with IBS. "


 http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12198695 It has nothing to do with not digesting fat properly!


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## SpAsMaN* (May 11, 2002)

Snookered


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## flux (Dec 13, 1998)

> quote: a. IBSr's are found to have imbalanced gut flora












> quote: owhere does it say that fat can't be digested.





> quote: It has nothing to do with not digesting fat properly!










*Every person with just IBS has totally normal digestion and absorption.*


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## bonniei (Jan 25, 2001)

i liked your graphic for me, flux







Talissa about the only reason you could get an impression that fat is a problem is because Creon has been recommended on the board for bloating. But the study of Creon was done on normal subjects and their symptoms were reduced and they did not know why Creon worked http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=10489912


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## Talissa (Apr 10, 2004)

Bonniei,I never said with IBS you can't digest fats.The research says that with bacterial overgrowth in the sm bowel, you have trouble digesting fats._____________And it's been proven that IBS patients have altered intestinal flora, in one bowel, in the other, or both:"Changes in Luminal Flora"(recognise 'luminal' from the 2nd fats article, or didn't you bother to read it???) http://www.medscape.com/viewarticle/457728_4 _________________"The faecal microflora in IBS has been shown to be abnormal with higher numbers of facultative organisms and low numbers of lactobacilli and bifidobacteria." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12215182 _________________Well, on a personal note, I've given up trying to figure out why you would fight the results of all this research, when it points to a way to getting better, and normal again. At least for those with PI IBS.It's bizarre.I've got guests coming soon, so have fun bickering, but you'll need to find a new partner.T-


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## bonniei (Jan 25, 2001)

Talissa,Didn't you bother to read that very people with iBS have small bowel overgrowth ? Your medscape link say this about SIBO "* Indirect* evidence for bacterial overgrowth of the small intestine (in the form of altered hydrogen breath test results) has been reported in patients with IBS, and a recent randomized controlled trial found evidence that antibiotic treatment was beneficial for IBS symptoms of bloating and discomfort.[38] [38] is Pimental's study. i remember posting a critique of pimental's studies. Didn't you bother to read that either? http://www.med.unc.edu/medicine/fgidc/bact...rowthandibs.htm And infact if it is SIBO then it is no longer IBS.And on this thread you are talking about absorption of nutrients and you posted the healthfinder link article in response to flux saying that in iBS digestion of fats is just fine. So i thought you were still saying digestion of fats is a problem. please explain the relevance of "Irritable Bowel Tied to Fat and Fructose" http://www.healthfinder.gov/news/newsstory.asp?docID=515488 to the flow of this thread.


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## bonniei (Jan 25, 2001)

Talissa you are the one who is bickering by making obnoxious statements like calling eric an idiot and asking me if I didn't bother to read your links. Whenever you don';t have anything to argue with you go on the offensive and then it is worse than bickering. You also bring up the escuse that you have guests coming. Otherwise you are very much a part of this bickering as you call it.


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## meribaibs (Jan 18, 2004)

Snookered,I was just asking Spas if he wanted fries with his SII. (That's French for IBS.) Au revoir. (That's French for _down but not out.)_


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## bonniei (Jan 25, 2001)

Here is another critique of Pimentals method (LBHT)"However, our unique approach of combining the LBHT with scintigraphy confirmed that all three instances of a positive LBHT occurring in the setting of a negative culture in surgically naï¿½ve patients in our study were false-positives, since breath hydrogen levels only increased well after the test solution had reached the caecum, presumably reflecting fermentation of lactulose by colonic, rather than small intestinal, bacterial flora (4). Since combined scintigraphic assessment has shown that a* LBHT result considered positive for SIBO according to current definitions may be the result of caecal fementation of lactulose*, even in surgically naï¿½ve patients (4), it follows that the LBHT cannot reliably be used to assess for eradication of SIBO after treatment with antibiotics, since any reduction in breath hydrogen levels may merely be the result of a suppressive effect of the antibiotics on caecal flora (3)." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15128374


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## kel1059 (Feb 28, 2003)

talissa has actually been very nice and helpful. the abstracts that she posts are from highly respected sources.eric could infuriate anyone with his marijuana clouded thinking style. i am still trying to figure out what exactly is going on with him -- is it the weed? is it financial? from the garbled sentences i think there might be some brain damage.there are dozens of people who think he is an idiot but they are not posting it. i have received about a dozen priv emails over the months stating this fact.hang in there talissa; eric fights with EVERYONE who has a different message than his. i can't stress this enough -- you are posting some excellent research.one other thing, there is a guy that used to post here named MNL and this MNL used to make a monkey of eric every time they debated but it did not stop eric from continuing. nothing will stop eric except when his hero drossman starts publishing more and more information about the things you are posting.


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## eric (Jul 8, 1999)

Tal, you don't even read an understand the articles you post. You have already posted so much inaccurate info as you personally try to figure it all out, then post things you only personally believe as facts. A sensible person would be listening to all the information and then sort it out, but you don''t have a strong enough background in the big picture to know what your talking about. You have not learned yet, what PI IBS is and how to seperate PI IBS from IBS.I don't believe I have called you any names.It would seem you and kel both have troubles reading and understanding the material your posting and talking about here and until that happens its all pointless and the information you think you know is inaccurate and bad information. You are posting information that is way more complex then you realize or have taken the time to actually study and understand.You so far have not understood fully inflmmation/infection in IBS!!!! And are giving out bad information on it."The experts at Medscape know this, with all of the reading you do there, why don't you know???"I have read every article in medscape for longer then you have had IBS and many of them more then a couple times. Before you call someone an idiot, and then post inaccurate information on things you think you understand and QUITE CLEARLY DO NOT, because of tunnel vision, you need to think hard before you post.all you two believe in is leaky gut and for kel the cure was sulphur and homeopathy. Okay we got it. How does homeopathy cure leaky gut or IBS? It is also already known how probiotics can be benefical in IBS by reducing gas producing bacteria in the gut and hence gas, which puts pressure on the pressure sensitive cells in the digestive system which are hypersensitive in most IBSer lining the gastro track, which in turn lessens gas producing bacteria and pain, exactly what they find in using them in IBS research so far. This is not something I have seen you say yet. Nor anything about the role of abnormal transit in IBSers and gas and bacteria. or "How IBS comes aboutThe cardinal symptoms of IBS are abdominal pain and altered intestinal activity - diarrhea or constipation. These are probably related to what is called visceral hypersensitivity; this means the nerve receptors in the intestines are super-sensitive, and fire off signals more readily than those in unaffected people.Visceral hypersensitivity can be demonstrated by inflating a balloon that's inserted in the rectum, and measuring the pressure that produces pain. The pain threshold is lowered in 60% of IBS patients. Interestingly, if the patient is led to anticipate pain, by a stepwise increase in balloon pressure, the pain threshold decreases; on the other hand, if the balloon pressure is randomly altered, there is no lowering of the pain threshold. This indicates that the brain can, indeed, play a part in the symptoms of IBS. And during the anticipation of, as well as actual, distension of the rectum in IBS patients, brain radiographs show increased blood flow in some parts of the brain.Patients with IBS may complain of diarrhea, constipation, or neither of these symptoms. The motility of the colon is clearly an important feature of the condition. Visceral hypersensitivity means the colon will react to a greater extent to stimuli that would produce no obvious effect in unaffected people. A worsening of symptoms after eating, for instance, might be an exaggerated response to the 'gastro-colic reflex', in which a full stomach releases a substance called cholecystokinin-1 that causes contractions of colon musculature.IBS sufferers are sometimes intolerant of certain foods, such as wheat products or milk. An irritant effect can lead, because of visceral hypersensitivity, to poor digestion, excessive gas, bloating, and intestinal 'hurry'.Visceral hypersensitivity implies increased nerve cell signals traveling from the intestines up to the brain (afferent signals), and increased signals going in the opposite direction (efferent signals). These signals are transmitted with the aid of a chemical called serotonin, or 5HT (short for 5-hydroxytryptamine).There are several reasons for believing that 5HT plays a central role in the way IBS symptoms are caused. First, in inflammatory intestinal conditions, such as food poisoning, enteritis, and colitis, the number of special cells that produce 5HT in the intestine wall are greatly increased, and there is increased intestinal motility and hurry. Second, a drug that antagonizes one type of 5HT receptors on the cells (alosetron) is effective in diarrhea-predominant ISB. And third, another drug that antagonizes another type of 5HT receptors (tegaserod) is effective in constipation-predominant IBS.Two other factors are important in how IBS occurs. Stress can make it worse. Acute stress situations are not likely to be a problem; chronic, unrelieved stress, such as separation or bereavement, are more likely triggers.Finally, genetic factors can play a role. Twin studies suggest that environmental factors are probably more important than genetic factors. However, there are some rare congenital conditions with abnormalities in intestinal motility, and others where the inflammatory reaction to infection is exaggerated.Psychological factors have been frequently blamed for IBS, and it's true that psychiatric diagnoses are increased in IBS patients referred to specialist clinics; however, there doesn't seem to be any association between psychiatric disorders and IBS in the general population." http://www.healthandage.com/Home/gid2=2071 Tal form your own post you just don't seem to understand or get, regardless of how many times we post it, you don't read it and comprehend it first, before drawing conculsions. an example of your cherry picking from your own post tilte?"However, it is generally accepted that IBS symptoms are multidetermined, and are generated from dysregulation at multiple levels of the brain-gut axis" Its alreay accepted and has been for years now. In IBS the brain and the gut are both operational to generate the symptoms!! You have not taken this into consideration yet, until you do you will always be behind in what your talking about, without the basics of the bigger picture."Inflammation, Infection, and Irritable Bowel Syndrome: An UpdateDisclosuresYehuda Ringel, MD Douglas A. Drossman, MDIntroduction Irritable bowel syndrome (IBS) is a chronic disorder of gastrointestinal function for which no specific pathophysiologic mechanism is known. *However, it is generally accepted that IBS symptoms are multidetermined, and are generated from dysregulation at multiple levels of the brain-gut axis.* They are manifest by abnormal motor reactivity to various stimuli, and low sensation and pain thresholds.1 The growing interest of clinicians and researchers in the pathogenesis of functional gastrointestinal disorders led to several research presentations during this year's Digestive Disease Week meeting. Although these presentations addressed various factors implicated in the pathogenesis of these disorders (ie, behavioral/psychosocial, central and peripheral contributors), this article focuses on some new insights into the possible contribution of gut infection and inflammation in the development of symptoms and other potential clinical consequences.Infection and Inflammation Stephen M. Collins2 provided a comprehensive review of the evidence suggesting the need to consider infection and inflammation in the pathogenesis of some patients with IBS. He presented data from clinical studies showing the development of IBS symptoms following acute gastroenteritis (ie, postinfectious PI IBS) and a higher than expected prevalence of IBS symptoms among patients with inflammatory bowel disease that was in remission. Additionally, data from animal studies demonstrated that *altered gut physiology can persist even after the infection and associated inflammation have resolved.* *Furthermore, studies of mucosal biopsies, from both human and animal models, have shown increased inflammatory cells and inflammatory mediators in patients with IBS and in previously sensitized/stressed animals. * Finally, some recent studies have shown proximity between nerve trunks and the inflammatory cells, suggesting a local neuroimmune interaction that may contribute to the pathogenesis of IBS. With respect to the latter, several key studies presented during these meeting proceedings provided some supportive evidence relating the role of infection and inflammation to IBS. Wheatcroft and colleagues3 *have shown a significant increase in serotonin-containing entero-endocrine cells (EC) * following Trichinella spiralis infection in mice. This finding suggests that the increased EC numbers that have previously been reported in humans after *Campylobacter enteritis are likely not specific to bacterial infections. These events may also occur after protozoan and other parasitic infections, and thus may contribute to postinfectious bowel dysfunction. * Dunlop and colleagues[4] compared the numbers of rectal mucosal lymphocytes, *EC, and mast cells from IBS patients* (n = 76) and healthy controls (n = 40). Although all biopsies were normal using conventional histology, immunohistochemical studies showed differences in patterns of mucosal pathology between several distinct subgroups of IBS. Patients with PI-IBS showed increased EC and CD3+ lamina propria lymphocytes (LPL),confirming previous findings. However, patients with constipation-predominant IBS were not significantly different from controls, and nonconstipated, non-PI-IBS patients showed increased CD3+, LPLs, and mast cells. These findings suggest that within the broad clinical grouping of IBS, there may be several distinct groups with different patterns of mucosal pathology. The clinical relevance of these findings needs further investigation. The growing interest and the emerging evidence supporting the role of infection and inflammation in the pathogenesis of at least a subset of IBS patients was also manifest in some key studies presented in the American Gastroenterological Association Research Forum on the "Medical Treatment of Functional GI Disorders." As discussed below, these studies explored possible new approaches in the treatment of IBS, while focusing on modulating and reversing infections and/or inflammation. A Role for Anti-inflammatory Agents? Dunlop and coworkers5 also presented the results of an intriguing multicenter study aimed at assessing the effect of a short course of steroids on intestinal inflammatory cell counts and clinical symptoms in patients with PI-IBS. Thirty-one patients with IBS symptoms 3 or more months after initial acute gastroenteritis were randomized in a double-blind fashion to receive oral prednisolone 30 mg per day or placebo for 3 weeks. Rectal biopsies were taken and symptom questionnaires (modified Talley, Gastrointestinal Symptom Rating Scale GSRS-IBS, QOL-IBS & Global Health) were completed prior to and after treatment. Rectal biopsies were immunostained for ECs, lymphocytes (CD3+ lamina propria cells, crypt and surface intraepithelial lymphocytes IELs), and mast cells. In addition, a symptom diary was kept throughout the study and a modified GSRS score incorporating pain, diarrhea, looseness, and urgency was used as the primary end point.Prior to treatment, the CD3 count in the lamina propria correlated with the EC counts (Spearman's coefficient 0.429, P = .036) and with the modified GSRS score (Spearman's coefficient 0.482, P = .015). Following treatment, there was a significant fall in CD3 counts. However, this fall was in both the placebo and the prednisolone groups (27, P =.05; and 20, P = .006 vs initial values, respectively) and there was no change in the EC, IEL, and mast cell counts in either group. The modified GSRS score did not change after prednisolone treatment. However, there was a surprising, and unexplained, decrease in GSRS score at the end of the treatment in the placebo group (P = .02 vs initial value). *The results of this study show that treatment with 30 mg of prednisolone started 3 or more months after the initial gastrointestinal infection is ineffective in PI-IBS.* It is not yet clear if anti-inflammatory treatment started in earlier stages, and/or with higher doses, and/or for longer duration would have other outcomes. *Therefore, despite preliminary evidence for an inflammatory/immune component in some patients with IBS, additional studies are needed before the use of anti-inflammatory agents can be considered in treatment. * Note: This is to stop PI IBS, from becoming full blown IBS after intial RESOLUTION of the infection!!!!A Role for Probiotics? Probiotics are live microbial food supplements or components of bacteria that alter the enteric microflora and have a beneficial effect on health. The most frequently used genera are Lactobacilli and Bifidobacteria. The potential mechanisms of their action include competitive bacterial interactions, production of antimicrobial metabolites, mucosal conditioning, and immune modulation. The emerging use of probiotics in several gastrointestinal disorders (eg, inflammatory bowel disease) has led to increased interest in their use in patients with IBS. Quigley and colleagues6 presented the results of a double-blind, placebo-controlled treatment study with probiotic bacteria in 77 patients (64% female) with IBS. Following a 2-week run-in period off all medication, patients were randomized to receive, once daily, either Lactobacillus spp, Bifidobacterium spp, each added to a milk drink, or the milk drink alone for 8 weeks. IBS symptoms were recorded daily throughout the entire study. In comparison to placebo, subjects randomized to Bifidobacterium experienced a significant reduction in pain, bloating, and bowel movement difficulty. Benefit with Lactobacillus was limited to an effect on pain in weeks 2 and 7 only, and *neither probiotic strain had any effect on the frequency of bowel movements.* A composite score, incorporating all symptoms, showed significant improvement in response to Bifidobacterium for all weeks. The improvement in the composite score response was greater with Bifidobacterium compared with placebo and Lactobacillus (Bifidobacterium vs Lactobacillus vs placebo = 3.70 +/- 0.59 vs 5.25 +/- 0.55 vs 5.68 +/- 0.56, P .05 for week 4). The symptomatic response with Bifidobacterium was associated with parallel improvement in quality of life as assessed by using an IBS-specific instrument.[7,8] A follow-up 4 weeks after discontinuation of the treatment (washout period) showed that both symptoms and quality of life returned to baseline. The results showed a beneficial effect of probiotic bacteria in IBS. However, it must be kept in mind that data on the use of these agents in IBS are still very limited and not always consistent. (For example, a previous double-blind, placebo-controlled, randomized study showed beneficial effect of Lactobacillus plantarium in IBS.9) In addition, as emphasized by the investigators, *it seems that the beneficial effect was short-term and strain-specific.* Additional information regarding the variability of strain-specific response was provided by the results of a study presented by another group from Ireland, as discussed below. Sheil and colleagues10 examined cytokine production by human mononuclear cells that were incubated in vitro in various strains of Lactobacilli and Bifidobacteria. They found strain-specific alterations in cytokine gene expression and strain-specific cytokine responses for both Lactobacilli and Bifidobacteria strains. As proposed by the investigators, these results suggest that experiments on the immunomodulatory effects of one bacterium cannot be extrapolated to other bacteria. Thus, each bacterial strain that is considered for use as a probiotic may need to be validated individually. The results of studies that have thus far been conducted with probiotics are encouraging. However, additional investigations that will better define the potential subgroup of patients, the specific strain, and the duration of treatment are required in order to establish the role of probiotics in the treatment of IBS. Until the latter is accomplished, their use will remain investigational. A Role for Antibiotics? Pimentel and associates11 tested the utility of antibiotic treatment in IBS. This study follows a recently published provocative report from the same group in which they identified an association between IBS and abnormal findings on lactulose breath test (LBT).12 However, this previous report had limitations due to its study design, primarily related to possible ascertainment bias, the lack of a control arm, and the unblended nature of the treatment. Thus, the results of this study and their clinical significance were uncertain. The current study was designed to test the effect of antibiotic treatment in patients with IBS in a randomized, double-blind, placebo-controlled fashion.One hundred-one consecutive IBS subjects recruited through advertising were randomized to receive neomycin 500 mg (n = 49) or placebo (n = 52) twice daily for 10 days. All subjects underwent LBT before and 7 days after completion of treatment. The LBT was read by a blinded reviewer, and the results remained blinded throughout the study. An IBS symptom questionnaire was administered before and after treatment and a true clinical response was defined as 50% improvement in symptoms. Abnormal LBT was found in 83% of IBS subjects who entered the study compared with 20% in sex-matched controls (P .01). In an intention-to-treat analysis, neomycin resulted in a 39.3% improvement in an IBS composite symptom score compared with 12.3% for placebo (P .05), and 40.1% bowel normalization compared with only 15.1% for placebo (P .001). Of the subjects receiving neomycin, 50% had a true clinical response compared with 17% given placebo (P .01). These results were even greater (up to 75%) in the group in which neomycin was successful in normalizing the breath test. The investigators concluded that abnormal LBT is very common in subjects with IBS and that IBS symptoms can be significantly improved with antibiotic treatment. Important concerns raised during the discussion of this paper related to the following: (1) the unusually high positive LBT rate in this population, possibly due to false-positives likely resulting from rapid transit of lactulose in the small bowel in IBS; (2) the use of a nonstandard measure of primary efficacy (ie, composite symptom score); (3) the significant effect being driven by an unusually low treatment and placebo response rate. The results of this study are provocative and interesting, and therefore deserve replication. They emphasize the need to consider performing LBT, when clinically indicated, as part of the evaluation of patients with IBS. In addition, the definition of IBS is a complex of symptoms that cannot be explained by other conditions. *Thus, the finding of positive LBT and positive response to antibiotic treatment suggests the presence of bacterial overgrowth that may be incorrectly diagnosed as IBS. * Concluding RemarksThe above discussion seeks to bring to the fore the current state of knowledge regarding the potential role of various factors in the pathogenesis of IBS. Within this context, new insight may be gleaned with respect to the clinical and therapeutic implications for patients with this functional gastrointestinal disorder." http://www.medscape.com/viewarticle/434527 why is it that not everyone who gets an enteric infection comes down with IBS. Post Infectious Irritable Bowel Syndrome This is one of the worlds leading expert in PI IBS if nt the leader. Robin C. Spiller, MDReader in Gastroenterology at the University Hospital, Nottingham, UKAn important subgroup of patients with Irritable Bowel Syndrome describe a previously entirely normal bowel habit with all their symptoms developing immediately after an acute bout of diarrhea and vomiting. This phenomenon has been recognized by clinicians for many years and was well described by Truelove and Chaudary who studied 130 patients with Irritable Bowel Syndrome, 34 of whom were described as having post-infective IBS. Most of the infections were bacillary dysentery but some were amoebic. *Interestingly, they found there was an important interaction between psychological problems and infection.* *They found that a post-infectious origin and absence of anxiety, depression or neurotic features both predicted a good outcome.* The commonest causes of gastroenteritis are viral, followed by Campylobacter, Salmonella and Shigella. Viral gastroenteritis typically heals rapidly with little residual injury, while the bacterial infections often produce ulceration and bleeding. They are generally associated with more prolonged illness and it is these infections which have been associated with post-infective Irritable Bowel Syndrome. The first prospective study was reported by McKendrick 1 who studied 38 individuals following a salmonella outbreak. He found that 11 out of the 38 met the Rome I criteria for IBS 6 months after the initial illness. Two further prospective studies of hospitalized patients from an infectious disease unit in Sheffield also confirmed this high incidence of post-infective IBS 2 3. Our own study of 386 cases of bacterial gastroenteritis obtained from a community survey showed a lower incidence of post infective IBS (7%) possibly reflecting a less severe illness, since only 1 in 10 of these patients were hospitalized However these were not trivial illnesses since the average duration of illness was 7 days with a third reporting bloody diarrhea and a median weight loss of 6kg. Interpreting this data requires knowledge of the normal incidence of new IBS, as was obtained in a large survey based on the British general practice database. This study of 584,308 patients found the incidence of new IBS per annum in non-infected patients to be 0.35%. However, in 300 patients who had a culture positive infectious gastroenteritis, the annual incidence was 4% giving a relative risk of 11.9% 95% CI (6.9-21) 4. Traveller's diarrhea is of course extremely common in Canadian citizens travelling to Mexico and Ilnyckyj prospectively surveyed this group. Nearly 50% developed travellers diarrhea and in this group the incidence of new IBS three months later was 17.5% compared with just 2.7% for those who did not get travellers diarrhea, a relative risk of 6.6(0.8-53) 5. Risk Factors *Most patients with bacterial gastroenteritis recover fully and only a small minority develop post-infective Irritable Bowel Syndrome.* *Female sex, hypochondriasis and adverse life events in the previous year all give an increased risk 6 7 with a relative risk of 3.4, 2.0 and 2.0 respectively.* A much stronger risk factor is the duration of the initial illness, with a steadily increasing relative risk for each week of illness, reaching 11.4 for those with diarrhea lasting more than 21 days. Bacterial factors are likely to be important since we found around 1 in 10 of Campylobacter infected individuals developed post-infective IBS compared with just 1 out of 100 with Salmonella. It is likely *therefore that the severity of tissue damage and ulceration is a major predictor.* PathophysiologyDiarrheal illnesses are characterized by accelerated GI transit and increased gut sensitivity. This gradually returns to normal but at a variable rate. By three months most of those who are going to recover will have done so and thereafter the rate of recovery is much slower. As Gwee found colonic transit is accelerated in all infected individuals at 3 months, but those who meet the Rome I criteria for IBS have a faster transit than those who do not. Similarly rectal sensitivity is increased in those meeting Rome criteria, though again all those infected show a similar trend. *Although conventional histological examination of mucosal biopsies in IBS shows no abnormality, when detailed quantification is undertaken changes are noted.* We performed serial rectal biopsies in individuals recovering from Campylobacter gastroenteritis at 2, 6, 12 and 52 weeks. *We note initial increases in both inflammatory cells and enteroendocrine cells, which mostly returned towards normal, but remained abnormal in a few markedly symptomatic individuals * 8. Similar abnormalities were noted in patients attending the outpatients with a history of post-infectious Irritable Bowel Syndrome. *There is a good correlation between the inflammatory cells and the enteroendocrine cells suggesting that cytokines might drive the enteroendocrine cell hyperplasia. * *The main content of the enteroendocrine cells is 5HT, an agent that stimulates peristalsis and intestinal secretion causing diarrhea in normal subjects.* Drugs, which inhibit the action of 5HT such as Alosetron, are likely to show benefit in this group thought they have not been specifically studied.Other authors have noted increased enteroendocrine cells in unselected irritable bowel patients 9 but this needs confirmation. *More important than increase in numbers may be the increase in release of 5HT.* *Several pilot studies 10 including some reported at DDW this year suggested that there was an exaggerated release of 5HT following a meal particularly in those who got meal related symptoms 11.* Management *It is important that patients should understand the important roles of anxiety, stress, and diet and persisting low-grade inflammation in this condition. * *Providing the Rome criteria are met and general physical examination is normal then the probability of another diagnosis is low.* However, infections can unmask other disease particularly coeliac disease, inflammatory bowel disease such as Crohn's and tropical sprue together with hypolactasia. Such patients should therefore undergo a minimum set of screening tests including endomysial antibodies, hemoglobin, CRP, ESR, albumin and stool culture. *In the absence of alarm features such as weight loss, fever, rectal bleeding and nocturnal diarrhea, only 5% of all these tests will be abnormal.* Since microscopic colitis has also been reported to develop acutely after an infectious illness it is important to do a colonic biopsy and, if suspicions are high, also a duodenal biopsy to exclude coeliac disease. Lactose intolerance developing after a viral gastroenteritis is well recognized by pediatrician. This occurs because lactase, the enzyme responsible for digesting lactose, is expressed fully only in the mature enterocyte at the tip of the villus. Since viral gastroenteritis generally specifically damages the villi, lactose levels remain low for some months. A low lactose diet is therefore worth trying, particularly in those racial groups with an a priori greater risk of lactose intolerance such as Asians, Africans and Chinese. A low lactose diet is only relevant if the subjects take more than 240 mls of milk. Even those with documented lactose intolerance can tolerate amounts smaller than this when spread throughout the day. *Since psychological factors are so important, it is necessary to make some formal assessment of this. Where anxiety and depression levels are high they should be treated on their own merits since it is unlikely the patient will recover without addressing these issues. * *There are no specific diets recommended for post infective IBS but reduction of poorly absorbed carbohydrates, particularly wheat, potatoes together with other items such as citrus fruits have been reported to be beneficial in patients with diarrhoea-predominant IBS and should be tried * 12. Loperamide and codeine are well tried treatments for diarrhea predominant IBS regardless of origin and are likely to be effective though at the risk of some side-effects, including sedation and nausea in the case of codeine and abdominal pain in the case of Loperamide. Alosetron has also been reported to be effective in diarrhea predominate IBS but again has not been specially tried in post infective patients. PrognosisWhatever treatments are offered, the clinician can afford to be reassuring since the prognosis is relatively good. Chaudary's original study found 77% had recovered within 2 years 13 while Harvey also found 82% of those with acute illness at onset had recovered by 5 years 14. In our own follow-up 5 to 6 years following the initial survey we found that 11 out of 17 post infective Irritable Bowel Syndrome patients had actually recovered though *we also noted that a past history of psychiatric disorder predicted a poor outcome.* Key PointsPost infective Irritable Bowel Syndrome *accounts for around 1 in 10 of all cases of IBS. * *Females with prolonged illnesses and previous adverse life events are more likely to develop post-infective IBS. * *Low-grade inflammatory changes may persist in some of these patients. * Overall prognosis is good with 2 out of 3 recovering over a period of 3-5 years. http://www.med.unc.edu/wrkunits/2depts/med..._infectious.htm "Low-grade inflammatory changes may persist in some of these patients."What does the above have to do with mast cells, which by the way secrete serotonin to fight infection in the gut?Inflammatory Mediators in Irritable Bowel Syndrome "Mast Cells and IBS The mast cell has potential to be a key player in IBS. Although mast cells are most widely known for their role in allergic responses, these cells are normally present throughout the gut and are involved in a range of physiological and pathological activities including mucosal defense mechanisms and inflammation. Mast cells may release an array of inflammatory mediators that act on smooth muscle, nerves and immune cells, which may ultimately result in gastrointestinal dysfunction and symptoms. In addition, mast cells in the gut are located close to nerves providing a structural basis for communication between the gut and the nervous system.""A Link between Inflamation and StressAn increase in inflammatory mediators alone is insufficient to explain the pathogenesis of IBS. From post-infective IBS, we know that the most people who have gastroenteritis and accompanying inflammation do not develop IBS. As discussed earlier, several factors may be important in interacting with the gut insult and in predicting those who develop symptoms - one interesting factor here is the role of stress. Psychological stress is known to affect gut function in normal healthy humans, and in people with IBS stress may trigger or exacerbate symptoms. More recently there is evidence of a link between stress and inflammatory responses. Exposure to stress in both animals and humans has been shown to result in the release of mast cell mediators in the colon 18,19 and in a recent study stress was capable reactivating previous inflammation in rats 15. An important challenge for future work will be to clarify the interaction between inflammation, stress and IBS symptoms." http://www.med.unc.edu/wrkunits/2depts/med...rymediators.htm Activated mast cells in proximity to colonic nerves correlate with abdominal pain in irritable bowel syndrome.Gastroenterology. 2004 Mar;126(3):693-702. Related Articles, Links Activated mast cells in proximity to colonic nerves correlate with abdominal pain in irritable bowel syndrome.Barbara G, Stanghellini V, De Giorgio R, Cremon C, Cottrell GS, Santini D, Pasquinelli G, Morselli-Labate AM, Grady EF, Bunnett NW, Collins SM, Corinaldesi R.Departmentof Internal Medicine and Gastroenterology, and CRBA, University of Bologna, Italy. gbarbara###med.unibo.itBACKGROUND & AIMS: The mechanisms underlying abdominal pain perception in irritable bowel syndrome (IBS) are poorly understood. Intestinal mast cell infiltration may perturb nerve function leading to symptom perception. We assessed colonic mast cell infiltration, mediator release, and spatial interactions with mucosal innervation and their correlation with abdominal pain in IBS patients. METHODS: IBS patients were diagnosed according to Rome II criteria and abdominal pain quantified according to a validated questionnaire. Colonic mucosal mast cells were identified immunohistochemically and quantified with a computer-assisted counting method. Mast cell tryptase and histamine release were analyzed immunoenzymatically. Intestinal nerve to mast cell distance was assessed with electron microscopy. RESULTS: Thirty-four out of 44 IBS patients (77%) showed an increased area of mucosa occupied by mast cells as compared with controls (9.2% +/- 2.5% vs. 3.3 +/- 0.8%, respectively; P 0.001). There was a 150% increase in the number of degranulating mast cells (4.76 +/- 3.18/field vs. 2.42 +/- 2.26/field, respectively; P = 0.026). Mucosal content of tryptase was increased in IBS and mast cells spontaneously released more tryptase (3.22 +/- 3.48 pmol/min/mg vs. 0.87 +/- 0.65 pmol/min/mg, respectively; P = 0.015) and histamine (339.7 +/- 59.0 ng/g vs. 169.3 +/- 130.6 ng/g, respectively; P = 0.015). Mast cells located within 5 microm of nerve fibers were 7.14 +/- 3.87/field vs. 2.27 +/- 1.63/field in IBS vs. controls (P 0.001). *Only mast cells in close proximity to nerves were significantly correlated with severity and frequency of abdominal pain/discomfort * (P 0.001 and P = 0.003, respectively). CONCLUSIONS: * Colonic mast cell infiltration and mediator release in proximity to mucosal innervation may contribute to abdominal pain perception in IBS patients.* PMID: 14988823


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## bonniei (Jan 25, 2001)

eric. Re ;overgrowth and lBHT there was a study in 2004 -"However, our unique approach of combining the LBHT with scintigraphy confirmed that all three instances of a positive LBHT occurring in the setting of a negative culture in surgically naï¿½ve patients in our study were false-positives, since breath hydrogen levels only increased well after the test solution had reached the caecum, presumably reflecting fermentation of lactulose by colonic, rather than small intestinal, bacterial flora (4). Since combined scintigraphic assessment has shown that* a LBHT result considered positive for SIBO according to current definitions may be the result of caecal fementation of lactulose, even in surgically naï¿½ve patients (4),* it follows that the LBHT cannot reliably be used to assess for eradication of SIBO after treatment with antibiotics, *since any reduction in breath hydrogen levels may merely be the result of a suppressive effect of the antibiotics on caecal flora (3)*." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15128374


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## bonniei (Jan 25, 2001)

> quote:Thus, the finding of positive LBT and positive response to antibiotic treatment suggests the presence of bacterial overgrowth that may be incorrectly diagnosed as IBS.


So eric after so many years of criticizing pimental are you actually saying pimental was right? Why have you not been giving exposure to this study if it was done in 2002?


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## Talissa (Apr 10, 2004)

Here's another pimental study from 2003 if anyone's interested: http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12591062


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## Talissa (Apr 10, 2004)

Er,I do apologize for coming right out and saying you're an idiot. I lost my temper & I'm sorry.It's just frustrating when when you argue, not specific points of what I say, but just to say I don't know what I'm talking about.And it's painfully clear you read everything on medscape, but fail to form logical conclusions from what you've read, nor do you see the big picture.Is it because you've had postinfectious IBS for 30 years & change is scary? This may mean you can get back to a normal life someday. No IBS. Fearing change is human, just like to er is human.Talissa


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## kel1059 (Feb 28, 2003)

see, i told you she was nice.but i think it is obvious to many people that eric could be one of the most stubborn and illogical people that we have ever come across.to be fair, i would say that he hits on a few interesting points but then makes the mistake of overblowing its importance, and also makes the huge mistake of disregarding hard evidence.then there is the mistake of continuing to slop around inside the murky definition of what constitutes an unknown condition. it is as though he selectively decides what is IBS and what is not IBS all based on unprovable murky beliefs.just a reminder eric, drossman still holds out the possibility that IBS COULD BE related to an organism. he has not ruled it out. i heard it from the horse's mouth.


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## kel1059 (Feb 28, 2003)

i have often suspected that he has been forced to carve out a special life that requires he stay home on the computer as opposed to leave the house for work. there is an extreme rigidity, inflexibility that suggests that he is still in the deep throes of this wretched curse -- IBS.i think that he may have hypnotized (through the tapes and weed) his way to a moderate amount of relief but the problem still simmers away underneath. this could explain his claim that IBS is INCURABLE.now if you will excuse me i need to leave the house for about 5 hours or so.leaving the house was something that i had extreme trouble doing just 8 months ago. there is hope -- it is NOT incurable.(eric, can you prove that all those antibiotics they put you on didn't screw up your system. i mean, what if they did.)


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## bonniei (Jan 25, 2001)

The American Journal of Gastroenterology Volume 98, Issue 11 , November 2003, Page 2572 Small intestinal bacterial overgrowth and irritable bowel syndrome Giancarlo Parisi M.D., a, Gioacchino Leandro M.Db, E. Bottona M.D.c, M. Carrara M.D.c, F. Cardin M.D.c, A. Faedo M.D.c, D. Goldin M.D.c, M. Pantalena M.D.c, G. Tafner M.D.c, G. Verdianelli M.D.c and M. Zilli M.D.c "The cause of the irritable bowel syndrome (IBS) is not known, and no standard treatment has been firmly established. Pimentel et al. [1 and 2] found that 78ï¿½84% of IBS patients also had small intestinal bacterial overgrowth (SIBO) diagnosed by means of lactulose hydrogen breath test (LHBT) and that antibiotic treatment effectively reduced IBS symptoms. However, the accuracy of LHBT is questionable for diagnosing SIBO because of low sensitivity [3].We recruited consecutive IBS patients among subjects referred to six GI clinics in Italy and diagnosed them according to the Rome II criteria. Preliminary data on 85 patients, 63 (74.1%) of whom were women, aged 44.7 ï¿½ 12.8 yr, enrolled from January to June, 2002 are reported. All patients underwent glucose breath test (GBT) for diagnosing SIBO according to the standard procedure for this examination. Specifically, patients were given 250 ml of an aqueous solution of 50 g glucose. A sample of alveolar air was subsequently taken every 10 min with the double-bag system (Quintron Instruments, Milwaukee, WI) for 3 h. The test was considered positive for SIBO when an increment of at least 10 ppm in the hydrogen concentration above the basal value was seen, followed by successive and sustained increases. No patient (0%) was found to be SIBO positive to GBT.The work of Pimentel et al. received a great deal of attention in the lay press but also several criticisms by clinicians and researchers, both on the Internet and in this journal. Criticism focused on different methodologic aspects of the article, including the use of LHBT for diagnosing SIBO. The dramatic discrepancy between the findings of Pimentel et al. [1 and 2] and ours is likely to be due to the use of different assessment methods. *The LHBT has been demonstrated to be ineffective in diagnosing SIBO, with only 16% sensitivity [3], *whereas the GBT is considered a reliable diagnostic tool for SIBO, with 93% sensitivity and 78% specificity for SIBO [4]. Treatment for IBS is likely to be long-term, and the use of antibiotics might be detrimental for intestinal bacteria or might also influence the development of functional bowel syndromes [5]. Therefore, the lack of positive cases for SIBO in our patients when a more sound assessment method was used strongly cautions against antibiotic treatment for IBS patients."References1. M. Pimentel, E.J. Chow and H.C. Lin, Eradication of small intestinal bacterial overgrowth reduces symptoms of irritable bowel syndrome. Am J Gastoenterol 95 (2000), pp. 3503ï¿½3506. SummaryPlus | Full Text + Links | PDF (76 K) | Full Text via CrossRef2. M. Pimentel, E.J. Chow and H.C. Lin, Normalization of lactulose breath testing correlates with symptom improvement in irritable bowel syndrome: A double-blind, randomized, placebo-controlled study. Am J Gastoenterol 98 (2003), pp. 412ï¿½419. SummaryPlus | Full Text + Links | PDF (106 K) | Full Text via CrossRef3. S.M. Riordan, C.J. McIver, B.M. Walker et al., The lactulose breath hydrogen test and small intestinal bacterial overgrowth. Am J Gastroenterol 91 (1996), pp. 1795ï¿½1803. Abstract-MEDLINE | Abstract-Elsevier BIOBASE 4. P. Kerlin and L. Wong, Breath hydrogen testing in bacterial overgrowth of the small intestine. Gastroenterology 95 (1988), pp. 982ï¿½988. Abstract-MEDLINE | Abstract-EMBASE 5. P.R. Maxwell, E. Rink, D. Kumar et al., Antibiotics increase functional abdominal symptoms. Am J Gastroenterol 97 (2002), pp. 104ï¿½108. SummaryPlus | Full Text + Links | PDF (42 K) | Full Text via CrossRef


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## bonniei (Jan 25, 2001)

While there is value in LBT (LHBT) and normalization of LBT, it is only because it attacks the cecal flora. No one has yet been able to confirm the positive LBT with SIBO by the golden standard of cultures.


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## flux (Dec 13, 1998)

> quote:And it's been proven that IBS patients have altered intestinal flora, in one bowel, in the other, or both:


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## Talissa (Apr 10, 2004)

Bonniei,Thanks for that info. I like how they concluded with cautions against antibiotic use to treat IBS. I caution ag that!When do you think they'll try antibiotics countered with probiotics? Oh yeh, they have had success with that, as was reported in the IBS/IBD medscape article. We're definitely moving in the right direction.Apparently, due to the location of the small intestine, it being very hard to access(below esophagus, before colon), there were high hopes for the LBT. Maybe someone will come up with a better way.But indirect evidence, though debatable in medical circles & on this bb, is enough for me. Especially since seeing the difference recently after taking Digestive Advantage. The LAB strains effect the small bowel & wow, it's so weird being able to eat freely again.So, seriously, I hope I do get someone's hopes up, someone who has PI IBS, because I & many others are proof that there's hope.


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## Talissa (Apr 10, 2004)

Regarding the hope--most of you know this, but just taking DA-IBS won't solve everything. Rarely could one product do that for our condition. But it's things like this that can improve the quality of your life, you just have to find what works for you!(Flux, that guy needs to widen his vocabulary--he never seems to say anything but wrong! Can he prove its wrong?)


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## kel1059 (Feb 28, 2003)

maurice (flux),if you know so much then why do you continue to suffer. obviously you do not know as much as you think you do. i hope i do not end up putting the hex on myself with a premature claim of recovery but i have never had a 3 month remission like i am enjoying right now.sure it could come back but maybe it won't.so i ask you again -- why do you play know-it-all when you are absolutely clueless in controlling your own symptoms.maurice,do you still believe this to be true?quote maurice -----"Extreme flatulence due to altered gut flora IS an infection!"http://groups.google.com/groups?hl=en&lr=&...hl%3Den%26lr%3D [/URL] %26ie%3DUTF-8%26selm%3D3317f25b.2714525%2540nntp.ix.netcom.com%26rnum%3D1


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## bonniei (Jan 25, 2001)

Talissa I don't know if you know the symptoms of SIBO are "A complex array of clinical symptoms ensues, resulting in chronic diarrhea, steatorrhea, macrocytic anemia, weight loss, and less commonly, protein-losing enteropathy." I don't know if you had all this.


> quote:The LAB strains effect the small bowel


I am not sure why DA-IBS would help small intestinal bacterial overgrowth. They seem to have done no research except through surveys. And i did not see any questions related to SIBO in their surveys.I have found only a couple of studies saying SIBO can be treated by probitics http://www.ncbi.nlm.nih.gov/entrez/query.f...st_uids=9702645


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## bonniei (Jan 25, 2001)

I found 6 studies mentioning that probiotics can be used for SIBO. But that is stll only a handful of studies http://www.ncbi.nlm.nih.gov/entrez/query.f...earch&DB=pubmed


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## Talissa (Apr 10, 2004)

Hi Bonniei,My own take on DA-IBS is that they work at manufacturing enzymes in the sm bowel. Because diff probiotics have diff functions, they seem to work in the small bowel, helping to deal with food intolerance. quote:-------------------------------------------------The LAB strains effect the small bowel -------------------------------------------------I said this because enzymes are mfr'd in the small intestine, where food intolerance occurs.I don't think DA-IBS on its own would be enough to combat SIBO that is moderate to severe, maybe not even mild. But it could help with food tolerance. (I also take the multi-strain probiotic--but am out right now(grrrr) & twice a year take natural anti's.) This is why I -think-my last step is figuring out how to naturally get the inflammation down. I have some references somewhere re: lactic acid bacteria and enzymes--will look for them later.T-


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## Talissa (Apr 10, 2004)

Here's some more info on how deconjugated bile acids affect the colon when they pass thru from the small intestine:"Most adverse effects of the indigenous gut flora are caused by the intense metabolic activity of luminal organisms. The following are associated with Putrefaction dysbiosis:1. The enzyme urease, found in Bacteroides, Proteus and Klebsiella species, and induced in those organisms by a diet high in meat, hy- drolyzes urea to ammonia, raising stool pH. A relatively high stool pH is associated with a higher prevalence of colon cancer(7).2. Bacterial decarboxylation of amino acids yields vasoactive and neurotoxic amines, including histamine, octopamine, tyramine and tryptamine; these are absorbed through the portal circulation and deaminated in the liver. In severe cirrhosis they reach the systemic circulation and contribute to the encephalopathy and hypotension of hepatic failure(1).3. Bacterial tryptophanase degrades tryptophan to carcinogenic phe- nols, and, like urease, is induced by a high meat diet(8).4. Bacterial enzymes like beta-glucuronidase hydrolyze conjugated es- trogens and bile acids. Hepatic conjugation and biliary excretion is an important mechanism for regulating estrogen levels in the body. Bacte- rial deconjugation increases the enterohepatic recirculation of estrogen. A Western diet increases the level of deconjugating enzymes in stool, lowers estrogen levels in stool and raises estrogen levels in blood and urine, possibly contributing to the development of breast cancer(6).5. Beta-glucuronidase and other hydrolytic bacterial enzymes also deconjugate bile acids.Deconjugated bile acids are toxic to the colonic epithelium and cause diarrhea. They or their metabolites appear to be carcinogenic and are thought to contribute to the development of colon cancer(6,9) and to ulcerative colitis(10). Gut bacteria also reduce primary bile acids like cholate and chenodeoxycholate to secondary bile acids like deoxycholate (DCA) and lithocholate. The secondary bile acids are ab- sorbed less efficiently than primary bile acids and are more likely to contribute to colon carcinogenesis. The prevalence of colon cancer is proportional to stool concentration of DCA.Not all bacterial enzyme activity is harmful to the host. Fermenta- tion of soluble flber by Bifidobacteria sp. yields SCFA. Recent interest has focused on the beneficial role of short-chain fatty acids like buty- rate in nourishing healthy colonic mucosal cells. Butyrate has been shown to induce differentiation of neoplastic cells(l1), decreased ab- sorption of ammonia from the intestine(1), decreased inflammation in ulcerative colitis(12) and, following absorption, decreased cholesterol synthesis in the liver(7). Butyrate lowers the stool pH. A relatively low stool pH is associated with protection against colon cancer(S). The principal source of colonic butyrate is fermentation of soluble fiber by colonic anaerobes. Thus, putrefaction dysbiosis results from the inter- play of bacteria and diet in their effects on health and disease." http://healthy.net/asp/templates/Article.a...=Article&Id=423 When they say luminal organisms, it's referring to the pathogens that alter the luminal cells of the intestinal wall--the first of 3 layers of the intestinal wall.The above info also appears in the "Texbook of Natural Medicine"_________________________Here's is some great info on SIBO and nutritional staus:http://216.239.41.104/search?q=cache:-vnys...+%2B+%27irritab le%22&hl=en&start=20[/URL]


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## Talissa (Apr 10, 2004)

This has to be quick, but re: LAB strains(there are 8 diff ones that I know of), I have some more info.However, it seems to contradict my simplistic theory re: digestive enzyme manufacturing.I think now that there's a correlation between the inflamed intestinal wall and the body's ability to mfr enzymes.I keep thinking in simplistic terms, when microflora is anything but!________________Here's 2 articles that talk about LAB and restoring homeostasis through downgraded abnormal inflammatin--& how it affects normal intestinal function & for ex, problems with malabsorption weight loss:"The enteric flora comprise approximately 95% of the total number of cells in the human body and are capable of eliciting immune responses while also protecting against microbial pathogens. However, the resident bacterial flora of the gastrointestinal tract (GIT) may also be implicated in the pathogenesis of several chronic conditions such as inflammatory bowel disease (IBD). The University College Cork-based Probiotic Research Group has successfully isolated and identified lactic acid bacteria (LAB) which exhibit beneficial probiotic traits. These characteristics include the demonstration of bile tolerance; acid resistance; adherence to host epithelial tissue; and in vitro antagonism of potentially-pathogenic micro-organisms or those which have been implicated in promoting inflammation. The primary objective of this report is to describe the strategy adopted for the selection of potentially effective probiotic bacteria. The study further describes the evaluation of two m embers of the resulting panel of micro-organisms (Lactobacillus salivarius subsp. salivarius UCC118 and Bifidobacterium longum infantis 35624) under in vitro conditions and throughout in vivo murine and human feeding trials. Specifically, an initial feeding study completed in Balb/c mice focused upon (i) effective delivery of the probiotic micro-organisms to the GIT and evaluation of the ability of the introduced strains to survive transit through, and possibly colonise, the murine GIT; (ii) accepting the complexity of the hostile GIT and faecal environments, development of a method of enumerating the introduced bacterial strains using conventional microbiological techniques; and (iii) assessment of the effects of administered bacterial strains on the numbers of specific recoverable indigenous bacteria in the murine GIT and faeces. Additional research, exploiting the availability of murine models of inflammatory bowel disease, demonstrated the beneficial effects of administering probi otic combinations of Lactobacillus salivarius UCC118 and Bifidobacterium longum infantis 35624 in prevention of illness-related weight loss. A further ethically-approved feeding trial, successfully conducted in 80 healthy volunteers, demonstrated that yoghurt can be used as a vehicle for delivery of Lactobacillus salivarius strain UCC118 to the human GIT with considerable efficacy in influencing gut flora and colonisation." http://www.kluweronline.com/article.asp?PIPS=236216&PDF=1 *********************************ABSTRACTBackground: Probiotic bacteria have a beneficial effect on intestinal inflammation. In this study, we have examined the effect of lactic acid and commensal Gram positive (+) bacteria conditioned media (CM) on tumour necrosis factor (TNF-) release and the mechanisms involved. Methods: Lipopolysaccharide (LPS) induced TNF- secretion by peripheral blood mononuclear cells or the THP-1 cell line was monitored in the presence or absence of bacteria CM obtained from two probiotic strains, Bifidobacterium breve (Bb) and Streptococcus thermophilus (St), and three commensal bacterial strains (Bifidobacterium bifidum, Ruminococcus gnavus, and unidentified Streptococcus). Bb and St bacteria CM were allowed to cross filter grown intestinal epithelial cell monolayers (HT29-19A) to assess intestinal transport of active bacterial products. These products were characterised and their effect on LPS binding to THP-1 cells and nuclear factor B (NFB) activation assessed. Results: Dose dependent inhibition of LPS induced TNF- secretion was noted for both probiotic bacteria CM (64% and 71% inhibition for Bb and St, respectively) and to a lesser extent commensal bacteria CM (21ï¿½32% inhibition). Active products from Bb and St were resistant to digestive enzymes and had a molecular mass <3000 Da. Their inhibitory effect was preserved after transepithelial transport across intestinal cell monolayers, mainly in inflammatory conditions. LPS-FITC binding to THP-1 cells and NFB activation were significantly inhibited by Bb and St CM. Conclusion: B breve and S thermophilus release metabolites exerting an anti-TNF- effect capable of crossing the intestinal barrier. Commensal bacteria also display a TNF- inhibitory capacity but to a lesser extent. These results underline the beneficial effect of commensal bacteria in intestinal homeostasis and may explain the role of some probiotic bacteria in alleviating digestive inflammation. http://gut.bmjjournals.com/cgi/content/abstract/53/6/821 ___________________________It looks like by helping to normalize inflammation, this helps the body to mfr the enzymes.And in DA-IBS, they added lysine, which may help as a catalyst for enzyme mfr.I really wish I wasn't out of iFlora right now, should come this week. I say this because it contains mutliple strains, plus Bifidum strains for the colon.I think some of us need both types.Now I'm late to teach my own class!T-


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## eric (Jul 8, 1999)

" there's a correlation between the inflamed intestinal wall "This is completely wrong in IBS, there is no inflammaed intestinal wall in IBS that can be seen with a conolonscopy or standard tests, it is only specific cells under a microscope embedded in the digestive wall after peeling back the layers of muscle in a subgroup of IBSers!!!!!!!!!!!!!!Very bad information!!!!!!!!!!!!!! And what Tal, continues to not understand!Bonniei"Thus, the finding of positive LBT and positive response to antibiotic treatment suggests the presence of bacterial overgrowth that may be incorrectly diagnosed as IBS. --------------------------------------------------------------------------------So eric after so many years of criticizing pimental are you actually saying pimental was right? Why have you not been giving exposure to this study if it was done in 2002?No if they find positive SIBO its SIBO, not IBS, although it could be misdiagnosed as IBS. That's what that says, SIBO is not IBS!!!"Quite apart from these concerns about the study design, there is a question whether these patients should be diagnosed as IBS. The Rome criteria [3] state that a patient should be diagnosed IBS if they have a sufficient number of a list of positive symptoms (which these patients had) and if there is no alternative, disease explanation for these symptoms. Many gastroenterologists are aware that small bowel bacterial overgrowth can produce symptoms similar to IBS, just as inflammatory bowel disease and lactose malabsorption can; they do not label a patient as IBS if there is evidence for one of these alternative diagnoses." http://www.aboutibs.org/Publications/bacteria2.html Something some members, a few here, do not understand yet. As well as not really understanding the kind of and the role of infection/inflammation in IBS. Understanding IBS (Irritable bowel Syndrome): A Primer for Patients Chapter 7: *Some Common Conditions Where Diarrhea and Gas with Bloating Can Be Misinterpreted as Evidence of IBS* James Christensen, M.D. and Robert W. Summers, M.D.Peer Review Status: Internally Peer Reviewed-------------------------------------------------------------------------------- *Organisms growing in the Gut that should not be there * *Bacterial Overgrowth in the Small Intestine * *Abnormalities in the Lining of the Intestine * *Intolerance to Lactose * *Celiac Disease, or Sprue * *Inflammatory Bowel Disease * *Things You Eat and Drink When Your Gut is Normal * *Intolerance to Fructose * *Unconscious Intake of Laxative Substances * Chapter 8: Some Common Conditions Where Abdominal Pain Can Be Misinterpreted as Evidence of IBSJames Christensen, M.D. and Robert W. Summers, M.D.Peer Review Status: Internally Peer Reviewed--------------------------------------------------------------------------------Abdominal Wall Pain Neuropathies and Trigger Points Abdominal Wall Hernias Intra-abdominal Diseases Chapter 9: Some Common Conditions Where Nausea and Vomiting Can Be Misinterpreted as Evidence of IBSJames Christensen, M.D. and Robert W. Summers, M.D.Peer Review Status: Internally Peer Reviewed--------------------------------------------------------------------------------Disordered Emptying of the Stomach Incomplete Small Intestinal Obstruction http://www.vh.org/adult/patient/internalme...ebowelsyndrome/ GI Disorders in Adults GERD | Functional GI Disorders | Motility Disorders Gastroesophageal Reflux Disease (GERD)The most frequent symptoms of GERD are so common that they may not be associated with a disease. Self-diagnosis can lead to mistreatment. Consultation with a physician is essential to proper diagnosis and treatment of GERD. Heartburn, the primary symptom of GERD, is a fairly consistent problem for about 15% of the global population.(1) An occasional bout of heartburn is generally nothing to worry about, but if heartburn occurs two or more times per week, a more serious medical condition, gastroesophageal reflux disease (GERD), may be the problem. Data on the impact of this debilitating disease indicates that it often is not treated optimally. The result is that many patients, from adolescents to senior citizens, continue to suffer pain and other symptoms so severe that the quality of their lives is significantly impaired and they run the risk of even more serious medical complications. This is unfortunate because GERD is generally a treatable disease. GERD is a chronic disease. Treatment usually must be maintained on a long-term basis, even after symptoms have been brought under control. Issues of daily living, and compliance with long-term use of medication need to be addressed as well. This can be accomplished through follow-up, support, and education. Various methods to effectively treat GERD range from lifestyle measures to the use of medication or surgical procedures. It is essential for individuals who suffer persistent heartburn or other chronic and recurrent symptoms of GERD to seek an accurate diagnosis, to work with their physician, and to receive the most effective treatment available. Functional GI DisordersThe term "functional" is generally applied to disorders described by symptoms when no organic explanation is detected using common diagnostic procedures. The Rome Diagnostic Criteria categorize the functional gastrointestinal disorders and define symptom based diagnostic criteria for each category.(2)Functional esophageal disordersGlobus - a sensation of a lump, something stuck, or a tightness in the throatRumination syndrome - effortless regurgitation of recently swallowed food Functional chest pain - the feeling of chest pain, presumably of esophageal origin (can be confused with cardiac pain which must be examined) Functional heartburn - persistent burning sensation in the absence of gastroesophageal reflux disease (GERD), a motility disorder, or a structural explanationFunctional dysphagia - the sensation of difficulty swallowingFunctional gastroduodenal disorders (symptoms generally attributable to the mid or upper gastrointestinal tract)Functional dyspepsia - pain or discomfort located in the upper abdomenAerophagia - repetitive air swallowing or ingesting air and belchingFunctional vomiting - recurrent vomiting in the absence of all known medical and psychiatric causes Functional bowel disorders and abdominal pain (symptoms generally attributable to the mid or lower gastrointestinal tract) Irritable bowel syndrome (IBS) - a group of bowel disorders characterized by abdominal discomfort or pain associated with defecation or a change in bowel habitFunctional abdominal bloating - a group of functional bowel disorders dominated by a feeling of abdominal fullness or bloatingFunctional constipation - a group of functional disorders characterized by persistent difficult, infrequent, or seemingly incomplete defecationFunctional diarrhea - continuous or recurrent passage of loose or watery stools without abdominal pain Functional abdominal pain - continuous or frequently recurrent abdominal pain, either not or infrequently related to gut function, and associated with some loss of daily activitiesFunctional disorders of the biliary tract and pancreas (symptoms generally attributable to the upper or upper right abdomen)Gall bladder dysfunction - characterized by episodes of severe steady pain accompanied by decreased gall bladder emptyingSphincter of Oddi dysfunction - a motility disorder characterized by severe steady pain with no structural abnormalities that explain the symptoms. It sometimes occurs following gall bladder removal, but also may occur with an intact gall bladder. Functional disorders of the anus and rectum Functional fecal incontinence - recurrent uncontrolled passage of fecal material where no structural or neurological cause is evident Functional anorectal pain - Levator ani syndrome is a dull ache in the rectum that lasts for hours to days. Proctalgia fugax is an infrequent sudden, severe pain in the anal area of short durationExamples of GI Motility Disorders"Motility" is a term used to describe the contraction of the muscles that mix and propel contents in the gastrointestinal tract. The gastrointestinal tract is divided into four distinct parts that are separated by sphincter muscles; these four regions have distinctly different functions to perform and different patterns of motility (contractions). They are the esophagus (carries food to the stomach), stomach (mixes food with digestive enzymes and grinds it down into a more-or-less liquid form), small intestine (absorbs nutrients), and colon (reabsorbs water and eliminates indigestible food residues). Abnormal motility or abnormal sensitivity in any part of the gastrointestinal tract can cause characteristic symptoms.(3)Intestinal dysmotility, intestinal pseudo-obstructionAbnormal motility patterns in the small intestine can lead to symptoms of intestinal obstruction. Symptoms of bloating, pain, nausea, and vomiting can result either from weak contractions or from disorganized (unsynchronized) contractions. Small bowel bacterial overgrowthToo many bacteria in the upper part of the small intestine may lead to symptoms of bloating, pain, and diarrhea. Symptoms occur immediately after eating because the bacteria in the intestine begin to consume the food in the small intestine before it can be absorbed. Small bowel bacterial overgrowth is a result of abnormal motility in the small intestine. ConstipationThe symptoms of constipation are infrequent bowel movements usually less than 3 per week, passage of hard stools, and sometimes difficulty in passing stools. One motility problem that can lead to constipation is a decrease in the number of high amplitude propagating contractions slow transit in the large intestine. The test used to detect this is a transit time (Sitzmark) study. Outlet obstruction type constipation (pelvic floor dyssynergia)The external anal sphincter, which is part of the pelvic floor normally stays tightly closed to prevent leakage. When you try to have a bowel movement, however, this sphincter has to open to allow the fecal material to come out. Some people have trouble relaxing the sphincter muscle when they are straining to have a bowel movement, or they may actually squeeze the sphincter more tightly shut when straining. This produces symptoms of constipation. DiarrheaThe symptoms of diarrhea are frequent, loose or watery stools, and a subjective sense of urgency. An excessive number of high amplitude propagating contractions rapid transit can be a cause of diarrhea; it reduces the amount of time food residues remain in the large intestine for water to be reabsorbed. Changes in the motility of the small intestine may also occur, but there is little information available on this. Fecal incontinenceFecal incontinence means involuntary passage of fecal material in someone over the age of 4 years. The most common causes are (a) weakness of the anal sphincter muscles; (







loss of sensation for rectal fullness; © constipation, in which the rectum fills up and overflows; and (d) stiff rectum, in which the fecal material is forced through the rectum so quickly that there is no time to prevent incontinence by squeezing the sphincter muscles. Diarrhea can also lead to fecal incontinence.Hirschsprung's disease There are actually two anal sphincter muscles: an internal anal sphincter that is part of the intestines, and an external anal sphincter that is part of the pelvic floor muscles. The internal anal sphincter normally stays closed to prevent the leakage of gas or liquid from the rectum, but when the rectum fills up with gas or fecal material, a reflex causes it to open to allow the bowel movement to pass through. The nerves that this reflex depends on are sometimes missing at birth, with the result that the internal anal sphincter stays tightly closed and bowel movements cannot occur. This congenital (birth) defect is called Hirschsprung's disease. GastroparesisGastroparesis is a disorder in which the stomach takes too long to empty its contents. Gastroparesis is most often a complication of type 1 diabetes. At least 20 percent of people with type 1 diabetes develop gastroparesis. It also occurs in people with type 2 diabetes, although less often. Symptoms of gastroparesis are nausea, vomiting, an early feeling of fullness when eating, weight loss, abdominal bloating, abdominal discomfort. These symptoms may be mild or severe, depending on the person. In most cases treatment does not cure gastroparesis -- it is usually a chronic condition. However, treatment does help manage the condition.AchalasiaAchalasia is an esophageal motility disorder. It is diagnosed when there is a complete lack of peristalsis within the body of the esophagus. The lower esophageal sphincter does not relax to allow food to enter the stomach. Symptoms are difficulty swallowing both liquids and solids. Many people also have associated regurgitation, vomiting, weight loss, and atypical chest discomfort. http://www.iffgd.org/GIDisorders/GIAdults.html


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## Talissa (Apr 10, 2004)

This is from the "flagyl" thread, but I'm posting here as well because it has to do with this threadostinfectious IBS and gut flora/gas:_____________________________Hi Sally Jane & Trac,This is what many MDs do--they Rx flagyl(metronidazole) without countering the bacterial die-off with multi-strain high quality probiotics. (you should always take a probiotic 3-4 hours after an anti, or one hour before the anti.)ie--"Currently under investigation are antibiotics such as ciprofloxacin, metronidazole, and doxycycline, *which can treat postinfectious IBS, a disorder believed to be caused by alterations in intestinal microflora.* " http://www.emedmag.com/html/pre/gic/consults/041501.asp >>But many people here & elsewhere have a worsening effect from flagyl because of having very imbalanced gut flora before the flagyl was given.Here's some more info on bad reactions to flagyl/metronidazole:"A second study in the European Journal of Gastroenterology and Hepatology shows that taking metronidazole kills the bacteria that cause the gas, and it takes around 50 days for the bacteria to return, so if you do not avoid refined carbohydrates, expect the irritable bowel syndrome to recur (2). " http://www.drmirkin.com/morehealth/9095.html Irritable Bowel SyndromeHunter and his colleagues have studied patients with the irritable bowel syndrome in whom diarrhea, cramps and specific food intol- erances are major symptoms(24). They have found abnormal fecal flora to be a consistent finding, with a decrease in the ratio of anaer- obes to aerobes, apparently due to a deficiency of anaerobic flora (25,26). Previous exposure to antibiotics, metronidazole in particular, was associated with the development of this disorder(27). http://healthy.net/asp/templates/Article.a...=Article&Id=423 ___________________So, ironically they are treating postinfectious IBS symptoms with a known cause of postinfectious IBS.It's maddening!Lots of research is going on right now on the intestinal ramifications of gut microflora, so hopefully, things will change!________________(ps--I reacted very badly to striaght aloe in the form of Molocure when I tried it)


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## kel1059 (Feb 28, 2003)

Molocure -- very interesting. i am deeply suspicious of that product and not only due to the outrageous price. however, i do hold out hope that it could help some people. i tend to think that Dr Peter d'adamo is correct on some of his theories on blood types and foods that should be eaten.i believe he only recommends aloe or aloe based products for people who have "B" type blood.


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## kel1059 (Feb 28, 2003)

talissa quote


> quote: So, ironically they are treating postinfectious IBS symptoms with a known cause of postinfectious IBS.It's maddening!Lots of research is going on right now on the intestinal ramifications of gut microflora, so hopefully, things will change!


it is unbelievably maddening. as i type these clueless butchers are killing my 13 year old nephew. he has crohns disease diagnosed last year. he is getting ready to have his ileum removed.13 months ago i was in the hospital with him and the doctor walked in -- i asked him why the boy was not on probiotics during (or shortly after) his 3 fold antibiotic therapy. the doctor looked at me and said, "there is no need, the original bacteria will just grow back".i was dumbstruck!!!however, my sister is very stubborn and gets defensive whenever you try to tell her anything. she was still at that point of "doctor-worship".finally she feels the same frustration as me.


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## eric (Jul 8, 1999)

""Currently under investigation are antibiotics such as ciprofloxacin, metronidazole, and doxycycline, which can treat postinfectious IBS, a disorder believed to be caused by alterations in intestinal microflora. " http://www.emedmag.com/html/pre/gic/consults/041501.asp Post infectious IBS leads to IBS!! *After the intial, infection inflammation HAS resolved.* You have had IBS for six years now Tal, you no longer have PI IBS, but IBS and the molecular cellular changes matter a lot in PI IBS leading to IBS. This is another thing your not comprehending.from your above postGI Consult: Irritable Bowel SyndromeTwo specialists discuss the pathophysiology, clinical characteristics, and management of this common ailment.By Christine L. Frissora, MD, and Lucinda A. Harris, MDThis series of discussions in question-and-answer form is edited by Dr. Maltz, who is an assistant professor of medicine at Cornell Medical School in New York City and is attending physician in the department of emergency medicine and division of gastroenterology and hepatic diseases in the department of medicine at New York Presbyterian Hospital. Dr. Frissora is assistant professor of medicine and Dr. Harris is assistant professor of clinical medicine in the department of gastroenterology at Cornell University. They are also consultants to Novartis Pharmaceuticals Corporation and Glaxo Wellcome Inc. 1. What is irritable bowel syndrome? Irritable bowel syndrome (IBS) is the most common functional gastrointestinal disorder. It accounts for 12% of all visits to primary care physicians and affects 15% of the population in the U.S. Like other functional disorders, IBS does not lead to cancer, nor is there an organic or infectious component; in fact, the involved anatomic structures are grossly normal. The situation is much like that of a light bulb that will not illuminate even though it is structurally sound. Likewise, IBS appears to be caused by an anomaly of the circuitry, specifically an abnormal communication between the central nervous system (CNS) and the enteric nervous system (ENS) mediated by serotonin. It should be noted, however, that there is a small subset of patients who have what is called postinfectious IBS, a disorder thought to be caused by an infectious process.2. What is serotonin and what role does it play in IBS?Serotonin, or 5-hydroxytryptamine (5-HT), is a peptide that is found throughout the body. Approximately 96% of serotonin is located in the gastrointestinal tract, 2% in platelets, and 2% in the CNS. More than 20 types of serotonin receptors at various locations in the human body have been described, but the receptors that seem to be most important in the gastrointestinal tract in general and in IBS in particular are the 5-HT3 and 5-HT4 receptors.Because the structure of the receptor determines the function of the peptide, serotonin has slightly different functions when paired with each different receptor. Generally, these receptors are involved in controlling the motility of and secretions in the gut and the perception of abdominal pain. Typically, 5-HT3 and 5-HT4 receptor agonists promote motility and the antagonists decrease motility. Although the exact mechanism is not known, these receptors do not function properly in IBS.3. What are the clinical features of IBS?Symptoms of IBS normally appear in late adolescence or early adulthood. The disorder is twice as likely to occur in women. In most patients with IBS, a particular symptom or pattern of symptoms will predominate. The predominant symptom in IBS can be pain or bloating, diarrhea, or constipation, or it may alternate between diarrhea and constipation. Patients with IBS have abdominal discomfort, which is normally relieved by defecation or associated with a change in stool frequency or consistency.Stress and certain foods often trigger and exacerbate symptoms of IBS. Dairy products, fatty food, alcohol, caffeine, lactose, sorbitol, and fructose have all been known to produce and aggravate symptoms of IBS. Other influences such as lack of sleep, decreased fluid intake, and a sedentary lifestyle can also affect the severity of symptoms.In a given patient, the dominant symptom usually remains constant. Studies have shown that 75% of patients have the same set of symptoms over a five-year period. If the dominant symptom changes, a new, separate disorder may have occurred and a reevaluation may be necessary.4. How is IBS diagnosed? Irritable bowel syndrome is no longer a diagnosis made only by exclusion. In the 1990s, a group of gastroenterologists and health professionals formed a committee in Rome, Italy, to develop clinical criteria that would enable physicians to make a reliable and focused diagnosis of irritable bowel syndrome. The criteria devised by the Rome II committee define IBS as abdominal pain or discomfort lasting twelve weeksï¿½consecutive or nonconsecutiveï¿½in the year before treatment is sought and that is associated with two of the following: pain relieved by defecation; pain associated with a change in frequency of the stool; or pain associated with a change in the form of the stool.In addition to a focused history and physical examination, the Rome committee recommended that the following laboratory tests be performed: complete blood count; erythrocyte sedimentation rate (ESR); chemistry panel, including liver function tests; and stool studies that include measurement of stool guaiac, ova and parasites, stool culture, and fecal leukocytes. A flexible sigmoidoscopy is also suggested, and for some patients, colonoscopy is recommended.Because thyroid disease is common in many young adults, measurements of thyroid-stimulating hormone and thyroxine may be necessary: hypothyroidism often occurs with constipation and, conversely, hyperthyroidism often accompanies diarrhea. Culture of a stool sample for Clostridium difficile should also be considered if clinically indicated, particularly in patients who have undergone antibiotic therapy, recent hospitalization, or a surgical procedure. Colonoscopy and flexible sigmoidoscopy can also be useful in the diagnosis of IBS; the appropriate technique will be determined by the clinical characteristics of each patient (see Question 6).5. Are there any "red flags" to look for in the history and on physical and laboratory evaluations that can be used to rule out IBS?Features that should lead the clinician to consider other diagnoses include older age, family history of colon cancer or inflammatory bowel disease (IBD), or a history of being awakened in the night by the need to have bowel movements. Surgical history should also be considered. For example, a patient who has undergone cholecystectomy may have-instead of IBS-bile salt diarrhea, which can be treated with cholestyramine. Likewise, fever, palpable abdominal masses, or guaiac positive stool are not features of IBS and could indicate IBD or a malignant process. Similarly, anemia, increased ESR, and abnormal results on metabolic or liver function tests are usually not seen in IBS.6. Is colonoscopy necessary for every patient suspected of having IBS?Whether to perform sigmoidoscopy or colonoscopy depends on the age, symptoms, and family history of the patient. The American College of Physicians recommends that routine colon cancer screening should begin at age 50. Some patients with a family history of IBD, colon cancer, or severe symptoms of IBS may require colonoscopy at a younger age. If a diagnosis of microscopic or collagenous colitis is suspected, a biopsy will be necessary during colonoscopy because the mucosa will appear normal. If flexible sigmoidoscopy is performed for a patient who has IBS in which diarrhea is the predominant symptom, then a biopsy will be necessary to rule out ulcerative colitis. In some patients, ulcerative colitis is not grossly obvious and can be confirmed only by microscopic examination.When sigmoidoscopy or colonoscopy is performed, stool specimens can be obtained for culturing and to determine the presence of C. difficile antigen or ova and parasites. In patients with a family history of sprue or stomach cancer, upper endoscopy may be indicated, depending on the clinical symptoms.7. Can a patient have both IBS and IBD?Patients and physicians alike can confuse IBS and IBD, and distinguishing the symptoms of IBS from a flare up of IBD can be clinically challenging. Crohn's disease and ulcerative colitis are two types of IBD. Some symptoms of IBD, such as gas and pain, can be similar to those of IBS. Patients with ulcerative colitis usually have fever and bloody diarrhea; those with Crohn's disease can have pain, diarrhea or constipation, perianal disease, strictures, or fistula. It is also known, however, that patients with IBD can have IBS as well.8. What is the approach to treatment in patients with IBS?For patients with mild disease, all that may be needed is education about the disease, reassurance from the physician, and lifestyle and dietary modification.Many patients may have previously been given an erroneous diagnosis, or their physician may have even dismissed their symptoms as psychosomatic. It is therefore important to explain to all patients the actual physiologic causes and processes of IBS-including the role of serotonin and the interaction between the ENS and CNS-and reassure them that the disorder won't lead to cancer or IBD.Patients with IBS should also understand that the disorder is chronic and its severity varies in response to several influences, including diet, stress, lifestyle, and medications such as antibiotics or other drugs meant for other conditions.In addition to the dietary triggers mentioned earlier, dairy products can produce and exacerbate symptoms. Women who must limit the dairy content in their diet should be encouraged to take calcium supplements. Women who have constipation may benefit from calcium combined with magnesium, whereas those who have diarrhea may do better with calcium carbonate. Stress may be relieved through regular exercise and a proper and consistent amount of rest. Stretching exercises and yoga in particular can be very beneficial for some patients.9. What role does dietary fiber have in the treatment of IBS?Dietary fiber is often advocated in the treatment of diarrhea, because it is believed to absorb excess water from the stool. In practice, however, dietary fiber has proved ineffective for that purpose, but studies have shown that it has a role in the treatment of constipation-predominant IBS. Soluble fiber helps reduce colonic transit time, thereby relieving constipation. Dietary fiber provides ancillary benefits as well, including the lowering of serum cholesterol levels, improving glucose control in diabetic patients, and perhaps preventing certain cancers by reducing the number of free radicals in the gastrointestinal tract.Patients with mild, constipation-predominant IBS must be careful to limit the amount of crude, insoluble fiber in their diet. Found in the bran layers of wheat and other grains and in cruciferous vegetables, insoluble fiber generates gas and bloating, which are the products of carbohydrate fermentation that occurs when the fiber reaches colonic bacteria in the large intestine. Soluble fiber, however, which is found in fruits, vegetables, oats, barley, legumes, and seaweed, produces less gas and is therefore the type that patients with constipation-predominant IBS are encouraged to include in their diet.Soluble fiber may also be derived from over-the-counter supplements. Those that contain calcium polycarbophil are often better tolerated than psyllium-based compounds, which can produce more gas.10. When is pharmacotherapy necessary?Patients with moderate IBS can benefit from drug therapy directed at either pain and bloating, diarrhea, or constipation, depending on which symptom predominates. Before beginning such therapy, however, patients should keep a symptom diary, in which they can track the progress of their symptoms and the relationship of those symptoms to diet, activity, and stress. From the information collected in the diary, the physician and patient can then determine the predominant symptom to treat and the appropriate regimen to begin.The available agents currently given for the treatment of the bloating and pain that accompany moderate IBS are, as a rule, minimally effective. Over-the-counter drugs that contain simethicone may be helpful in eliminating gas in the upper gastrointestinal tract, but they are mostly ineffective in treating flatulence and bloating. Activated charcoal is sometimes recommended to relieve gas in the lower tract, but it too is not very effective. In addition, it turns stools black and can even cause constipation.Anticholinergic/antispasmodic drugs may have a role in treating severe intestinal spasm, but they also produce drowsiness, urinary retention, and dry mouth, adverse effects that limit the medications' acceptance among patients. Examples include hyoscyamine, dicyclomine, methscopolamine bromide, and clidinium/chlordiazepoxide. Selective serotonin reuptake inhibitors (SSRIs) can relieve pain and bloating, but these drugs should be reserved for patients with moderate to severe IBS.In the treatment of diarrhea, agents such as diphenoxylate, loperamide, and cholestyramine have all been used with varying success. Through their anticholinergic effects, tricyclic antidepressant agents, such as amitriptyline and desipramine, can be helpful in treating diarrhea. When given in low doses, they may also help relieve the abdominal pain of IBS, but these drugs also produce drowsiness and weight gain, which limits their usefulness and acceptance. Currently under investigation are antibiotics such as ciprofloxacin, metronidazole, and doxycycline, which can treat postinfectious IBS, a disorder believed to be caused by alterations in intestinal microflora.In addition to dietary or supplementary soluble fiber, the standard treatment for constipation has included laxatives, usually milk of magnesia or lactulose. Polyethylene glycol agents are often more effective, however, and produce less bloating than does lactulose.The latest advance in the treatment of moderate constipation-predominant IBS are the neuroenteric modulator agents, which affect the 5-HT3 and 5-HT4 serotoninergic receptors. Variants are targeted specifically at either diarrhea or constipation, but all neuroenteric modulator agents can also control the pain and bloating that often accompany these symptoms. Tegaserod, expected to be released in 2001, is a 5-HT4 partial agonist that increases intestinal motility and is meant for the treatment of constipation-predominant IBS. Alosetron, a 5-HT3 antagonist intended for the treatment of diarrhea-predominant IBS, was removed from the market because it was found to cause constipation and possibly ischemic colitis.It is important to know which neuroenteric modulator agents treat diarrhea and which treat constipation; they are not dietary supplements, and patients who take them must be monitored more closely.11. What are the options for patients with severe IBS?Along with the pharmacotherapy described above, patients with severe IBS-and even those with moderate IBS-may try short-term psychotherapy, which may consist of cognitive or relaxation therapy or hypnosis. For such patients it is important to establish realistic treatment goals that require their understanding, participation, and cooperation with the physician. They should be made aware that because a cure is not likely, their attention should be focused on health, not illness, with an aim toward controlling the symptoms and improving overall functioning. Physicians should also be aware that a high proportion of patients with severe IBS have been victims of child or sexual abuse.When stronger pharmacologic agents for the treatment of pain are necessary, the SSRIs and tricyclic antidepressants, mentioned earlier, can be tried. The SSRIs, which include citalopram, sertraline, fluoxetine, and paroxetine, are given when pain and bloating or constipation predominates, whereas the tricyclic agents are given when diarrhea is the predominant symptom.Until recently, SSRI therapy was usually administered empirically, but research has begun to confirm some of the benefits of these drugs in the treatment of severe IBS. In one study, for example, citalopram was associated with increased pain tolerance and decreased sensitivity to rectal distension. To allay any fears of addiction or mind-altering effects, physicians should explain to their patients that the drugs only inhibit the sensation of intestinal pain and are neither addictive nor psychotropic. For all patients given antidepressant drugs or neuroenteric modulators, monitoring and follow-up are essential.As with any chronic illness, severe IBS can be complicated by anxiety or depression, for which a longer period of psychotherapy or admission to a pain management clinic may be beneficial. http://www.emedmag.com/html/pre/gic/consults/041501.asp IBS FACT SHEETIrritable Bowel Syndrome (IBS)Fact SheetIrritable bowel syndrome (IBS) is a disorder characterized by abdominal pain or discomfort, and altered bowel habit (chronic or recurrent diarrhea, constipation, or both in alternation).IBS affects between 25 and 45 million people in the United States (10 to 15% of the population). Approximately 60 to 65% of IBS sufferers are female; 35 to 40% are male. IBS affects people of all ages, even children. *The exact cause of IBS is not known. Symptoms appear to result from a disturbance in the interaction between the gut, brain, and nervous system that alters regulation of bowel motor or sensory function. IBS is not caused by stress. However, because of the connection between the brain and the gut, symptoms can be exacerbated or triggered by stress. * The impact of IBS can range from mild inconvenience to severe debilitation, controlling many aspects of one's emotional, social and professional life. Those with moderate to severe cases, affecting an estimated 10 to 15 million people, must struggle to overcome symptoms that often impair their physical, emotional, economic, educational and social well-being.IBS is unpredictable. Symptoms vary and are sometimes contradictory, such as diarrhea alternating with constipation. Chronic and recurrent symptoms can disrupt personal and professional activities, upset emotional well-being and limit individual potential. Treatments are available for IBS to help manage symptoms. However, research is needed to provide greater relief and more treatment options.Although IBS is very common in the general population, few seek medical care for their symptoms. On average, patients report it takes more than three years from onset to diagnosis, and see nearly three healthcare professionals before their condition is diagnosed as IBS.Approximately 20 to 40% of all visits to gastroenterologists are due to IBS symptoms.For those with IBS an additional burden comes from living in a society where the word "bowel" may scarcely be spoken. Individuals are left to cope with multiple symptoms that affect every aspect of their lives while those around them may be unaware of the true impact, or even the existence, of the disorder. IBS can only be diagnosed by a medical professional. http://www.aboutibs.org/publications/IBSFactSheet.html Characteristicsof IBS Most people with IBS have mild symptoms. Many people don't recognize IBS symptoms. Yet, IBS is one of the most common disorders seen by physicians. Irritable bowel syndrome is characterized by symptoms of abdominal discomfort or pain, usually in the lower abdomen, and altered bowel habit (change in frequency or consistency) -- chronic or recurrent diarrhea, constipation, or both in alternation. The abdominal discomfort or pain are usually relieved with a bowel movement."Irritable Bowel" refers to a disturbance in the regulation of bowel function that results in unusual sensitivity and muscle activity."Syndrome" refers to a number of symptoms and not one symptom exclusively.Everyone suffers from an occasional bowel disturbance. However, for those with IBS the symptoms are more severe, or occur more often -- either continuously or off and on. IBS affects men and women of all ages. Some or all of IBS symptoms can occur at the same time -- some symptoms may be more pronounced than others.The Rome II Diagnostic Criteria (a system for diagnosing functional gastrointestinal disorders based on symptoms) for IBS is as follows:At least 12 weeks or more, which need not be consecutive, in the preceding 12 months of abdominal discomfort or pain that is accompanied by at least two of the following features: 1) It is relieved with defecation, and/or2) Onset is associated with a change in frequency of stool, and/or 3) Onset is associated with a change in form (appearance) of stool.Other symptoms that are not essential but support the diagnosis of IBS:Abnormal stool frequency (greater than 3 bowel movements/day or less than 3 bowel movements/week); Abnormal stool form (lumpy/hard or loose/watery stool); Abnormal stool passage (straining, urgency, or feeling of incomplete evacuation); Passage of mucus; Bloating or feeling of abdominal distension. Bloating, feelings of urgency, a feeling of "incomplete" emptying, and nausea may also be experienced. Symptoms can vary and sometimes seem contradictory, such as alternating diarrhea and constipation. *The symptoms of IBS are produced by abnormal functioning of the nerves and muscles of the bowel. In IBS there is no evidence of an organic disease, yet, something -- a "dysregulation" between the brain, the gut, and the central nervous system -- causes the bowel to become "irritated," or overly sensitive to stimuli. Symptoms may occur even in response to normal events. * IBS is not caused by stress. It is not a psychological or psychiatric disorder. It is not, "All in the mind." IBS is not caused by stress. It is not a psychological or psychiatric disorder. It is not, "All in the mind." Because of the connection between the brain and the gut, symptoms in some individuals can be exacerbated or triggered by stress. Dietary and hormonal factors can affect symptoms of IBS.IBS is not an indication of another more serious disease, like cancer. Irritable bowel syndrome can, however, seriously compromise a person's quality of life. Chronic and recurrent symptoms can disrupt personal or professional activities, upset emotional well being, and limit individual potential.A significant proportion -- 35% to 40% -- of individuals who report IBS in the community are male. Approximately 60% to 65% of individuals who report IBS in the community are female.IBS is a major women's health issue. Data reveals an increased risk of unnecessary surgery for extra-abdominal and abdominal surgery in IBS patients. For example, hysterectomy or ovarian surgery has been reported in female patients with IBS as high as 47% to 55% and has been performed more often in the IBS patient than in comparison groups.There is a pressing need to support educational programs about IBS to the public and health care providers. Anemia, bleeding, weight loss, or fever are not characteristic of IBS. You should alert your physician immediately if you are experiencing these symptoms. http://www.aboutibs.org/characteristics.html


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## bonniei (Jan 25, 2001)

Talissa I believe one of the sites selling DA-IBS has also posterd that it works on the small bowel flora"Digestive Advantageï¿½ IBS helps normalize the small intestine supporting normal bowel functions. It is formulated for the dietary management of Irritable Bowel Syndrome. "PRESIDENT of DA-IBS, Can you elaborate on this please?Talissa I will try to l0ok at your info later when I have time.


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## bonniei (Jan 25, 2001)

eric, so does UNC think that LBT is reliable for SIBO?


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## Talissa (Apr 10, 2004)

Post infectious IBS leads to IBS!! After the intial, infection inflammation HAS resolved. Really?"Role of Immune or Inflammatory MediatorsIBS-like symptoms have been reported in 7% to 30% of patients who have had a recent history of proven bacterial gastroenteritis; this has been termed postinfectious IBS (PI-IBS).[41] A subset of patients with IBS can trace the development of their symptoms to an episode of infectious diarrhea, primarily bacterial[42] or amebic,[43] and possibly even viral,[44] in etiology. Risk factors for PI-IBS include female sex, duration of acute diarrheal illness, and the presence of significant life stressors occurring around the time of the infection.[41]Investigators have found that there are colonic mucosal abnormalities in PI-IBS. One study compared rectal mucosal cellularity and intestinal permeability in patients at 2, 6, and 12 weeks and 1 year after an acute infection with Campylobacter enteritis with those of patients with a history of PI-IBS and healthy controls.[45] Compared with controls, patients with a previous Campylobacter infection were found to have increased numbers of intraepithelial lymphocytes and EC cells and increased intestinal permeability, even after 1 year, as did the patients with PI-IBS. When the secretory granules of the EC cells were evaluated, patients with PI-IBS had granules containing mainly serotonin. The EC cells in healthy control subjects had granules containing primarily PYY, a peptide associated with antisecretory effects. It is conceivable that these findings play a role in the GI symptoms (eg, diarrhea, mucus in the stool) in at least a subset of patients with IBS." http://www.medscape.com/viewarticle/463521_3 _______________Stop making things up Eric, seriously. One year after the infection, the wall is still inflamed.You find anything recent that shows after six years, there is no more abnormal inflammation, or leave it alone.Cells renew themselves Eric. Did you know that?A "molecular change" is never permanent.I'm trying not to get frustrated again._________________________And THIS kind of thinking is why the allopathic methods of MDs is failing(I'm quoting an MD here)& why naturopathic methods are succeeding:


> quote: For such patients it is important to establish realistic treatment goals that require their understanding, participation, and cooperation with the physician. They should be made aware that because a cure is not likely, their attention should be focused on health, not illness, with an aim toward controlling the symptoms and improving overall functioning. Physicians should also be aware that a high proportion of patients with severe IBS have been victims of child or sexual abuse.


Grrrrr. These people should be sued. I personally was never molested or abused as a child, but I was given TETRACYCLINE for a bloody year to treat zits.Tetracycline is a broad spectrum bacterial killer. Good & bad bacteria.There are many other ways to kill good bacteria in the gut.Things are changing Eric, & it's pointing to gut flora.This is the knowlegde that gets people better:


> quoteostinfectious IBS, a disorder believed to be caused by alterations in intestinal microflora."


 http://www.emedmag.com/html/pre/gic/consults/041501.asp


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## Talissa (Apr 10, 2004)

For people with postinfectious IBS, Eric, you are as helpful as the average MD.This is not a good thing.


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## kel1059 (Feb 28, 2003)

eric,talissa is doing the same to you as Mike NoLomotil (NML) used to do to you. they are doing circles around you as you stumble from one claim to the next. bonniei was correct -- you can't interpret what you read. please stick to the HT end of the problem.


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## Talissa (Apr 10, 2004)

To be specific about how I percieve our differences in perception, here's some of the info you are reading:" Although such a mechanism could be protective, prolonged hyperexcitability of submucosal neurons may contribute to detrimental symptoms, like those often seen in post-infectious IBS. Recent studies of patients with IBS have demonstrated that a proportion of them display increased numbers of colonic mucosal mast cells (Chadwick et al. 2002). In preliminary studies, we have found increased spontaneous release of mast cell tryptase from colonic tissue obtained from patients with IBS (Barbara et al. 2002)." http://jp.physoc.org/cgi/content/full/547/2/531 This is inflammation, increased mucosal mast cells, in my mind along the brush border of the luminal layer of the intestinal wall._______________________________It can be reduced by ending the dysbiosis & with targeted anti-inflammatories/immune system regulators, such as "Colostrum" which has been used successfully in clinical trials against Colitis:2000Donald R. Henderson, MD, MPHChief of StaffDaniel Freeman Memorial Hospital;Assistant Clinical Professor of Medicine and GastroenterologyUCLA School of MedicineLos Angeles, California


> quotehysicians also should note that IBS recently has been linked to possible infection or bacterial imbalance. Thus the use of antibiotics and probiotics may prove to be of value. *In addition, nutritional supplements like bovine colostrum have been proved to be of great value in treating colitis and, I believe, similarly may be of value in treating IBS.* *The allopathic model for treating IBS has failed miserably * because we do not have much understanding or agreement about how to manage this problem. Therefore, from a therapeutic standpoint, I believe we should look toward the alternative models and further investigate the mindï¿½gut interaction.


 http://www.medicalcrossfire.com/debate_arc...er_Exchange.htm


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## bonniei (Jan 25, 2001)

kel, I don't think I have ever said that eric can't interpret what he reads. I would however appreciate summaries instead of long articles post after post. I don't think I read as much as I have read from eric's posts even when I did my PHD. However these days he seems to be highlighting parts of the articles he posts so that I atleast know what points he wants to make. So that's all for the good.


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## Talissa (Apr 10, 2004)

Eric,You say PI iBS either clears up w/i 5-6 years, or turns into IBS, right?Medline Gastroenterology says(May 2003):


> quote: PI-IBS is associated with modest increases in mucosal T lymphocytes and serotonin-containing enteroendocrine cells. *Both the histologic changes and symptoms in humans may last for many years with only 40% recovering over a 6-year follow-up. *


 http://www.ncbi.nlm.nih.gov/entrez/query.f...4&dopt=Abstract Also, the chances of recovering from PI IBS are much lower if the infection(bringing on PI IBS) lasted more than 21 days.This was unfortunately the situation in my case because I was on vacation when I got the Giardia bacteria._______________________________So please, leave it alone. *Most people have PI IBS long after 6 years.* And it has nothing to do with psychological factors.


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## Talissa (Apr 10, 2004)

Sidenote--More irony--I got a traveller's infection traveling in the US, from my home in the tropics.You know the term "tropical sprue"?Maybe I got "American Sprue" !


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## Talissa (Apr 10, 2004)

For clarification:"histological" refers to "histology" which means the microscopic study of human cells.For instance, microscopic inflammation caused by increased mucosal cells.Inflammation along the wall doesn't mean the cells of the wall "inflame" or puff up, it means there's an increase in the number of cells along the wall.This can be downgraded with anti-inflammatories.But if anyone knows a sure-fire way to decrease the inflammation along the wall, I'd love to know!!I'm trying just ibsacol right now, but also have NZ Colostrum ordered.I will report any results from my own biochemical testing lab(aka--my intestines).T-


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## flux (Dec 13, 1998)

> quote:"Most adverse effects of the indigenous gut flora are caused by the intense metabolic activity of luminal organisms. The following are associated with Putrefaction dysbiosis:


Make that the following are associated with *normal * activities of gut flora.


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## Talissa (Apr 10, 2004)

Hmmmm, so you're saying everyone gets the intense metabolic activity of luminal organisms in the way of improper immune response--abnormally inflamed brush border from the interaction with pathogens not kept in check by beneficial bacteria(probiotics that should naturally be present)?>>>"...The significance of appropriate interactions between intestinal cells and bacteria in creating a healthy intestinal immunity was also demonstrated by this research.With this knowledge, researchers have a better perspective on what goes awry in some intestinal diseases." http://www.niddk.nih.gov/federal/advances/2004/ddn.pdf ___________________________Probiotics and immunity Regarding the influence of probiotics on cell-mediated immunity, research has shown that intake of probiotic bacteria increases the production of IgA antibodies. (1) (2) (3) (4) The activity of macrophages and NK-cells also increase (5) (6) (7), which leads to an increased killing of bacteria. It has also been shown that probiotic bacteria modulate the cytokine activity. Cytokines are signal substances in the immune system, which regulate the activity of the immune cells. Cytokines also work as a link between the immune system and the nervous system. Probiotics and the intestinal barrier The mucosa of the intestines is a selective barrier which, when functioning normally, prevents the penetration of potentially noxious agents into the bloodstream, while still enabling the passage of useful substances, such as nutrients. The health of the intestinal wall is totally crucial to our health. Probiotic bacteria have a healing effect on the intestinal mucosal membrane by the stimulation of the formation of epithelial cells and by decreasing inflammation in the intestinal mucosa, shown by a decreased production of inflammatory cytokines during the intake of probiotic bacteria.(8) It has been shown that atopic eczema is associated with intestinal inflammation and increased antigen transfer over the intestinal barrier.(9) Treatment of food-allergies with probiotics has shown good results.(8) Allergy The intestine has an important function in working as a barrier against the surrounding world. This barrier is maintained by tight-junctions between the epithelial cells, by production of IgA antibodies and by the normal microbial flora. It is extremely important that only harmless substances are absorbed while the harmful substances are secreted via the faeces. Studies show that individuals allergic to cowï¿½s milk have defective IgA production (10) and an increased permeability of the intestinal mucosa.(11) This results in an increased absorption of macromolecules through the intestinal mucosa.(12) The increased permeability is most probably caused by local inflammations due to immunological reactions against the allergen. This damages the intestinal mucosa.(8) Probiotics and allergy Research has shown that probiotics have a healing effect on cowï¿½s milk allergy both regarding the symptoms of eczema and the intestinal inflammation.(8) Probiotics have a healing effect on the intestinal mucosa and decrease the passage of macromolecules over the intestinal wall, thus preventing and adjusting what is referred to as a ï¿½leaky gutï¿½. A study done by Kalliomaki & Co shows that the supplementation of probiotics during pregnancy and breast-feeding decreases the frequency of allergy among the children of allergic mothers.(13) http://www.probiohealth.nu/pdf/probiotics_res.pdf


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## Talissa (Apr 10, 2004)

MEDSCAPE--"The demonstration that immune and epithelial cells can discriminate between different microbial species has extended the known mechanism(s) of action of probiotics beyond simple barrier and antimicrobial effects. It has also confirmed that probiotic bacteria modulate mucosal and systemic immune activity and epithelial function."(this is what I said above, but in medicalese)..."Level II evidence is emerging in support of the use of probiotics in other gastrointestinal infections, in the prevention of postoperative bacterial translocation, in IBS, and in both ulcerative colitis and Crohn disease. "..."The use of probiotics and prebiotics as therapeutic agents for gastrointestinal disorders is rapidly moving into the mainstream." http://www.medscape.com/viewarticle/470571_4


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## eric (Jul 8, 1999)

Those cell are connected to serotonin. You remember our serotonin discussion you dismissed out of hand, which are connected to mast cells and EC cells found in PI IBS?"Post infectious IBS refers to cases of IBS, which can be shown to have arisen after a distinct case of gastroenteritis caused by an infection. This lecture gave a comprehensive review of the literature on the subject, including a large amount of data from R. Spiller and his group.Studies have looked at patients with IBS, and shown a large proportion with an acute stage of onset, suggesting an infectious cause:Many IBS studies have been performed on patients seeking medical treatment and within Gastrointestinal units. More recent studies have used databases of patients within the community as a whole, and *have suggested that an acute episode of gastritis can lead to IBS.* Several studies have focused on communities and the incidence of post-infectious IBS seen within patients visiting their doctors. A study published in the British Medical Journal by Rodriguez and Ruigï¿½mez *showed that in the year following an episode of gastritis, patients were 10 times more likely to have IBS then patients in the general population. * This study used patients identified using the British General Practice Research Database, containing data on patients recorded by general practitioners (Rodriguez and Ruigï¿½mez 1999, BMJ 318: pp. 565-566), allowing this study to contain 584 308 subjects in the general cohort and 318 in the gastroenteritis cohort.Other studies with smaller patient groups have shown similar results:28 (7%) of the patients *went on to develop functional IBS. However, a further 78 of the cases developed altered bowel habits, with similar symptoms to that of the new IBS cases, lacking the pain.* As a result they did not meet the Rome criteria for IBS (Neal et al, BMJ 1997, 314(7083): pp. 779-782).Other studies have looked at specific infections; McKendrik (McKendrik and Read, J Infect. 1994; 29(1)







p. 1-3) presented a study of patients with salmonella infections, 31% of the patients acquired IBS post infection. Gwee et al (Gwee et al, Lancet. 1996; 347(8995): pp. 150-3) looked at cases of gastroenteritis, and found that *29% of patients suffered from new IBS after resolution of the infection. * One of the major problems with this type of study results from the fact that people often have a bout of vomiting or stomach distress due to food. Consequently few people specifically remember having a *bacterial infection that rapidly resolves.* This would suggest that the number of cases of IBS resulting from a bacterial infection is actually higher than that shown in studies.Several groups have compared differing factors with an increased risk of IBS. One new method involves using specific cells (e.g. Hep2 cells) and reacting them with bacteria. If you get an increased elongation of the cell, then the bacterial strain used can be considered to be capable of inducing IBS. This induced elongation gives a much higher risk of IBS than other factors, such as gender or life stress.Prospective studies have shown that there are elevated CD8+ lymphocytes in patients with post-infectious IBS after 1 year. *This coincides with an increased permeability DURING a bacterial infection,* and an increase in inflammatory cells in IBS patients, *suggesting that PI-IBS patients suffer from a lack of down regulation of the inflammatory response.  Indeed, some studies have shown that some IBS patients are deficient in TGFb and IL-10.* Following infections with campylobacter enteritidis there is an *increase in entero-endocrine cells. In the case of IBS patients this increase does not return to normal, * remaining up to 10 fold higher then that seen in normal controls.Long-term prognosis for PI-IBS patients: *This study, and others like it, suggests that 2/3 of PI-IBS patients recover within 6 years. The majority of recovering patients showed no anxiety, while the persistent sufferers did, suggesting that anxiety impairs recovery from PI-IBS.* The take home message from this lecture what that there appears to be significant evidence leading to the role of post-infectious IBS, although host factors play a large role in susceptibility. However, *PI-IBS has a reasonably high chance of recovery over the long term, if there are no other contributing factors (such as anxiety)."* http://wwwhost.gu.se/cgf/fouschema.html#Robin graphs are on the site.From - Report on the 5th International Symposium onFunctional Gastrointestinal DisordersApril 4, 2003 to April 7, 2003 Milwaukee, Wisconsin By: Douglas A. Drossman, M.D., UNC Center for Functional GI and Motility Disorders at Chapel Hill, and William F. Norton, IFFGDBasic Principles -- Brain-Gut Moderators: Emeran Mayer MD; Robin Spiller MD. Panel: Robin Spiller MD; Jackie Wood PhD; George Chrousos MD; Yvette Tachï¿½ PhD; Lisa Goehler PhD; G.F. Gebhart PhD; Emeran Mayer MD. "Robin Spiller, University Hospital, Nottingham, England began the session by noting the difficulty in separating disorders of structure ("organic") from disorders of function. He noted, "The difference is based on how high the power of your microscope is." This was elaborated upon in his presentation on Post-infectious Functional GI Disorders. *It has been observed that IBS-like symptoms, that persist for 6 months to a year or longer, may appear after a bout with an acute infection in the gastrointestinal tract (e.g., food-poisoning).* *This is termed, "post-infectious IBS." A study by Gwee et al showed that the presence of unusual or amplified life stress at the time of onset of infection increased the chances of developing IBS symptoms. * * Inflammation persisted in patients with IBS-like symptoms but did not in patients whose symptoms resolved. This suggests that the brain's management of certain stressful stimuli (i.e., psychologic distress) affects the brain-gut system's ability to inhibit inflammation. "* " *An initial response to an infection in the gastrointestinal tract can involve the neurotransmitter, serotonin, which acts as a messenger (mediator) to cells involved with the immune response.* Immune cells -- mostly in the blood, but also in the lymphatic system -- enter the infected area and remove the invader. Additionally, the body adaptively removes the infection (e.g., via vomiting or diarrhea -- normal beneficial responses that help the body expel an infecting organism). Persistence of the underlying inflammatory response may lead to post-infectious disorders of function. A variety of neuroimmune responses can lead to intestinal over-responsiveness (sensitization) and other clinical effects. These responses include direct toxicity to nerves that influence intestinal contractions, alteration in gut immune activation, abnormalities of serotonin metabolism, and persisting low-grade inflammation. IBS developing after infective gastroenteritis is associated with subtle increases in enteroendocrine : *note serotonin containing cells * and chronic inflammatory cells *note: Mast cells * in the gut mucosa. *The net effect may be to increase serotonin availability in the gut and enhance secretion and propulsive motility patterns. * Serotonin antagonists may be beneficial in such "" *Major inflammatory responses have not been observed in most IBS patients.* *However, in some studies subtle changes associated with inflammation have been noticed, such as increased presence of mast cells * (a type of immune system cell present in blood and tissue). Jackie Wood, Ohio State University College of Medicine discussed the Effects of Inflammation on the Gut Enteric Nervous System, specifically noting the importance of mast cell degranulation ( *the release from within the cell of granules, or small sacs, containing chemicals that can digest microorganisms and fight infection)." * " *In tissue mast cells accumulate around nerve endings of nerves that contain the neurotransmitter serotonin. * The release of substances that can induce activity in excitable tissue (i.e., *histamine* , Interleukin-1 (IL-1), and bradykinin) *by mast cells can affect receptor and neurotransmitter function in the enteric nervous system - the part of the autonomic nervous system that controls function of the gastrointestinal tract.* *In other words, when mast cells in the intestinal lining empty their contents in response to an infection, they activate nearby nerve endings. In a subgroup of patients, this can have significance in terms of resulting clinical consequences of diarrhea and abdominal discomfort.2* "Yvette Tachï¿½, University of California Los Angeles discussed *Stress and Inflammation* . *The experience of stress is an adaptive behavior common to all living organisms. The activation of corticotropin releasing factor (CRF) signaling pathway, is the major mediating mechanism involved with the body's stress response system in which gastric emptying is inhibited (with possible loss of appetite) while colonic motor activity is stimulated (producing a loose stool or a sensation of bowel urgency). * *There is growing evidence that activation of this CRF pathways impacts on inflammation, autonomic nervous system function, immunity, and clinical behavior or illness, all of which may be linked to the pathophysiology of the functional gastrointestinal disorders. * http://www.iffgd.org/symposium2003brain-gut.html "Central activation -- the rapid short-term biophysical and biochemical changes in neurons that make possible such activities as thought, perception, and voluntary movement -- appears to increase as intensity of stimulus increases. However, repeated exposure can lead to adaptation, as the brain adjusts to the stimuli, with decreased central activation. *In studies, IBS patients are differentiated from healthy controls by showing greater activation of an area of the brain essential for conscious pain (the anterior mid-cingulate component of the anterior cingulate cortex).* *It is in this region in the brain where the systems concerned with emotion or feeling, attention, and working memory interact. On the other hand, controls (and also patients with inflammatory bowel disease who have adapted to the visceral signals) show greater activation of the descending pain inhibitory pathways in areas of the brain involved in the suppression of pain (in the brain stem in the region of the periaqueductal gray). * In summary, brain imaging is a rapidly growing new technology for studying how pain is processed as well as how pain treatments may work. Although there are many similarities between the brain response to visceral and somatic pain some consistent differences have emerged with visceral stimulation showing greater affective responses. *Patients with IBS show some differences in how their brains respond to a visceral event and these effects may relate directly to both the hypersensitivity and hypervigilance associated with this disorder.* http://www.iffgd.org/symposium2003imaging.html IBS a misunderstood condition.Dr. Brian Lacy, an assistant professor of medicine at Johns Hopkins University School of Medicine in Baltimore, defines IBS and explains its symptoms, possible causes and treatments. "Do we know what is wrong with the digestive systems in people with IBS?Over the last 50 years, there has been a dramatic change in our thinking about IBS. We used to attribute IBS only to abnormal gut motility. That means that patients may have muscle or nerve abnormalities in the gastrointestinal tract. *Over the last 20 to 30 years, however, we learned that patients with IBS sense things in their gut differently. * *Their body may interpret normal gut function as abnormal; this is called visceral hypersensitivity.* During the day, we all have the stomach growling, mixing, churning and emptying of things in the colon, as well as movement in the small intestine. *Most of us are not affected by those signals. But many patients with IBS, for whatever reason, seem to feel those signals and find them painful. It is uncomfortable and frustrating for the patient.* *Finally, we learned in the last decade, through studies using MRI and CAT scans of the brain, that patients with IBS seem to sense pain in their brains differently. * What are neurotransmitters and what role do they play in IBS?Neurotransmitters are substances that transmit nerve impulses. *Serotonin is a major neurotransmitter throughout the nervous system in the gut.* *Serotonin has been shown to be very important in gut peristalsis, which relates to the movement of contents in the intestinal tract from the mouth through the stomach, through the small intestine and colon.* Gut peristalsis occurs all the time: it's how we empty our food and digest our meals. *It also seems to be important in gut sensation. As a result, we believe that serotonin may play a major role in IBS and may be a unifying link in these patients who have disordered gut motility and disordered sensation. * http://dhn-online.healthology.com/focus_ar...i_misunderstood The Neurobiology of Stress and EmotionsBy: Emeran A. Mayer, M.D., UCLA Mind Body Collaborative Research Center, UCLA School of Medicine, California "We often hear the term "stress" associated with functional gastrointestinal (GI) disorders, such as irritable bowel syndrome (IBS). Many patients experience a worsening of symptoms during times of severely stressful life events. But what is stress? How often does it occur? How does our body respond to stress? This article explores the mechanisms that link stress and emotions to responses that have evolved to ensure survival and that, in the modern world, affect healthï¿½including gastrointestinal function. ""Stressors are internal or external factors or stimuli that produce stress. Stress is the neurophysiological and subjective response to the stimuli. ""In order to understand how a chronically enhanced stress response can produce the cardinal symptoms of IBS (abdominal pain and discomfort associated with altered bowel habits) we have to go back to the earlier section on the emotional motor system: activation of the stress system will stimulate contractions and secretion in the sigmoid colon and rectum. Depending on the specific emotional context (fear vs. anger), the upper GI tract will be either inhibited (fear) or stimulated (anger). In addition, recent research in animals has demonstrated a phenomenon referred to as stress-induced visceral hyperalgesia. What this means is that in vulnerable animals, exposure to an acute moderate stressor will make the colon more sensitive to distension (and the perception of discomfort or pain). "Perceptions of pain, muscle tensions, and other somatic symptoms can cause stress levels to spiral upward. Self-regulation strategies that reduce unpleasant symptoms offer both physical and psychological relief." ï¿½R. Sovik Why do the symptoms go away after one stressful situation has resolved and persist in another? Amongst many factors, anxiety and fear generated by IBSsymptoms themselves are sufficient in many patients to maintain the stress responsiveness in a chronically enhanced state. Some of the more common symptom related anxieties include: *Am I close enough to a bathroom when my symptoms come on? Will I be OK for the rest of the day, unless I completely empty my colon in the morning before leaving the house? * http://www.aboutibs.org/Publications/stress.html *Tal, this is the same DR Mayer/author you qoute from this article.* Inflammatory Bowel Disease and Irritable Bowel Syndrome: Separate or Unified? (07/15/03)"Comment from Emeran Mayer, M.D. -- In contrast to the common interpretation of the term "stress" as a psychological phenomenon, it should be understood as any real or perceived perturbation of an organism's homeostasis, or state of harmony or balance. For example, in this viewpoint a severe hemorrhage, starvation, extreme temperature, or worry about the unpredictable onset of abdominal pain all qualify as stressors -- some as "physical" stressors, others as "psychological" stressors. The fear to leave the house in the morning without knowing if one can make it to work without having to stop on the freeway because of an uncontrollable bowel movement, or the fear of experiencing uncontrollable abdominal discomfort during an important business meeting are sufficient stressors to activate the central stress system. *The central stress system involves the release of chemical stress mediators in the brain (such as corticotropin releasing factor), * which in turn *orchestrate an integrated autonomic, behavioral, neuroendocrine, and pain modulatory response. * *This biological response in turn will alter the way the brain and the viscera interact, and this altered brain-gut interaction can result in worsening of IBS symptoms. * *Thus, pain and discomfort, fear of these symptoms, activation of the stress response, and modulation of the brain-gut interactions by stress mediators are part of a vicious cycle which need to be interrupted to produce symptom relief. "* http://www.aboutibs.org/Publications/StressDefined.html Mast Cells and Stressï¿½A PsychoneuroimmunologicalPerspectivehttp://216.109.117.135/search/cache?p=ibs+...7841D0&c=482&yc =53349&icp=1[/URL]The link between IBS and bladder problems and the mast cell."Nevertheless, IC patients with nonulcerative IC showed mast cells to be highly activated. 'The increase in bladder mast cells was recently related to possible high local levels of *corticotrophin- releasing factor* .... Thus, it appears that the mast cell has a pathogenic role in at least a subset of patients with interstitial cystitis.'""Functional interactions have been suggested to have association with the *central and peripheral nervous system. * It is currently being invoked in the pathophysiology of certain inflammatory diseases. Studies have shown by using Electron Microscopic methods *that the mast cells can be related to sensory nerve fibers, moreover, direct nerve stimulation results in mast cell activation, and the histamines as we know can stimulate the peripheral nerves. "* "IBS is similar to IC, as it occurs more in women than in men. The symptoms are , abdominal pain and can be associated with urinary frequency, dyspareunia and fatigue. *IBS is also exacerbated by stress and shows hypersensitivity to visceral stimuli,' a process that is also selectively activated by the sympathetic nervous system.* *Stress is KNOWN to affect the development of inflammation, and the contribution of the nervous system to the regulation of immune and inflammatory processes is now accepted.' "* http://www.ic-network.com/sant/sant12.html Histimine and mast cellsColonic mucin release in response to immobilization stress is mast cell dependent "These findings provide direct evidence for a link between mast cells and the intestinal epithelium in the pathogenesis of stress-related responses. Our findings could be of importance for understanding the pathophysiology of irritable bowel syndrome, in which intestinal mast cell activation (17, 21, 38) and mucus discharge (8) have been reported. " http://ajpgi.physiology.org/cgi/content/full/274/6/G1094 Gut Feelings: The Surprising Link Between Mood and Digestion"If you've ever felt your insides twist in knots before a big speech, *you know the stomach listens carefully to the brain. In fact, the entire digestive system is closely tuned to a person's emotions and state of mind,* says William E. Whitehead, PhD, a professor of medicine and an adjunct professor of psychology at the University of North Carolina."" *People with irritable bowel syndrome often suffer flare-ups during times of stress and anxiety, and even perfectly healthy people can worry their way to stomach pain, nausea, diarrhea, constipation, or other problems.* Even if a doctor can't find anything physically wrong, the misery is real. ""Listening to your gut It may surprise many people to learn that the gut actually contains as many neurons (nerve cells) as the spinal cord. In an article in the medical journal Gut, author J. D. Woods and colleagues compare this network -- known as the *enteric nervous system, or ENS -- to a "local mini-brain" storing a library of programs for different patterns of gut behavior." Woods and colleagues compare the ENS to a microcomputer with its own independent software, "whereas the brain is like a larger mainframe with extended memory and processing circuits that receive information from and issue commands to the enteric computer."* With all these messages, the connection between the brain and the digestive system is a busy two-way street. *The central nervous system releases chemicals (acetylcholine and adrenaline) that tell the stomach when to produce acid, when to churn, and when to rest. Similar signals help guide the movements of the intestines. The digestive system responds by sending electrical messages to the brain, creating such sensations as hunger, fullness, pain, nausea, discomfort, and possibly sadness and joy."* "The stress alarm Whatever messages may be passing back and forth, they can easily become garbled in times of stress. *When the brain senses a threat, real or imagined, it sounds the alarm by flooding the body with adrenaline and another hormone called CRF (short for corticotropin-releasing factor). * *These hormones trigger the "fight or flight" response * helpful back in the days when humans had to run from lions, but a potential liability when we lose a job or go through a divorce.If you suffer from frequent emotional distress -- perhaps because of extreme stress, depression, or anxiety -- the unrelenting flood of *adrenaline* and CRF will *take a toll on your digestive system. For one thing, the hormones can make the cells in the stomach and intestines extra-sensitive to pain. As a result, normal contractions and movements can become excruciating. The new signals can also disrupt the motion of the intestines, causing bouts of constipation or diarrhea."* " *In a similar manner, strange messages along the gut-brain axis also seem to be a major cause of "functional" dyspepsia, or indigestion.* People with dyspepsia often experience the discomfort of constant ulcer pain without actually having ulcers. *Stress definitely makes the symptoms worse, but the effect isn't nearly as dramatic as with irritable bowel syndrome. If adding stress to functional dyspepsia is like throwing woodchips on a fire, combining stress with IBS is like dousing a blaze with gasoline.* "The influence of the mind on the gut goes beyond functional diseases. For instance, people with Crohn's disease or ulcerative colitis -- two conditions with clearly physical origins -- often suffer flareups during times of emotional stress. And in a recent survey, 68 percent of people with basically healthy digestive systems said stress gives them stomachaches.""The two realms constantly exchange streams of chemical and electrical messages, and anything that affects one is likely to affect the other. *The connections between the two systems are so tight that scientists often refer to them as one entity: the brain-gut axis.* (The brain-gut axis is a hot topic in medicine. In the summer of 2001, more than 100 researchers from around the world gathered in Los Angeles for a convention called "2001: A Brain-Gut Odyssey.") For people suffering from persistent digestive troubles unconnected to disease, such research suggests that reducing stress, depression, and anxiety may go a long way toward calming the gut." http://www.ahealthyme.com/article/primer/101186767 The Sympathetic NerveAn Integrative Interface between Two Supersystems: The Brain and the Immune System "The brain and the immune system are the two major adaptive systems of the body. *During an immune response the brain and the immune system "talk to each other" and this process is essential for maintaining homeostasis."* "hypothalamic-pituitary-adrenal (HPA)-axis. This axis involves corticotropin releasing factor (CRF) and this axis is operative in a series of situations in which "stress" appears to play a role. These include responses to environmental and social factors, psychiatric and psychological adaptation, and immunologic and inflammatory responses to infectious agents such as viruses, bacteria and parasites. " http://pharmrev.aspetjournals.org/cgi/content/full/52/4/595 "Emeran Mayer, M.D. has applied Dr. LeDouxï¿½s concepts regarding the emotional brain to the gastrointestinal tract (Mayer EA, Naliboff B, and Munakata. The evolving neurobiology of gut feelings. Prog Brain Res 2000;122:195-206). Click here to read an abstract of this medical journal article. Even though we may be completely unaware of any associated emotional feeling, such as fear, anxiety, or anger, the programmed emotional responses are generated in our internal organs, particularly the gastrointestinal tract (gut). For example, the emotion of fear is associated with the inhibition of the upper gut (stomach and duodenum) contractions and secretions, leading to the symptoms of fullness, bloating, loss of appetite, nausea, and even vomiting. The emotional gut response of fear stimulates the lower gut (sigmoid colon and rectum), which can cause diarrhea, cramping, and abdominal pain. From the perspective of evolution, this response program or pattern evolved in order to reduce exposure of the gut to ingested food and waste material while energy is shunted to the cardiovascular and musculoskeletal systems in order to maximize the effects of the fight and flight response and survival potential. In other words, the last thing that your body needs to be doing when your life is threatened is to be digesting your lunch! And to emphasize the point again, all of this emotional gut response can occur without your being consciously aware of the emotional feeling of fear. ""These remarkable and complex programs that have evolved to activate the stress response are counterbalanced by mechanisms to turn it off when the threat has passed or to blunt the response with repeated occurrences of the same stressor. These systems of activation and deactivation of the stress response have evolved over millions of years and have been perfected in order for animals to deal with survival threats in the cycle of prey and predators. But our lives are usually not threatened in modern society. Instead, these same mechanisms are turned on by the hassles and hustles of every day living. Unfortunately, this good stress can become bad stress through the process of allostatic load, which is the wear and tear of severe, repeated, or sustained chronic stress. Symptoms, syndromes, illness, and disease can result." http://www.parkviewpub.com/parksub/n5.html "The Little Brain in the GutThis is supplemental information for this topic marked by the little computer icon on page 83 of the book, Irritable Bowel Syndrome and the MindBodySpirit Connection, by William B. Salt II, M.D. and Neil F Neimark, M.D. (Columbus: Parkview Publishing, 2002). *You have two brains: one in your head and another in your gut. * Dr. Jackie D. Wood is a renowned physiologist at The Ohio State University. He calls the second brain, "the-little-brain-in-the-gut." This enteric nervous system is part of the autonomic nervous system and contains over one hundred million neurons, which is as many as are in the spinal cord. This complex network of nerves lines the walls of the digestive tract form the esophagus all the way down to the colon. *This little brain in the gut is connected to the big brain by the vagus nerves, bundles of nerve fibers running from the GI tract to the head. All neurotransmitters, such as serotonin that are found in the brain are also present in the gut.* *Dr Wood has discovered that this little-brain-in-the-gut has programs that are designed for our protection and which are very much like computer programs. They respond to perceived threats in the same way that the limbic system or the emotional brain does. So the threat of a gastrointestinal infection can activate the program that increases gut contractions in order to get rid of the infection. The symptoms are abdominal cramping and diarrhea. * *Dr. Wood has determined that a type of cell found in the body and the gut, called the mast cell, is a key to understanding the connection of the big brain in the head with the little-brain-in-the-gut. * *Mast cells are involved in defense of the body. In response to certain threats or triggers, such as pollen or infection, mast cells release chemicals, such as histamine, that help to fight off the invader. * Histamine is one of the chemicals that causes the symptoms of an allergy or a cold. When an infection of the gut occurs, such as food poisoning or gastroenteritis, *the mast cells of the gut release histamine. The little-brain-in-the-gut interprets the mast cell signal of histamine release as a threat and calls up a protective program designed to remove the threat ï¿½ at the expense of symptoms: abdominal pain and diarrhea. * *The brain to mast cell connection has a direct clinical relevance for irritable bowel syndrome and other functional gastrointestinal syndromes. * *It implies a mechanism for linking allostasis and the good stress response to irritable states (e.g., abdominal pain and diarrhea) of the gut. Mast cells can be activated to release histamine in response to perceived psychological stress, whether the stressor or trigger is consciously perceived or not.* *So the end result is the same as if an infection activated the program in the-little-brain-in-the-gut: abdominal pain and diarrhea. "* http://www.parkviewpub.com/parksub/n5.html Rome CommitteeFunctional GI Disorders Coordinating Committee Douglas A. Drossman, MDChairChapel Hill, NC USA "Dr. Drossman is a Co-director of the Center and Professor of Medicine and Psychiatry at UNC-CH. He established a program of research in functional gastrointestinal disorders at UNC more than 15 years ago and has published more than 250 books, articles, and abstracts relating to epidemiology, psychosocial and quality of life assessment, design of treatment trials, and outcomes research in gastrointestinal disorders. Dr Drossman's comments on foods for IBS Health.Shawn Eric,To say that people with IBS may get symptoms from food intolerances is an acceptable possibility, *since the gut will over react to stressors of all types * including food (high fat or large volumes of food in particular). Futhermore, there can be specific intolerances. So if you have a lactose intolerance for example, it can exacerbate, or even mimic IBS. Other examples of food substances causing diarrhea would be high consumers of caffeine or alcohol which can stimulate intestinal secretion or with the latter, pull water into the bowel (osmotic diarrhea). The same would be true for overdoing certain poorly absorbed sugars that can cause an osmotic type of diarrhea Sorbitol, found in sugarless gum and sugar substituted foods can also produce such an osmotic diarrhea. Even more naturally, people who consume a large amount of fruits, juices or other processed foods enriched with fructose, can get diarrhea because it is not as easily absorbed by the bowel and goes to the colon where it pulls in water. So if you have IBS, all of these food items would make it worse. *However, it is important to separate factors that worsen IBS (e.g., foods as above, stress, hormonal changes, etc.) from the cause or pathophysiology of IBS. Just like stress doesn't cause IBS, (though it can make it worse), foods must be understood as aggravating rather than etiological in nature. * *The cause of IBS is yet to be determined. * *However, modern research understands IBS as a disorder of increased reactivity of the bowel, visceral hypersensitivity and dysfunction of the brain-gut axis. There are subgroups being defined as well, including post-infectious IBS which can lead to IBS symptoms.* *Other work using brain imaging shows that the pain regulation center of the brain (cingulate cortex) can be impaired, as well as good evidence for there being abnormalities in motility which can at least in part explain the diarrhea and constipation. * *So finding a specific "cause" of IBS has grown out of general interest in place of understanding physiological subgroups that may become amenable to more specific treatments.* Hope that helps.Doug http://www.ibshealth.com/ibs_foods_2.htm


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## kel1059 (Feb 28, 2003)

> quote: Eric just demonstrated what propagandistic tool he knows how to use best: stacking the deck. His amateurish cut and paste jobs look like it too.quote:--------------------------------------------------------------------------------Stacking the Deck: One stacks the deck when he/she leaves out relevant information, tells half-truths, exaggerates, or otherwise tampers with the facts. We often see this technique used in the presenting of statistics and polling results.Reference: http://rhetorica.net/propaganda.htm Card Stacking. "Stack the cards" or "arrange the deck" of facts against the truth. Use under-emphasis and over-emphasis. Suppress facts that don't support your side.Reference: http://brainstorm-services.com/wcu/propaganda.html --------------------------------------------------------------------------------Eric wrote:quote:--------------------------------------------------------------------------------Well that's funny he wrote these then"IBS PublicationsAnother look at bacteria and IBSBy Douglas A. Drossman, M.D. http://www.aboutibs.org/Publications/bacteria.html "Bacterial infection as a possible factor in irritable bowel syndrome (IBS) has long been a subject for research."Bacterial Overgrowth in IBS http://www.med.unc.edu/wrkunits/2depts/med...rowthandibs.htm --------------------------------------------------------------------------------Eric why are you quoting outdated information? Dr. Drossman's critiques on the SIBO study is outdated and moot. With the gobs of time you spend compiling your database of articles and links, I'd expect you to be up to snuff on this.


eric it is obvious that you are hiding your lack of intellect (or understanding of the problem at hand) behind these monstrously long cut and pastes. you have no shame do you?


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## eric (Jul 8, 1999)

Understanding IBS (Irritable bowel Syndrome): A Primer for Patients Chapter 7: *Some Common Conditions Where Diarrhea and Gas with Bloating Can Be Misinterpreted as Evidence of IBS* James Christensen, M.D. and Robert W. Summers, M.D.Peer Review Status: Internally Peer Reviewed *Organisms growing in the Gut that should not be there * *Intestinal Parasites, Especially Giardia * *Bacterial Overgrowth in the Small Intestine * *Abnormalities in the Lining of the Intestine * *Intolerance to Lactose * *Celiac Disease, or Sprue * *Inflammatory Bowel Disease * *Things You Eat and Drink When Your Gut is Normal * *Intolerance to Fructose * *Unconscious Intake of Laxative Substances * http://www.vh.org/adult/patient/internalme...rome/chap7.html You really need to read the ROME Book Kel. Wait it wouldn't matter.


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## bonniei (Jan 25, 2001)

Fructose intolerance and lactose intolerance are caused by bacteria moore than the inability to digest or absorb lactose and fructose. Because not every one who maldigests or absoorbs these things develop intolerance or symptoms."A significant negative correlation, however, was found between the individual symptom scores of the (lactose)intolerant persons and the numbers of total hybridizable bacteria (r(s) = -0.42, P = 0.03). The results suggest that an increased number of bacteria might contribute--by means of a higher fermentative capacity--to the reduction of lactose intolerance symptoms." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=14992439 "However, the interesting correlation with the SCFA raises questions regarding possible connections between colonic bacteria, carbohydrate malabsorption, and the beneficial effect of this pattern of SCFA in several colonic diseases." http://reviews.bmn.com/medline/search/reco...85&refer=scirus


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## Talissa (Apr 10, 2004)

kel, there really is no reasoning with ctn people, is there? Facts be dam*ed, they'll believe what suits them. And drossman's critique IS outdated, because it's regarding the first pimental study(2000, I believe), which has since been replicated & meets drossman's criteria for a valid study(double blind, placebo, etc).Bonniei, very interesting info, thanks!


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## bonniei (Jan 25, 2001)

*eric hasn't answered my question.* Does the medscape http://www.medscape.com/viewarticle/434527 article in which Dr Drossman says that they found Pimental's study provovcative mean that UNC agrees that LBHT should be used in the diagnosis of SIBO?


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## flux (Dec 13, 1998)

> quote: which has since been replicated


Where, here?









> quote:UNC agrees that LBHT should be used in the diagnosis of SIBO?


I think his logic is that SIBO could conceivably be an clinical entity in the general population (I'm not convinced it is). I'm also not sure it could be used as a definitive diagnosis because LBHT isn't that reliable a test for SIBO.


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## bonniei (Jan 25, 2001)

flux, thanks. Is there value in doing the LBHT and normalizing it if it is abnormal? I have done lactose, fructose and thee glucose test for SIBO? Do you think it is worthwhile doing the LBHT? Even if it did reflect cecal bacteria, it could be that those are causing problems with FI.


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## eric (Jul 8, 1999)

Bonniei, from Drossman article This is not outdated!!"In summary, I believe that while the findings being reported are *not a major breakthrough* , they should increase awareness of one disorder *that can mimic or worsen IBS.* In our experience at the UNC Center for Functional GI and Motility Disorders, the frequency is much lower (maybe 10% or less) of people who come to us with IBS. But when we suspect bacterial overgrowth *based on certain clinical features* , we then test for it, and of course, there is a greater chance the test will be positive. In those cases we treat, and many (but not all) will respond; however, the symptoms may return. *Patients with IBS should consider a diagnosis of bacterial overgrowth if you have diarrhea, abdominal swelling and increased gas production within 30-45 minutes after eating. But these symptoms are also quite typical just for IBS. Your physician will work with you to determine if breath testing for bacterial overgrowth may be helpful."* also"Small Bowel Bacterial Overgrowth *This means that there are too many bacteria in the upper part of the small intestine. This leads to symptoms of bloating, pain, and diarrhea that occur immediately after eating because the bacteria in the intestine begin to consume the food in the small intestine before it can be absorbed. * *These bacteria give off hydrogen and other gases which cause bloating and diarrhea.* *Small bowel bacterial overgrowth is a result of abnormal motility in the small intestine; when the housekeeper waves do not keep the bacteria swept out because the contractions are too weak or disorganized, the bacteria grow out of control. Bacterial overgrowth is most easily detected by the hydrogen breath test: The patient drinks a sugar solution and breathes into a bag every 15 minutes for two hours. If the bacteria are present in large amounts in the small intestine, they give off hydrogen, some of which is absorbed into the blood, carried to the lungs, and breathed out where it can be detected. "* http://www.med.unc.edu/wrkunits/2depts/med...smintestine.htm Again" *is a result of abnormal motility in the small intestine; when the housekeeper waves do not keep the bacteria swept out because the contractions are too weak or disorganized, * SIBO IS NOT IBS. The UNC Breath Testing Center http://www.med.unc.edu/wrkunits/2depts/med...gidc/breath.htm The cluster of IBS symptoms for a diagnoses of IBS.The Rome II Diagnostic Criteria (a system for diagnosing functional gastrointestinal disorders based on symptoms) for IBS is as follows:At least 12 weeks or more, which need not be consecutive, in the preceding 12 months of abdominal discomfort or pain that is accompanied by at least two of the following features: 1) It is relieved with defecation, and/or2) Onset is associated with a change in frequency of stool, and/or 3) Onset is associated with a change in form (appearance) of stool.Other symptoms that are not essential but support the diagnosis of IBS:Abnormal stool frequency (greater than 3 bowel movements/day or less than 3 bowel movements/week); Abnormal stool form (lumpy/hard or loose/watery stool); Abnormal stool passage (straining, urgency, or feeling of incomplete evacuation); Passage of mucus; Bloating or feeling of abdominal distension. "Bloating, feelings of urgency, a feeling of "incomplete" emptying, and nausea may also be experienced. Symptoms can vary and sometimes seem contradictory, such as alternating diarrhea and constipation.The symptoms of IBS are produced by abnormal functioning of the nerves and muscles of the bowel. In IBS there is *no evidence of an organic disease,* yet, something -- a "dysregulation" between the brain, the gut, and the central nervous system -- causes the bowel to become "irritated," or overly sensitive to stimuli. Symptoms may occur even in response to normal events. " http://www.aboutibs.org/characteristics.html Spasman, emailed a Italian gastroenterologist and got this full study, which is excellent.Activated Mast Cells in Proximity to Colonic Nerves CorrelateWith Abdominal Pain in Irritable Bowel SyndromeI am sure he might email it to people if you asked him nicely. Irritable Bowel Syndrome (IBS)"WHAT IS IT?IBS is characterized by a combination of persistent and recurrent abdominal pain and abnormal bowel habit (diarrhea, constipation, or both). The pain often begins after eating and goes away after a bowel movement. Other symptoms are bloating, passage of mucus, and a feeling of incomplete emptying.""CAUSEIBS is not caused by structural, biochemical, or *infectious abnormalities* . Rather, IBS is considered a dysregulation, or abnormality of brain-bowel function. There is increased pain sensitivity and abnormal motility (increased or irregular muscular movement of the gut). In IBS, diarrhea comes from an increased rate of passage of stool through the colon. Constipation is the result of a decreased speed of stool passing through the colon. Spasms, which are very strong contractions, also occur in IBS. Increased pain sensitivity results from the increased sensitivity of the nerves. Sometimes, the nerves are so sensitive that normal contractions, even with digesting a normal meal, bring on pain or discomfort. " http://www.med.unc.edu/wrkunits/2depts/med...e/fgidc/ibs.htm This points to a more positive diagnoses of IBS and less to an organic disease"It is relieved with defecation"


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## bonniei (Jan 25, 2001)

* eric as usual you have not answered my question!!!!!! Is the LBT used for SIBO in UNC?Keep rambling. flux answered it for me better.*


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## eric (Jul 8, 1999)

I posted the link to the tests for you.The UNC Breath Testing Center http://www.med.unc.edu/wrkunits/2depts/med...gidc/breath.htm Hydrogen Breath Test:for bacterial overgrowth tests for bacteria in the small bowel. Preparation The patient must fast 12 hours prior to the test and the patient must NOT be taking any antibiotics, lactose, milk of magnesia, or sorbitol. The patient may NOT eat, drink, smoke or sleep during the test. Indications diarrhea, abdominal bloating Procedure The patient drinks 80 grams of sucrose dissolved in water and breathes into bag once every 15 minutes for 2 hours. Hydrogen Breath Test for lactose:intolerance tests for intolerance to milk. Preparation The patient must fast 12 hours prior to the test and the patient must NOT be taking any antibiotics, lactose, milk of magnesia, or sorbitol. The patient may NOT eat, drink, smoke or sleep during the test. Indications abdominal pain, abdominal bloating, diarrhea, nausea and/or vomiting Procedure The patient drinks 50 grams of lactose dissolved in water and breathes into bag once every 15 minutes for 3 hours. Hope that helps.


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## Talissa (Apr 10, 2004)

SIBO is a factor for many with IBS Eric. It is a huge factor in food intolerances & more. Addressing the SIBO brings improvements in symptoms. Is that wrong to do? Get better?Where did someone type that SIBO IS IBS?


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## bonniei (Jan 25, 2001)

i knew that UNC used sucrose. Now that Dr Drossman thinks that Pimental's study is interesting, I was wondering how much he believed in the LBHT- whether enough for UNC to change to lactulose. As long as UNC does not change the test for SIBO, there is really not much sense in talking about Pimental's study is it? It has always been known that SIBO should be one of the things that should be ruled out. What are UNC's figures- 10% of the patients have SIBO? What I don't understand is why PImental's study was mentioned in the article at all except perhaps to say it deserves to be replicated. I was trying to figure out the significanceof Pimental's study to Dr Drossman. That UNC still does sucrose settles it in my mind.


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## flux (Dec 13, 1998)

> quote:SIBO is a factor for many with IBS Eric


SIBO is *not* a factor for anyone with just IBS.


> quote: It is a huge factor in food intolerances & more.


SIBO has *nothing* to do with food intolerance, whatever that is.


> quote: Addressing the SIBO brings improvements in symptoms


For someone who has SIBO, I would think so.


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## kel1059 (Feb 28, 2003)

> quote: SIBO has nothing to do with food intolerance, whatever that is.


maurice,can you prove it beyond a shadow of a doubt?you are still in denial of food intolerance. --or that people are having strange reactions to various foods. dizzyness, spaciness, fatigue, anxiety, worsening of GI symptoms, asthma, low blood sugar, ADD, ADHD symptoms, depressionyou don't believe in anything do you?what is your opinion on gut sterilization? http://groups.google.com/groups?q=gut+ster...G=Google+Search


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## bonniei (Jan 25, 2001)

I will have to agree that SIBO doesn't have to do with food intolerance. If you had SIBO you would be intolerant of * all* carbs and fat and then that wouldn't be true food intolerance. You are intolerant of all food.Food intolerance in IBS seems to have more to do with colonic fermentation http://www.ncbi.nlm.nih.gov/entrez/query.f...st_uids=9777836


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## flux (Dec 13, 1998)

> quote:Food intolerance in IBS seems to have more to do with colonic fermentation


Did you notice they used Christl's air-leak (er, I meant tight) chamber?


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## bonniei (Jan 25, 2001)

Hi flux, LOL! I think King used some kind of a plastic canopy which is more likely to have leaked but Christl used an air tight room if I remember Levitt's description of it correctly. King's paper is being cited all over the place soI think that research has gained acceptance insofar as to says abnormal colonic fermentation of carbs seems to be present in IBS. You may not agree with the details like what exactly the excretion rate was but most people seem to concur with the general thrust of his research. I guess you don't agree?


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## Talissa (Apr 10, 2004)

Food intolerance caused by SIBO explained: http://www.healthsystem.virginia.edu/inter...idelArticle.pdf


> quote:SIBO decreases brush border enzyme activity as a result of this change and further exacerbates carbohydrate intolerance in patients (28). As carbohydrates fail to be assimilated proximally, these substrates continue to be fermented by the gut bacterial flora, and are therefore not available to the host. Mucosal injury further interferes with carbohydrate uptake.


Here's more if interestedRACTICAL GASTROENTEROLOGY ï¿½ JULY 2003 30"EFFECTS OF SIBO ON DIGESTION AND ABSORPTIONThe adverse effects of SIBO on nutrition involve a number of factors including bacterial metabolism, injury of the mucosa of the host, and altered food intake secondary to gastrointestinal symptoms of SIBO. One of the most common clinical manifestations of SIBO is chronic diarrhea secondary to fat maldigestionand malabsorption. This complication primarily occurs through the step of deconjugation of bile acids by intraluminal bacteria (19). *Because fat solubilization and absorption require a critical concentration of conjugated bile acids for the formation of mixed micelles, when the* Similar to patients with maldigestion secondary to pancreatic insufficiency, the abnormal presentation of nutrients that occurs in the setting of bacterial overgrowth may lead to altered postprandial motility (22) which inturn, may worsen the patientï¿½s gastrointestinal symptoms.The change in motility and transit may be related to a displacement of nutrients from the transit control mechanism located in the proximal small intestine known as thejejunal brake (23) to the transit control located in the distal small intestine known as the ileal brake (24ï¿½26). Electron microscopic studies have confirmed such morphologicaldamage to enterocytes in animals with SIBO, providing direct evidence that absorptive cell injury contributes to malabsorption in this condition (27).SIBO decreases brush border enzyme activity as aresult of this change and further exacerbates carbohydrate intolerance in patients (28). As carbohydrates fail to be assimilated proximally, these substrates continue to be fermented by the gut bacterial flora, and are thereforenot available to the host. Mucosal injury further interferes with carbohydrate uptake.Although hypoproteinemia maybe seen in SIBO,severe protein malnutrition is rare (29). Bacteria do compete with the host for protein substrates, much as they do with carbohydrates, producing fatty acids and ammonia. However, bacterial products do not contribute significantly to host protein catabolism. The absorptive dysfunction and mucosal injury seen in SIBO may also contribute to decreased amino acid and peptide uptake. In addition, decreased levels of enterokinases have been demonstrated in patients with SIBO, which may impair the activation of proteases in pancreatic secretions (30).Protein-losing enteropathy has also been described in both animal and human models of SIBO. Vitamin B12 deficiency occurs in SIBO as a result of utilization of the vitamin by bacteria. When bacteria take up the vitamin, it is partially metabolized to inactive analogues,which compete with normal vitamin B12 bindingand absorption (31,32). Folate levels, however, are usually normal or elevated in the context of SIBO because bacteria are able to synthesize folate (33).Through the complication of steatorrhea associated with fat maldigestion and malabsorption, SIBO is complicated by malabsorption of fat-soluble vitamins. VitaminA, D, and E deficiencies can all be seen in SIBO. Because vitamin K is synthesized by luminal bacteria, deficiency of this vitamin is rarely seen in the context of SIBO."


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## Talissa (Apr 10, 2004)

> quote: Recent studies have shown a link between SIBO and irritable bowel syndrome (IBS). In a recent randomized, double blind, placebo controlled study of 101 patients with IBS, 83% were found to have an abnormal LactuloseHydrogen Breath Test (LBT), suggesting the presence of SIBO, compared with 20% in sex matched controls. The causative role of SIBO in IBS was supported by the response of patients to antibiotic treatment. If antibiotic treatment succeeds in normalizing the breath test to demonstrate eradication of SIBO, IBS patientsreported 75% improvement in symptoms. Thus, SIBOmay be found even in patients without abnormal intestinal anatomy or severely impaired intestinal motility.


 http://www.healthsystem.virginia.edu/inter...idelArticle.pdf Let's just say the breath test is unreliable.Nevertheless,*When IBS patients are treated for SIBO, they see a 75% improvement in symptoms.* I know I did! It was awful, getting better.It would be so horrible if most of the folks here on this bb saw at least a 75% improvement in symptoms by effectively treating SIBO.___________________________________(This is sarcasm, in case someone takes this literally!)It really seems that some of you, you know who you are, like to hear the sad stories, & don't want people to get better.It's criminal.There are others of us that have gotten better, and we try to share how we got better by treating the source naturally & we get slammed.It ain't right.


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## Talissa (Apr 10, 2004)

PS--Please note their explanation of how bacterial overgrowth in the small intestine can affect motility in the large intestine. (& colonic fermentation)The knowledge of intestinal microflora is growing everyday.


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## kel1059 (Feb 28, 2003)

talissa,i would have to say that you are the first person that i have ever seen who can assemble the information, interpret it, and present it in a way that almost all of us can understand.i agree it is mind boggling when a couple of life long malcontents can only come here and rip on it.flux can not stand your information because he is incredibly sick. everything in his life is negative. he is just one very toxic person. he believes in nothing and is convinced that he is doomed to suffer forever; therefore, he wants others to suffer with him.maurice volaski (flux of the famous gut sterilization procedure),why don't you go back to the pain/gas forum and keep telling all those people that they need to go to the doctor and get that worthless standing xray procedure to see if they are inhaling their gas. what a joke you are.


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## Nath (Jan 5, 1999)

Personally my pain is associated with areas of my colon, or what feels like areas, rather than my entire large intestine. I think this would most likely rule out a flora problem as the little critters would not localize themselves to specific areas and stay put for years on end.I would think that there is a localized change at some level to these sections of bowel which can be aggrivated by a number of factors.


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## kel1059 (Feb 28, 2003)

"Personally my pain is associated with areas of my colon, or what feels like areas"mycobacterium is a slow growing organism that confines itself to specific areas of the intestines.if MAP can do this then i imagine other organisms can do this also.but who really knows what is going on.


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## Poor Boy (Feb 13, 2003)

KEl & Talissa Thank you so much for your hard work....The others are devils advocates for sure but they are helpful in that they push us to look harder and longer at what we are doing.....3 weeks on Dr. Dahlmans approach, but really only a couple of honest fructose, lactose, and wheat free....seeing some improvement.....I am praying that everyone who is on this probiotic track can bring about some positive change, maybe even remission..... fingers are crossed....keep the good stuff in and the bad stuff out....later Eric and Flux


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## calid (Aug 4, 2003)

PoorBoy: You are currently on Dr. Dahlman's program? Please post your updates on this thread Dr. Dahlman Update Thread so we can all compare notes and let everyone watching know how we're doing. Glad you're doing well also!!!!


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## kel1059 (Feb 28, 2003)

> quote: KEl & Talissa Thank you so much for your hard work


talissa is doing all the work. excellent work if i don't say so myself. the research is impeccable.me on the other hand -- i am just coasting. i am in remission and that is causing me to be lazy. i'm just here to try and keep eric in check. his bad information is downright dangerous to many people.just ask the person who was carrying around a couple of nasty P-A-T-H-O-G-E-N-S about the harm that eric is capable of.poor boy,i sure am glad that i went through the DMSA lead/mercury chelation therapy last year. i believe in covering all the bases. when the lead came out there seemed tpo be a noticeable difference in brain function but nothing i can be 100% certain of.the mercury is a little more suspect. can't be certain of anything but i am glad it is gone. i do know that i had a very bad time on the days that it was coming out --- lots of shaking and bad anxiety.


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## bonniei (Jan 25, 2001)

> quote:When IBS patients are treated for SIBO, they see a 75% improvement in symptoms


Make that when IBS patients are treated for an abnormal LBHT they see a 75% improvement in it. LBHT is most probably due to *cecal fermentation and not SIBO from the info there is so far* BTW like I said with SIBO you have problems with all foods. That is not what you typically call food intolerance. Food intolerance is like lactose, fructose, sucrose intolerance. It is a much *narrower* term.


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## bonniei (Jan 25, 2001)

If SIBo was connected to food intolerance you would think that if you typed in Food intolerance and small intestine bacterial overgrowth in Pubmed there would be more thasn the two irrelevant studies which come up while typing that in.


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## Talissa (Apr 10, 2004)

Hi Bonniei,The referenced article in my post this am details how bacterial overgrowth affects the 3 categories of food--fat, carb, protein.Problems then arise in the colon, due to the lack of proper digestion in the small bowel.So if you say food intolerance occurs in the small intestine, you're correct. If you say it occurs in the large intestine, you're also correct.Seems to originate in the sm. int. due to bacterial overgrowth & the interaction of pathogens on the wall, which cause mucosa cells to build up to protect the wall, since the beneficial bacteria are depleted & can no longer protect it adequately. This causes the food maldigestion.Then the unweildy symptoms of intolerance occur because of what then transpires in the large intestine. Abnormal fermentation--causing build up of anaerobic pathogens, changes in motility are possible, along with gas formation, cramping, changes in transit time due to colonic absorption malfunctioning.At least this is my oversimplified interpretation of what I've read.It just seems to involve both intestines to me.


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## flux (Dec 13, 1998)

> quote:Nevertheless,When IBS patients are treated for SIBO, they see a 75% improvement in symptoms.


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## bonniei (Jan 25, 2001)

Talissa, What I got from, the article is that there are inflammatoiry changers and anything which involcves the immune system is not a food intolerance,


> quote:So if you say food intolerance occurs in the small intestine, you're correct. If you say it occurs in the large intestine, you're also correct.


You are missing the point. When you are intolerant to all food it is not true food intolerance. By intolerance one generally means lactose, fructose or sucrose. By intolerance we mean a much narrower range of foods.* I posted before you posted the article that there is intolerance to all food in SIBO* So I am well aware of that. When you can't tolerate any food you have a serious disease not food intolerance. Also the problems that I talk about are those which start in the colon and * nothing * to do with the small intestine. Where the breath tests sjhow that there is nothing wrong with the Small intestine but have everything to do with the colon. You might want to read breath tests to understand that


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## eric (Jul 8, 1999)

Food intolerence is not connected to the immune system!National Institute of allergy and infectious diseases."Food Allergy and IntolerancesFood allergies or food intolerances affect nearly everyone at some point. People often have an unpleasant reaction to something they ate and wonder if they have a food allergy. One out of three people either say that they have a food allergy or that they modify the family diet because a family member is suspected of having a food allergy. But only about three percent of children have clinically proven allergic reactions to foods. In adults, the prevalence of food allergy drops to about one percent of the total population. This difference between the clinically proven prevalence of food allergy and the public perception of the problem is in part due to reactions called "food intolerances" rather than food allergies. A food allergy, or hypersensitivity, is an abnormal response to a food that is triggered by the immune system. *The immune system is not responsible for the symptoms of a food intolerance, even though these symptoms can resemble those of a food allergy. * It is extremely important for people who have true food allergies to identify them and prevent allergic reactions to food because these reactions can cause devastating illness and, in some cases, be fatal. http://www.niaid.nih.gov/factsheets/food.htm The below article goes over throughly many issues very releavant in IBS.Irritable Bowel Syndrome: Taking Concepts Into Clinical Practice CME Chairperson: Michael D. Gershon, MD; Faculty: Kevin W. Olden, MD; Walter L. Peterson, MD; Nicholas J. Talley, MD, PhD; Gervais Tougas, MD, CM, FRCPCMy brief is to review 6 main points:Look at how a phenomenon, a set of symptoms, relates to, or at least begins to relate to, a definable pathophysiologyTry to see to some extent how and why patients with irritable bowel syndrome (IBS) experience visceral painGet back to this area of mind and gut, and how events that seem to influence primarily psychological constraints, such as stress and psychological factors, will play a role in the perception of symptoms originating from the gutRemind us that in addition to these factors, primarily luminal and enteric factors, such as certain food types, infection, or inflammation, can also interact with these central nervous system (CNS) factors to produce painBegin to look at the role and the place of serotoninergic mechanisms in the modulation of these thingsLook at this in the broader sense of IBS *We know that in terms of its phenomenology, IBS is a condition that's associated with altered brain-gut communication.* Pain plays a major role so that we have alterations, or at least generation of abnormal sensation within the gut. Emotions can modulate these symptoms to a large extent, but at the end they also have alterations of function characterized in general by either constipation or diarrhea. This is largely due to alterations of neuromodulation at the level of the enteric neurons and also at the level of central and autonomic pathways."IBS has many dimensions. The symptom complex itself is characterized by abdominal discomfort associated with altered bowel habits. In addition to these, though, there is a substantial psychological comorbidity in many patients. At the same time, we have frequent extraintestinal manifestations associated with poor sleep, fatigue, changes in libido, and loss of energy, and a number of other symptoms, that often overlap with symptoms in the gut, outside of the colon, such as dyspeptic symptoms or noncardiac chest pain.We also know from increasing literature that many of these patients have other symptoms including irritable bladder, chronic fatigue, fibromyalgia, headaches, and a number of other symptoms. This is related to a number of abnormalities, some of them having to do with autonomic dysregulation and visceral hypersensitivity, altered pain modulation, abnormal health-seeking behavior and, to some degree, iatrogenesis."If we try to integrate this into a coherent map, we have symptoms that are subjectively definable, which then are associated with a series of complaints, either diarrhea, constipation, or abdominal pain, the whole spectrum of IBS. There is a pathophysiological basis to these symptoms that will vary in individual patients but seems to involve abnormalities of perception, epithelial function, and in some patients, motility, which then leads to symptom generation, and involves both external stressors, psychological stress, as well as genetic abnormalities and inflammation at the peripheral level.To summarize, we know that there is alteration of visceral perception. There are good data to that effect and increasingly sophisticated ways to measure this, but in most patients, visceral hypersensitivity seems to play a role. In a substantial group of patients, luminal events, in particular infection and some degree of mild irritation, can alter visceral perception and lead to symptoms. Psychological factors also play a role in altering visceral perception and the vigilance to symptoms originating from the gut.Involvement of the Brain-Gut Axis in Central and Visceral HypersensitivityOne of the most convincing studies was done by Bradette and coworkers. This was a simple study that looked at differences in visceral perception to balloon distension in patients with IBS and compared it to healthy subjects. Both the threshold to discomfort and the threshold to pain were much lower in patients with IBS than in healthy controls, suggesting that, in fact, there was visceral hypersensitivity in those patients.Things have progressed a fair bit since then and we can demonstrate that, in addition to symptomatic abnormalities, there are significant differences that we can see between IBS patients and control subjects using functional magnetic resonance imaging (fMRI), brain imaging, during colonic distension. These abnormalities are in 2 main parts. One is the somatosensory areas of the brain and the other is the prefrontal cortex region of the brain, each of which deals with different aspects of pain symptomatology.Up to 95% of patients with IBS will have altered pain perception. They will have lower thresholds, so they experience symptoms at much lower volumes than healthy controls. They also have an increased intensity of the sensation elicited by distension at a given volume, and they have increased referral of these sensory perceptions in response to rectal distension when compared with healthy patients.This is not something that we see very often in normal subjects and there's also different somatic pain perception in a subset of IBS patients, but by no means all. Why would that be? There are 2 regions in the brain that are involved with the perception of visceral sensation. The first one is the somatosensory cortex that is associated with the perception of noxious stimulation and painful stimuli. This region closely interacts with the limbic system, which is the part of the brain that is involved with the neuroendocrine and autonomic responses associated with the perception of pain. This is more of a hard-wired reflex area, but it plays a very important role in modulating responses in areas involved more directly with pain perception. These areas are also associated with aspects such as mood, hedonic behavior, and motivation, which play a very important role in the psychological make-up and modulation of these visceral sensations.Visceral Pain and the Autonomic PathwayA lot of this is mediated through autonomic responses, and the important aspect here is that perception of pain in itself elicits responses that will then, in turn, alter the response and the reactivity of the gut. Eliciting painful visceral sensation will involve activation of sympathetic spinal afferents that, in turn, will lead to homeostatic visceral responses that will be associated with vagal afferent responses leading to symptoms such as satiety, nausea, and even bloating. These afferent pathways will then lead to efferent responses that are associated with visceral perception. And this is important because these pathways can in turn modulate the intensity of the afferent input.To summarize, IBS patients display evidence of a central hyperresponsiveness to visceral stimuli and events, and this occurs at the level of the brain. In response to these pain stimuli, IBS patients have a visceral hyperresponsiveness to luminal events and also to central, more psychologically derived events, and this is occurring at the level of the gut. The understanding of these mechanisms is still evolving and begins to explain the 2 dimensions that we see with IBS patients, pain and altered bowel function.Psychological and Enteric Factors Associated With the Symptoms of Irritable Bowel SyndromeEmotions modulate pain perception by several dimensions. One of them is that if you've experienced unpleasant or uncomfortable symptoms, you will have an increased vigilance to these visceral stimuli. And to some degree, the same seems to be occurring at the level of visceral pain. This involves both cortical and brain stem nuclei and a large degree of autonomic modulation. The central nervous system increases the perception of symptoms at the level of the gut. There is a clear presence of visceral hyperalgesia that can be related in many situations and experimental paradigms to very early trauma during childhood or infancy, and also seems to be associated with very stressful, psychological events, such as abuse or posttraumatic stress disorder. This raises the issue of whether there is an element of neuroplasticity involving altered perception in addition to the cortical activation that comes from altered symptoms.Furthermore, a number of studies have shown that patients with IBS have altered autonomic activity. While this is not completely described yet, it is associated with an increase or altered visceral responsiveness in many of these patients. A final aspect is that these symptoms lead to increased health-seeking behavior and use of healthcare.One of the best studies looking at this is a study that looked at auditory stress and showed that an unpleasant external stressor, a noise in this case, altered both the perceptual and emotional rating that you experience in response to a visceral stimulus. In this study published a year ago, a control subject had responses that were measured in response to either a relaxing stimulus or a stressful stimulus, a conflicting sound in both ears. In patients with IBS, the same stimulus led to an increased degree of unpleasantness at set pressure distension. Similarly, it had the same effect on the anger rating, a psychological measure of psychological stress.When we look at this in clinical practice, we see that many patients will relate the fact that stress seems to trigger or exacerbate their symptoms. While in most patients this is not of a pathological or psychopathological dimension, certainly disorders such as depression, anxiety, and somatoform disorders play an important role in some patients, whereas in most of us, life stress will be the primary precipitant. It seems to be more important in referral populations, in tertiary care but, nevertheless, it's present across the whole spectrum of IBS. And we know that psychological factors affect outcome. The more severe the psychopathology, the more difficult it is to successfully treat many of these patients. In particular, physical and sexual abuse is a major determinant of adverse outcome or more severe symptomatology.When we look at the other dimension, enteric factors, many patients tell us that certain foods will produce symptoms. It is difficult to determine whether this is a pharmacological, a chemical, or even an immune mechanism. Also, low-grade inflammation is present in a small subset of patients with functional symptoms. There is increasing awareness that in the substantial group of patients, although the proportion remains to be determined, *infectious events seem to lead to the subsequent development of IBS. * *Sometimes this occurs as a single precipitant, but in many studies the biggest predictor of the subsequent development of symptoms following an enteric infection is other factors, such as psychological stress or an adverse life event a few weeks or a few months preceding the infection. Clearly, there is a role for infections but this is in association with central factors.* Pathophysiology of Postinfectious IBSIn postinfectious IBS patients, there is accelerated gut transit in many patients, increased visceral sensitivity, and evidence for alteration of intestinal permeability, something very relevant to chronic diarrhea in these patients. *There's clear evidence in many patients of increased presence of enterochromaffin (EC) cells in the colon. Therefore, there is the possibility of increased release of serotonin (5-HT) in these patients.* Potential Pathogenetic Role of Serotoninergic Mechanisms in the Symptoms of Irritable Bowel SyndromeSerotonin and the Neural Control of Digestive FunctionsSerotonin is involved at just about every level of the communication between gut and brain, both going from gut to brain and then from brain to gut. One appealing therapeutic avenue is to focus on the site where most of the 5-HT is being released and try to affect outcome and symptoms by modulating symptoms at the level of the gut trying to avoid the possible side effects that may come with more central modulation of serotoninergic pathways. *We know that 5-HT release is actually increased in IBS patients with the diarrhea-dominant component, suggesting that, again, 5-HT may play a role in subsets of patients with IBS.* *This may be further demonstrated in the sense that there is increased circulating 5-HT in patients with diarrhea-dominant IBS and increased EC cell population in the gut, whereas in some subgroup of patients with chronic constipation, there appears to be a decreased number of EC cells suggesting that, if we stimulate serotoninergic pathways, we might be able to improve symptoms in these patients.* Integrating Current Concepts of Causality: Towards a Unifying Hypothesis *In summary, IBS is affected and modulated by many factors. Some of them have to do with emotional dimensions, others are more related to visceral function and sensation. This is probably, to some extent, associated with a dysfunction or a disorder of gut-brain communication involving both afferent and efferent pathways going to and from the gut. There is good evidence to suggest that 5-HT is a central mediator in the regulation of these visceral functions, and its modulation may provide an appealing form of therapy for a proportion of patients with IBS.* You can read the rest of the article and see the graphs here.Slides with transcript and RealAudio:The Incidence and Socioeconomic Burden of the IllnessEpidemiology of Irritable Bowel SyndromeAnnual Visits to Office-Based PracticesUtilization of Healthcare Resources by Patients With Irritable Bowel SyndromeNegative Impact of Irritable Bowel Syndrome on Quality of Life, Work-Related Issues, and ProductivityEconomic Burden of Irritable Bowel Syndrome: Direct, Indirect, and Intangible CostsSummaryIntegrating Current Concepts of Causality: Towards a Unifying HypothesisPhenomenology, Pathophysiology, and Symptomatology of Irritable Bowel SyndromeInvolvement of the Brain-Gut Axis in Central and Visceral HypersensitivityPsychological and Enteric Factors Associated With the Symptoms of Irritable Bowel SyndromePotential Pathogenetic Role of Serotoninergic Mechanisms in the Symptoms of Irritable Bowel SyndromeSummaryCurrent Treatments: Do They Meet the Clinical Need?Current Symptomatic Treatments of Irritable Bowel SyndromeEffect of High Placebo Response in Irritable Bowel Syndrome Clinical TrialsInitial Therapeutic Management of Irritable Bowel Syndrome: Education and ReassuranceReview and Assessment of Treatment Trials in Irritable Bowel SyndromeInitial Therapeutic Management of Irritable Bowel Syndrome: Dietary AdviceCurrent Pharmacologic Treatment of Irritable Bowel Syndrome: Smooth Muscle Relaxants and AnticholinergicsCurrent Pharmacologic Treatment of Irritable Bowel Syndrome: AntidepressantsCurrent Pharmacologic Treatment of Irritable Bowel Syndrome: Other AgentsCurrent Nonpharmacologic Treatment of Irritable Bowel Syndrome: Psychological InterventionConclusionsAn Evidence-Based Approach to the Management of IBSRome Criteria for Clinical Study MethodologyStudy Designs of Tegaserod Phase III Clinical TrialsTherapeutic Efficacy of Tegaserod Using the Subjective Global Assessment of Symptom ReliefMeta-Analysis of Randomized Controlled Trials of Tegaserod in Irritable Bowel SyndromeEffect of Tegaserod on the Incidence of Abdominal Surgery/Cholecystectomy in Patients With Irritable Bowel SyndromeSafety and Tolerability of Tegaserod in Patients With Irritable Bowel SyndromeConclusions http://www.medscape.com/viewprogram/1985 Probiotics and Prebiotics in Gastrointestinal DisordersIntroductionThe mammalian intestinal tract contains a complex and diverse society of both pathogenic and nonpathogenic bacteria. Most research to date has focused on the mechanism by which pathogenic bacteria achieve their detrimental effects. However, more recent research has unveiled a glimpse into the mechanisms of action and potential therapeutic role of indigenous nonpathogenic microorganisms (probiotics). Probiotics, prebiotics, and synbiotics are moving from snake oil into the mainstream of medical therapy. This evolution has been facilitated by our ever-increasing understanding of the mechanism of action of these agents and by the development of molecular methods for analyzing and identifying complex bacterial communities within the mammalian intestine. A series of review articles have been published in the past year outlining the efficacy of probiotics and prebiotics in human health.Mechanisms of Action of Probiotic BacteriaPrevious research into the protective mechanisms associated with probiotic bacteria focused on the bacteriology of the gut and concentrated on intestinal colonization and probiotic-induced suppression of pathogen growth and/or invasion.14 Indeed, the concept of a microbiologic balance existing in the intestine, involving competition between probiotic and pathogenic bacteria for specific binding sites on intestinal epithelial cells, has been well established in the literature. However, recent research has turned toward understanding the role of probiotic bacteria and their secreted products in enhancing and modulating innate and adaptive immune responses in the host by other mechanisms. With the demonstration that immune and epithelial cells can discriminate between different microbial species through activation of Toll-like receptors,15* the idea that probiotics may exert some of their protective functions through modulation of immune activity and epithelial function in both the large and small intestine has arisen.Effects on Barrier FunctionTwo papers in the past year have demonstrated that some strains of probiotic bacteria can enhance barrier function through distinctly different mechanisms. Resta-Lenert and Barrett16 showed that live Streptococcus thermophilus and Lactobacillus acidophilus could inhibit the adhesion and invasion of enteroinvasive Escherichia coli into human intestinal cell lines. Epithelial cells exposed to these probiotic bacteria demonstrated enhanced phosphorylation of actinin and occludin in the tight junction region.16 A second novel mechanism of maintaining barrier function was identified by Yan and Polk.17* These investigators showed that Lactobacillus rhamnosus GG was able to prevent cytokine-induced apoptosis in intestinal epithelial cell models through the inhibition of a tumor necrosis factor (TNF)-induced activation of the proapoptotic p38/mitogen-activated protein kinase.Effects on Immune FunctionIt has been well documented that probiotic bacteria can interact with epithelial and immune cells and alter signal transduction pathways in the presence or absence of pathogenic bacteria and cytokines. Epithelial cells respond to whole bacteria and bacterial components in a differential manner, releasing interleukin-8 in response to pathogenic bacteria such as E. coli but not to probiotic strains.18 Bacterial DNA is also recognized in a differential manner by epithelial cells, with pathogenic strains evoking a phosphorylation of the extracellular signal-regulated kinase pathway and activation of activator protein-1,19* and probiotic strains modulating the nuclear factor-κB pathway in response to TNF-α.20 However, bacterial DNA has been shown to be both beneficial21* and detrimental22 in the treatment of murine colitis. An interesting paper by Ibnou-Zekri et al.23* highlights the idea that activity of probiotic strains in vitro may not translate into similar in vivo behavior. Two strains of Lactobacillus that exhibited very similar in vitro properties demonstrated distinct differences in colonization patterns and resultant host immune response at both the mucosal and systemic levels.23*Effects on Systemic ImmunityOral administration of probiotics has been shown to result in altered immunity at distant mucosal sites, including the female genital tract, the respiratory tract, the skin, and the nasal passages. Specific strains of Bifidobacterium and Lactobacillus appear to be promising in the treatment and/or prevention of eczema/dermatitis in infants24,25 and children.26 It is interesting to note that in these studies, supplementation with the probiotic did not appear to alter bacterial numbers in the colon. This suggests that these results are owing to altered immunity rather than altered colonization.Probiotic ColonizationWhether colonization is critical for probiotics to have their effect remains unresolved. Agarwal et al.27* studied the ability of Lactobacillus GG to colonize the neonatal gut. Colonization with Lactobacillus GG occurred in 21% of infants who weighed less than 1500 g versus 47% of larger infants. Colonization was limited to infants who were not on antibiotics within 7 days of treatment of Lactobacillus GG. Thus, the neonatal response to probiotic preparations is dependent on gestational and postnatal age and prior antibiotic exposure.27*Clinical Therapeutic Effects of ProbioticsHelicobacter Pylori InfectionPrevious reports have suggested a role for probiotics in the treatment and prevention of Helicobacter pylori infection through both a probiotic-induced inhibition of H. pylori growth and adhesion to epithelial cells and an effect on the host immune system. Three reviews have been published that examine the role of probiotics in the treatment and prevention of H. pylori infection. They also provide a summary of the 13 published clinical trials examining the potential of probiotics to modify eradication rates and antibiotic-associated gastrointestinal side effects.28,29*,30In the presence of clarithromycin-resistant H. pylori, eradication is significantly attenuated. Ushiyama et al.31 demonstrated that Lactobacillus gasseri inhibited both the in vitro growth of clarithromycin-resistant H. pylori and the release of interleukin-8 from epithelial cells. In addition, in an in vivo mouse model, H. pylori colonization was significantly decreased by L. gasseri.31 Chatterjee et al.32* also demonstrated an inhibitory effect of Lactobacillus (L. acidophilus) on H. pylori growth but only if the colonization ratio was 1:1 or higher. Both of these studies support the complementary effect of probiotics in the management of H. pylori infection.In a double-masked, randomized, controlled clinical trial, 326 school children from a low socioeconomic area of Santiago, Chile, with H. pylori infection were treated with both live and heat-killed strains of Lactobacillus johnsonii, Lactobacillus paracasei, or vehicle once daily for 4 weeks. A 13C-urea breath test demonstrated a significant decrease in H. pylori colonization in children receiving live L. johnsonii but not the other groups. Once again, this study implies a probiotic species specificity for the therapeutic effect.33In an attempt to identify why some strains of probiotics are effective in altering H. pylori colonization and others are not, Mukai et al.34 examined the binding of Lactobacillus reuteri and H. pylori to the putative H. pylori glycolipid receptor molecules. Among the nine L. reuteri strains tested, only two were shown to bind to the same glycolipid receptors as H. pylori and thereby inhibit H. pylori binding. The investigators suggested that the sharing of glycolipid specificity was required for the Lactobacillus strains to have a therapeutic effect on H. pylori eradication.In addition to their direct role in H. pylori, probiotics have been suggested to increase efficacy of eradication therapy by preventing antibiotic-associated side effects and thus increasing compliance. Cremonini et al.35 randomized 85 patients with H. pylori undergoing eradication with triple therapy to one of four groups:Lactobacillus casei subspecies rhamnosus, Saccharomyces boulardii, L. acidophilus plus Bifidobacterium lactis, or placebo. In all probiotic-supplemented groups, there was a significantly lower incidence of antibiotic-associated diarrhea and taste disturbance relative to placebo. Nevertheless, there was no difference in H. pylori eradication or compliance rates between the various groups.35CancerThere is no direct experimental evidence for cancer suppression in humans as a result of consumption of probiotics. However, there is significant indirect and mechanistic evidence, based largely on laboratory animal and in vitro studies, that has been reviewed.36,37 The mechanisms by which lactic acid bacteria inhibit colon cancer may include alteration of the metabolic activities of intestinal microflora, alteration of physicochemical conditions in the colon, binding and degradation of potential carcinogens, quantitative and/or qualitative alterations in the intestinal microflora incriminated in the production of carcinogens, production of antitumorigenic or antimutagenic compounds, enhancing the host's immune response, and effects on the physiology of the host. During the past year, there were no human studies published that examined the effects of probiotics on colon cancer.Covalent binding of carcinogens, or their metabolites, to DNA yield cancer potential DNA adducts. Horie et al.38 found that a probiotic mixture consisting of Streptococcus faecalis, Clostridium butyricum, and Bacillus mesentericus could decrease DNA adduct formation induced by a food mutagen in the colonic epithelium of a human flora-associated mouse model of colon cancer. The fact that this was a human flora-associated animal model carries the science beyond models with animal-associated flora and raises the specter that these probiotics may have similar anticancer effects in humans.38There is an ongoing human clinical trial to examine the effect of synbiotic preparation on colon cancer risk biomarkers. The SYNCAN project, funded by the European Union, began in August 2001 and involves eight research centers in Europe. It will test human dietary intervention in a 12-week, randomized, double-masked, placebo-controlled trial of a food supplement containing Lactobacillus GG, Bifidobacterium Bb-12, and Raftilose Synergy1 (ORAFTI Active Food Ingredients, Oreye, Belgium) in patients with adenoma. Raftilose Synergy1 is the prebiotic inulin enriched with oligofructose. Colon cancer risk biomarkers, including mucosal markers, fecal water markers, and immunologic markers, are being measured (www.syncan.be). Using an azoxymethane-induced colon cancer mouse model, Femia et al.39 demonstrated that the prebiotic (Raftilose Synergy1), in combination with probiotics, was more effective than probiotics alone in decreasing colon cancer in this mouse model. *Irritable Bowel Syndrome* Between 1996 and 2001, there were five clinical trials that examined various species of Lactobacillus in the treatment of irritable bowel syndrome (IBS).40-44 These studies, along with the role of microflora in IBS, have been reviewed during the past year.45,46In a recent clinical trial, Kim et al.47* examined the effects of a probiotic formulation containing eight different probiotic species, VSL#3 (VSL Pharmaceuticals Inc., Fort Lauderdale, FL), on gastrointestinal transit and symptoms of patients with diarrhea-predominant IBS. After 8 weeks of treatment, there was no significant difference in mean gastrointestinal transit measurements, bowel function scores, or satisfactory global symptom relief between the two treatment groups. However, abdominal bloating was significantly reduced in the VSL#3 treatment group.47* *The mechanism of action of probiotics in IBS is poorly understood and has been thought to be attributable to changes in fermentation products.* In 10 patients with diarrhea-predominant IBS, administration of VSL#3 probiotics improved the clinical picture without significant alterations in indigenous enterococci, coliforms, Bacteroides, or Clostridium perfringens flora.48 In a similar open-label study, Bazzocchi et al.49 demonstrated that VSL#3 probiotic induced changes in the composition of the colonic microflora together with improvement in colonic dysmotility and visceral perception. In contrast, in a double-masked, placebo-controlled, crossover 4-week trial in 12 patients with IBS, Lactobacillus plantarum 299v did not alter colonic fermentation or improve symptoms compared with placebo.50 Once again, these discordant results support the concept of specific probiotic strains being more effective than others across varied disease states.Postoperative ComplicationsProbiotics for treatment of postoperative complications (pouchitis and recurrence) after intestinal surgery for Crohn disease has been reviewed.51 Using in vitro Ussing chambers, Mangell et al.52 demonstrated that rats pretreated with L. plantarum 299v were protected against E. coli-induced increases in intestinal permeability. Carrying these observations in animals forward to a human clinical study, Rayes et al.53 found that liver transplant recipients receiving fiber-containing enteral formula plus living L. plantarum 299v developed fewer bacterial infections (13%) than those receiving standard enteral formula (48%) or fiber-containing enteral formula plus heat-killed L. plantarum 299v (34%). A larger prospective, randomized trial of 172 patients, which also included the 95 liver transplant recipients referred to previously, demonstrated that the incidence of bacterial infections after liver, gastric, or pancreatic resections was 31% in the conventional enterally or parenterally treated group. This compared with 4% in the fiber-containing enteral formula plus live L. plantarum 299v group and 13% in the fiber-containing enteral formula plus heat-killed L. plantarum 299v group.54Patients with short bowel syndrome have bacterial overgrowth and increased gut permeability. In an animal model of short bowel syndrome (80% resection), B. lactis administration reduced bacterial translocation from 93% in the placebo-treated group to 44% in the B. lactis group.55 However, the same degree of success was not observed in human studies. McNaught et al.56 studied patients undergoing elective abdominal surgery and found that there was no difference in bacterial translocation into mesenteric lymph nodes between patients pretreated for 1 week with L. plantarum or placebo.An interesting study used probiotics to inhibit S taphylococcus aureus infection in surgical implants in rats. Lactobacillus fermentum RC-14, but not L. rhamnosus GR-1, inhibited S. aureus infection in surgical implants situated under the skin.57 Once again, therapeutic specificity of a specific probiotic strain was identified.PancreatitisPancreatic necrosis and associated pancreatic infection are determinants of poor outcome in patients with severe acute pancreatitis. The mortality rate after pancreatitis is five to 10 times higher if the necrotic tissue becomes infected. Antibiotics and various proinflammatory cytokine inhibitors have failed to have a significant impact on the outcome. Colonization of the lower gastrointestinal tract and oropharynx with gram-negative organisms often precedes contamination of the pancreas. Olah et al.58 conducted a randomized, double-masked study in which patients with acute pancreatitis received L. plantarum 299v for 1 week by nasojejunal feeding tube. The control group received a similar preparation but with L. plantarum 299v heat inactivated. Infected pancreatic necrosis in abscesses occurred in one of 22 patients in the live Lactobacillus group compared with seven of 23 in the killed Lactobacillus group (P = 0.023). In addition, there was a trend toward a shorter mean length of stay in the live (13.7 days) versus the killed Lactobacillus group (21.4 days).58,59 In a similar randomized clinical trial conducted by the same research group, 45 patients admitted with severe acute pancreatitis were randomized to receive either live or dead L. plantarum 299v. Pancreatic infection/abscess rates were 4.5% and 30%, respectively.59 These human findings were supported by trials of probiotics (L. plantarum 299v and S. boulardii) in animal models of acute pancreatitis in which intestinal microbial translocation was reduced.60,61Infectious diarrheaThe evidence in support of the use of probiotics to shorten the duration of diarrhea, especially in children, and prevent recurrence of diarrhea is robust, with the highest level of evidence of treatment of acute infectious diarrhea. Well-controlled clinical trials have shown that probiotics L. rhamnosus GG, L. reuteri, L. casei, and B. lactis can shorten the duration of acute rotavirus diarrhea.62**,63** Two recent reviews outline the role of probiotics as therapy64 and their role in limiting malnutrition associated with diarrhea.65 In a metaanalysis of 18 probiotic therapy clinical trials involving children younger than 5 years of age with acute-onset diarrhea, Huang et al.66 demonstrated that coadministration of probiotics with standard rehydration therapy reduced the duration of diarrhea by approximately 1 day. This metaanalysis went on to perform subanalysis of inpatient trials (reduction of diarrhea by 0.7 days); double-masked, randomized, placebo-controlled studies (reduction of diarrhea by 0.6 days); and Lactobacillus-only studies (reduction of diarrhea by 1.1 days). This metaanalysis was further supported by three recent additional randomized, placebo-controlled trials demonstrating the effect of probiotics on infant diarrhea. Rosenfeldt et al.67 described the effect of L. rhamnosus and L. reuteri administered twice daily for 5 days to a cohort of children with acute diarrhea in local daycare centers. In children treated with a mixture of the two Lactobacillus strains, the mean duration of diarrhea was reduced by 40 hours (P = 0.05). Rotavirus infection was found in 63% of the children. This same group randomized 69 children hospitalized for acute diarrhea to the same mixture of L. rhamnosus and L. reuteri twice daily for 5 days. The duration of diarrhea was reduced by 19 hours and the length of hospitalization by 48% in the probiotic-treated group. Although this primary end point did not reach statistical significance, 10% of the probiotic group versus 30% of the control group still had loose stools at the end of the study period (P = 0.03). Rotavirus infection was identified in 66% of patients, and at the end of intervention, rotavirus antigen persisted in 12% of patients in the probiotic group versus 46% of patients in the control group (P = 0.02).68 Once again, these two studies confirm that both inpatients and outpatients with primarily rotavirus-induced diarrhea can be successfully treated with probiotic preparations.In contrast, Duggan et al.69 used prebiotics to perform two consecutive randomized, masked, controlled clinical trials on infants with acute diarrhea in Lima, Peru. The first trial examined the effects of dietary supplementation with the prebiotic oligofructose in the prevention of acute diarrhea. The second trial added zinc to the prebiotic and then examined the outcomes. In the first trial, there were 282 infants, and there were 369 in the second. The mean number of days with diarrhea (approximately 10) was the same whether the infants were fed the prebiotic, prebiotic plus zinc, or nonsupplemented cereals. It is important to note that all these infants were breast-fed and thus may have already represented a protected cohort.Costa-Ribeiro et al.70 similarly measured the effect of L. casei subspecies rhamnosus GG on male children younger than 2 years of age admitted to a metabolic unit in Brazil with moderately severe dehydration (by World Health Organization criteria) and severe acute diarrhea. In their randomized, double-masked, placebo-controlled trial, Lactobacillus GG did not reduce diarrhea duration or stool output. Whether this signifies the fact that probiotics are not effective in more severe forms of diarrhea or whether the short duration of diarrhea (approximately 39 hours) meant that the duration of probiotic administration was too short to permit colonization remains to be determined.An Italian group led by Dani et al.71 evaluated the effectiveness of Lactobacillus GG supplementation in reducing urinary tract infections, bacterial sepsis, and necrotizing enterocolitis in preterm infants. In a double-masked, placebo-controlled study, 585 newborn infants, of gestational ages less than 33 weeks or birth weight less than 1500 g, were randomized to receive standard milk feed supplemented with Lactobacillus GG or placebo once daily until discharge. Unfortunately, both the probiotic and placebo group had the same number of infections and episodes of necrotizing enterocolitis.71 Nevertheless, these results may have simply been a consequence of limited probiotic colonization in preterm infants.27* Infant rhesus monkeys fed a formula supplemented with L. reuteri from birth to 4 months of age demonstrated reduced diarrhea severity and recovered from diarrheal episodes more quickly than those with placebo-supplemented formula feeding.72Clostridium Difficile DiarrheaThe efficacy of probiotics in both C. difficile diarrhea and antibiotic-associated diarrhea has been reviewed.73* The current largest, randomized, controlled trial with C. difficile-associated colitis74 demonstrated that S. boulardii was able to prevent disease recurrence, but only in those individuals who had more than one C. difficile sequential infection. It did not have a beneficial effect on the first C. difficile infection. In a double-masked, placebo-controlled trial conducted in 2003, Wullt et al.75 examined the ability of L. plantarum 299v to prevent recurrent episodes of C. difficile-associated diarrhea. Recurrence of clinical symptoms was seen in four of 11 patients treated with metronidazole plus L. plantarum 299v and in six of nine treated with metronidazole combined with placebo.75 Although a small study, it does support the earlier findings.In a novel study, Sambol et al.76 colonized hamsters with nontoxigenic C. difficile strains and found that these nontoxigenic strains were able to prevent diarrheal disease in 87% to 97% of hamsters subsequently challenged with toxigenic C. difficile. This novel probiotic strategy needs to be explored for C. difficile-associated disease in humans.76Antibiotic-Associated DiarrheaTwo metaanalyses have been published that examine the randomized, double-masked, controlled trials of probiotics in the prevention of antibiotic-associated diarrhea.77*,78* These metaanalyses confirm an odds ratio of 0.39 and 0.37, respectively, in favor of probiotic treatment over placebo in preventing diarrhea associated with antibiotics.In a randomized trial, Seki et al.79 found that the concomitant use of the probiotic Clostridium butyricum in 110 children receiving antibiotics for upper respiratory tract infections reduced diarrhea from 59% in the placebo-treated group to 5% in the Clostridium-treated group. Similarly, concomitant S. boulardii used in the treatment of 57 adult patients with acute amoebiasis reduced the duration of diarrhea from 48 hours in the placebo-treated group to 12 hours in the Saccharomyces-treated group (P 0.001). After 4 weeks, amebic cysts were detected in 18% of the placebo-treated group but in none of the probiotic-treated group.80 In a double-masked, controlled trial, 740 patients undergoing cataract surgery received preoperative treatment with ampicillin and cloxacillin, with or without Lactobacillus. The incidence of diarrhea in patients receiving antibiotic alone was 13% compared with 0% in patients receiving antibiotics plus Lactobacillus.81Two studies examined the mechanism of the probiotic effect and antibiotic-associated diarrhea. Sullivan et al. demonstrated that the probiotics (administered as yogurt) prevented antibiotic-induced changes in Bacteroides fragilis microflora cultured from human feces.82 Using an anaerobic culture system, Payne et al.83 demonstrated that L. plantarum 299v diminished antibiotic-induced overgrowth of Candida albicans.Radiation-induced DiarrheaVSL#3 is a high-potency probiotic preparation that contains eight different probiotics. The efficacy of VSL#3 to prevent radiation-induced diarrhea was examined in 95 patients undergoing pelvic radiation. More patients in the placebo group (55%) had radiation-induced diarrhea compared with the VSL#3 group (38%) (P 0.001). Furthermore, patients treated with placebo had more severe radiation injury, increased mean daily number of bowel motions, and increased use of loperamide compared with those who received VSL#3.84*Nonalcoholic Fatty Liver DiseaseStudies in rodent models of alcoholic fatty liver disease have demonstrated that intestinal bacteria, bacterial endotoxin, and TNF-α modulate alcohol-induced liver damage. Furthermore, treatment with agents that inhibit TNF-α activity has been shown to be beneficial in patients with severe alcoholic steatohepatitis. Given this, the question has been raised as to whether the fatty liver associated with obesity also has a relation with intestinal bacteria and TNF-α. Using the ob/ob mouse as a model for nonalcoholic fatty liver disease, Li et al.85** fed ob/ob mice either a high fat diet alone or the same diet plus VSL#3 probiotic or anti-TNF antibodies for 4 weeks. Treatment with VSL#3 or anti-TNF antibodies improved liver histology, reduced total hepatic fatty acid content, and decreased serum alanine aminotransferase levels. These benefits were associated with decreased hepatic expression of TNF-α in mice treated with anti-TNF antibodies but not in mice treated with VSL#3. These results support the concept that intestinal bacteria induce endogenous signals other than TNF-α, which play a pathologic role in nonalcoholic fatty liver disease, and suggest a role for novel probiotic therapy in this common condition.85**In a recent review on hepatic encephalopathy, Solga86 hypothesized that probiotic compounds might be ideally suited to treat this condition because of their effects on colonic pH, intestinal permeability, and the immune system. In keeping with this hypothesis, Chiva et al.87 and an accompanying editorial88 reported that oral administration to cirrhotic rats of L. johnsonii with a vehicle of antioxidants, compared with antioxidants alone, suppressed bacterial translocation to the mesenteric lymph nodes, reduced ileal and cecal counts of enterobacteria and enterococci, and reduced intestinal malondialdehyde levels (used as an index of intestinal oxidative damage). Unfortunately, no group of cirrhotic rats received L. johnsonii alone, thus precluding direct comparison with the probiotic. Nevertheless, in an earlier study by Bauer et al.,89 bacterial translocation rates, acidic fluid infection, and enteric bacterial load were unchanged after an 8- to 10-day course of L. rhamnosus GG.Inflammatory Bowel DiseaseA disturbance in the gastrointestinal microflora, or the host response to this flora, has been demonstrated to play a critical role in the pathogenesis of inflammatory bowel disease (IBD). This has led to attempts to modify the bacterial flora with probiotics. Animal models of IBD have provided proof of principle that probiotics can prevent and/or treat established intestinal inflammation. Clinical trials have demonstrated the efficacy of probiotics in the maintenance or remission of pouchitis, prevention of pouchitis after surgical formation of the ileal-anal reservoir, maintenance or remission of ulcerative colitis, and treatment of active ulcerative colitis and Crohn disease. However, many of these clinical trials in IBD are small and open-label and remain in abstract form. The role of probiotics in IBD was presented in several large, well-written reviews.90*,91*,92,93Animal Models of Inflammatory Bowel DiseaseThe various gene-deficient, transgenic, and chemically induced models of IBD have significantly advanced our understanding of the role of probiotics and prebiotics in this disease. It is clear that not all models of experimental colitis respond the same to probiotics. Shibolet et al.94 demonstrated that both VSL#3 and Lactobacillus GG prevented colitis induced by the sulfhydryl blocker iodoacetamide but had no effect on immune-mediated dinitrobenzene sulfonic acid-induced colitis. Oral administration of various probiotic bacteria has been shown to be effective in ameliorating colitis in the interleukin-10 gene-deficient mouse model (Lactobacillus salivarius subspecies salivarius and Bifidobacterium infantis),95 the dextran sulfate sodium chemically induced model (lysed E. coli and Bifidobacterium longum),96,97 and the HLA-B27 rat model (Lactobacillus GG).98 Finally, Setoyama et al.99 induced inflammation in luminally sterile axenic mice with a single Bacteroides vulgatus strain. It was found that coadministration of B. vulgatus with Bifidobacterium reduced both the growth of the B. vulgatus strain and the intestinal inflammation. It is important to note that the Bacteroides strains were isolated from patients with ulcerative colitis.99Ulcerative ColitisPatients with mild to moderate active colitis, who had been unresponsive or intolerant to standard therapy, received 20 to 30 g of a prebiotic germinated barley drink in a nonrandomized, open-label fashion. At 4 weeks, this treatment resulted in significant clinical and endoscopic improvement.100 Previous studies with this prebiotic demonstrated positive effects on epithelial cell restitution, suppression of nuclear factor-κB binding activity, increased short chain fatty acid production, and enhanced growth of probiotic bacterial strains.101 Ishikawa et al.102 conducted a randomized trial of the use of Bifidobacterium-fermented milk in the treatment of ulcerative colitis. Eleven subjects received the Bifidobacterium-fermented milk for 1 year, whereas the control group did not. Exacerbation of symptoms was seen in three of the 11 subjects in the group treated with Bifidobacterium-fermented milk and in nine of 10 in the control group (P = 0.01). Analysis of the microflora and the organic acids of the feces demonstrated significant reduction in the relative proportion of B. vulgatus and in Bacteroidaceae. In an open-label pilot trial with S. boulardii, a group of 25 patients with mild to moderate ulcerative colitis received S. boulardii for 4 weeks in addition to the treatment with mesalamine. Of the 24 patients who completed the study, 17 attained clinical remission.103Finally, human fecal rectal infusions in six selected patients with ulcerative colitis were carried out in a novel protocol.104 Fecal flora donors were healthy adults. Fecal suspensions were administered as a retention enema daily for 5 days. Full clinical remission and cessation of ulcerative colitis medication were achieved in all patients. Interestingly, at 1 to 13 years after human fecal infusi


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## calid (Aug 4, 2003)

OMG, what in the heck is Eric doing? Only hit the ADD REPLY button once Eric, it's bad enough we have to scroll over 20 pages of your cut and pastes, but to do over 60 is totally ridiculous.


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## kel1059 (Feb 28, 2003)

er eric, quit spamming. there is no need to post that 3 times. you are learly in violation of the rules of this forum. when jeff gets back i am going to report you.when the new moderator takes over i am going to make certain she kicks your rear to the curb.


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## bonniei (Jan 25, 2001)

> quoteroblems then arise in the colon, due to the lack of proper digestion in the small bowel


I read this article http://www.healthsystem.virginia.edu/inter...idelArticle.pdf thrice and didn't find that. Although due to the double peaks you see in SIBO it is quite likely that undigested carbs enter the colon and cause a problem there.


> quote:the interaction of pathogens on the wall, which cause mucosa cells to build up to protect the wall,


That sounds like an immune reaction and immunological reactions and food intolerance are supposed to e mutually excclusive


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## kel1059 (Feb 28, 2003)

calid i just reported him by clicking on the 'report post' icon.


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## Talissa (Apr 10, 2004)

"Biotherapeutic Agents in the Treatment of Gastrointestinal Disorders"Current Treatment Options in Infectious Diseases 2003


> quote: "It is becoming increasingly evident in gastrointestinal disorders that colonic bacterial flora are implicated in the initiation and maintenance of intestinal dysfunction, such as inflammatory bowel diseases and irritable bowel syndrome [1ï¿½],]. "


 http://www.biomedcentral.com/1523-3820/5/183 This one's so good, & I'm short on time, so I'm going to pull an Eric(pls don't report me!)____________The complex interactions that occur between dietary components, indigenous and transient microflora, and the host within the dynamic environment of the digestive tract are poorly understood [1ï¿½]. However, recent advances in molecular biology (in particular, the emergence of methods based on 16S ribosomal RNA gene sequences [2]) and confocal microscopy [3] have facilitated an improved understanding of the alimentary tract microbial structure [2]. These innovations have complemented conventional, culture-based microbiologic techniques and have enabled scientists to elucidate the host-mediated influences exerted by bile juices, pancreatic secretions, and an active mucosal immune system on gut-associated microbial species (1) [1ï¿½]. Precise and adaptable techniques will soon allow us to assess the influences exerted by gut-associated microbes on their host [4]. Many reports have attributed the normal development and homeostasis of the humoral and cellular mucosal immune systems to the presence of a complex gastrointestinal microbial load [5]. The interactions between the mucosal immune systems and the enteric microflora maintain the physiologically normal state of inflammation or activation of gut-associated lymphoid tissue (Peyer's patches, lymphoid follicles, lymphocytes, and mesenteric lymph node cells) throughout life [6]. It is becoming increasingly evident in gastrointestinal disorders that colonic bacterial flora are implicated in the initiation and maintenance of intestinal dysfunction, such as inflammatory bowel diseases and irritable bowel syndrome [1ï¿½],]. The hypothesis that it may be the failure of immunologic tolerance toward indigenous microflora that facilitates disease--associated dysregulation of the immune system [12,13] has been supported by the identification of gene mutations (NOD2) in patients with Crohn's disease [14-16]. The NOD2 protein has a repeating, leucine-rich, C-terminal domain, as found in many sensing components of the innate immune system, and its functional role may be as a cytosolic receptor for bacterial lipopolysaccharide or endotoxin. Disruption of this system in predisposed individuals may result in aberrant immune activation to commensal or other enteric microbial species. Other intestinal disease states involving altered microflora (in addition to impaired gut barrier and/or intestinal inflammation) include small-bowel bacterial overgrowth [17], colorectal cancer [18], and children's, traveler's, and antibiotic/Clostridium difficile-associated diarrhea [19,20]. In recent years, these conditions (in addition to gastritis, urogenital and respiratory tract infections, and atopic eczema) have been the subject of biotherapeutic management strategies, with varying levels of success [21,22,23ï¿½ï¿½,24-26,27ï¿½,28,29ï¿½].Biotherapeutic management of patients with intestinal disorders predominantly takes the form of probiotic administration. Probiotics have been defined as live microbial food supplements that benefit the host by improving the intestinal microflora balance when ingested in sufficient numbers [1ï¿½]. However, despite their widespread availability [30-34] and their historical safety (combinations of various microorganisms, particularly species of Lactobacillus and Strepto-coccus, have been used traditionally in fermented dairy products to promote human health) [35-38], probiotics are not yet accepted in modern clinical practice [39,40]. Several issues must be resolved completely for their use to become widespread. Those involved in the selection, in vitro assessment, manu-facturing, and distribution of these products have defined their needs (as discussed earlier [41]). Candidate probiotic microbes should be of human origin, be nonpathogenic, be resistant to technologic processes (ie, retain viability and activity in delivery vehicles), be resistant to physiologically relevant levels of gastric acid and bile, adhere to gut epithelial tissue, be able to persist in the gastrointestinal tract (albeit for short periods), produce antimicrobial substances, and modulate beneficial immune responses. However, it is unlikely that skepticism regarding probiotics will be overcome through innovative fermentation processes, enhanced shelf-life, or improved organoleptic properties, despite their obvious benefits. An understanding of prokaryotic-host physiologic and molecular inter-actions, and clinical validation of publicized claims, are essential.Mechanistically, the beneficial influence of probiotics requires the ingestion of sufficient numbers of cells (whether these must be viable is a topic of much discussion [42]) that then transit, or persist within, the distinct physiologic and chemical environments of the gut [1ï¿½]. There are many proposed mechanisms through which the consumed microorganisms may benefit their host (1), including competition for nutrients and competitive exclusion of opportunistic pathogenic organisms, the production of antimicrobial factors, transformation of toxins or eukaryotic toxin receptors, and immunomodulation [1ï¿½,42-45].In vitro assessments and studies involving animal models of infection, inflammation, and cancer feature prominently in a wide range of reports that describe the sometimes successful application of wild-type and genetically enhanced probiotic bacteria [8,9,46ï¿½ï¿½]. Although a report by Steidler et al. [46ï¿½ï¿½] (detailing the use of transgenic Lactococcus lactis conferred with the ability to deliver bioactive interleukin-10 to mediate inhibition of spontaneous colitis development in interleukin-deficient mice) may have predicted the future of probiotics as delivery vehicles of therapeutic moieties rather than as active agents, most attention has focused on clinical studies.Numerous studies have attributed strains of lactic acid bacteria, Saccharomyces boulardii, and Escherichia coli with the ability to influence the microbial ecology of the host, in addition to affecting lactose intolerance, incidence of diarrhea, mucosal immune response, levels of blood cholesterol, and cancer [1ï¿½,44]. Unfortunately, the observations detailed are often marred by inconsistencies, mainly because of inappropriately selected organisms, inability to track the consumed biologic agents, and failure to comply with the standards of good clinical practice. Although these studies do not provide the necessary evidence for probiotic-based biotherapy to become a treatment modality within the standard of care, the near total absence of adverse events anecdotally demonstrates the safety of these approaches, and their results continue to contribute to our understanding of fundamental aspects of -probiotic-eukaryotic inter-actions [47ï¿½,48].Of the recently reported studies, those by Zoppi et al. [49] and Gionchetti et al. [50] are the most noteworthy. Zoppi et al. [49] described the assessment of multiple probiotic cocktails, representing consortia of up to nine separate bacterial and Saccharomyces species in children who were prescribed ceftriaxone for respiratory tract infections. Zoppi et al. [49], recognizing that studies with greater numbers of subjects will be required to validate the effects of probiotics on dysbiosis associated with antimicrobial therapy, present a study that emphasizes the requirement to select probiotic microbes/products appropriate to the treated disorder. They also emphasize that prudent selection of probiotics with otherwise suitable beneficial traits should also take into account their tolerances to clinically complementary antimicrobials and inherent antibiotic sensitivities. Gionchetti et al. [50] demonstrated that consumption of a combination probiotic product resulted in 85% of the test cohort remaining in remission throughout the 9-month study period (compared with no patients in the control limb), thus promoting the prophylactic use of probiotic consortia against relapse of chronic pouchitis. The results of the trial are convincing. However, the strength of the reported data is undermined by the lack of information regarding transit of the introduced probiotics (a product similar to that evaluated by Zoppi et al. [49]) through the gut.____________________


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## Talissa (Apr 10, 2004)

Bonniei, I think that it's just clear to me from what I've read from other sources. For ex, I posted the info on what deconjugated bile salts do in the colon. (fat maldigestion)I think you'll find more from the article this am really, really interesting & here's the link: http://www.healthsystem.virginia.edu/inter...idelArticle.pdf. The main point is, though, that food reactivity in IBS stems from bacterial overgrowth--the pathogens interaction with the intestinal wall & the mucosal cells that develop in response.Both intestines need to be addressed when treating bacterial overgrowth, and then the abnormal inflammation needs to be addressed.(At least that's how I'm approaching it.)Gotta run! T-


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## Poor Boy (Feb 13, 2003)

Ok Eric your now what I consider a real Royal Pain In The Ass.... Why don't you go play in your own sandbox and while your at it ask yourself why you and flux are becoming so disliked on this BB....Get a grip dude, chick, or whatever you are...


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## bonniei (Jan 25, 2001)

talissa I suggest you start reading what I post instead of asking me to read. *I have already said that I read the article you posted thrice* I did not find anything new in it.


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## kel1059 (Feb 28, 2003)

> quote: Mechanistically, the beneficial influence of probiotics requires the ingestion of sufficient numbers of cells (whether these must be viable is a topic of much discussion [42]) that then transit, or persist within, the distinct physiologic and chemical environments of the gut [1•]. There are many proposed mechanisms through which the consumed microorganisms may benefit their host (1), including competition for nutrients and competitive exclusion of opportunistic pathogenic organisms, the production of antimicrobial factors, transformation of toxins or eukaryotic toxin receptors, and immunomodulation [1•,42-45].


more good information. i have assumed all along that the bifidus from Metagenics played a very positive role in my recovery. i guess that in days past i was not taking enough bifidus from my store bought probiotics. possibly the homemade bifidus yogurt that i used to make is far inferior to probiotics. i actually read that probiotics might be better.


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## Talissa (Apr 10, 2004)

"immunological reactions and food intolerance are supposed to be mutually exclusive"They aren't in IBD.Immunological reactions happen due to pathogens threating the intestinal wall, & food intolerances are one of the consequences.______________Hey Bonniei, tell me what you REALLY think.I'm sorry, I thought you just read the "entire article"--what was posted. Silly of me. Pls accept my apology. And I really did think you'd find it interesting & referenced, & a reliable source--just the way you like it.btw--I only linked it twice.______________Hey kel,I've also read that's its much better from a treatment standpoint to use a probiotic in the billions than consuming homemade yogurt.But the yogurt is pretty good!


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## bonniei (Jan 25, 2001)

Talissa, here is the definition of food intolerance for you from an online dictuionary http://www.hyperdictionary.com/medical/food+intolerance Definition: an adverse food-induced reaction that does not involve the immune system (i.e., lactose intolerance). This is what I mean by mutually exclusive. The definition of food intiolerance does not involve inflammatory reactions.


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## kel1059 (Feb 28, 2003)

> quote: "immunological reactions and food intolerance are supposed to be mutually exclusive"They aren't in IBD.Immunological reactions happen due to pathogens threating the intestinal wall, & food intolerances are one of the consequences.


interesting. a couple of things need to be pointed out-- our nemesis, spammer-e, posted something a while ago that showed that some IBSers are actually in the murky area of IBD.also, talissa posted something from medline that made the claim that IBS can be considered as a disease entity in some cases where they are seeing physical differences -- extra mast cells in caecal region???? drossman was one of the ringleaders of the article.***************************************i think that some people spend too much time quibbling over definitions of things that are not entirely clear to the medical people themselves. therefore to be splitting hairs over murky theories seems to be a waste of time. and i am not referring to T as the person who is doing this.********************i never could understand the yogurt vs probiotics problem, but i think that i am going to assume that probiotics may be better.


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## bonniei (Jan 25, 2001)

Well without definitions misunderstandings happen. Perhaps this is why thie thread gas gone on for so long. flux, already said, "food intolerance whatever that is" and Talissa hasn't bothered to define it but conti nues talking about it.I guess I am too scientific for you kel. My background is scientific. Too bad you can't handle it


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## kel1059 (Feb 28, 2003)

> quote:interesting. a couple of things need to be pointed out-- our nemesis, spammer-e, posted something a while ago that showed that some IBSers are actually in the murky area of IBD.also, talissa posted something from medline that made the claim that IBS can be considered as a disease entity in some cases where they are seeing physical differences -- extra mast cells in caecal region???? drossman was one of the ringleaders of the article.


the conclusion of this is that eric is posting misleading information once again.


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## Talissa (Apr 10, 2004)

"FOOD INTOLERANCE An intolerant food aggravates the immune systemï¿½s mast cells in the gutï¿½s mucous membrane, causing the gut to leak. Particles of partially digested food then pass into the blood stream setting up a chain reaction. This gives rise to symptoms such as migraine, excessive weight and arthritis. The onset of a food intolerance is often insidious and thought to be the result of normal absorption failing to take place. The foods which cause subtle but adverse reactions may slowly build up in number and severity. Symptoms are usually multiple, not consistent and may be affected by the suffererï¿½s general state of health. They may take hours or even days to appear and include anxiety, mouth ulcers, aching joints and muscles, fatigue, headaches/migraine, sinus and mucus problems, digestive disturbances (indigestion, discomfort, bloating, gas, etc.), hyperactivity weight gains, etc.. The most common food intolerances are wheat and dairy products, and stimulants (coffee, sugar, chocolate, etc.). At a recent ION (Institute of Nutrition) Conference, Dr James Brahy stated that food intolerance is associated with at least 92 common diseases. *The immune system reacts giving rise to fatigue, weight gain, arthritis, IBS and headaches etc. *" http://www.bromleyhealthmanagement.com/allergies.htm _________________Food intolerance involves an indirect immune response, where with food allergies, there's a direct & immediate immune response.


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## bonniei (Jan 25, 2001)

Talissa thanks for providing us with the definition you are using. There are many doctors even who will call an allergy an intolerance. Then there are people like MNL who claim LEAP tests catch intolerance.Now if I was using a term I would try to use it as a medical dictionary defines it. But hey that's just me.Anyway now that we are clear what the other means by intolerance perhaps we can make progress.


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## Talissa (Apr 10, 2004)

Here's more~"It now appears that the most likely subgroup of IBS patients for whom the inflammatory process is involved are those whose illness began after an enteric infection for even a low grade mucosal inflammation has been shown to lead to significant and persistent dysfunction in enteric nerves and smooth muscle. Food allergy that is IgE mediated and delayed food allergy such as that that occurs in IgG immune responses or food intolerance are another important subgroup with diarrhea-predominant IBS.7 8 " http://www.gutdoc.org/IBS.htm


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## kel1059 (Feb 28, 2003)

the problem with flux and eric is that they do not see the bigger picture.tal does see the bigger picture and it is presented in the post that she just made which i will repeat.(tal-- don't go away. you are the only person on this board that i have ever seen who can dispell all the BAD INFORMATION being put out by flux and eric. although i fully expect you to get burned out. afterall you are thinking and eric is just posting from his library w/out any thought )


> quote:FOOD INTOLERANCE An intolerant food aggravates the immune system's mast cells in the gut's mucous membrane, causing the gut to leak. Particles of partially digested food then pass into the blood stream setting up a chain reaction. This gives rise to symptoms such as migraine, excessive weight and arthritis. The onset of a food intolerance is often insidious and thought to be the result of normal absorption failing to take place. The foods which cause subtle but adverse reactions may slowly build up in number and severity. Symptoms are usually multiple, not consistent and may be affected by the sufferer's general state of health. They may take hours or even days to appear and include anxiety, mouth ulcers, aching joints and muscles, fatigue, headaches/migraine, sinus and mucus problems, digestive disturbances (indigestion, discomfort, bloating, gas, etc.), hyperactivity weight gains, etc.. The most common food intolerances are wheat and dairy products, and stimulants (coffee, sugar, chocolate, etc.). At a recent ION (Institute of Nutrition) Conference, Dr James Brahy stated that food intolerance is associated with at least 92 common diseases. The immune system reacts giving rise to fatigue, weight gain, arthritis, IBS and headaches etc. " http://www.bromleyhealthmanagement.com/allergies.htm


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## bonniei (Jan 25, 2001)

Firstly, food intolerance that is IgE mediated does not fit the definition you posted in the next to last post, Talissa. It is an allergy by that definitionSecondly IBS is not generally associated with Ig-E mediated intolerances.


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## Talissa (Apr 10, 2004)

Bonniei,I don't make things up like some people.And kel overestimated my ability to interpret what I've read in a way that allows others to comprehend it.The delayed immune response in IBS is complicated & I'm lousy at explaining it.But it's real.


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## bonniei (Jan 25, 2001)

Delayed immune responses are not Ig-E mediated. Ig-E mediated responses are immediate. I am quibbling with this statement" *Food allergy that is IgE mediated* and delayed food allergy such as that that occurs in IgG immune responses or food intolerance *are another important subgroup with diarrhea-predominant IBS.*"


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## kel1059 (Feb 28, 2003)

i agree bonniei. i have always thought that you do good research. i asked you back in nov if you would like to join our team. how 'bout it?


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## bonniei (Jan 25, 2001)

Ha ha kel I suppose joining your team means flux and eric are on different teams


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## Talissa (Apr 10, 2004)

"Food allergy that is IgE mediated and delayed food allergy such as that that occurs in IgG immune responses or food intolerance are another important subgroup with diarrhea-predominant IBS.7 8 "I'm reposting this because it's the best I can do without spending the rest of the night on it--but it seems to be the situation in my case, as part of the "sub-group" of postinfectious IBSr's._________________________Thanks kel, but this is too time-consuming. I need to cut back!!!Talissa


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## bonniei (Jan 25, 2001)

Where are the references for that statement that ig-E mediated responses make up a subset of IBS'ers? It says 7 and 8 are the references for it but it provides no reference list for it.


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## kel1059 (Feb 28, 2003)

yeah, this is driving me crazy. it is an addiction. okay i am out of here for the rest of the night.*************b,we are the good side. we stand for all that is good and right in the world.


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## Talissa (Apr 10, 2004)

I have time for this one--It's saying that food intolerance is DELAYED food allergy such as that occurs in IgG immune responses.(This is also what happens in IBD.)It isn't saying they are the same thing.It's saying both can occur.Luckily in my case, I just have DELAYED, IgG response.


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## bonniei (Jan 25, 2001)

Finally you have got it right, Talissa."Researchers have employed both skin tests and serum immunoglobulins (IgG and IgE) as markers of food hypersensitivity in various disorders including irritable bowel syndrome, but published data are equivocal." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=11284772 MikeNl would agree with you that it may be IgG but I am sitting on the fence.


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## Talissa (Apr 10, 2004)

Gee, thanks Bonniei







Hey poor boy--just wanted to say to you it's nice to know you're out there!!! Your imput here was greatly appreciated. T-


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## meribaibs (Jan 18, 2004)

Anyone familiar with this man?Dr. Nigel Plummer has his doctorate in microbial physiology and has worked at Pfizer in antibiotic research and development. His research on the use of normal flora in the prevention and treatment of genitor-urinary candidiasis has won numerous awards. His current research includes the study of natural antimicrobials and the interaction between antibiotic usage, normal flora and the spread of antibiotic resistance. Dr. Plummer lectures extensively in North America and Europe on the use of human microflora and essential fatty acids in degenerative diseases. Dr. Plummer resides in Wales. http://www.immunesupport.com/library/showarticle.cfm/id/5550


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## meribaibs (Jan 18, 2004)

From what I understand, probiotic therapy has marginal benefits on a diet of processed foods.


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## kel1059 (Feb 28, 2003)

this dr plummer sounds like one of the rare good doctors. he believes in using probiotics especially when antibiotics are involved.-----"From what I understand, probiotic therapy has marginal benefits on a diet of processed foods"the typical Western diet could be a strong contributor for many of the troubles.


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## Talissa (Apr 10, 2004)

Sounds like Dr Plummer is one of the good guys too....Regarding food--I know after my 365+ days of tetraccycline in hs, I ate primarily junk food throughout college--probably didn't help at all. ( post-IBS--I only eat whole foods now--or 99% of the time.)_______________________Guess what? You can get a gsdl diagnostic stool test without going through a doctor! I just got a response back from crohns.net saying that I do the 3 samples, and send it directly to gsdl myself.When I emailed gsdl directly last month, I asked if I could send it in myself since I'm a CN, and they said it had to be through a doctor.Hmmm. Well, I guess crohns.net must have worked out a special deal. This is from their email this am:"Once you order the test, we send you the kit which you then send directly to Great Smokies once you have obtained 3 days of samples via Airborne Express. It is prepaid.The results are sent to us and we will forward them to you as soon as we receive them. If you require any assistance with interpretation we will be happy to help." In good health!Pamela Nathanpamela###crohns.net www.crohns.netwww.buyprobiotics.net877 240-7528 - Toll free in US_______________________Will probably do this in July or August, when we're through with all the company coming down.


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## eric (Jul 8, 1999)

The triple post was just an accident and a problem with my ISP at the time.Not spam and I was NOT doing it on purpose."Bacteria and IBSMany have wondered if IBS is caused by an infection. To date, no virus, bacteria, or parasite has been found to directly cause IBS. It has, however, been hypothesized that these microbes may indirectly cause IBS or at least exacerbate its symptoms. Some researchers question whether IBS begins with a common bacterial gastroenteritis. [Gastroenteritis is an inflammation of the lining of the stomach and intestinal tract often caused by a bacterial infection. Symptoms may include vomiting, abdominal pain, and diarrhea.] Other investigators question whether the number or type of bacteria that normally live in the colon affects symptoms.Some individuals with IBS recall that their symptoms began with a gastroenteritis. The first theory of a "post-infection diarrhea" as a possible link has been explored in greater depth this past year. A post-infection diarrhea is a common, temporary phenomenon resulting from the destruction of intestinal digestive enzymes during an infection. Even after the infection has cleared, certain foods will cause the persistence of loose stools for several weeks until the intestine rebuilds its digestive enzymes.One recent Canadian study looked at the occurrence of IBS in people who travel overseas and acquire a "traveler's diarrhea." These investigators found that 10% of travelers who acquired an infectious gastroenteritis subsequently developed IBS. Those who did develop a traveler's diarrhea, compared to those who did not, had an approximate 6-fold increased risk of developing IBS.Another study from England found that 23% of their patients hospitalized for an infectious gastroenteritis went on to develop IBS. Regardless of whether these individuals developed IBS, they all had increased rectal sensitivity and increased colon movements several weeks after their infection had cleared. However, the researchers also found that the individuals who developed IBS reported more life events suggesting that that there may have been a psychological component to their symptoms in addition to the infectious component.Can bacteria cause IBS without a preceding infection? There are trillions of bacteria that normally reside in the gastrointestinal tract where they help digest nutrients. [Fermentation and intestinal gas are a byproduct of this digestive process.] Some investigators have questioned whether the number or type of bacteria normally present is different in individuals with IBS. A group of German investigators found that the tissue taken from the colons in people with IBS had higher bacterial concentrations than the tissue from individuals without IBS. The researchers believe that this finding suggests that the colons of some people with IBS are colonized by a greater number of bacteria than those without IBS. This may alter how nutrients are fermented in the colons of IBS patients.A group of British investigators also believe that colonic fermentation (gas production) is different in some people with IBS. They confirmed this in one study, which may explain why some individuals respond to dietary restriction and why some do not. The investigators went on to measure gas production in IBS patients before and after antibiotic treatment. The antibiotics appeared to reduce the total volume and rate of hydrogen gas production in the people studied. The investigators felt that this second study provided additional evidence of the role of colonic fermentation in IBS symptoms and supported the use of dietary modification or antibiotics to reduce gas production and improve symptoms in people with IBS.These findings are promising. It is too early however, to say conclusively that bacteria and antibiotics have a role in the development of IBS symptoms and in effective treatment." http://www.aboutibs.org/Publications/resea...ml#anchor143049 Dr Wood is an expert in food allergies and also a top expert in IBS. He is responsible for coining the term for the enteric nervous system as the "brain in the gut""You have two brains: one in your head and another in your gut. *Dr. Jackie D. Wood is a renowned physiologist at The Ohio State University. He calls the second brain, "the-little-brain-in-the-gut." This enteric nervous system is part of the autonomic nervous system and contains over one hundred million neurons, which is as many as are in the spinal cord.* *This complex network of nerves lines the walls of the digestive tract form the esophagus all the way down to the colon. This little brain in the gut is connected to the big brain by the vagus nerves, bundles of nerve fibers running from the GI tract to the head. All neurotransmitters, such as serotonin that are found in the brain are also present in the gut. * *Dr Wood has discovered that this little-brain-in-the-gut has programs that are designed for our protection and which are very much like computer programs. They respond to perceived threats in the same way that the limbic system or the emotional brain does. So the threat of a gastrointestinal infection can activate the program that increases gut contractions in order to get rid of the infection. The symptoms are abdominal cramping and diarrhea. * *Dr. Wood has determined that a type of cell found in the body and the gut, called the mast cell, is a key to understanding the connection of the big brain in the head with the little-brain-in-the-gut. Mast cells are involved in defense of the body. In response to certain threats or triggers, such as pollen or infection, mast cells release chemicals, such as histamine, that help to fight off the invader. Histamine is one of the chemicals that causes the symptoms of an allergy or a cold.* *When an infection of the gut occurs, such as food poisoning or gastroenteritis, the mast cells of the gut release histamine. The little-brain-in-the-gut interprets the mast cell signal of histamine release as a threat and calls up a protective program designed to remove the threat ï¿½ at the expense of symptoms: abdominal pain and diarrhea. * *The brain to mast cell connection has a direct clinical relevance for irritable bowel syndrome and other functional gastrointestinal syndromes. It implies a mechanism for linking allostasis and the good stress response to irritable states (e.g., abdominal pain and diarrhea) of the gut. Mast cells can be activated to release histamine in response to perceived psychological stress, whether the stressor or trigger is consciously perceived or not. So the end result is the same as if an infection activated the program in the-little-brain-in-the-gut: abdominal pain and diarrhea. " * http://www.parkviewpub.com/parksub/n5.html


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## Poor Boy (Feb 13, 2003)

Eric your apology is ridiculous....just take a hike and leave the people who can contribute positively alone......Talissa, thank you for your kind words....was wondering what your personal take on the probability of finding a state of remission, with resumption of a somewhat normal diet might be....? Hope your still Feeling well Kel....peace


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## kel1059 (Feb 28, 2003)

poor boy fill me in sometime on your thoughts concerning your heavy metal chelation therapy.i am glad i did it but uncertain how much it helped.


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## kel1059 (Feb 28, 2003)

> quote: and a problem with my ISP at the time.


oh please!







your apology is accepted. however you need to quit attacking us with those long posts. it is ridiculous. all you do is make people hostile towards you.i did report you for it, but since you apologized i would undo it if i could but can't.


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## calid (Aug 4, 2003)

> quote:The triple post was just an accident and a problem with my ISP at the time.Not spam and I was NOT doing it on purpose.


I didn't read an apology, just more excuses.


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## Talissa (Apr 10, 2004)

MEDSCAPE:"ConclusionThe demonstration that immune and epithelial cells can discriminate between different microbial species has extended the known mechanism(s) of action of probiotics beyond simple barrier and antimicrobial effects. *It has also confirmed that probiotic bacteria modulate mucosal and systemic immune activity and epithelial function."* http://www.medscape.com/viewarticle/470571_print _________________It's all about mucosal immunity in dysbiosis. Here's an example of probiotic research going on relevant to endotoxin(pathogen) effects on mucosal immunity(along the intestinal wall):Abstract: The aim of the present study was to examine the effects of oral supplementation of newborn Balb/c mice with bifidobacteria (B. infantis, B. bifidum) and iron-free apo-lactoferrin (bovine, human) *on gut endotoxin concentration and mucosal immunity.* Endotoxin concentration was measured in ileocecal filtrates at 7, 14, 21, and 28 days postdelivery by a quantitative limulus amebocyte lysate test. While endotoxin levels in bifidobacteria-fed mice showed a steady rise over time, they were consistently lower than that observed in control animals. Results of lactoferrin supplementation varied depending on the specific time point, but overall by day 28, all treatment groups showed lower intestinal endotoxin concentrations compared to saline fed animals.Neither bifidobacteria nor lactoferrin stimulated an increase in B or T cells, or in cytokine production (IL-6, TNF-, INF-), (T: this is good--the immune response to endotoxins/pathogens is a cause of IBS symptoms)...Bifidobacteria and lactoferrin were well tolerated as dietary supplements and showed promising potential to reduce gut endotoxin levels. http://www.ingenta.com/isis/searching/Expa...0000004&index=8 ______________They do these tests in mice, because you can't go around doing intestinal biopsies(the only sure-fire way to assess pathogen over-populations) to test people's endotoxin levels--especially on controls with no digestive problems...And it looks like they're going to be genetically altering mice specifically for digestive disorder studies--"Future studies with genetically altered (i.e., transgenic) mice that become models for studying specific human diseases and their treatments may further increase our understanding of IBS mechanisms.[6]" http://www.iffgd.org/symposium2003brain-gut.html Crazy!____________________In case any one wants to split hairs of "endotoxin"~Endotoxin Definition: "Any of a group of poisonous lipopolysaccharides found in the outer membranes of Gram-negative bacteria. These toxins cause illnesses such as diarrhea and hemorragic shock. "(pathogens are gram-negative)


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## eric (Jul 8, 1999)

My above post was helping to explain the VICIOUS CYCLE in IBS, which is extremely well known.symtoms=stress/anxiety/emotions=syptomsThe nice comments are appreciated. This is a fact in all this.THE CAUSE OF IBS IS UNKNOWN. American Gastroenterological AssociationAmerican Gastroenterological Association medical position statement: Irritable bowel syndrome"Pathophysiology of IBS symptoms TOP The symptoms of IBS have a physiological basis. *Although no specific physiological mechanism is unique to, or characterizes IBS* , there are at least 3 interrelated factors that affect symptoms to varying degrees in individuals with IBS: (1) altered gut reactivity (motility, secretion) in response to luminal (e.g., meals, gut distention, inflammation, bacterial factors) or provocative environmental (psychosocial stress) stimuli, resulting in symptoms of diarrhea and/or constipation; (2) a hypersensitive gut with enhanced visceral perception and pain; and (3) dysregulation of the brain-gut axis, possibly associated with greater stress-reactivity and altered perception and/or modulation of visceral afferent signals. *Brain-gut axis dysregulation may also play a role in the subgroups of patients who have gut inflammatory and immune factors persisting following infection or inflammation of the bowel.* Further studies are needed to characterize the precise role of these factors in IBS and to identify physiological subgroups more amenable to specific treatments. "" Role of psychosocial factors in IBS TOP Although IBS patients show enhanced stress responsiveness, and more severe and prolonged impairment of bowel function related to various inciting factors, specific psychosocial factors are not characteristic of the disorder; they are not considered in diagnosis. However, their identification may help in planning psychological or psychopharmacological treatment, particularly for those with more moderate or severe symptoms, where psychosocial factors contribute to the clinical presentation. *Psychological stress and other psychosocial factors may exacerbate gastrointestinal (GI) symptoms via alterations in gut motility, epithelial function, or perception of visceral stimuli or may modify illness experience and behaviors including pain reporting, physician visits, medication use, or the seeking of alternative medical treatment.* A history of major life stress (e.g., abuse, family death, or divorce), comorbid psychiatric disorders, or maladaptive coping style *strongly influence the clinical outcome.* Because psychosocial factors affect health care seeking, patients with IBS seen at referral centers usually have greater psychological disturbances than patients seen in primary care or nonpatients in the community. Finally, IBS adversely affects health-related quality of life, including impairment of physical, psychosocial, emotional, and role function to a degree exceeding that found in most patients with other medical disorders. " *An integrative biopsychosocial model3 is needed to understand the multiple factors contributing to symptom generation and experience.* The challenge faced by clinicians and investigators is to determine for each individual the degree to which each of these interacting factors are identifiable and remediable using current therapeutic options. http://www2.gastrojournal.org/scripts/om.d...id=agast1232105


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## Poor Boy (Feb 13, 2003)

Kel, I did the dumb thing when I went through the Merc Removal, found a friend Doc and just did it one Tooth at a time but I did not have the outside air or rubber dam used to keep the mercury exposure limited as possible...I mentioned this to Dr. D, he does not think that Merc has anything to do with the IBS, he might be right, but I am happy to get it out of me anyway, as I said before my hair levels were three times normal levels. I only consumed minimal amounts of fish, so who knows where it came from..The chelation I used was all that the Homeopaths say to do minus the intervenus stuff... Many supplements...I just had a blood and urine level test of Mercury exposure done, and the results were non-detectable.... Good I suppose, though it could mean that the Merc does not easily chelate from our fat cells...not that I have much fat..but you know what I mean....I lost alot of strength after the amalgam removal, but of course my diet was still pretty much low carb...I am slowly getting stronger, but I need to have some carbs to gain some muscle mass back....the all protein and low carb veggies does not do it....for me anyway.... Now its your turn...I just would like to get your opinion as to what will be the time period needed before the mucosal membrane can be healed....how long before I can start adding some carbs back into the diet...? Your experience Kel & Calid will be greatfully appreciated...


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## eric (Jul 8, 1999)

Okay, lets cover all the bases for the BIG PICTURE.Pathophysiology of IBS and Serotonin SignalingAbnormal GI MotilityThe pathophysiology of IBS has evolved tremendously over the last 50 years. IBS was previously considered a disorder primarily due to abnormal intestinal motility. In the 1950s, a study by Thomas Almy22 demonstrated that gut motility was increased in both normal individuals and patients with IBS when presented with a stressful situation. Subsequent research demonstrated that patients with IBS had increased motility abnormalities related to meals (ie, after eating) compared with control subjects.23,24 Studies have also demonstrated GI motility abnormalities, such as clustered contractions, prolonged propagated contractions, and high-amplitude propagating contractions more commonly in patients with IBS compared with healthy individuals.25-28 Although these motility abnormalities may be, but are not always, associated with IBS symptoms, there does not appear to be a consistent motility abnormality to explain the etiology of symptoms in all patients, and therefore, they are not currently used as diagnostic markers.Visceral HypersensitivityThe initial clinical observations that led to the hypothesis that patients with IBS have visceral hypersensitivity include recurring abdominal pain, tenderness during palpation of the sigmoid colon on physical examination, and excessive pain during endoscopic evaluation of the sigmoid colon. Experimental evidence suggests that a variety of perceptual alterations exist in patients with IBS: visceral hypersensitivity involving the upper and lower GI tract, as well as a heightened perception of physiologic intestinal contractions. Multiple studies using various balloon distension paradigms have reported lowered colorectal perceptual thresholds, increased sensory ratings, and viscerosomatic referral areas in patients with IBS compared with healthy individuals.29-33 By contrast, most studies have demonstrated that patients with IBS do not exhibit generalized hypersensitivity to noxious somatic stimulation.30,34,35 At least 2 underlying, distinct mechanisms contribute to the visceral hypersensitivity in IBS: a hypervigilance towards expected aversive events arising from the viscera, and a hyperalgesia that is inducible by sustained noxious visceral stimulation.32Central Nervous System Modulation *In the 1980s and 1990s, a greater appreciation for the role of the "brain-gut" axis was achieved, and it was recognized that patients with IBS had a dysregulation between these 2 areas.* 36 In general, brain-gut interactions play a key role in the modulation of GI functioning in health and disease. *Signals from the brain to the gut play an important role in ensuring optimal digestive function, reflex regulation of the GI tract, and modulation of mood states. Proposed alterations in the brain-gut axis in IBS are best supported by recent findings in functional neuroimaging studies. * Using distal colonic stimulation, several studies have demonstrated alterations in regional brain activation in patients with IBS compared with healthy control subjects.37,38 These brain regions include the anterior and midcingulate cortices, insula, and dorsal pons (in the region of the periaqueductal grey) -- which are some of the most consistently activated brain areas in response to visceral as well as somatic nociceptive stimuli.One area that is consistently activated to a greater degree in patients with IBS compared with control subjects is the anterior midcingulate cortex, a brain region concerned with cognitive processing of sensory input, including attentional processes and response selection. Furthermore, midcingulate activation correlates with the subjective unpleasantness of visceral and somatic pain. These observations suggest that patients with IBS may fail to use central nervous system downregulating mechanisms in response to incoming or anticipated visceral pain. They further show altered activation or deactivation of brain areas involved in the emotional or cognitive processing of visceral stimuli, ultimately resulting in the amplification of pain perception. *Role of Stress and Psychological Factors in IBS* It has been postulated that in the predisposed individual, sustained stress can result in permanent increased stress responsiveness of central stress circuits and vulnerability to develop functional and affective disorders.39 Stress may be central (eg, psychological distress) or peripheral (eg, infection, surgery) in origin. Numerous studies indicate that patients with IBS report more lifetime and daily stressful events, including abuse, compared with patients with organic GI conditions or healthy individuals.1 In addition, in patients with IBS, *stress is strongly associated with symptom onset, exacerbation, and severity. Even though the effects of stress on gut function are universal, patients with IBS appear to have greater reactivity to stress compared with healthy individuals.* 40A large proportion of patients with IBS or other functional bowel disorders have concurrent psychological disturbances, particularly those with severe symptoms or those seen in tertiary care referral centers. Psychosocial factors have been recognized to modify the illness experience and influence healthcare utilization and treatment outcome. These psychosocial factors include a history of emotional, sexual, or physical abuse, stressful life events, chronic social stress, anxiety disorders, or maladaptive coping styles.1 A current conceptual model regarding the role of psychosocial factors and stress in IBS suggests that adverse life experiences (past and present) influence stress responsiveness, physiologic responses, and susceptibility to developing and exacerbating this functional disorder via amplification of brain-gut interactions.Role of Immune or Inflammatory MediatorsIBS-like symptoms have been reported in 7% to 30% of patients who have had a recent history of proven bacterial gastroenteritis; this has been termed postinfectious IBS (PI-IBS).41 A subset of patients with IBS can trace the development of their symptoms to an episode of infectious diarrhea, primarily bacterial42 or amebic,43 and possibly even viral,44 in etiology. Risk factors for PI-IBS include female sex, duration of acute diarrheal illness, and the presence of significant life stressors occurring around the time of the infection.41Investigators have found that there are colonic mucosal abnormalities in PI-IBS. One study compared rectal mucosal cellularity and intestinal permeability in patients at 2, 6, and 12 weeks and 1 year after an acute infection with Campylobacter enteritis with those of patients with a history of PI-IBS and healthy controls.45 Compared with controls, patients with a previous Campylobacter infection were found to have increased numbers of intraepithelial lymphocytes and EC cells and increased intestinal permeability, even after 1 year, as did the patients with PI-IBS. *When the secretory granules of the EC cells were evaluated, patients with PI-IBS had granules containing mainly serotonin.* The EC cells in healthy control subjects had granules containing primarily PYY, a peptide associated with antisecretory effects. It is conceivable that these findings play a role in the GI symptoms (eg, diarrhea, mucus in the stool) in at least a subset of patients with IBS.Role of Serotonin in GI Function and IBSThe ENS plays a key role in regulation of both gut motility and secretion. A number of neuropeptides are involved in regulation of motility and secretion, including serotonin, which can modulate both of these functions. Ninety-five percent of serotonin is found in the gut, with 90% localized within the EC cells and 10% in the enteric neurons. *Serotonin is an important mediator of the peristaltic reflex. * The excitatory 5-HT1P, 5-HT3, and 5-HT4 receptors have been found to be particularly important in modulating this motor activity. Following mucosal stimulation (eg, mechanical or chemical stimulation), serotonin is released from EC cells. Serotonin acts on the 5-HT1P receptor located on the terminals of IPANs within the submucosal plexus. 5-HT4 receptors are located on the presynaptic terminals of these afferent nerves and, when activated, facilitate the release of acetylcholine and calcitonin gene-related peptide (CGRP).3 Following activation of interneurons within the ENS, acetylcholine and substance P are released from enteric motor neurons proximally (orad), which leads to a contractual response. Release of vasoactive intestinal peptide and nitric oxide distally (caudad) result in relaxation in the gut. Peristaltic activity of the gut then occurs. 5-HT3 receptors are located on enteric nerves within the myenteric plexus as well as on vagal and spinal afferents. These receptors are thought to play a role in other intestinal reflexes and modulation of nonpainful (eg, nausea) and painful sensations, respectively.Serotonin Reuptake TransporterThere is likely an evolutionary advantage to having physiologic mechanisms that regulate serotonin levels and activity, because it could be quite harmful without these regulatory mechanisms.3 One of the primary mechanisms the body has for regulating availability of serotonin within the extracellular space is the serotonin reuptake transporter (SERT). SERT is present in the brain and gut. The amount of serotonin reuptake that occurs from the extracellular space is genetically determined and is based on whether there are long, short, or heterozygous polymorphisms in the promoter for synthesis of SERT. For instance, homozygosity for the short variant and presence of the heterozygous variant result in less transcript, less protein expression, and thus, less reuptake of serotonin. SERT activity is obviously an important factor influencing serotonin availability to act on postsynaptic receptors, and would possibly affect the response to serotonergic medications such as SSRIs, in the treatment of depression, and to the novel agents tegaserod and alosetron, for IBS.Camilleri and colleagues46 hypothesized that differences in SERT polymorphisms in patients may influence a patient's response to the 5-HT3 antagonist alosetron. It was noted that there were both sex effects and interindividual effects in the way that the medication worked in patients, slowing intestinal transit in some with IBS more than in others. Therefore, a small study of 30 patients (15 women) with IBS with diarrhea was performed in which the patients were given alosetron 1 mg orally twice daily for 6 weeks and their colonic transit measured via scintigraphy at the end of treatment. Only 23 (12 women) of these patients actually submitted blood for analysis, but 8 long homozygous, 4 short homozygous, and 11 heterozygous SERT polymorphisms were identified. When colonic transit was measured, the patients with a long homozygous polymorphism (associated with more serotonin reuptake, ie, there is conceivably less serotonin around to stimulate the gut and peristalsis and therefore gut motility is slowed) had greater slowing of colonic transit with alosetron than heterozygotes. The importance of SERT and its effect on colonic transit response to alosetron on its clinical efficacy, as well as the vulnerability to adverse events associated with the drug, such as constipation and ischemic colitis, need to be examined. http://www.medscape.com/viewprogram/2750


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## Talissa (Apr 10, 2004)

This is just too easy.


> quote:The chemical mediators responsible for the permeability changes include histamine, serotonin (5-HT), bradykinin and leukotreines and prostaglandins.


 http://www.nurseminerva.co.uk/immunity.html This sounds like something I read from one of kel's posts....So serotonin, as part of the immune function in the gut, & THE BIG PICTURE, is indeed very important--along with histamine, bradykinin and leukotreines and prostaglandins --WHEN PERMEABILITY of the intestinal wall comes into play due to altered mucosal response from intestinal cells exposure to endotoxins._________________________Here's an example backing up the link from the uk:"We have investigated the influence of mast cells on the barrier function of intestinal epithelium during nematode infection. Trichinella spiralis infection induces a strong type 2 cytokine-mediated inflammation, resulting in a critical mucosal mastocytosis that is known to mediate expulsion of the parasites from the intestine. The host response to infection is also characterized by an increase in mucosal leakiness. *We show here that intestinal epithelial permeability is markedly elevated during infection, with kinetics that mirror the adaptive immune response to primary and secondary infection.* ...Their further work (37) revealed an increase in chloride ion secretion by infected tissue in response to externally applied *histamine, serotonin, and prostaglandin E2, three factors produced by mast cells.* ...Various stimuli including cytokines, allergens, and bacterial products have been implicated in enhancing mucosal permeability " http://www.pubmedcentral.nih.gov/articlere...gi?artid=164661 (the whole article is great, if anyone's interested)________________________So essentially, whenever -himself- talks about serotonin(his idea of the big picture), he's actually talking about the effects of (the body's immune response to) cytokines, allergens, and bacterial products on the intestinal wall--& more specifically -it often points to leaky gut!What a hoot.


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## kel1059 (Feb 28, 2003)

ahh, the irony. spammer-e is the cook yet he is the one being diced and sliced.


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## Talissa (Apr 10, 2004)

If anyone's confused about mast cells & immune response~Quick Biology Lesson(Kmottus-I'm sure you & many others know this already!):The principal characteristics of inflammation:"BASOPHILS AND MAST CELLS These are virtually identical cells, except Basophils are found in blood and Mast cells are found mainly in mucosal and connective tissues. These cells have IgE receptors on their surface. Once bound to IgE + Antigen, these cells degranulate. The granules contain large amounts of heparin (link to role), serotonin and histamine (link). In addition, these cells can produce a variety of Cytokines that enhance the inflammatory response. The predominant consequence of mast cell degranulation is vasodilation, and the enhanced leakiness of blood vessels allowing the extravasation of cells and fluid, causing edema.These are the principal characteristics of acute inflammation." http://sprojects.mmi.mcgill.ca/immunology/cell_non_spec.htm And the cycle continues because of the permeability(leakiness) so the "acute" inflammation becomes "chronic inflammation".Lucky for us--the altered mucosal wall is NOT as damaged as in IBD.


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## kel1059 (Feb 28, 2003)

> quote: So essentially, whenever -himself- talks about serotonin(his idea of the big picture), he's actually talking about the effects of (the body's immune response to) cytokines, allergens, and bacterial products on the intestinal wall--& more specifically -it often points to leaky gut!What a hoot.


i bet 10 to 1 that he fails to get any of this.this is almost similar to spammer-e's Dr esther sternberg post. he posts information that i am able to use against him.which i do --- but then he turns around and tells me that i don't understand it, and that i am the one missing out on the big picture.mind numbing!!!


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## Talissa (Apr 10, 2004)

kel--here's more~"In a subgroup of patients with IBS, their condition appeared to be preceded by an enteric infection, such as Campylobacter jejuni, with increased inflammatory cell response.19,20 IBS and small-intestinal bacterial overgrowth may share similar symptoms. In a study of 202 patients with IBS, 157 (78%) had small-intestinal bacterial overgrowth. Eradication of bacterial overgrowth improved patients' abdominal symptoms.21 Intraepithelial lymphocytes, lamina propria CD3 cells and CD25 cells, neutrophils, and mast cells are increased in patients with IBS.20 Exact mechanisms by which the inflammatory changes cause the symptomatology are not clear. The inflammatory response may be associated with activating enterochromaffin cells to produce 5-hydroxytryptamine (5-HT) and CD3 cells to produce cytokines, which in turn leads to enhanced motility, increased intestinal permeability, and lowered visceral sensation thresholds.19,20,22 " http://www.clevelandclinicmeded.com/diseas...tro/ibs/ibs.htm Serotonin really is part of the picture--as part of the gut's immune response to pathogens!Bacterial overgrowth=serotonin release=leakiness=serotonin in blood=vicious cycle


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## Kathleen M. (Nov 16, 1999)

But what bacteria...that is the important part.There is a recent article that methane producers (NORMAL BACTERIA IN THE GUT) and Hydrogen producers (NORMAL BACTERIA IN THE GUT).Neither one of these needs to be OVERGROWTH BTW.And their post-prandial serotonin release.In this case certain bacteria (methanogens) seem to LOWER serotonin post-prandially.But who is a methane producer and who is not varies although IBSers are somewhat less likely to be methane producers, but a substantial number are. Unlike crohn's where there are virtually no methane producers.K.


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## kel1059 (Feb 28, 2003)

some how, some way i think that some of this resembles our old friend H. Pylori.why is it that people can have h pylori yet be asymptomatic. i suppose that there could be dozens of bacteria or even mycobacterium (or fungi) that cause some people to react in violent ways similar to what an ulcer sufferer might experience. (i am not talking about actual ulcers but other odd occurrences like uncontrolled cytokine release)pure speculation but the h pylori example has always made me wonder.the mayo clinic findings on sinusitis and "odd immune reaction" with respect to various fungi has always made me wonder.


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## kel1059 (Feb 28, 2003)

http://www.mayoclinic.org/ent-rst/chronicsinus.html Many studies at Mayo Clinic have added evidence to the thinking that chronic rhinosinusitis is caused by an immune reaction to fungi in the nose. Our original study linking chronic rhinosinusitis to fungi in the nose, which was published in the Mayo Clinic Proceedings in September 1999, has been reproduced and confirmed by a sinus center in Europe (ENT University Hospital in Graz, Austria).There are currently 16 studies at Mayo Clinic Rochester to further investigate the role of fungi in inflammatory diseases of the respiratory tract.In addition, researchers from the Allergic Diseases Research Laboratory at the Mayo Clinic in Rochester found that certain white blood cells called T-Lymphocytes are reacting to the fungi and were producing the kind of inflammation we see in the sinuses, and that healthy people did not react in that way. This work was presented at the 2001 Annual Meeting of the American Academy of Allergy, Asthma and Immunology and will be published soon.The evidence was so convincing that the National Institute of Health (NIH) has given Mayo Clinic a $2.5 million grant to further investigate the mechanisms behind this *immunologic response to the fungi.*****************************************i guess this is the followup to the original study back in 1999.it is really interesting!!!it has been referred toi as an "odd" immune reaction.i believe that it could certainly occur in the intestines and NOT just the sinuses.flux thinks i am wrong.


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## Talissa (Apr 10, 2004)

My last one today-promise.What about when they say STRESS causes the IBS/serotonin problem?Stress, just like antibiotics, can cause the # of beneficial bacteria to decline, aloowing opportunistic pathogens to over-populate~"Stress causes the adrenal glands to release cortisol into circulation. As cortisol levels increase human performance decreases as found in military cadets subjected to five day training course of heavy physical exercise and food and sleep deprivation. These effects persist well beyond the actual cessation of the stressful event resulting in lowered levels of natural killer cell activity, secretory IgA activity, lowered healthy gut bacteria and elevations of unhealthy gut bacteria. Natural killer cell activity plays a vital role of the immune system to fight against viral and cancer cells in the body. Secretory IgA is the first line of defense of the immune system lining the gastrointestinal tract, mouth, lungs, urinary tract and other body cavities. Any decline in these levels decreases oneï¿½s resistance to bacteria, viruses and parasites. A single five minute experience of anger can produce a significant decrease in secretory IgA up to five hours afterwards! Intestinal microflora is a delicate balance of millions of flora as numerous as the stars and once imbalanced very difficult to restore. Under high stress situations such as found in astronauts before and after a launch into space, healthy gut bacteria decreased and unhealthy bacteria increased. A simple acidophilus/bifidus supplement can optimize gut flora." http://www.island.net/~ipincott/article53.htm


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## eric (Jul 8, 1999)

Serotonin is released from EC cells in the gut to intiate digestion in all humans and this process has nothing to do with bacteria. IN IBS this process is abnormal.The release of serotonin from mast cells has to do with fighting bacteria.


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## Talissa (Apr 10, 2004)

Somebody's making things up again!!


> quote: The enterotoxins attach to endocrine (enterochromaffin) cells on the villus surface of the intestinal epithelium, causing an increase of cAMP or cGMP. cAMP or cGMP triggers these cells to release serotonin, neurotensin, and possibly other peptides into the subepithelial space.


 http://akabaslab.aecom.yu.edu/pdf/JCI%2011...20-%20Field.pdf p. 8*Enterotoxin definition: A toxin affecting the intestine. *enterochromaffin cell= "EC Cell"___________________ There's *much* more from the above link,including a scientific explanation for malabsorption of carbs & fat from a bacterial overgrowth, but will have to dissect it later.Once again, short on time.


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## flux (Dec 13, 1998)

> quote:Somebody's making things up again!!


It's not us.


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## ohnometo (Sep 20, 2001)

I wouldnt be sure of that !!! After all you was the one on here telling many people for years that with their IBS they couldnt feel sick...If I am correct I believe they are going to put nausea in one of these new Rome Criteria...So see you really dont know as much as you think you doFlux's quoteIt's not us.


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## Poor Boy (Feb 13, 2003)

Talissa, Thanks for the great info...Hows the weather in St. Kitts...? Wish I was there....I'm in Atlantic City....Not quite Tropical....Oh and thanks for disregarding the crackers....It's difficult keeping the lunatics inside the aslyum, but they love to show up on posts like these...


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## kel1059 (Feb 28, 2003)

donna,i am not sure but i think flux was actually taking our side on this issue.talissa's link was from the albert einstein school of medicine where flux works. --so flux was just validating that talissa's information was indeed accurate.eric,when flux agrees with something then you know you are cooked because he does not believe in ANYTHING. (i don't even think he believes he had all that gas a while ago) flux quote:"Hmm, are you saying that passing gas 100 times a day (that's about once> every ten minutes, excluding sleeping hours) with enough pain to> significantly interefere, and prevent altogther in some cases, with life> activities, such as being forced to live on diet of virtually no> carbohydrates is healthy?> > --> -- http://groups.google.com/groups?hl=en&lr=&...hl%3Den%26lr%3D %26ie%3DUTF-8%26selm%3D3317f25b.2714525%2540nntp.ix.netcom.com%26rnum%3D1[/URL]what i want to know is if you were imagining all this gas. you claim that gas production is normal in IBS, yet you claim that you passed gas 100 times per day.what have you discovered since then to work. i imagine you have not solved it as of yet because you are still here but in case you have --do share it with others.


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## eric (Jul 8, 1999)

Gut. 2004 Jun;53(6):829-837. Related Articles, Links Association of distinct alpha(2) adrenoceptor and serotonin transporter polymorphisms with constipation and somatic symptoms in functional gastrointestinal disorders.Kim HJ, Camilleri M, Carlson PJ, Cremonini F, Ferber I, Stephens D, McKinzie S, Zinsmeister AR, Urrutia R.Clinical Enteric Neuroscience Translational and Epidemiological Research (CENTER) Program, Gastroenterology Research Unit, Mayo Clinic College of Medicine, Rochester, Minnesota, USA. Department of Health Sciences Research, Division of Biostatistics, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.BACKGROUND: The role of genetics in the phenotypic manifestations of irritable bowel syndrome (IBS) is unclear. Our aims were: (1) to compare the prevalence of polymorphisms of alpha 2 (alpha(2)) adrenoceptors, norepinephrine transporter, and serotonin transporter protein (soluble carrier protein member 4 (SLC6A4)) promoter in patients with lower functional gastrointestinal disorders (FGID) and in healthy controls; and (2) to test associations of these genetic variations with symptoms of IBS and high somatic symptom scores. METHODS: Validated bowel and somatic symptom questionnaires characterised the phenotype: 90 with IBS constipation (IBS-C), 128 IBS diarrhoea, 38 IBS alternating bowel function, and 20 chronic abdominal pain. Logistic regression analyses assessed associations of different polymorphisms for alpha(2) adrenoceptor and SLC6A4 with IBS or chronic abdominal pain phenotypes and high somatic score. RESULTS: Two distinct polymorphisms independently appeared to be associated with the phenotype IBS-C: alpha(2C) Del 322-325 (odds ratio (OR) 2.48 (95% confidence interval (CI) 0.98, 6.28); p = 0.05) and alpha(2A) -1291 (C--G) (OR 1.66 (95% CI 0.94, 2.92); p = 0.08) relative to wild-type. Overall, the alpha(2C) Del 322-325 polymorphism (alone or combined with other polymorphisms) was also significantly associated with a high somatic symptom score (OR 2.2 (95% CI 1.06, 4.64); p = 0.03). Combinations of polymorphisms were also associated with high somatic scores. CONCLUSION: Functionally distinct alpha(2A) and alpha(2C) adrenoceptor and serotonin transporter polymorphisms are associated with constipation and high somatic symptoms in patients with lower functional gastrointestinal disorders, although the strength of the genetic contribution to the phenotype is unclear.PMID: 15138209


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## eric (Jul 8, 1999)

"Dr esther sternberg post. he posts information that i am able to use against him."Does Stress Make You Sick and Believing Make You Well? The Science Connecting Body and MindEsther M. Sternberg M.D., National Institutes of Health, Bethesda, MD, USA.The notion that stress makes you sick and believing makes you well has been part of the popular culture for thousands of years. These ideas are universal throughout all cultures. In Western culture these beliefs held sway from before the time of Hippocrates, when the Greeks built temples to Aesclepius, the God of healing, all the way through to modern times, when Norman Cousins and Norman Vincent Peale espoused the idea that laughter and positive thinking heals. Perhaps because these ideas were so much a part of the popular culture most scientists have until very recently rejected the concept that emotions can affect disease and that disease can affect our emotional health. In part this may be because until recently, scientists have not had the technological tools to prove these connections. But, in the last decade we have finally developed the technology in immunology and neuroscience to prove that these connections between emotions and disease, between the brain and the immune system, the mind and the body, are real. Thus, with molecular biology we can prove that immune molecules, the interleukins, signal the brain through many routes - through the blood stream and through nerve pathways. And we can prove that when the brain receives such signals we experience a set of feelings and behaviors that, lumped together, are called "sickness behavior". We know that immune molecules can also stimulate the brain's hormonal stress response and start a cascade of hormones that finally result in the adrenal glands' release of anti-inflammatory corticosteroid hormones. Thus, the brain's stress response keep the immune system tuned down when an immune response is no longer needed to fight off a foreign invader. This can be good or bad, for too much of these anti-inflammatory stress hormones at the wrong time, such as during chronic stress, can predispose a stressed host to more infection. On the other hand, too little can predispose to autoimmune diseases such as arthritis, since the immune response is not shut off and can go on unchecked. Many studies have now proven that a blunted hormonal stress response in animals and humans, whether present on a genetic basis, because of drug therapy or because of surgical intervention, can all lead to increased susceptibility to inflammatory disease. These diseases include arthritis, systemic lupus erythematosus, allergic asthma and atopic dermatitis. Knowing this can help treat such diseases, or can lead to development of new treatments for such illnesses based on stimulating various parts of the hormonal stress response. But immune molecules, the interleukins do not simply act as hormones to stimulate brain function. They also act as growth factors when expressed in brain. These molecules are made by the scaffolding cells in the brain - those cells that are not nerve cells that provide an essential milieu to help nerve cells survive or kill them off. So through this science we know that interleukins play an important role in nerve cell death and survival and therefore in nerve regeneration and repair. Thus, interactions between the immune and nervous system play a role in diseases such as Alzheimer's, stroke, neuroAIDS and nerve trauma. Understanding exactly how such molecules and immune cells interact with nerve cells is helping us develop new treatments for these diseases. Interactions in the other direction are also true - that is, nerve chemicals play a role in keeping the immune system active. In this way, adrenalin-like molecules released from nerve endings in the spleen can help restore lost immune cell function that occurs during aging. Drugs which stimulate growth of such nerve endings can thus be used to enhance the diminished immune responses seen in aging. There are still more communications between these systems that occur at a local level, where nerve endings feed tissues, such as the lining of joints. Nerve chemicals released from such nerve endings during inflammation can increase inflammation, and thus drugs that block such nerve chemicals can be used to treat arthritis. What does the future hold? All of these discoveries just touch the surface, and each leads to many more questions, which when answered in depth will lead to more specific ways to manage stress effects on immune function, local effects of nerve chemicals on inflammation, effects of immune molecules on nerve growth and death. Studies showing the effects of interleukins on sickness behavior raise the question whether these molecules play a role in illnesses such depression, in the absence of infection. We now have the tools to answer these questions by combining molecular biology and modern imaging technologies. With such technologies we should also be able to take studies of the effects of stress on immune responses to the next level, by asking how learning and memory and early experience and development affect the stress response. With sophisticated new genetic and mathematical modeling techniques, we can determine what part of our stress responsiveness we are born with, and how much is under environmental control. These sorts of studies will help us understand not only the reasons for individual differences in stress responsiveness that affect susceptibility to inflammatory disease, but will also point the way to using old and developing new behavioral strategies that can change the set point of different individual's stress responses. So this science can help explain why meditation, crystals or other alternative therapies do work to ameliorate disease. By studying the neurobiology of the placebo effect, we can not only understand such phenomena that have been around for thousands of years in all cultures, but physicians can also shed the bias that has stigmatized the lowly placebo effect, and rather than trying to control for it and exclude it, can use this very powerful biological effect judiciously to help heal. More than anything else this field of neuroimmunomodulation - the brain-immune connection, the science of the mind-body connections, embodies the marriage of the beliefs of the popular culture with technological advances across many disciplines, from the molecular through to the systems interaction levels. That is the most important contribution of this field to modern science and medicine - it pushes and pulls science out of a narrow reductionist view rooted in the 16th century philosophy of Descartes, back into the holistic view of body and soul entwined, embodied by Hippocrates. But it does so with a modern technological twist that empowers us to apply this science to discover new treatments for a whole host of diseases. So, this very old science, born before recorded history, has now, with modern scientific technology been reborn. Not only can this science help physicians and scientists believe their patients when they say that stress makes them sick and believing makes them well, but it can help us develop new therapies to treat many diseases, from arthritis to Alzheimers' and stroke, from nerve trauma to the immunosuppression of aging. http://psydoc-fr.broca.inserm.fr:16080/col.../Sternberg.html


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## kel1059 (Feb 28, 2003)

nice try eric but that is not the sternberg article that i am referring to.once again ----nice try!!!


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## eric (Jul 8, 1999)

FYI"Br J Pharmacol. 2004 Apr;141(8):1285-93. Related Articles, Links Role of serotonin in the pathophysiology of the irritable bowel syndrome.Crowell MD.Mayo Clinic College of Medicine and Mayo Foundation, Scottsdale, AZ, U.S.A.The irritable bowel syndrome (IBS) is a complex disorder that is associated with altered gastrointestinal motility, secretion, and sensation. *Serotonin (5-HT) is an important neurotransmitter and paracrine signalling molecule in the gastrointestinal tract. 5-HT release from enterochromaffin (EC) cells initiates peristaltic, secretory, vasodilatory, vagal and nociceptive reflexes.* The enteric nervous system (ENS) comprises a semiautonomous effector system that is connected to the central autonomic network. Parasympathetic and sympathetic nerves modulate the ENS via afferent and efferent communications. Ongoing, bidirectional brain-gut interactions involving 5-HT pathways occur that significantly influence the effector systems. Altered 5-HT signalling may lead to both intestinal and extraintestinal symptoms in IBS. 5-HT directly and indirectly affects intestinal motor and secretory function and abnormalities may lead to either constipation or diarrhea. 5-HT modulates sensation and perception of visceral stimulation at peripheral and central sites. Therapeutic agents targeting altered 5-HT signalling may provide new, effective treatments for patients with IBS.British Journal of Pharmacology (2004) 141, 1285-1293. doi:10.1038/sj.bjp.0705762PMID: 15100164Curr Opin Investig Drugs. 2004 Jan;5(1):55-60. Links Enterochromaffin cells and 5-HT signaling in the pathophysiology of disorders of gastrointestinal function.Crowell MD, Shetzline MA, Moses PL, Mawe GM, Talley NJ.Mayo Foundation and Mayo Clinic, GI Physiology & Motility, Division of Gastroenterology & Hepatology, 13400 E Shea Blvd, Scottsdale, AZ 85259, USA. crowell.michael###Mayo.eduDisorders of gastrointestinal function are common and significantly reduce quality-of-life, as well as negatively impacting healthcare costs. Consequently, there is much interest in understanding the pathogenesis of these disorders. Increasing, albeit as yet limited, evidence has implicated alterations in 5-hydroxytryptamine (5-HT) release, and the subsequent interaction of 5-HT with specific 5-HT receptor subtypes, in the altered gut function of patients with irritable bowel syndrome (IBS) and other functional bowel diseases. *Alterations to enterochromaffin cells and/or 5-HT signaling can result in gastrointestinal dysmotility, visceral hypersensitivity and secretomotor abnormalities in the gut. Evidence is beginning to link disturbed 5-HT physiology with the pathophysiology of diarrhea and constipation in IBS, and with slow-transit constipation. This review discusses the current evidence on the pathobiology of these systems.* PMID: 14983974


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## flux (Dec 13, 1998)

> quote:i am not sure but i think flux was actually taking our side on this issue.


Nope, us includes eric


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## Poor Boy (Feb 13, 2003)

If Fungi can be the source of some of these problems what are the methods of testing this and possibly erradicating this....I personally believe the connection of the GI tract, Sinus, and soft tissue joints is well made....Any positive input....?


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## Talissa (Apr 10, 2004)

Okay, so now himself is saying it could be genetic. Well, there would be a great reason to never do the things necessary to get better, & just take drugs & hypnotise yourself!But himself should read the last sentence of his "genes" post & let that sink in.He'd also learn something from this info:"The intestinal barrier function test was developed since mucosal barrier dysfunction may result in gastrointestinal, cardiovascular, systemic immunity and autoimmunity. Human beings harbor an incredibly complex and abundant ensemble of microbes...Colonized bacteria modulated expression of genes involved in important intestinal function including:Nutrient absorption Lipid absorption capacity Mucosal barrier fortificationXenobiotic metabolismAngiogenesis This article emphasizes the importance of host-microbial relationships in the GI tract and how gut bacteria and their products play a role in the induction and expression of normal immune responses, suggesting that changes in this flora may mediate abnormalities of system immunity.In addition to measurement of antibodies against dietary proteins, yeast, aerobic and anaerobic bacteria, antibodies against secretin are measured. Similar to DPP IV, secretin is *involved not only in digestion of peptides but also in neuroimmune communication.* http://www.immuno-sci-lab.com/2003_cat_page105.htm ________________________________________________And then we're back to stress.We all should know by now that stress can cause imbalanced gut flora. It causes a lowering of beneficial bacteria as a result of the "flight or fight response"(~ cortisol & low blood circulation), allowing opportunistic pathogens to overpopulate.Here's a nice abstract~ *"Critical role of mast cells in inflammatory diseases and the effect of acute stress"* 8. Gastrointestinal inflammation The role of mast cells and their interaction with local nerve endings in gastrointestinal pathology , * especially in the intestinal response to bacterial infections * has been reviewed extensively. Mast cells are located close to intestinal neurons. Even though mucosal mast cells cannot be commonly activated by neuropeptides, it was recently shown that mucosal-like mast cells could make functional associations with neuronal processes through SP at distinct points of contact, and could express NK-1 receptors. Moreover, in rats, NT has been shown to play a significant role in Clostridium difficile-induced colonic inflammation and the accompanying activation of mast cells. Neuroimmune interactions have been implicated in food allergies as well as in IBS._______________________ Summing it up--The neuroimmune response seen in IBS can be caused by bacterial overgrowths, such as C. Difficile. (aside-the overgrowth of which is also found in conjuction with yeast overgrowth in IBS)_____________________Here's more on neuroimmune interactions & bacterial instigators:" *Neuroimmune intercommunication, central opioids, and the immune response to bacterial endotoxin.* " http://www.ncbi.nlm.nih.gov/entrez/query.f...5&dopt=Abstract (when they talk about "lipopolysaccharide", this is another word for endotoxin)Just an interesting connection--this next article is captioned under "Chronic Neuroimmune Disease" & it's all about intestinal permeability: http://www.cndsinfo.net/pdf-files/m4-leakygut.pdf Here's one showing neuroimmune interactions after C. Difficile overgrowth(& it doesn't have to be a substantial overgrowth to make a difference in bowel function):"Introduction""Over the past few years, our understanding of the pathophysiology of enterotoxin actions(bacterial actions) has evolved from a classic cell-oriented model to an integrated model incorporating neuronal and immune mediators" (neuroimmune interactions)"Synopsis""Bacterial enteric toxins are incredibly potent molecules that are capable of disrupting the normal function of the bowel at nanomolar or even lower concentrations. Even a few molecules per cell of certain toxins like diphtheria toxin or C. difficile toxin B are sufficient to "intoxicate" target cells.... *It is likely that other enteric pathogens(Bacteria!) elicit specific amplification pathways involving neurons, neuroimmune cells* , vascular endothelium, and circulating inflammatory cells. Dissecting out these complex pathways for specific pathogens and devising ways to interrupt them may provide new weapons for disease control." http://nips.physiology.org/cgi/content/full/13/2/58


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## Talissa (Apr 10, 2004)

Hey PB,It's supposed to be tropical--it's felt like Ohio though for the past week & a half--very overcast, w/ off & on rain. Have never seen it like this before down here.The locals say it means we may get hit with a major hurricane this year.I REALLY hope they're wrong!Btw, Atlantic City sounds great to me! I miss civilization. Did you catch any of the taping of "The Apprentice" up there?


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## Talissa (Apr 10, 2004)

PB,


> quote:If Fungi can be the source of some of these problems what are the methods of testing this and possibly erradicating this


I think this is why treatments for IBD have been shown effective in treating IBS(medscape): "In conclusion, regardless if the presumed infective agent in Crohn's disease is Mycobacterium paratuberculosis or Helicobacter species, clinical studies have shown the following similarities with H pylori (and H hepaticus): -dual therapy is superior to monotherapy (two vs. one antibiotic) -clarithromycin and metronidazole have been shown effective -both infections exist as a chronic process with slow onset http://www.geocities.com/HotSprings/Spa/7959/antibiotics.htm Wish they'd mention the need for probiotics during antibiotic treatment & for at least 2 months after, so that the condition doesn't return.What can you do.


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## eric (Jul 8, 1999)

I am already well aware of the gentic link to IBS.







also Tal, you need to pay some more attension to NONE IMMUNE ISSUES IN IBS! They are just as important as the immune issues. Again tunnel vision.And you and Kel were wrong about the EC cells!"Gut-Brain Connection -- The gut and the brain develop from the same part of the human embryo. So it is not surprising that the intestinal tract has such a rich nerve supply that it is sometimes referred to as "the little brain." The gut shares many of the same kinds of nerve endings and chemical transmitters as the brain to which it remains linked through a large nucleus. This collection of nerve cells is partly responsible for controlling anxiety and fear, which explains why these emotions can sometimes be associated with bowel function."They both develop at the same time and there are looking at serotonin and other abnormalities at the start of this development for clues. I have also heard they are trying to clone 5ht cells.Alsosocial learning seems to be as important as the gentic link.Gastroenterology. 2001 Oct;121(4):799-804. Related Articles, Links Irritable bowel syndrome in twins: heredity and social learning both contribute to etiology.Levy RL, Jones KR, Whitehead WE, Feld SI, Talley NJ, Corey LA.University of Washington, Seattle, Washington 98195, USA. rlevy###u.washington.eduBACKGROUND & AIMS: Heredity has been suggested to explain the finding that irritable bowel syndrome (IBS) tends to run in families. Research in this area has been limited. The aim of the present study was to assess the relative contribution of genetic and environmental (social learning) influences on the development of IBS by comparing concordance rates in monozygotic and dizygotic twins to concordance between mothers and their children. METHODS: Questionnaires soliciting information on the occurrence of more than 80 health problems, including IBS, in self and other family members were sent to both members of 11,986 twin pairs. RESULTS: Analysis is based on 10,699 respondents representing 6060 twin pairs. Concordance for IBS was significantly greater (P = 0.030) in monozygotic (17.2%) than in dizygotic (8.4%) twins, supporting a genetic contribution to IBS. However, the proportion of dizygotic twins with IBS who have mothers with IBS (15.2%) was greater than the proportion of dizygotic twins with IBS who have co-twins with IBS (6.7%, P 0.001), and logistic regression analysis showed that having a mother with IBS and having a father with IBS are independent predictors of irritable bowel status (P 0.001); both are stronger predictors than having a twin with IBS. Addition of information about the other twin accounted for little additional predictive power. CONCLUSIONS: Heredity contributes to development of IBS, but social learning (what an individual learns from those in his or her environment) has an equal or greater influence.Publication Types: Twin StudyPMID: 11606493 Wed Dec 10 14:48:40 2003 Pacific TimeIrritable Bowel Syndrome's Possible Genetic Link Studied by Mayo Clinic ResearchersROCHESTER, Minn., Dec. 10 (AScribe Newswire) -- Researchers at Mayo Clinic studying irritable bowel syndrome say their study of people with this disorder suggests genetic factors may play a role. Irritable bowel syndrome is a common problem affecting about one in 10 adults. However, many people don't talk about irritable bowel syndrome, which causes abdominal cramping, constipation and diarrhea. The study, which is published in the December issue of Gut, an international journal in gastroenterology, shows that the risk of having irritable bowel syndrome is nearly double in the families of people with the disorder. "The next challenge is determining nature versus nurture," said G. Richard Locke, M.D., a Mayo Clinic gastroenterologist and one of the authors of the study. "Is this due to a gene or genes or is it due to a shared environmental factor? Our group is active in investigating these issues." In developing the study, researchers noted that people with irritable bowel syndrome often report family members with similar symptoms. The researchers hypothesized that if there is a familial connection, there would be an increased frequency of irritable bowel syndrome in direct relatives of irritable bowel syndrome patients compared to relatives of people without irritable bowel syndrome. Others who conducted the study include Jamshid Kalantar, M.D., Alan Zinsmeister, Ph.D., Christopher Beighley, and Nicholas Talley, M.D., Ph.D. Dr. Kalantar was a research fellow at Mayo Clinic during the study, but is now with the Department of Medicine, University of Sydney, Australia. Mr. Beighley now works in West Virginia. The others are with Mayo Clinic in Rochester. In the study, patients with irritable bowel syndrome seen at Mayo Clinic and their spouses filled out a bowel disease questionnaire and provided the names and addresses of their direct relatives. Researchers then sent a bowel disease questionnaire to 355 relatives of the patients and their spouses, and 71 percent responded. Irritable bowel syndrome occurred in 17 percent of the patients' relatives compared with 7 percent in spouses' relatives. http://www.ascribe.org/cgi-bin/spew4th.pl?...r=2003&public=1 Mast cells again *"The brain to mast cell connection has a direct clinical relevance for irritable bowel syndrome and other functional gastrointestinal syndromes. It implies a mechanism for linking allostasis and the good stress response to irritable states (e.g., abdominal pain and diarrhea) of the gut. Mast cells can be activated to release histamine in response to perceived psychological stress, whether the stressor or trigger is consciously perceived or not. So the end result is the same as if an infection activated the program in the-little-brain-in-the-gut: abdominal pain and diarrhea. " * *Major inflammatory responses have not been observed in most IBS patients.* However, in some studies subtle changes associated with inflammation have been noticed, such as increased presence of mast cells (a type of immune system cell present in blood and tissue). Jackie Wood, Ohio State University College of Medicine discussed the Effects of Inflammation on the Gut Enteric Nervous System, specifically noting the importance of mast cell degranulation (the release from within the cell of granules, or small sacs, containing chemicals that can digest microorganisms and fight infection). http://www.iffgd.org/symposium2003brain-gut.html "Well, there would be a great reason to never do the things necessary to get better, & just take drugs & hypnotise yourself!"This is totally riducluous. For one I am pro probiotics in IBS!HT is a safe and natural treatment for IBS, and I know you don't understand HT and IBS."Hypnosis is only one of several approaches to treating irritable bowel syndrome and may not be the most suitable option for all patients (click here for discussion of treatment options for IBS). However, hypnosis treatment has some advantages which makes it an attractive option for many IBS sufferers with chronic and severe symptoms:- It is one of the most successful treatment approaches for chronic IBS. The response rate to treatment is 80% and better in most published studies to date. - The treatment often helps individuals who have failed to get improvements with other methods (see for example: Whorwell et al., 1984, 1987; Palsson et al., 1997, 2000).- It is a uniquely comfortable form of treatment; relaxing, easy and generally enjoyable.- It utilizes the healing power of the person's own mind, and is generally completely without negative side effects. - The treatment sometimes results in improvement in other symptoms or problems such as migraine or tension headaches, along with the improvement in IBS symptoms.- The beneficial effects of the treatment last long after the end of the course of treatment. According to research, individuals who improve from hypnosis treatment for IBS can generally look forward to years of reduced bowel symptoms. http://www.ibshypnosis.com/whyhypnosis.html Drugs are needed for some people and some people just look for a pill to make it all go away. Drugs have a role in IBS, but you don't even listen to what we are saying a combination approach with stress reduction and diet changes are the first step in IBS treatment and then drugs if needed or requested by the person.Phycological and standard medical care has repeatedly shown to be more benefical then standard medical treatment alone. You also don't understand the placebo responce in IBS which is another factor or the fact that some people's IBS just goes away on it own. You don't have a bigger picture, because of the tunnel vision on bacter and the immune system and the lack of understanding the hugely important role of the brain in IBS."And then we're back to stress.We all should know by now that stress can cause imbalanced gut flora. It causes a lowering of beneficial bacteria as a result of the "flight or fight response"(~ cortisol & low blood circulation), allowing opportunistic pathogens to overpopulate."This proves your not reading what I am posting or not understanding it.Levels of 5-Hydroxytryptamine Increase After Meals in Women With Irritable Bowel SyndromeNEW YORK Reuters Health May 05 - Platelet-depleted plasma 5-hydroxytryptamine 5-HT levels increase after meals in women with diarrhea-predominant irritable bowel syndrome d-IBS whose symptoms increase following food ingestion, according to a report in the May issue of Gut.In small studies, 5-HT concentrations in platelet-poor plasma appear higher in women with d-IBS than in healthy women, the authors explain, suggesting a possible link between 5-HT and postprandial symptom exacerbations or IBS itself.Dr. L. A. Houghton from University Hospital of South Manchester, UK and colleagues assessed 5-HT and 5-HIAA its metabolite concentrations, 5-HT turnover, and platelet 5-HT stores in 39 women with d-IBS and 20 healthy female volunteers before and after a standard carbohydrate meal.Although there was no difference in the ratio of postprandial to fasting 5-HT levels between d-IBS patients and healthy controls, the authors report, d-IBS subjects did have higher postprandial concentrations of 5-HT with earlier peak 5-HT levels than did healthy women.Women with d-IBS who reported symptoms following the meal also tended to have higher 5-HT concentrations and higher peak concentrations than did other women, the report indicates, though there was no difference in the time to peak levels compared with asymptomatic women with d-IBS.Fasting 5-HIAA levels were higher in d-IBS women than in healthy controls, the researchers note, but postprandial concentrations did not differ.Fasting and postprandial 5-HT turnover the ratio of 5-HIAA to 5-HT levels did not differ between healthy controls and women with d-IBS, the results indicate, but d-IBS subjects with postprandial symptoms tended to have a lower 5-HT turnover than did d-IBS women without symptoms.Women with d-IBS had significantly higher platelet 5-HT stores than did healthy women, the investigators find, though levels did not differ between d-IBS patients with and without postprandial symptoms."Our results have shown for the first time that symptom exacerbation following meal ingestion in female subjects with d-IBS is associated with increased levels of plasma 5-HT, together with a reduction in 5-HT turnover," the authors conclude. "In addition, baseline platelet stores of 5-HT are elevated in female subjects with d-IBS compared with healthy subjects, supporting increased exposure of platelets to 5-HT in the systemic circulation.""Platelet 5-HT concentrations may have a potential role to play as a marker in the diagnosis and management of d-IBS," the researchers suggest. "This would be similar to the way glycosylated hemoglobin is used to reflect mean blood glucose concentration over a prolonged time period in patients with diabetes mellitus."The investigators add, "Further studies addressing both mucosal 5-HT concentrations and enteroendocrine cell numbers in subjects with d-IBS, as well as similar studies to the present one conducted in subjects with constipation predominant IBS and assessing the transient relationship between symptoms and the 5-HT system need to be performed."Gut 2003;52:663-670.www.medscape.com/viewarticle/45348915 minutes after eating in the sigmoid colon n normals and IBS. The ACT OF EATING CAN TRIGGER IBS! This also has to do with an altered gastro coloniic response to nutrients which is exaggerated in IBS. Look it up and what it is about.














PathophysiologyAltered Serotonin Signaling?The pathogenesis of IBS remains obscure, and in particular, an explanation for alternating diarrhea and constipation has been elusive. In arguably one of the most important papers presented during this year's meeting, Moses and colleagues21 studied potential deregulation of the gut's serotonin transporter in IBS. It is known that serotonin (5-hydroxytryptamine or 5HT) is released from enteroendocrine (or enterochromaffin) cells in response to either chemical or mechanical stimulation of the gut mucosa. Serotonin in turn initiates peristalsis, and then the serotonin released is taken up in health by a highly selective serotonin transporter (SERT). One potential mechanism that could explain altered bowel function in IBS is an abnormality in the serotonin transporter itself. The study authors evaluated this hypothesis in patients with IBS with constipation and IBS with diarrhea compared with patients with ulcerative colitis and healthy controls. They were able to convincing show on blinded review that SERT immunoreactivity was less intense in patients with IBS with constipation and patients with ulcerative colitis. If these findings are indeed correct, they represent a landmark observation. The findings suggest that patients with constipation and IBS may have a reduced capacity to reuptake serotonin, leading to excess free serotonin and then desensitization of these receptors, thus reducing motor function. In contrast, in the setting of diarrhea, serotonin uptake was normal. If the underlying abnormality in serotonin transporter function alternated, then this would in turn explain alternating constipation and diarrhea. These data strongly suggest that IBS is a "real" gut disease and a potential diagnostic disease marker. They also suggest that it is valid to subdivide IBS into constipation and diarrhea symptom subgroups. This study also provides additional rationale for the use of serotonin-modulating agents in IBS and provides a new target for drug modulation. Confirmation of these very exciting initial findings in larger patient samples is awaited with great interest.Ask The Expert.Image of a cadeusus. .General Medical Questions.Q: I have suffered from irritable-bowel syndrome for many years. I get diarrhea. The doctors I've seen have offered little help. Recently, my daughter suggested I try an over-the-counter medicine called "5-Hydroxy-tryptophan," made by a company called Natrol Inc. My daughter says it is a mild antidepressant. It seems to have helped quite a bit, but it also seems to slow me down and make me feel tired. Can you give me any information on this? What is it, exactly, and are there any serious side effects? The only other medicine I take is Synthroid....The Trusted Source..Harold J. DeMonaco, M.S.Harold J. DeMonaco, M.S., is senior analyst, Innovative Diagnostics and Therapeutics, and the chair of the Human Research Committee at the Massachusetts General Hospital. He is author of over 20 publications in the pharmacy and medical literature and routinely reviews manuscript submissions for eight medical journals...June 19, 2001.A:Irritable bowel syndrome is now recognized as a disorder of serotonin activity. Serotonin is a neurotransmitter in the brain that regulates sleep, mood (depression, anxiety), aggression, appetite, temperature, sexual behavior and pain sensation. Serotonin also acts as a neurotransmitter in the gastrointestinal tract.Excessive serotonin activity in the gastrointestinal system (enteric nervous system) is thought to cause the diarrhea of irritable-bowel syndrome. The enteric nervous system detects bowel distension (expansion) on the basis of pressure-sensitive cells in the bowel lumen (opening). Once activated, these pressure-sensitive cells promote the release of serotonin, which in turn promotes both secretory function and peristaltic function (the contractions of the intestines that force the contents outward). At least four serotonergic receptors have been identified to be participants in the secretory and peristaltic response.Patients with diarrhea-predominant IBS may have higher levels of serotonin after eating than do people without the disorder. This recognition led to the development of the first drug used specifically to treat diarrheal symptoms of IBS, alosetron (also known as Lotronex). Alosetron blocked the specific serotonin receptors responsible for recognizing bowel distention. In doing so, it blocked the effects of serotonin and reduced both bowel secretions and peristalsis. Constipation was the most common side effect seen. (Note: Alosetron was removed from the market by the manufacturer after repeated reports of a dangerous condition known as ischemic colitis became known.) Tegaserod (Zelmac) is another drug under development and under review by the U.S. Food and Drug Administration for approval. Tegaserod is indicated for the treatment of constipation-predominant IBS and works to increase enteric nervous system serotonin activity.So, increasing serotonin activity in the enteric nervous system produces increased bowel secretions and peristalsis (and potentially diarrhea), whereas depressing serotonin activity produces reduced secretions and reduce peristalsis (and potentially constipation). Increasing serotonin activity in the brain would increase awareness and, in higher doses, produce anxiety, insomnia and restlessness. So I would have expected exactly the opposite effects of those that you experienced.I am unable to identify any possible drug interactions between 5-HTP and Synthroid (levothyroxine) but the symptoms described suggest a check with your doctor may be in order. Persistent feelings of tiredness and constipation may be signs of an underactive thyroid (hypothyroidism).June 19, 2001 The cardinal symptoms of IBS are abdominal pain and altered intestinal activity - diarrhea or constipation. These are probably related to what is called visceral hypersensitivity; this means the nerve receptors in the intestines are super-sensitive, and fire off signals more readily than those in unaffected people.Visceral hypersensitivity can be demonstrated by inflating a balloon that's inserted in the rectum, and measuring the pressure that produces pain. The pain threshold is lowered in 60% of IBS patients. Interestingly, if the patient is led to anticipate pain, by a stepwise increase in balloon pressure, the pain threshold decreases; on the other hand, if the balloon pressure is randomly altered, there is no lowering of the pain threshold. This indicates that the brain can, indeed, play a part in the symptoms of IBS. And during the anticipation of, as well as actual, distension of the rectum in IBS patients, brain radiographs show increased blood flow in some parts of the brain.Patients with IBS may complain of diarrhea, constipation, or neither of these symptoms. The motility of the colon is clearly an important feature of the condition. Visceral hypersensitivity means the colon will react to a greater extent to stimuli that would produce no obvious effect in unaffected people. A worsening of symptoms after eating, for instance, might be an exaggerated response to the 'gastro-colic reflex', in which a full stomach releases a substance called cholecystokinin-1 that causes contractions of colon musculature.IBS sufferers are sometimes intolerant of certain foods, such as wheat products or milk. An irritant effect can lead, because of visceral hypersensitivity, to poor digestion, excessive gas, bloating, and intestinal 'hurry'.Visceral hypersensitivity implies increased nerve cell signals traveling from the intestines up to the brain (afferent signals), and increased signals going in the opposite direction (efferent signals). These signals are transmitted with the aid of a chemical called serotonin, or 5HT (short for 5-hydroxytryptamine).There are several reasons for believing that 5HT plays a central role in the way IBS symptoms are caused. First, in inflammatory intestinal conditions, such as food poisoning, enteritis, and colitis, the number of special cells that produce 5HT in the intestine wall are greatly increased, and there is increased intestinal motility and hurry. Second, a drug that antagonizes one type of 5HT receptors on the cells (alosetron) is effective in diarrhea-predominant ISB. And third, another drug that antagonizes another type of 5HT receptors (tegaserod) is effective in constipation-predominant IBS.Two other factors are important in how IBS occurs. Stress can make it worse. Acute stress situations are not likely to be a problem; chronic, unrelieved stress, such as separation or bereavement, are more likely triggers."http://216.109.117.135/search/cache?p=pres...A3D53EB061&c=48 [/URL] 2&yc=28196&icp=1Current insights into the pathophysiology of irritable bowel syndrome.Schwetz I, Bradesi S, Mayer EA.Center of Neurovisceral Sciences and Women's Health, CURE: Digestive Diseases Research Center, David Geffen School of Medicine at UCLA, VAGLAHS, Bldg. 115, Room 223, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA. emayer###ucla.eduRecent reports have emphasized the possible role of mucosal immune activation and inflammation in neuropathic changes in the pathophysiology of irritable bowel syndrome (IBS). However, novel findings using functional brain imaging techniques have underlined the importance of altered perception of visceral stimuli to symptom generation in IBS. These new developments have rekindled an old debate on peripheral versus central mechanisms in the pathophysiology of IBS. In this review we discuss the latest findings in light of these two concepts. In addition, we provide evidence for the hypothesis that, in the absence of alterations in endogenous pain modulation systems and changes in visceral perception, chronic *inflammatory mucosal changes in the gut are not a plausible mechanism to explain the presence of chronic abdominal pain, a cardinal IBS symptom. * Publication Types: Review Review, Tutorial PMID: 12864964" *Both central and peripheral serotonergic modulators are used in the treatment of irritable bowel syndrome. The majority of patients with irritable bowel syndrome presenting to a gastroenterologist demonstrate affective dysregulation. Serotonin may play a regulatory role in both gastrointestinal motility and sensitivity, as well as in affective dysregulation, in irritable bowel syndrome.* http://www.medscape.com/viewarticle/462728 *There seems to be increasing evidence that the pathology in IBS is not limited to the gut, brain, or autonomic nervous system only. Rather there may be an involvement of all three systems.* Therefore, any potential new therapy should be aiming at this widespread pathology. http://www.aboutibs.org/Publications/resea...ml#anchor147531 From Medscape GastroenterologyMEDLINE Abstracts: Serotonin Signaling and Visceral Hypersensitivity in IBSPosted 10/23/2003 What's new concerning the role of serotonin signaling and mechanisms of visceral hypersensitivity in the pathophysiology of irritable bowel syndrome (IBS)? Find out in this easy-to-navigate collection of recent MEDLINE abstracts compiled by the editors at Medscape Gastroenterology.--------------------------------------------------------------------------------Serotonin and Its Implication for the Management of Irritable Bowel SyndromeGershon MDRev Gastroenterol Disord. 2003;3(suppl 2):S25-S34Our understanding of the enteric nervous system (ENS) has evolved from the "classical" view, in which the brain controls all enteric behavior, to the current view, which holds that enteric innervation is one of local control within the bowel, modified by a bidirectional "dialogue" with the brain. The ENS independently controls enteric reflexes through intrinsic primary afferent neurons, which monitor intraluminal conditions. This monitoring is accomplished through the use of enteroendocrine cells in the mucosa, the best known of which are the serotonin-containing enterochromaffin cells. This article describes the roles that serotonin, specific serotonin-receptor subtypes, and the serotonin reuptake transporter play in the ENS and in the communication between the ENS and central nervous system. The way in which these findings have implicated serotonin in irritable bowel syndrome is discussed.Systematic Review: Serotonergic Modulators in the Treatment of Irritable Bowel Syndrome--Influence on Psychiatric and Gastrointestinal SymptomsKilkens TO, Honig A, Rozendaal N, Van Nieuwenhoven MA, Brummer RJAliment Pharmacol Ther. 2003 ;17:43-51Background: Both central and peripheral serotonergic modulators are used in the treatment of irritable bowel syndrome. The majority of patients with irritable bowel syndrome presenting to a gastroenterologist demonstrate affective dysregulation. Serotonin may play a regulatory role in both gastrointestinal motility and sensitivity, as well as in affective dysregulation, in irritable bowel syndrome.Aim: To analyse, systematically, randomized controlled trials studying the influence of serotonergic modulators on both gastrointestinal and psychiatric symptoms in irritable bowel syndrome, in order to elucidate baseline irritable bowel syndrome symptomatology and possible differential effects of serotonergic modulation on this symptomatology.Methods: A standardized qualitative analysis was performed of studies investigating the influence of serotonergic modulators on both gastrointestinal and psychiatric symptoms in irritable bowel syndrome using a blind review approach. The studies were ranked according to their total quality score (maximum 100 points).Results: Eleven studies fulfilled the entry criteria, six of which scored above 55 points. An association between gastroenterological and psychiatric changes was present in five of the six studies.Conclusions: The results strengthen the serotonergic association between gastroenterological and psychiatric symptoms. Adjusted guidelines for combined gastrointestinal and psychiatric assessments are recommended in order to further elucidate the serotonergic interaction between gastrointestinal and psychiatric symptoms.Tegaserod and Other Serotonergic Agents: What Is the Evidence?Chey WDRev Gastroenterol Disord. 2003;3(suppl 2):S35-S40Through effects on gastrointestinal motor and secretory function as well as visceral sensation, serotonin (5-HT) plays a key role in the pathogenesis of irritable bowel syndrome (IBS). In particular, 5-HT3 and 5-HT4 receptors appear to be very important in IBS. This article critically appraises the evidence supporting the use of the 5-HT3 receptor antagonist alosetron in the treatment of women with diarrhea-predominant IBS. The safety profile and restricted-use program for alosetron is also reviewed. This discussion is followed by a comprehensive review of the efficacy and safety data in support of tegaserod for women with constipation-predominant IBS.Sex Differences of Brain Serotonin Synthesis in Patients With Irritable Bowel Syndrome Using Alpha-[11C]Methyl-L-Tryptophan, Positron Emission Tomography and Statistical Parametric MappingNakai A, Kumakura Y, Boivin M, et alCan J Gastroenterol. 2003;17:191-196Background: Irritable bowel syndrome (IBS) is the most common functional bowel disorder and has a strong predominance in women. Recent data suggest that the brain may play an important role in the pathophysiology of IBS in the brain-gut axis. It is strongly suspected that serotonin (5-HT), a neurotransmitter found in the brain and gut, may be related to the pathophysiology of IBS. It is reported that a 5-HT3 antagonist is effective only in female patients with diarrhea-predominant IBS.Objective: In the present study, 5-HT synthesis was measured using positron emission tomography, with alpha-11Cmethyl-L-tryptophan as the tracer, in patients with IBS. The aim of the present study was to compare 5-HT synthesis in the IBS patients with that in the controls, and to compare 5-HT synthesis between male and female IBS patients.Methods: Six male and six female nonconstipated IBS patients were scanned. Age-matched healthy volunteers were scanned as controls. Eighty minute dynamic scans were performed. Functional 5-HT synthesis images were analyzed using statistical parametric mapping.Results: 5-HT synthesis was greater only in the female IBS patients in the right medial temporal gyrus (multimodal sensory association cortex) compared with the female controls (P 0.001).Conclusions: The greater brain 5-HT synthesis in the female IBS patients than in the controls may be related to the pathological visceral pain processing of the IBS patients, a larger female predominance of the disorder, and the sex difference of the efficacy of the 5-HT3 antagonist in treatment.Sex-Related Differences in IBS Patients: Central Processing of Visceral StimuliNaliboff BD, Berman S, Chang L, et alGastroenterology. 2003;124:1738-1747Background & Aims: Women have a higher prevalence of irritable bowel syndrome (IBS) and possible differences in response to treatment, suggesting sex-related differences in underlying pathophysiology. The aim of this study was to determine possible sex-related differences in brain responses to a visceral and a psychological stressor in IBS.Methods: Regional cerebral blood flow measurements using H(2)(15)O positron emission tomography were compared across 23 female and 19 male nonconstipated patients with IBS during a visceral stimulus (moderate rectal inflation) and a psychological stimulus (anticipation of a visceral stimulus).Results: In response to the visceral stimulus, women showed greater activation in the ventromedial prefrontal cortex, right anterior cingulate cortex, and left amygdala, whereas men showed greater activation of the right dorsolateral prefrontal cortex, insula, and dorsal pons/periaqueductal gray. Similar differences were observed during the anticipation condition. Men also reported higher arousal and lower fatigue.Conclusions: Male and female patients with IBS differ in activation of brain networks concerned with cognitive, autonomic, and antinociceptive responses to delivered and anticipated aversive visceral stimuli.Functional Brain Imaging in Irritable Bowel Syndrome With Rectal Balloon-Distention by Using fMRIYuan YZ, Tao RJ, Xu B, et alWorld J Gastroenterol. 2003;9:1356-1360Aim: Irritable bowel syndrome (IBS) is characterized by abdominal pain and changes in stool habits. Visceral hypersensitivity is a key factor in the pathophysiology of IBS. The aim of this study was to examine the effect of rectal balloon-distention stimulus by blood oxygenation level-dependent functional magnetic resonance imaging (BOLD-fMRI) in visceral pain center and to compare the distribution, extent, and intensity of activated areas between IBS patients and normal controls.Methods: Twenty-six patients with IBS and eleven normal controls were tested for rectal sensation, and the subjective pain intensity at 90 ml and 120 ml rectal balloon-distention was reported by using Visual Analogue Scale. Then, BOLD-fMRI was performed at 30 ml, 60 ml, 90 ml, and 120 ml rectal balloon-distention in all subjects.Results: Rectal distention stimulation increased the activity of anterior cingulate cortex (35/37), insular cortex (37/37), prefrontal cortex (37/37), and thalamus (35/37) in most cases. At 120 ml of rectal balloon-distention, the activation area and percentage change in MR signal intensity of the regions of interest (ROI) at IC, PFC, and THAL were significantly greater in patients with IBS than that in controls. Score of pain sensation at 90 ml and 120 ml rectal balloon-distention was significantly higher in patients with IBS than that in controls.Conclusion: Using fMRI, some patients with IBS can be detected having visceral hypersensitivity in response to painful rectal balloon-distention. fMRI is an objective brain imaging technique to measure the change in regional cerebral activation more precisely. In this study, IC and PFC of the IBS patients were the major loci of the CNS processing of visceral perception.Role of Visceral Sensitivity in the Pathophysiology of Irritable Bowel SyndromeDelvaux MGut. 2002;51(suppl 1):i67-i71Visceral hypersensitivity has been recognised as a characteristic of patients with irritable bowel syndrome (IBS). It may be involved in the pathogenesis of abdominal pain/discomfort, and seems to result from the sensitisation of nerve afferent pathways originating from the gastrointestinal tract. From a clinical point of view, hypersensitivity, although frequent, is not a constant finding among patients with IBS and cannot therefore be considered as a diagnostic marker of the condition. The advances made in understanding visceral hypersensitivity in patients with IBS are reviewed: the factors that influence abdominal distension are defined and different therapeutic perspectives are examined.www.medscape.com/viewarti...02/7001/-1 *Neuroimaging has provided evidence of physiological differences between normal individuals and those suffering from IBS in the way a visceral stimulus (ie, rectal distention) is processed in the brain. *







But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it. " *With regard to IBS, the gut-related effects of microscopic inflammation may be only one component of a dysfunctional brain-gut system. * In addition, and often in response to stress, there may be a failure to activate descending pain inhibitory systems that enable the clinical experience of pain and other symptoms that typify this disorder (25). In one prospective study of post-infectious IBS, it was found that those who retained their symptoms 3-months after an enteric infection had not only increased mucosal cellularity, but also had increased psychosocial distress at the time of the infection. Furthermore, lowered visceral sensation thresholds and increased motility were present after the infection regardless of whether or not the patients retained their symptoms (26). *Therefore, the microscopic inflammation and its physiological effects on motility and sensation contribute to, but are not always sufficient for the clinical expression of IBS pain.* At least for post-infectious IBS this provides some evidence that psychological distress alters brain pain regulatory pathways to amplify incoming visceral signals leading to the full clinical expression of this syndrome. http://www.romecriteria.org/reading1.html


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## Poor Boy (Feb 13, 2003)

Well Eric the spam Guy you are to be pitied....Anger gets you know where..... so why do you just like to **** us off.....?


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## Talissa (Apr 10, 2004)

Angry & unable to grasp the concept of being "succinct".It does come across as some psychological issue.Himself might consider meditation instead of the hypno....Anyways,


> quote:And you and Kel were wrong about the EC cells!


Hey, I'm just citing solid references as to what EC cells do upon contact with bacteria/toxins/enterotoxins/exotoxins in the gut.It seems the mast cells react when in contact with endotoxins.****************************What about the nerves?Can't be a bacterial connection to that, or could there be? http://www.ucalgary.ca/~ksharkey/what.html


> quote: *To protect the body from parasitic, bacterial and other agents the mammalian GI tract has evolved a complex and effective system of barriers.* These include the secretion of acid in the stomach, mucus along the length of the GI tract and a resident immune cell population in the epithelium and in the underlying lamina propria of the mucosa. The enteric and autonomic nervous systems play an important role in signalling or responding to alterations in luminal content and coordinating these events along the length of the GI tract. The repertoire of responses elicited by nerves includes altered patterns of motility, changes in blood flow and increased secretion. In addition, there is recent evidence for a direct innervation of mast cells and other immune cells in the mucosa suggesting that homeostatic regulation involves not only conventional neuroeffector functions but also neuroimmune interactions.


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## Talissa (Apr 10, 2004)

This about sums up my stance~MEDSCAPE: http://www.medscape.com/viewarticle/434526


> quote:Mast Cells Park and colleagues[5] applied electron microscopy and found that mast cell counts were significantly higher in the cecum among patients with IBS, and that the number of activated mast cells close to nerves was increased in IBS patients vs controls.Similarly, Barbara and coworkers[6] employed immunofluorescence and found that tryptase-containing mast cells were increased 3-fold in IBS patients compared with controls. *They also found evidence of mast cell degranulation. * Therapeutic Intervention* In view of the increasing evidence of histologic abnormalities in IBS, *and providing that this is indeed a true organic bowel disease* , might intervention to reduce the inflammation have utility? *If such intervention was able to prevent the development or progression of IBS, then this would be of major clinical importance. *


Definition of "mast cell degranulation": the release from within the cell of granules, or small sacs, containing chemicals that can digest microorganisms and activate other cells to fight infection._______________Also, mast cells are not the only cells increased with bacterial overgrowths--so are EC cells~ http://www.ncbi.nlm.nih.gov/entrez/query.f...1&dopt=Abstract


> quote:CONCLUSIONS: Current evidence shows a strong association between colonic infection and inflammation with development of IBS. Microbial agents related with PI-IBS include bacteria (Campylobacter, Salmonella) and parasites (Trichinella spiralis). Increased number of *enteroendocrine cells* , CD3 lymphocytes and mast cells within the colonic muscle wall, release of pro-inflammatory substances, and increased number of inflammatory cells with intestinal nervous endings are the most common histopathologic findings.


(EC Cells=enteroendocrine cells=enterochromaffin)But there are literally countless different strains of pahogenic bacteria that can over-populate the gut.


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## Talissa (Apr 10, 2004)

One last point~They may have tried to superficially correct inflammation with the use of dangerous steroids, & it was unsuccessful--but this is because it was a band-aid approach.They didn't simultaneously balance bacterial flora with anti's & probiotics. And natural anti-inflammatories should be used in place of steroids.Also patients in the study should be on a whole foods diet--no processed foods allowed.That's the kind of study I'd like to see!


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## eric (Jul 8, 1999)

Poorguy, you have shown more anger towards me on your posts and I don't believe I have ever shown any hostility towards you. So who has the problem?Tal, you need to do a whole lot more homework on IBS, that is all there is to it period.You don't understand the basics yet, before you go off on very complex systems and interactions, then go around telling people IBS is leaky gut or misunderstanding the real roles of bacteria in IBS and even bacteria gut flora in general, which even that you don't even have the basics for that down yet.People's environments help shape their gut flora, someone in Forida, does not have the same gut flora as someone in California. There is whats called passive immune system responce also, where cells learn to create antibodies to pathogens in a persons own environment. Many things shape gut flora, stress, med's, foods, fiber, all kinds of things.Also, there is evidence that the more pathogens your exposed to when your young actually boosts your immune system. They have recently found that people raised on farms and exposed to more pathogens had better immune systems then people raised in sterile environments with less exposure to pathogens. Everyday people are exposed to pathogens, and the body has evolved for millions of years to fight them off. Its like talking to a brick wall.Until recently you didn't even know much about serotonin in IBS and that was very clear then and now. Remember the big picture and tunnel vision? Remmember being proactive first before being reactive? All you are doing is guessing about majorally complex issues and a lot of it is inaccurate.Do you understand the link between the brain and the gut and communication via serotonin? Why there is so much evidence in its involvement? You need to ask yourself the above very important question.Do some homework on other factors then the immune system in IBS. Not that there not connected, but they still need to be put in context. Get rid of the tunnel vision for a while and look at the whole big picture. Very importantly learn to understand how the body works first.The ec cells and serotonin intiating digestion has nothing what so ever to do with bacteria. This happens in every human and is how the body works!!!!!!yes serotonin is used to fight bacteria. but this is completely different then its role in intiating digestion. They can already in part explain the symptoms of D and c and d/c through those mechanisms, your way behind in IBS research.


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## Talissa (Apr 10, 2004)

Eric,Did you even notice Medscape is even saying it's looking like postinfectious IBS is an organic disease?Yeh, I've given bad info~from Medscape, universities & the like.Seriously, I've said it before, you've got issues. Especially since all this new info on gut flora regulating intestinal function means we can get better! You're fighting facts, and the chance to get well.Did you know that degranulated mast cells is due to infection(bacterial contact)?I have to tell you, one of my best friends here is a biology teacher. She read this thread.And got a good laugh.Says you're like one of her worst students--but worse because you're so over-emotionally involved in being right. When you're really, really wrong.Have a good wkd everybody!


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## kel1059 (Feb 28, 2003)

eric you don't have a clue.of all people you should be the one who should NOT be talking about pathogens. if you had your way --calid would still have the citrobacter freundii and the proteus mirab. in her intestines.let me guess --from your post above you are likey to conclude that those pathogens would just make her immune system stronger ---right?--and h pylori bacteria is there to make the ulcer sufferer's immune system "rise to the challenge"?


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## kel1059 (Feb 28, 2003)

all i can say is that there seems to be some type of pathology involved here. some untreated mental illness or too much reefer smoking. --or maybe the HT really does mask symptoms in certain people. maybe spammer-e really is like the girl with her arm in a pot on the stove with the hypnotist telling her that her arm is as cool as a cucumber.he claims to be an english major but i just don't believe it. the garbled sentence structure, misused words, poor spelling -- it paints a picture of someone with a very confused mind.i don't know people, i am just trying to figure it all out. so don't mind me (and forgive me if this seems harsh)"bizzare" as one person put it. could it be that we have a real loon on our hands?


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## SpAsMaN* (May 11, 2002)

Leaky gut and leaky bladder seemes to exist,see this link,a MD explain. http://www.ichelp.com/RelatedDiseases/ICAn...sturbances.html


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## bonniei (Jan 25, 2001)

Recent prospective studieshave further clarified the concept of post-infectious IBS. Thefirst included 75 patients with acute gastroenteritis who werefollowed for at least 6 months (66). At 3 months, 22 haddeveloped irritable bowel syndrome. Similar risk factors wereagain identifiedï¿½female gender and a prolonged episode ofgastroenteritis. In addition, they noted that the patients whodeveloped IBS had higher scores for anxiety, depression,somatization and neurosis."IBS+ patients reported more life events and had higher hypochondriasis scores than IBS- patients. The predictive value of the life event and hypochondriasis measures was highly significant and independent of anxiety, neuroticism, and somatisation scores, which were also elevated in IBS+ patients. " "Psychological factors most clearly predict the development of IBS symptoms after gastroenteritis " http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=10026328


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## Talissa (Apr 10, 2004)

Spasman--That was an interesting discussion. Thanks. Itï¿½s amazing to me how far-reaching the effects of gut permeability are to the body. _______________________________Bonnie--Theyï¿½re learning now that another MAJOR predictor of getting post infectious IBS is when treatment for the gastroenteritis is not sought w/i 3 weeks of getting the infection. Also stress may proceed the infection--because stress lowers beneficial bacteria, allowing the opportunistic pathogen to overgrow:ï¿½ï¿½ A much stronger risk factor is the duration of the initial illness, with a steadily increasing relative risk for each week of illness, reaching 11.4 for those with diarrhea lasting more than 21 days. Bacterial factors are likely to be important since we found around 1 in 10 of Campylobacter infected individuals developed post-infective IBS compared with just 1 out of 100 with Salmonella. It is likely therefore that the severity of tissue damage and ulceration is a major predictor.ï¿½ http://www.med.unc.edu/medicine/fgidc/post_infectious.htm PubMed 2003~ï¿½More toxigenic organisms increase the risk 11-fold, as does an initial illness lasting more than 3 weeks.ï¿½ï¿½PI-IBS is associated with modest increases in mucosal T lymphocytes and serotonin-containing enteroendocrine cells.ï¿½ http://www.ncbi.nlm.nih.gov/entrez/query.f...4&dopt=Abstract ********************However, this newer study refutes both the psychological risk of PI IBS and the duration of acute infection as a risk of developing PI IBS~ ï¿½ *Relationship of Campylobacter Toxigenicity In Vitro to the Development of Postinfectious Irritable Bowel Syndrome * ï¿½ï¿½Campylobacter enteritis is associated with a significant risk of developing irritable bowel syndrome, but the mechanism is unknown. This study ascertained bowel symptoms in 93 patients 3 months after Campylobacter jejuni enteritis infection. ï¿½.Thus, long-term symptoms that occur Campylobacter infection are significantly associated with bacterial toxicity.Persons whose illness lasted 21 days had a relative risk (RR) of 11.4 of developing new IBS, compared with those with an initial illness lasting 7 days [2]. Although others have reported an association between postinfectious IBS and adverse life events and psychoneuroticism [3], we thought that bacterial pathogenic factors were probably the most important determinant of initial illness and, hence, long-term outcome. *We believe that this study is the first to show that bacterial factors are important determinants for the development of chronic gastrointestinal symptoms after bacterial gastroenteritis.* The mechanism by which these toxic effects are associated with prolonged bowel disturbance is uncertain. *Greater inflammation, local tissue destruction, and slower resolution of injury are probably important. Residual changes might include increased inflammatory and enteroendocrine cells, both of which could result in altered bowel patterns [4]* . In addition, Shiga-like toxin is neurotoxic, and we have shown that Campylobacter enteritis induces a profound loss of neural staining [5]. The lack of any clear association between cytotoxicity and clinical features of the initial illness seems at first paradoxical. However, persons who provide a stool sample are not a random selection of all cases of Campylobacter infection. Thus, sampling bias toward more severe cases as a threshold of severity and duration must be reached before the patient sees a physician and stool cultures are arranged. ...A range of Campylobacter toxins have been described elsewhere [7], including enterotoxins [8] and cytotoxins [9]. The detection of toxins depends on precise culture conditions and whether polymyxin B was present or cultures were sonicated [10]. This may explain why their prevalence in clinical series is highly variable, with poor correlation with clinical features of the initial illness. http://www.journals.uchicago.edu/JID/journ...067/010067.html __________________________From these sources, it seems to me that PI IBS risk is dependent on the degree of toxicity of the infectious organism, the duration of infection w/o treatment, &/or the degree of stress at the time of infection, allowing the organism to proliferate in the intestines when beneficial bacteria arenï¿½t in high enough # to fight it off--which means the EC & mast cells have to step in, in an immune response.


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## Talissa (Apr 10, 2004)

HOW STRESS ALTERS INTESTINAL MICRO FLORA:ï¿½Along with other endogenous and exogenous factors which may interfere in the regulation of various pathways that control the intestinal microflora, physical and psychological stress seem to play a crucial role. ï¿½ï¿½In order to estimate the influence of psychological stress on the intestinal microflora composition, repeated restraint stress was used as a stress paradigm. Faecal indicator bacteria (aerobic and anaerobic) were used to assess the microbiological profile of the intestinal flora.ï¿½ï¿½Numbers of C. perfringens were estimated and compared to those of E. coli. Higher numbers of vegetative forms of the anaerobic bacterial indicator C. perfringens were found in stress-exposed animals as compared with controls and with pre-stress conditions.ï¿½ http://taylorandfrancis.metapress.com/app/...ults,1:102100,1 ï¿½Stress also results in increased bacterial adherence and decreased luminal lactobacilli. As a result of all these changes luminal antigens may gain access to the epithelium, causing inflammation.ï¿½ http://www.blackwell-synergy.com/links/doi...36.2002.01359.x ï¿½The balance between host defenses and normal flora (organisms present to some degree in healthy individuals) may be upset by stress and lead to pathological conditions.ï¿½ http://www.indstate.edu/nurs/mary/pnipost.htm ï¿½Natural killer cell activity plays a vital role of the immune system to fight against viral and cancer cells in the body. Secretory IgA is the first line of defense of the immune system lining the gastrointestinal tract, mouth, lungs, urinary tract and other body cavities. Any decline in these levels decreases oneï¿½s resistance to bacteria, viruses and parasites. A single five minute experience of anger can produce a significant decrease in secretory IgA up to five hours afterwards.ï¿½ http://www.island.net/~ipincott/article53.htm ï¿½Thus it seems that stress can also alter the microenvironment for resident bacteria and change the conditions for enterocyte bacterial contacts.ï¿½ï¿½The stress-induced barrier defect results in enhanced passage into the mucosa of both small molecules, including chemotactic peptides derived from bacteria, and macromolecules, such as intact proteins with antigenic potential.ï¿½ï¿½Rapid mucin release during acute stress would increase barrier properties and provide a degree of protection against invasion of a leaky epithelium. However, over a longer time period, goblet cell depletion would be deleterious because of the reduced capacity to respond to ongoing or new threats.ï¿½ http://ajpgi.physiology.org/cgi/content/full/280/1/G7 (there are more sources to this, but you get the point...)


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## Talissa (Apr 10, 2004)

Eric--pls read this(again) and let it sink in:ï¿½Inflammatory Bowel Disease and Irritable Bowel Syndrome: Separate or Unified?ï¿½MEDSCAPE JULY 2003 "*Several recent independent studies have demonstrated alterations in the gut-associated immune system.* Quantitative assessment in unselected patients with IBS have shown increased mast cell numbers in the ileum[5] and colonic mucosa.[6] Preliminary evidence suggests an increase of overall cellularity in the colonic mucosa[7] and a higher number of mast cells containing tryptase (known to have proinflammatory effects) in the colonic lamina propria of patients with IBS.[8] Additional preliminary results indicate a significant increase of inducible nitric oxide synthase (iNOS) expression in the colonic mucosa from unselected patients with IBS compared with control patients.[9] In the human colon, upregulation of iNOS has been implicated in inflammatory processes, and increased expression has been documented in IBD.[10] More recently, a study by Chadwick et al.[11*] demonstrated intestinal mucosal immune activation in 77 symptomatic patients meeting the Rome criteria (the authors did not specify Rome I vs II criteria). The study included patients with diarrhea, constipation, or both. In 38 of the patients (50%), a normal conventional histologic appearance was seen, but the immunohistologic results were abnormal (intraepithelial lymphocytes-IEL, lamina propria CD25+ and CD3+ lymphocytes). In 40% of patients, nonspecific microscopic inflammation was seen, whereas immunohistologic results showed similar increases in lymphocyte populations as in the first group. However, in contrast to the first group, they also showed increased numbers of neutrophils and mast cells. Ten percent of patients fulfilled the histologic and immunohistologic criteria for lymphocytic colitis. Even though the magnitude of changes in cell numbers was far less than observed in patients with IBD, the increased numbers of IEL, T cells, IL-2 receptor expressing cells, suppressor/cytotoxic T cells, and NK cells were consistent with an increased inflammatory cell presence in a subset of patients with altered bowel habits who met the symptom-based Rome criteria. *Because a significant number of patients meeting the Rome criteria also met the histologic criteria for a diagnosis of lymphocytic colitis, the findings highlight a major problem with the way we currently diagnose IBS. By definition, the diagnosis of an organic disease such as lymphocytic colitis is inconsistent with a diagnosis of IBS. * Furthermore, it is unclear whether the patients met the Rome criteria because of the presence of discomfort (urgency, bloating) relieved by bowel movements, or whether they reported abdominal pain. Using the current Rome criteria, a diagnosis of IBS can be made in any patient experiencing abdominal discomfort (for example, in the form of urgency or bloating-type symptoms), that is relieved by a bowel movement. In the absence of mucosal histology to rule out macroscopic or microscopic forms of colitis, such a symptom cluster is likely to include a wide range of syndromes with different causes and pathologic mechanisms." http://www.medscape.com/viewarticle/457728_print ___________________And please, stop saying my sources are dated. It's classic "transference"--you're transferring your dated thinking on IBS onto me.Everything I'm discussing here re:infection, inflammation, flora & its importance to intestinal regulation & immune response is the NEW information on PI IBS. _The Rome Criteria & your line of thinking is what isn't up-to-date._ *PI IBS is more in-line with an ORGANIC disease as all of this new info comes to light. (as stated in the above Medscape article, dated July of last year)* "Old school thinking" takes time to change their stubborn views.______________________________I really hope this sinks in this time.(Stress tip from someone who's studied yoga--Calm deep inhale to the bottom of the belly, with a slow exhale twice as long as the inhale. It's more relaxing this way. It'll help keep any beneficial bacteria count up in times of stress.)


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## bonniei (Jan 25, 2001)

Talissa- I have always wobdered if stress increased gas apart from a rushed intestinal transit. It looks like it may by changing the bacteria.{quote]HOW STRESS ALTERS INTESTINAL MICRO FLORA:[/quote]However one thing I am unclear about. I thought youi started out by saying stress has nothing to dO with it but now you have made a turnaround and are admitting that stress playa a tole, am I right?


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## bonniei (Jan 25, 2001)

Also this is an example of how animal studies don't translate into human ones http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12848628


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## Talissa (Apr 10, 2004)

Hey Bonnie,"Also this is an example of how animal studies don't translate into human ones"That was a study using steroids. "CONCLUSIONS: Prednisolone does not appear to reduce the number of enterochromaffin cells or cause an improvement in symptoms in post-infectious irritable bowel syndrome. Other approaches to this persistent condition are indicated."They were trying to superficially address the inflammation w/o fixing the cause--no wonder it didn't work. You reduce the # of EC cells by reducing what's causing the immune reaction. But how does that study show that animal studies don't translate into human ones?________________Re: stress...I knew that stress inhibited the immune system, and thatï¿½s why I took up doing yoga regularly after being diagnosed. But now, itï¿½s fascinating to really learn the research behind the micro flora mechanisms.I also didnï¿½t think that high stress in & of itself could cause IBS in some people, but now Iï¿½m beginning to think thatï¿½s wrong--prolonged stress can cause pathogen overgrowths, which can cause IBS. Itï¿½s mind-boggling.Everything is explained by pathogen overgrowths & their interaction with gut epithelial immune cells--not just gas & motility, but the hormonal changes, the nerve actions, genetic alterations, the depression & anxiety, even the brain-gut axis~Itï¿½s no longer technically a brain-gut axis problemï¿½itï¿½s the ï¿½brain-gut-immune axisï¿½ problem & itï¿½s due to the immune response of imbalanced gut flora/overgrowth of pathogens. Amazing:2002ï¿½Review article: mechanisms of initiation and perpetuation of gut inflammation by stress.ï¿½ï¿½Elucidation of the *gut-brain-immune axis * has provided insight into the mechanisms by which stress may result in gut inflammation. Stress can alter intestinal physiological function. Stress can increase gut permeability, increase ion secretion by a mechanism involving neural stimulation or mast cells, increase mucin release and deplete goblet cells.(T: all immune response to pathogens)Stress causes parasympathetic activation via a mechanism involving corticotropin releasing factor, ultimately affecting mucosal mast cells. (T: again: immune response--this is the cortisol release that lowers beneficial bacteria)Stress also results in increased bacterial adherence and decreased luminal lactobacilli. (T:decreased luminal lactobacilli is the lowered beneficial bacteria) *As a result of all these changes luminal antigens may gain access to the epithelium, causing inflammation.* http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12452934 ****************************Also PubMed 2004~ï¿½Increased antigen and bacterial uptake in follicle associated epithelium induced by chronic psychological stress in rats.ï¿½ï¿½These results show that the barrier function of follicle associated epithelium can be modulated, and that *chronic stress enhances the uptake of luminal antigens and bacteria via the follicle associated epithelium.* ï¿½ http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15016742


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## bonniei (Jan 25, 2001)

> quote:But how does that study show that animal studies don't translate into human ones?


If you read the abstract you will see it says "Animal studies have suggested that steroids reduce the lymphocyte response and suppress some of the post-infectious changes in neuromuscular function"But their concluson when they tried it on humans was"Prednisolone does not appear to reduce the number of enterochromaffin cells or cause an improvement in symptoms in post-infectious irritable bowel syndrome. "Obviously steroids worked in animal studies and not in humans


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## Talissa (Apr 10, 2004)

Actually Bonnie, it says that


> quote:Animal studies have *suggested* that steroids reduce the lymphocyte response and suppress some of the post-infectious changes in neuromuscular function"


It never said the steroids did in fact lower the EC cells in the animals.You need to come up with a better example.I'll give you one--in studying drugs to inhibit storage of fat for people trying to lose weight.Didn't translate. This is the only example according to a news story I saw.And it seems to be irrelevant to the intestines, or the FDA wouldn't allow all of these studies for new drugs(band-aids) on rats & mice before trial on humans.And if these studies on mice rendered the studies invalid, as you seem to be suggesting, for one, they wouldn't do them. What would be the point. And two, they wouldn't be cited in prestigous journals.Does make me feel sorry for the little critters, though.


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## bonniei (Jan 25, 2001)

Another fact from the study which is not in the abstract"Although there was a significant reduction in the number of lamina propria T lymphocytes after prednisolone (22.0% ï¿½ 5.6%, P = 0.003), but not after placebo (11.5% ï¿½ 8.6%, P = 0.1), these differences were not statistically significant."Obviously in animal studies steroids led to a reduction in the number of lymphocytes which was statistically significant but not in humans


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## Talissa (Apr 10, 2004)

Btw, T Lymphocytes are a direct immune response and Enterochromaffin Cells are an indirect immune response.It's the actions of the mast cells & EC cells that cause the inflammation leading to permeability.However, this study probably explains why they thought up to a 22% reduction in T cells would effect mast & EC cell counts--accounting for the word "suggested":"nevertheless, the increases in mast cells, immunoglobulin E, eosinophils, and goblet cell mucin production are consistent with a Th2 host response (21)." http://iai.asm.org/cgi/content/full/69/7/4417#Abstract Aside--from the same study~"The concept that parasitic infection can modulate the course or severity of nonparasitic disease is not unprecedented.."


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## bonniei (Jan 25, 2001)

I think they always say "suggest" when referring to anuimal studies because that is all animal studies can do- suggest and not prove anything for humans beyond doubtSecondly" enterochromaffin cell numbers correlated with lymphocyte counts"Gut. 2000 Dec;47(6):804-11. Increased rectal mucosal enteroendocrine cells, T lymphocytes, and increased gut permeability following acute Campylobacter enteritis and in post-dysenteric irritable bowel syndrome.Spiller RC, Jenkins D, Thornley JP, Hebden JM, Wright T, Skinner M, Neal KR.


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## Talissa (Apr 10, 2004)

I obviously know they correlate--but they also found out that there need to be a larger reduction in T cells to effect the mast & EC cells.


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## bonniei (Jan 25, 2001)

Well they may have been wrong in your study about how much of a reduction in lymphoicytes to affect mast cells and EC cells. But your study isd unrelated to mine. However I will try to go to thre library today or tomorrow and find out the exact detailsof my study


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## bonniei (Jan 25, 2001)

Well I am in the library right now and the reference my study gavemy study is definitive that it has been demonstrated that corticosteroid suppressed the inflammatory response.


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