# The cause of IBS?



## eric (Jul 8, 1999)

This I believe is important.Especially to new people who have been recently diganosed but to all people diagnosed with IBS and worrying about what causes it.The exact cause of IBS is unknown.However"American College of Gastroenterology 70th Annual Scientific Meeting and Postgraduate Course Advances in Functional Gastrointestinal Disorders "Honolulu, Hawaii; Monday, October 31, 2005 Functional gastrointestinal (GI) disorders are extremely common conditions encountered in both primary and referral-based specialty care settings. It has been estimated that these disorders affect between 10% and 20% of the general population.[1] Over the last several years, our understanding of multiple epidemiologic and pathophysiologic aspects of the functional GI disorders has dramatically increased, and these advances have led to important developments in diagnostic approach and increasingly effective treatments for these disorders. During this year's annual meeting of the American College of Gastroenterology (ACG), the field of functional GI disorders continued to have a prominent role in both the plenary and poster sessions."Often times people specualte on the cause or causes of IBS. However there are things to consider in regards to IBS that are important.For example, IBS can present as mild, moderate or severe.IBS is pretty common.More women then men have it.It does not lead to a serious disease.When a person thinks about the cause or causes of IBS, these things should be taken into account. It is easy to worry about a zillion things that could be wrong with your gut, but learning about IBS is an important step in what is going on with IBS and how to treat it the most effectively.Although it is extremely complex and not completely understood by researchers for the vast majority of IBSers it is treatable.Of course there are other conditions that overlap and that to is very important.


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## eric (Jul 8, 1999)

FYIIBS Misconceptions Abound, Studies Show http://ibsgroup.org/eve/forums/a/tpc/f/71210261/m/987102671


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## eric (Jul 8, 1999)

I am thinking of some of these things as I go.







Why does it wax and wane or can be seasonal?How does the weather set it off?Why for some when you wear tight pants or move wrong it can set it off.Why does lack of sleep effect it?Why the high placebo rate in IBS?Some of these things may also apply differently depending on how bad you have it also, its estimated 70 percent are mild, 25 moderate and 5 percent severe. I know I fell into severe.Why sometimes does just lying down and relaxing make it go away for a lot of people?What do the majority of treatments that are shown to be effective have in common ?Important things to ponder?


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## eric (Jul 8, 1999)

The red flag symptoms are important to the cause as well."Red Flag symptoms which are NOT typical of IBS: Pain that awakens/interfers with sleep Diarrhea that awakens/interfers with sleep Blood in your stool (visible or occult) Weight loss Fever Abnormal physical examination "


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## 20250 (Jul 14, 2005)

Yeah, 2 things... I don't wear tight pants, but also have not buttoned them for 18 years because I get instant pain when I do. Also get upset gut easily when painting with an extension pole for more than an hour(happens often). I'm twisting or moving side to side in motion and notice that it sets me off from time to time.Come on Eric, I know you know why.By the way, I asked Jeff to come up with a special smiley for you and a few others.


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## Popp (May 31, 2004)

Here's my thoughts on IBS.I had supra ventricular tachycardia and they performed a electrophysiology(spelling?) in my heart and found the nerves that caused my rapid heart beats(spasms) and zapped them. It has worked now for almost 2 years now.I know the nerves in bowels might be a tad harder to pinpoint, but seems something along those lines should be done for those of us with IBS.Possible?


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## Screamer (Aug 16, 2005)

Huh, I'm the opposite of a lot of those things. The one that first springs to mind is tight pants. Now I don't like my pants real tight but when I'm feeling sick I always put pressure on my tum. It makes it feel a lot better. Mostly I use a hot water bottle but in summer I press a cushion on it real tight (maybe I'm just weird though). Another is that when I am feeling rotten no amount of lying down and relaxing makes me feel better. It just means I have further to get up when I have to dash to the loo, although feeling sick makes me SOOO tired and drained







Another thing I don't get for me, is why one day I can down 4 cups of coffee and be fine and others 1 cup will have me running like my pants are on fire


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## eric (Jul 8, 1999)

already some interesting things are imerging from the thread.let me say this and think about it some. This is all not written in stone.Some of these symptoms, are different then say an organic disease or infection. Infections usally get worse and can cause a fever and weight loss. If it bacteria, then it never gets worse and you don't keep getting sicker.Its not foods either.It doesn't cause any serious tissue damage or growths ect..But if you look at it as a "neuro-muscular" or "brain gut" issue it starts to make more sense really.Brettclensr, this is one reason tight pants can set it off for some people. Your putting pressure on the muscles, especially around the waist and lower abdomen, which is basically "classic IBS". Popp, they are researching the tachycardia rythm and IBS and also the autonomic nervous system.http://www.ibs.med.ucla.edu/Articles/Patie...icleSm02ANS.htmTreatments like that may happen in the future and there is already one similar available for certain people.Screamer, "I always put pressure on my tum" or heatthis is consistent with muscle activity also and relief. This probably wouldn't work well pain wise if it was an infection, single bacteria, parasite or virus, then its quite likely the symptoms would be 24/7 and also cause red flag issues.also this is important.Irritable Bowel Syndrome: How far do you go in the Workup?"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."http://www.romecriteria.org/reading1.htmlSomethings here like people with IBS/IBD maybe different of course or other conditions, then overlap makes diagnoses more difficult.


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## Screamer (Aug 16, 2005)

I have a couple of red flag symptoms however tests have not shown anything. For one it's nothing for me to lose 10kg in a week. I can put it on just as fast but there's never a reason other than D that I lose it. I lost about 15kg a couple of years ago. I've managed to put on 10 recently but that was due to the help of an anti dep which put the weight on. Nothing was found as to why I lost it.The other red flag is that every 3 or 4 months I become anemic. No reason for that either. My colonoscopy was clear. Tends to happen more often in winter than summer but can happen at either time. I also wake up a lot in the night in pain and other than my daily misery of IBS my "attacks" are most often during the small hours of the morning when normal peeps are in bed


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## Talissa (Apr 10, 2004)

Interesting topic Eric...Here's 2 MDs views..."...Other potential causes of continued low-level inflammation in the GI tract include food allergies and changes in bacterial microflora. Allergic reactions can evoke inflammatory cell infiltration in the GI tract (41), but the prevalence of food allergies in IBS is unclear (42). Gut microflora may be altered in patients with IBS (43); some findings suggest that IBS patients may have intestinal bacterial overgrowth (44) and increased colonic fermentation (45). Further information is needed to elucidate the role of these environmental factors in promoting and perpetuating the putative low-grade inflammatory process.Much remains unknown about the potential causes of IBS. There may not be a unifying hypothesis to link all the aspects of this diverse syndrome. *Nevertheless, markers of low-grade inflammation, which were initially found in diarrhea-predominant and postinfectious cases of IBS, are increasingly being found in constipation-predominant patients as well. Thus, inflammation may figure as an underlying factor in visceral hypersensitivity in more cases of IBS than previously was suspected. * These intriguing inroads may be the key to our understanding of the basis for the IBS and may yield exciting therapeutic possibilities."http://www.pulsus.com/Gastro/18_10/andr_ed.htm


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## 20250 (Jul 14, 2005)

Gotcha Eric, Although I'm pulling mine up all day because I can't button then because of the painy thingy. What to do, What to do?


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## Guest (Nov 3, 2005)

The painy thingy is allodynia, sensitive tissues and I have had that for years. No tight clothes for me and even the car seat belt causes pain. But my IBS really got going after 2 small bowel surgeries for adhesion obstuction. Char


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## eric (Jul 8, 1999)

Screamer, have you ever been tested for celiac?Brettclensr, I try not to wear tight clothing either. When they say life style changes it incorporates a lot.







Gardentime, it could have been there underlying all along and the surgery kicked it into high gear or perhaps the surgery somehow started it, this has been reported before.TalissaI am very familiar with this centers work and the work others are doing in sub clinical, macroscopic inflammation in subsets of IBS.The first paragraph is talking about low-level inflammation and the general causes of this in the gi tract."Allergic reactions can evoke inflammatory cell infiltration in the GI tract (41), but the prevalence of food allergies in IBS is unclear "These food allergic reactions effect the mast cell. You can have both IBS and a food allergy of course and foods might trigger these cells even without a flull blown allergic reaction.But there are major problems with this causing everything seen in IBS.IBS is not caused by foods though.There has been quite a bit of work recently on mast cells and IBS.New research shows mast cells can be degrandulated from chronic stressors, WITHOUT A PATHOGEN, the same as a allergic reaction can degrandulate them. However, The pathophysiology of irritable bowel syndrome.Schwetz I, Bradesi S, Mayer EA.Center of Neurovisceral Sciences and Women's Health (CNS), Division of Digestive Diseases and Brain Research Institute, Department of Medicine, Los Angeles, CA, USA."that, in the absence of changes in visceral perception and alterations in endogenous pain modulation systems, chronic inflammatory mucosal changes in the gut are not a plausible mechanism to explain the presence of chronic abdominal pain, a clinical hallmark of IBS."What this means is without the changes (cingulate cortex) they see in brain processing in IBS that is different then normals this does not explain chronic pain in IBS. It can contribute to it however, by releasing toxins, onto the smooth muscle, on of these is histimine and its know that the HPA axis is involved in IBS. The HPA axis is also the bodies stress system."Gut microflora may be altered in patients with IBS " It maybe, but not much evidence to support it as the cause of IBS. It can for sure be for many reasons in IBS. I wonder if they have ever done a food study and eating habits in IBS and gut flora, that would be interesting.Also since the colon in IBS can contract anywhere along its length due to altered motility it can create pockets where bacteria are trapped and cause more gas.For example.how it normally workshttp://arbl.cvmbs.colostate.edu/hbooks/pat...i_motility.htmland







An important chemical the neurotramsmitter serotonin is important here, because its involved in gut function and sensations from the gi tract to the central nervous system and brain.But we are back to looking at specifics here and there are abnormalites in different systems.Part of why I posted this though is a bigger picture because it gives some insight into the whole problem problems.Do women have more altered bacteria in their guts? Why the men and women differences seen in IBS?Women have more serotonin and their systems for stressors are set up slightly differently then mens, that seems to be important in research.One of the first things in Talissa posting theat paper is"Not so long ago, physicians construed the irritable bowel syndrome (IBS) as being a neurotic trait: it was all in the head. Today most clinicians believe that the main abnormality lies in the brain (and spinal cord), which reacts abnormally to stimuli from the gut. "However you look at it nowadays it is a brain gut problem, both are operational to cause the symptoms. Both are end organ targets for treatment, targeting both organs has shown to help the condition.They can also already partially explain the d and c and d/c in IBS. But those are just symptoms of a bigger issue.


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## eric (Jul 8, 1999)

Just fyi here alsoYou are receiving this email from the UNC Center for Functional GI & Motility Disorders because, at one time, you requested information from the Center. The reason for this email is to remind you of the Centers quarterly on-line "Chat with the Experts." This month's topic is "What is a Functional GI Disorder?" If you have an interest in this topic, the link to the chat room is on the Center's home page http://www.med.unc.edu/ibs. The chat room will open on Tuesday, November 8, 2005 at 7:45. ESTWe hope that you will join us this month at 7:45 and take this excellent opportunity to learn more about "Functional GI Disorders". Dr. Douglas Drossman, Co-Director of the UNC Center for Functional GI and Motility Disorders, Chapel Hill, will be our guest host. Enter the chat room on November 8th. from our Center's web page: http://www.med.unc.edu/ibs.I highly recommend these and they are free.


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## eric (Jul 8, 1999)

FYINat Clin Pract Gastroenterol Hepatol. 2005 Feb;2(2):82-8. Related Articles, Links Treatments targeting putative mechanisms in irritable bowel syndrome.Cremonini F, Talley NJ.F Cremonini is a Senior Research Fellow and NJ Talley is Professor of Medicine and Director of the Clinical Enteric Neuroscience Translational and Epidemiological Research (CENTER) Program, Mayo Clinic College of Medicine, Rochester, MN, USA.The pathophysiology of irritable bowel syndrome (IBS) is heterogeneous; it is possible for several mechanisms to be disturbed in the same patient. Isolating a single target for pharmacological manipulation is also difficult because of the complexity and overlap of the neural circuitry in the enteric and central nervous system. This review summarizes the rationale and efficacy of current and future therapies for IBS, on the basis of putative pathophysiological models. The modulation of gastrointestinal sensorimotor function, intestinal gas handling, the gastrocolonic reflex, neurohormonal stress responses, central processing of afferent information, and microbial flora are the current frontiers for experimental therapeutics for IBS. Patients presumed to have POSTINFECTIOUS IBS have also been targeted as a distinct group. In the very near future, it is unlikely that a single drug will come to the fore as a suitable and successful treatment for everyone with IBS, but new data on potential therapeutic targets lend hope for the improved long-term management of IBS. Disease modification rather than just symptom-based treatments must remain the goal.PMID: 16265125


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## Screamer (Aug 16, 2005)

Hi Eric, yep, they've tested me for coeliac twice (with the scope) and I also went on a totally gluten free diet for 4 months just to see if gluten was a problem. But both tests came back clear and taking gluten out of my diet did nothing







My doctor thinks I'm a total mystery


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## 20250 (Jul 14, 2005)

Thanks char, I have another thing to write down on my list for next doc visit.


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## Guest (Nov 4, 2005)

Hey Brett, allodynia is pain from stimuli which are not normally painful. Drives me crazy and I even had it before the last 2 surgeries, it started after a childhood surgery. Must have something to do with damaged nerves from those surgeries. Anyhow there is not a cure, some Rx meds might lessen the pain. Now I am trying Inositol.Char


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## 20250 (Jul 14, 2005)

So sorry that happened to you from your surgery. I guess once nerves are damaged theres no way to repair them. I've never had any surgery but will def tell my doc about it. Thank you and where is winterhaven? My daughter just moved to winterpark for school


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## Guest (Nov 4, 2005)

Allodynia can also occur from injury, such as sport injuries. Anyhow Winter Park is very close to Orlando, Winter Haven is mid state, south of Orlando. (Lakeland area) We still get the hurricane winds, Wilma did no damage. My house has survived up to 100 mph, price we pay for living in paradise.Char


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## 20250 (Jul 14, 2005)

aaah, Paradise! Thanks for the info and enjoy sunny florida. Me and the Mrs are going back next Friday to visit our girl for the weekend.Hope it's Sunny


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## eric (Jul 8, 1999)

Screamer are you a light sleeper?Do you eat regularly?Gardentime, I was once at a gi lecture and they mentioned low dose amitriptyline for Allodynia.I have relatives in Kissimmee-St. Cloud and use to live myself in Boyton Beach for a while. Glad you were spared from Wilma.


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## 17176 (Mar 31, 2005)

eric im sure you posted in a piece about stress i cant seem to find it now, either that or im losing the plot


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## 16132 (Nov 4, 2005)

If you use Splenda, check out this website, it's a huge finding! http://www.splendasickness.blogspot.com/


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## Screamer (Aug 16, 2005)

Eric I'm a terrible sleeper! I can never get to sleep in the first place and when I finally do I have the strangest vivid dreams all night long. I usually wake up feeling more tired than when I went to bed or like I've been hit by a bus







(my GP said he's checked me for fibro though and I don't have it). I do tend to skip breakfast but other than that I eat well. I also have a snack (try to keep it fairly healthy like yoghurt or cereal) after dinner and before sleep (but not too close too sleep or I end up with reflux).Don't worry, I don't expect you to have the answers for me. If my doctor and specialist have no idea no one else could either


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## eric (Jul 8, 1999)

Screamer did you know this by any chance?This article is worth reading in general."The Sleep-Gut ConnectionAs light is shed on the circuitry between the two brains, researchers are beginning to understand why people act and feel the way they do. The brain and gut are so much alike that during our sleeping hours, both have natural 90-minute cycles. For the brain, this slow wave sleep is interrupted by periods of rapid eye movement sleep in which dreams occur. For the gut, the 90-minute cycles also involve slow waves of muscle contractions but, as with REM intervals, these are punctuated by short bursts of rapid muscle movement. Could it be that both brains influence each other? The answer is probably yes. REM sleep is a sleep phase characterized by arousal, altered activity of the autonomic nervous system and altered colon (large intestine) function.We also know that patients with bowel problems tend to have abnormal REM sleep. Poor sleep has been reported by many perhaps a majority of, patients with irritable bowel syndrome (lBS) and non-ulcerative dyspepsia (also known as "sour stomach") who complain of awakening tired and unrefreshed in the morning. Even after patients awake from what they describe as a "sound sleep," they report a general feeling of tiredness and fatigue.Abnormal REM sleep is reduced by low-dose treatment with the anti-depressant amitryptiline, which has also been shown to be effective in treating lBS and non-ulcerative dyspepsia. Many drugs designed to affect the brain also affect the gut. For example, the gut is loaded with the neurotransmitter serotonin. In fact, more serotonin is produced there than anywhere else in the body. Serotonin is linked with initiation of peristalsis."http://immune.altmedangel.com/gutbrain.htm


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## Guest (Nov 5, 2005)

Hey Eric, I have tried those useless Rx drugs such as Elavil for the allodynia. They mess up my head, cause nausea, some of them give me diarrhea. I am more miserable and still have the pain. Try getting off of that stuff. I do not recommend those type of meds, off label use for pain. (Zoloff, Paxil, Cymbalta, Effexor etc.)Char


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## Kathleen M. (Nov 16, 1999)

These drugs can be very effective for some people, but there are those that do not tolerate them well. There is no way of knowing without a test with the individual which camp you end up in.For me they work well, but I have to watch blood pressure types of side effects with some of them, particuarly the tricyclics. Even with that, they can be very effective for pain control for me.K.


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## eric (Jul 8, 1999)

I agree char that the meds are not for everyone and I would rather people take a more holistic approach first, but sometimes meds are useful for sure.


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## Arnie W (Oct 22, 2003)

I'm not sure where you're coming from with the high placebo rate. If this is so, why are so many of us still frequenting this board and scratching our heads because we're still in the same old place despite trying out all the therapies and medications and supplements which are recommended here?I have tried everything from probiotics and GSE to anti-depressants to laxatives and, despite starting off with the expectation that this could be the one to give me relief, it never happens.And I do feel that bad dietary choices over the years, as well as excessive use of several types of medication, including antibiotics, have a lot to answer for in the development of IBS symptoms.


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## eric (Jul 8, 1999)

FYICurrent TherapiesIrritable Bowel Syndrome Remains a Difficult Condition to Manage"Irritable bowel syndrome (IBS) remains challenging to manage, with no universally agreed treatment protocol. Complicating the treatment picture is the placebo response, which can vary from 20% to 70% and can be sustained long term. "http://www.medscape.com/viewarticle/482425_print


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## Screamer (Aug 16, 2005)

Hmmm interesting that my brain and gut are connected and acting up at the same time. It does explain quite a lot, thanks for that Eric. Yep, no anti deps for me. After the last 5 they've tried on me the doctor says the only one left to try is Effexor and after coming off Aropax (paxil) I'm way too scared to give it a go!


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## eric (Jul 8, 1999)

This is another very good one.Complex and Hidden Brain in Gut Makes Bellyaches and Butterflieshttp://www.aikidoaus.com.au/dojo/docs/2nd_braina.htm


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## Guest (Nov 6, 2005)

Hey Screamer, I concur about the anti depressants and the reaction of Effexor is the same as the others. All of those nasty drugs gave me no relief, only the side effects. I still had the pain and I could hardly function from the side effects.Char


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## Arnie W (Oct 22, 2003)

I'm having a terrible time with Paxil too and I don't think it's helping my indigestion at all.As for the placebo effect, I can't open the link that was given - I just get the Medscaape page - so I'm going to continue to doubt that it really does work so widely with IBSers. In such a study I would expect to read how many had been clinically diagnosed with IBS, for how long, what the symptoms were (and how debilitating) and whether diet or other interventions such as hypnotherapy and counselling had been incorporated. Out of interest, how would a placebo work when other things which were supposed to help didn't give any relief?


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## eric (Jul 8, 1999)

Arnie, it is well known in IBS research and has been for years there is a high placebo rate.Here is the link again you should be able to read.Irritable Bowel Syndrome Remains a Difficult Condition to Managehttp://216.109.125.130/search/cache?p=Irri...&icp=1&.intl=usThe placebo effect depends on the person, but when you have a condition so closely connected to brain gut function, the brain has a powerful effect.Again this is well known to IBS researchers for years now. Its also well known to the Pharm companies and drug studies.Arnie, the medscape site has major IBS info, just sign up its free and they don't spam you. They have a huge IBS resource section with a lot of valuable IBS info and CME articles.


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## Screamer (Aug 16, 2005)

I was watching something interesting on placebo effects the other night on telly here. A lady who had had clinical depression for years and years went in this trial for some new anti dep and her (along with many others) were positive they'd been given the anti dep when in actual fact they got the placebo. The number of people on the placebo who improved were almost as many as those who took the actual pill which is leading the medical community to believe that things such as cognitive (sp?) behavioural therapy and the willingness of the mind to believe that you can get better are major contributors in gaining optimum health. I found it fascinating and wondered how much of this would be true for IBS suffers (not that I'm saying it's all in our heads, goodness knows I know that it is not). Yep I too get the most awful side effects from all anti deps. The minor mood improve and the lack of D just don't make up for the side effects I have! Arnie, sorry to hear that Paxil's giving you a rough time. I found it to be one of the worst side effects wise. Most of them made my D worse, one of them almost gave me an early heart attack (at 25), one of them had me so doped out I could barely remember my name (not good when you have kids) but the Paxil, well those side effects were totally insane! Talk to your doctor about it. They might have something that's better suited to you if you still want to try another. Some people do have a lot of success with them.


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## Arnie W (Oct 22, 2003)

My main problem with the paxil is insomnia. Couple that with my frequent bathoom visits during the night to pee and I feel like something that the dog has dragged up. Still getting to the gym though. I was meant to start on 10mg and go up to 20mg after 2 weeks, but I think I'll go the opposite way - down to 5mg, then maybe stop it.The Medscape article is very interesting, but didn't answer any of my questions. With depression and IBS, there can be an inexplicable recovery. A friend of my mother's had D so badly several years ago that he hardly dare to leave the house. It suddenly disappeared, but returned about 7 years later (last year). He had GI appointments ( I don't know whether he took any medication or anything) and it disappeared again. I really think that the placebo effect could depend on what caused the IBS. Spasman and also someone I know attribute it to NSAIDS. They've tried all sorts of remedies, but to no avail.Hypnotherapy is like a placebo in that if you can get your mind to believe you can get relief, you often will, but it never worked for me.


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## eric (Jul 8, 1999)

Arnie, oddly enough there are a small percentage of IBSers that just get better regarless of what they do.Nsids may contribute to developing IBS, that would make sense, some peoples IBS seems to develop from some sort of shock or damge to the gi system.It would be hard to tell why your friends mother recovered.Again, you also have to take into account mild, moderate and severe IBS.HT is not a placebo, because they have mechanisms of action, both physiologically and psychologically.However both the placebo and HT seem to work on the ACC of the brain.Was it Mike's tapes you did? How many times did you try, just courious, it does not work for everyone however.Screamer, did your doc mention this?Iron-Deficiency Anemia http://news.yahoo.com/s/kidshealth/2005110...ficiency_anemia


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## eric (Jul 8, 1999)

FYI"Post-Infectious IBSProfessor Robin Spiller, Wolfson Digestive Diseases CentreUniversity Hospital, Nottingham, NG7 2UH, UKDefinitionWe have defined Post infectious IBS (1) as acute onset Rome II criteria positiveIBS developing after an infectious illness characterised by two or more of thefollowing; fever, vomiting, acute diarrhoea, positive stool culture. Post infectiveIBS is of particular interest because it is â€œnatureâ€™s experimentâ€. Unlike mostother IBS there is a clearly defined start date, and the condition is morehomogenous, being mostly D-IBS.EpidemiologyThere have been at least 5 prospective studies of patients with culture positiveinfective gastroenteritis showing that 7 -31% progress to develop post infectiveIBS (PI-IBS) when assessed 3-6 months after infection (Table 1). Whencompared with uninfected controls two studies have shown an increased risk ofdeveloping IBS OR = 10.1, 95% CI = 3.32-30.69 (2;3)."http://ibsgroup.org/eve/forums/a/tpc/f/71210261/m/557105561


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## Arnie W (Oct 22, 2003)

I haven't done Mike's tapes. By the time you do the exchange rate to antipodean currency, it gets a bit expensive, but maybe one day I'll consider it. I've been with 4 different hypnotherapists, one of whom was a medical doctor.I still would like a link to a study which will answer my questions about the IBS histories of those who responded to the placebo in the trial.


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## Screamer (Aug 16, 2005)

Yeah, he did look into it however we established that my diet is okay as far as iron goes, my periods are way too light to be of any concern and he sent me for the colonoscopy to check for chrone's or UC the 2nd time it happened. Now it's just another one of my unexplainable symptoms







Very frustrating to know that not even my doctor knows what's going on with me or why but I guess I might get some answers eventually. Well I hope I do.


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## eric (Jul 8, 1999)

Arnie, maybe try his tapes someday.Some HT people are better at it then others of course and some know IBS better, but perhaps you just didn't respond to it as well.On the placebo I am looking into it. Like I said its pretty coomon knowledge to researchers and drug companies trying to show what works or doesn't.If you can make the UNC chat on Tuesday you can ask or I will ask them. I would think these IBSers were diagnosed onunder the rome criteria as having IBS. Also"The multifactorial pathophysiology of IBS, the waxing and waning of both colonic and noncolonic symptoms, and inordinate placebo effect noted in this population make it difficult to develop a therapeutic plan and evaluate its efficacy.11,26"This paper is pretty good anyway and this is also interesting."Patients with IBS may have alterations in GI tract motility in response to both psychological and physical stimuli such as meals, balloon distention, and cholecystokinin, a hormone released from the small-bowel mucosa in response to the ingestion of fats and proteins."Which is connected to"impaired gastrocolonic reflex that delays but prolongs activity"http://www.uspharmacist.com/index.asp?page...832/default.htmFor d people this is one reason right after you eat your lower colon over reacts. This is sometimes, blamed on the food for the wrong reasons.


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## Arnie W (Oct 22, 2003)

Maybe we can agree on this? Would there not be a higher placebo rate in patients with IBS precipitated by stress, anxiety and general trauma (as in your 'Changing Your Thoughts' thread) than those who got it from post infection, surgery, use of certain medication, etc?Interesting that there is a higher use of psychiatric services from people with IBS and functional bowel disorders than with other digestive diseases.


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## eric (Jul 8, 1999)

Arnie"percipitated by stress, anxiety "most cases of IBS can be triggered by"percipitated by stress, anxiety "regarless of the cause, but stress, anxietydon't cause IBS. more importantly IBS can be triggered by emotions themselves.surgery or medications would be the cause of gi problems themselves as defineable causes. In the case of surgery structural reasons and medications perhaps damage or chemical reasons."The limbic system is involved in emotion, mood, and visceral autonomic control. Limbic abnormalities are seen in depression and IBS. Thus, this system is a possible site of convergence where emotional disturbance provokes intestinal dysfunction. "http://www.fdhn.org/html/education/gi/ibs_nosology.htmPsychosocial Factors in IBS:http://ibsgroup.org/eve/forums?a=tpc&s=500...03771#714103771


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## eric (Jul 8, 1999)

Excerpts from the UNC chat with the experts.Drossman"symptoms are generated by abnormalities in motility (movement of the muscles), sensation (a lower pain threshold) or perception (how the brain interprets and modifies the nerve input from the bowel). To varying degrees, these disorders are characterized physiologically by any of 3 components. The first as shown here for IBS is that of increased motility or muscle contractions. In this slide, after eating a meal, the pressure generated in the lower bowel (sigmoid motility index) is similar to but greater in intensity for IBS (shown in yellow) compared to normal subjects. The second physiological component, is that of visceral hypersensitivity or a lower pain threshold. Here with IBS, after progressive rectal distension using a balloon, there is a predictable rise in the number of people reporting pain with greater distension. "The 3rd component is that of brain-gut dysfunction or difficulties with the brain controlling gut function or painful sensation. This slide shows that there is a 2-way connection between brain and gut. Pain in the intestines goes up the spinal cord to the brain where it is experienced as pain." when you eat or get increased motility from stress the bowel increases motilty and can cause pain. It's called increased gut reactivity. Anyone if they eat a large meal or are stressed can get diarrhea, those with IBS get it sooner because they are more sensitive to the stretch of the bowel."Diet can aggravate the symptoms, but in addition, and almost separately, people can go in and out of episodes. So when you have an episode, maybe anything you eat is a problem and other times when not having an episode you can eat anything. "


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## 13542 (Nov 10, 2005)

Whats with the right side pain Eric?You seem like an intelligent guy. I am new here - just today actually. Home from work due to another attack of IBS. Stress seems to bring on my attacks - but they almost always start with right side lower abdom pain (at times during sleeping - followed by an attack of urgent watery D. in the morning and then I am out of commission for most of the day.) Had a colonscopy a few years ago - showed nothing. Had a laporscopy also and the Gyne said I had scar tissue around the ilium and that something had been going on there for a few years. Sent me to GI specialist and he diagnosed me with IBS. Put me on Lorazepam to help with the anxiety - but I went off it when others told me it was addicting. Now I seem to suffer more often. Help from Canada. Any knowledge you have would be helpful.


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## eric (Jul 8, 1999)

freelily read thiskeep following to the next sectionhttp://hopkins-gi.nts.jhu.edu/pages/latin/...se=43&lang_id=1


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## 13542 (Nov 10, 2005)

Eric - good reading but not much I haven't already read about. Is there nothing specific to right sided pain?


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## eric (Jul 8, 1999)

Because there are so many nerve fibers in the gut, pain can radiate and causes all kinds of different sensations. Some with IBS have pain on the left, some on the right and some basically all over. The "feeling of pain" like crampy and short bursts, or dull aching pain are consistant with IBS, but that is a good question to ask your doctor about and see if other conditions cause right sided pain.You can have right sided pain in IBS though.


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## eric (Jul 8, 1999)

this requires a registration to medscape, but its free and they don't spam you, they also have a great IBS resource center.This Doctor is an expert on PI IBS.From Medscape GastroenterologyIBS and Chronic Constipation Expert ColumnRationale for the Use of Serotonin-Modulating Agents in the Management of IBS and Chronic ConstipationPosted 11/01/2005Robin C. Spiller, MD IntroductionClinical Features of Irritable Bowel Syndrome"Evidence of Abnormal Serotonin Metabolism in IBSAnimal studies have indicated that acute inflammation increases EC cell numbers,[50] enhances 5-HT release,[41] and depresses the serotonin transporter.[51] Studies of 5-HT availability in humans have been limited so far to measurements of peripheral 5-HT in platelet-poor plasma following a test meal. This is a very indirect measure of intestinal 5-HT because most 5-HT released is taken up locally or by the liver or lung and metabolized. However, 4 studies have reported increased postprandial 5-HT in patients with IBS-D.[52-55] In one of these studies, the patients had PI-IBS, whereas in the other investigations, the mode of onset of IBS was not specified. Two studies agreed that in patients with IBS-C, the release of serotonin is abnormally depressed.[53,54] Dunlop and colleagues[53] reported reduction in the 5HIAA (5-hydroxyindoleacetic acid [metabolite of 5-HT])/5-HT ratio, an indication of impaired serotonin turnover compatible with the reduced blood levels noted postprandially. This study also showed that constipated IBS patients have more 5-HT per EC cell, in keeping with the idea of impaired release."http://www.medscape.com/viewarticle/514413


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## SpAsMaN* (May 11, 2002)

Eric,what was the response from Dr.Drossman to my idea of using mast cell stabilizers?Perhaps histamine meds?


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## eric (Jul 8, 1999)

They weren't sure why anti histimines drugs were not that effective, even though in IBS research the HPA axis and mast cells were an issue so far in subgroups of IBS, especially PI IBS, but now also in some IBSers in general.I think I have mentioned this to you before also, chronic stressors degrandulates mast cells without a pathogen. The HPA axis is also the body's stress system and is also closely tied to emotions and the limbic system.Mast cells however are different then the above EC cells and serotonin problems.


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## eric (Jul 8, 1999)

FYIfrom Drossman in the chat"the work on serotonin has been studied now in terms of there being decreaseed SERT reuptake of 5HT3"


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## eric (Jul 8, 1999)

this requires a registration to medscape, but its free and they don't spam you, they also have a great IBS resource center.This Doctor is an expert on PI IBS.From Medscape GastroenterologyIBS and Chronic Constipation Expert ColumnRationale for the Use of Serotonin-Modulating Agents in the Management of IBS and Chronic ConstipationPosted 11/01/2005Robin C. Spiller, MD IntroductionClinical Features of Irritable Bowel Syndrome"Evidence of Abnormal Serotonin Metabolism in IBSAnimal studies have indicated that acute inflammation increases EC cell numbers,[50] enhances 5-HT release,[41] and depresses the serotonin transporter.[51] Studies of 5-HT availability in humans have been limited so far to measurements of peripheral 5-HT in platelet-poor plasma following a test meal. This is a very indirect measure of intestinal 5-HT because most 5-HT released is taken up locally or by the liver or lung and metabolized. However, 4 studies have reported increased postprandial 5-HT in patients with IBS-D.[52-55] In one of these studies, the patients had PI-IBS, whereas in the other investigations, the mode of onset of IBS was not specified. Two studies agreed that in patients with IBS-C, the release of serotonin is abnormally depressed.[53,54] Dunlop and colleagues[53] reported reduction in the 5HIAA (5-hydroxyindoleacetic acid [metabolite of 5-HT])/5-HT ratio, an indication of impaired serotonin turnover compatible with the reduced blood levels noted postprandially. This study also showed that constipated IBS patients have more 5-HT per EC cell, in keeping with the idea of impaired release."http://www.medscape.com/viewarticle/514413


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## eric (Jul 8, 1999)

bump


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## eric (Jul 8, 1999)

two excellent glossaries for medical terminology.http://arbl.cvmbs.colostate.edu/hbooks/glossary.htmlandhttp://www.iffgd.org/GIDisorders/glossary.htmland a really good site on how digestion works.http://arbl.cvmbs.colostate.edu/hbooks/pat...sics/index.html


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## SpAsMaN* (May 11, 2002)

The spasman theory:IBS occurs mostly overtime."Stress" in the sensitive nerves in the belly accumulate the "stress".I quote stress since it could be post-infection or bladder cross-neural communication stress.For the bladder related stress,it's because a too full bladder influence the brain-gut signal to the bowel resulting in urgency and sensitization.So now i need a pacemaker to settle these nerves ending.


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## SpAsMaN* (May 11, 2002)




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## eric (Jul 8, 1999)

There is physical stressors and there are mental stressors.A theory and one they are researching.The gut brain may signal to the main brain via serotonin and that signal gets sent to the prefrontal cortex(a brain area associated with anxiety) and the anxiety gets "turned up) instead of the signal going where its suppose to, to the ACC part of the brain that sends anti pain measures back to the gut. The anxiety then sends a signal back to the gut and may degrandulate mast cells contributing to pain and altered motility, which then sends the signals back to the brain.


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## 20139 (Jun 4, 2005)

Hello,Eric, I want to see if you could ascertain this.I cant sweat. I have run 3 miles in 100 degree weather at about 7 minutes a mile. All I get it pricks where I'm suppose to sweat. My Gallbadder went bad and it was taken out. My aunt has a pituitary disorder. My prostates enlarged and I have a cyst on my kidney. Theres two blemishes on my ankle that never go away. I used to get kicked punched in the gut constantly (martial arts). I had 3rd degree burns on my abdomen. I had a tooth infection which I fought off without antibiotics somehow. I took bags of crushed asprin for the pain. It came back and had the tooth removed.Doctors dont see any correlation between this evidence and whats been happening to me. I have gerd, gastritis, D occasionally and basic pain in aorta section of my chest and abdomen. Also I have pain where the gallbladder is to my shoulder and arm.Ive been diagnosed with IBS by the doctor that said not sweating was normal.Ive looked in all different directions to the cause and can find no answers. Let me know if you have any ideas. Thanks


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## eric (Jul 8, 1999)

Pickelebarrel, sorry this took so long.I am not sure about the sweating or why that maybe, I didn't find much trying to look it up.Have you ever been checked for a "pituitary disorder?""My Gallbadder went bad and it was taken out."Did they put you on questran? "My prostates enlarged and I have a cyst on my kidney.""Theres two blemishes on my ankle that never go away."Can't really help you there either, but probably not big connections to IBS."I used to get kicked punched in the gut constantly (martial arts). I had 3rd degree burns on my abdomen. I had a tooth infection which I fought off without antibiotics somehow."Probably not to involved with IBS either."I took bags of crushed asprin "Now that might be something, some peoples IBS develop or is made worse by a "shock" to the digestive system.a lot of people have gerd and IBS, my wife does for one, both can effect each other." basic pain in aorta section of my chest and abdomen"Has this been checked out? There is something called "Functional chest pain - the feeling of chest pain, presumably of esophageal origin (can be confused with cardiac pain which must be examined) "http://www.iffgd.org/GIDisorders/GIAdults.htmla lot of these functional disorders can and do overlap in people."Also I have pain where the gallbladder is to my shoulder and arm."On a regular basis, what did the doctor say about that with you.on the Gastritis, that may have been caused by the aspirn, but you also have gerd.Info Gastritis http://www.gicare.com/pated/ecdgs46.htmDo you have lower abdomen pains or discomfort?


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## eric (Jul 8, 1999)

The ANS or autonomic nervous system is connected to the enteric nervous system that runs digestion.You don't have to conciously think about digesting your food."The autonomic nervous system (ANS) is the portion of the nervous system that controls the body's visceral functions, including, but not limited to action of the heart, movement of the gastrointestinal tract and secretion by different glands, among many other vital activities. ""To summarize:Thoughts and even subtle emotions influence the activity and balance of the autonomic nervous system (ANS).The ANS interacts with our digestive, cardiovascular,immune and hormonal systems and is therefore ideally suited to translate mind states into organ functions/dysfunctions Negative reactions create disorder and imbalance in the ANS. Positive feelings such as appreciation and a state of relaxation create increased order and balance in the ANS, resulting in increased hormonal and immune system balance and more efficient brain function. It has been shown in a number of studies that during mental or emotional stress and physical stress, there is an increase in sympathetic activity and a decrease in parasympathetic activity. This results in increased strain on the heart as well as on the immune and hormonal systems. Increased sympathetic activity is associated with a lower ventricular fibrillation threshold and an increased risk of fibrillation, in contrast to increased parasympathetic activity, which protects the heart."


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## eric (Jul 8, 1999)

http://ibs.med.ucla.edu/Articles/PatientArticleSm02ANS.htm


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## eric (Jul 8, 1999)

bump


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## eric (Jul 8, 1999)

Post-Infectious IBSProfessor Robin Spiller, Wolfson Digestive Diseases CentreUniversity Hospital, Nottingham, NG7 2UH, UKDefinitionWe have defined Post infectious IBS (1) as acute onset Rome II criteria positiveIBS developing after an infectious illness characterised by two or more of thefollowing; fever, vomiting, acute diarrhoea, positive stool culture. Post infectiveIBS is of particular interest because it is â€œnatureâ€™s experimentâ€. Unlike mostother IBS there is a clearly defined start date, and the condition is morehomogenous, being mostly D-IBS.Epidemiologyhttp://ibsgroup.org/eve/forums/a/tpc/f/71210261/m/557105561


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## eric (Jul 8, 1999)

"Irritable Bowel Syndrome: A Postinfectious and Inflammatory Disorder? CMEDisclosuresNicholas J. Talley, MD, PhD IntroductionThe pathophysiology of the functional gastrointestinal disorders remains obscure, but there is increasing evidence that, in at least a subset of patients, infection and inflammation may play key roles.[1] After an episode of severe gastroenteritis requiring hospitalization, it has been observed that approximately 1 in 4 patients has long-standing irritable bowel syndrome (IBS)-like symptoms on follow-up 6 months later.[2,3] A topic forum was therefore devoted to infection and inflammation in functional bowel disease. A number of other key abstracts were also presented on this topic, and a review of the new data and the clinical implications will be highlighted.Can Infection Change Gut Sensory Perception?It is established that patients with IBS usually have visceral hypersensitivity, particularly in the colon, although pan-gut involvement has been documented. A key question is whether infection can directly alter colonic sensory pathways. A useful model developed in mice involves infection with the parasite Trichomonas spiralis, which results in neuromuscular abnormalities in both the colon and small bowel that persist despite healing of the initial injury and loss of the organism.[1]Dr. Yukang Mao and colleagues from McMaster University in Hamilton, Ontario, Canada, examined the acute and chronic effects of T spiralis on colonic sensory function by measuring the dorsal root ganglion single-unit discharges in adult male NIH Swiss mice.[4] The investigators placed a latex balloon in the colon distally following the introduction of T spiralis. There was jejunal enteritis at 6 days postinfection, which returned to normal in 28 days. There were no T spiralis remaining in the bowel after 3 weeks. The investigators found postinfection hyperalgesic sensory response following distension of the colon that persisted despite healing of the acute inflammation. Furthermore, the authors were able to show that the induced response was blocked by a neurokinin (NK)-1 receptor antagonist (SR140333). The results confirm that postinfection inflammation can alter visceral sensitivity and imply that NK-1 antagonists may be therapeutically useful in this situation. There is increasing interest in NK receptor antagonists as visceral analgesics,[5] and these drugs are currently being tested in IBS.Is There Evidence of Increased Inflammation in IBS?Direct evidence of an active inflammatory component in IBS remains to be confirmed. Earlier reports suggested that there is a small, albeit significant, quantitative increase of colonic inflammatory cells in patients with IBS as well as an increase in terminal ileal mast cells.[1,6] More direct evidence has become available during this year's DDW. "http://66.218.69.11/search/cache?p=immunol...&icp=1&.intl=us


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## eric (Jul 8, 1999)

Personal Reporter: Answers About Irritable Bowel Syndrome webmdOur experienced medical journalist Jennifer Warner took your questions about IBS to specialists. Here's what she found out. WebMD Personal Reporter "Question: What progress has been made in finding a theory in the development of IBS? Answer: IBS occurs when there is a dysfunction in the regulation of how the brain and gut talk to each other. Diet, stress, hormones, and infection can all affect a person's sensitivity to this condition. There's a brain-gut connection, and if the bowel is distressed, it's not unusual to get anxious. Mental stress may also cause the bowel to become distressed. -- Douglas Drossman, professor of medicine and psychiatry at the University of North Carolina, Chapel Hill and co-director of the UNC Center for Functional GI and Utility Disorders. What's happening now is that there is an increasing recognition that IBS is a problem that is occurring in both the central nervous system and the gut and the interplay between the two. That is giving us a much better handle on mechanisms involved. Therefore, we now have a lot of new ideas and more scientific evidence that are leading to more effective treatments. -- Ray E. Clouse, MD, professor of medicine and psychiatry in the division of gastroenterology at the Washington University School of Medicine in St. Louis. "http://www.webmd.com/content/article/65/79519.htmPersonal Reporter: Answers About Irritable Bowel SyndromeOur experienced medical journalist Jennifer Warner took your questions about IBS to specialists. Here's what she found out. WebMD Personal Reporter http://www.webmd.com/content/article/65/79522.htm


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## eric (Jul 8, 1999)

FYIFrom UNC "Digest" with permission.Emeran Mayer, MD, visited the UNCCenter for Functional GI & MotilityDisorders on August 30-31, 2004. Heis Professor of Medicine and Directorof the Center for NeurovisceralSciences & Womenï¿½s Health, DavidGeffen School of Medicine at UCLA,and the following is his report on hisvisit to UNC."included a presentation to the Division on Gastroenterologyand Hepatology titled ï¿½Progress in IBS Biology: One Diseaseor Many Mechanisms Leading to Similar Symptoms.ï¿½Functional GI disorders, including IBS, are currently defined byGI symptom-based criteria, yet every experienced clinicianis aware of the multiplicity of symptoms and complaints thatmost IBS patients report when asked appropriately. Someof these symptoms may be attributed to other parts of theGI tract (such as heartburn or chest pain) while others mayattributed to other organs (urinary urgency, pelvic pain) orthe skeletomotor system (headaches, muscle and joint pain).To explain such ï¿½co-morbidities,ï¿½ several theories have beenproposed: (1) IBS as defined by the Rome criteria is a diseaseof the intestine, but can co-occur with other syndromes.( 2) The GI tract related symptoms are just one of severalpossible somatic manifestations of disorders that primarilyimpact affect and mood (anxiety and depression). ( 3) IBS isa reflection of an altered perception of so-called homeostaticafferent signals from the GI tract and resulting alteredautonomic responses. In my presentation, I briefly addressedthe following two hypotheses:Is IBS a disease related to inappropriate immune activationof the intestine?Is IBS a somatic manifestation of psychiatric disease?Evidence was reviewed showing that currently availabledata does not support the immune activation hypothesis. Inthe absence of altered perceptual responses to a chronically,mildly inflamed intestine, typical IBS symptoms would be quiteunlikely. Similarly, current evidence does not support that IBSsymptoms only occur in patients with depression or anxiety,and that IBS symptoms in the normal population are generallynot associated with DSM-4 diagnoses. As an alternative, thefollowing hypothesis was proposed:IBS reflects an alteration in the perception of and responseto homeostatic feelings."http://ibsgroup.org/eve/forums/a/tpc/f/71210261/m/51210084


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## eric (Jul 8, 1999)

Curr Opin Gastroenterol. 2006 Jan;22(1):13-7. Related Articles, Links Post-infectious irritable bowel syndrome.Spiller R, Campbell E.Wolfson Digestive Diseases Centre, University Hospital, Nottingham, UK.PURPOSE OF REVIEW: Irritable bowel syndrome patients form a heterogeneous group with a variable contribution of central and peripheral components. The peripheral component is prominent in irritable bowel syndrome developing after infection (post-infectious irritable bowel syndrome) and this has proved a profitable area of research. RECENT FINDINGS: Recent studies have overthrown the dogma that irritable bowel syndrome is characterized by no abnormality of structure by demonstrating low-grade lymphocytic infiltration in the gut mucosa, increased permeability and increases in other inflammatory components including enterochromaffin and mast cells. Furthermore, increased inflammatory cytokines in both mucosa and blood have been demonstrated in irritable bowel syndrome. While steroid treatment has proved ineffective, preliminary studies with probiotics exerting an anti-inflammatory effect have shown benefit. SUMMARY: The study of post-infectious irritable bowel syndrome has revealed the importance of low-grade inflammation in causing irritable bowel syndrome symptoms. It has suggested novel approaches to irritable bowel syndrome including studies of serotonin and histamine metabolism which may be relevant to other subtypes of of the disease.PMID: 16319671


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## eric (Jul 8, 1999)

Neurology. 2005 Oct 25;65(8):1268-77. Related Articles, Links Abnormal forebrain activity in functional bowel disorder patients with chronic pain.Kwan CL, Diamant NE, Pope G, Mikula K, Mikulis DJ, Davis KD.Institute of Medical Science, University of Toronto, Ontario, Canada.BACKGROUND: Abnormal cortical pain responses in patients with fibromyalgia and conversion disorder raise the possibility of a neurobiologic basis underlying so-called "functional" chronic pain. OBJECTIVE: To use percept-related fMRI to test the hypothesis that patients with a painful functional bowel disorder do not process visceral input or sensations normally or effectively at the cortical level. METHODS: Eleven healthy subjects and nine patients with irritable bowel syndrome (IBS) underwent fMRI during rectal distensions that elicited either a moderate level of urge to defecate or pain. Subjects continuously rated their rectal stimulus-evoked urge or pain sensations during fMRI acquisition. fMRI data were interrogated for activity related to stimulus presence and to specific sensations. RESULTS: In IBS, abnormal responses associated with rectal-evoked sensations were identified in five brain regions. In primary sensory cortex, there were urge-related responses in the IBS but not control group. In the medial thalamus and hippocampus, there were pain-related responses in the IBS but not control group. However, pronounced urge- and pain-related activations were present in the right anterior insula and the right anterior cingulate cortex in the control group but not the IBS group. CONCLUSIONS: Percept-related fMRI revealed abnormal urge- and pain-related forebrain activity during rectal distension in patients with irritable bowel syndrome (IBS). As visceral stimulation evokes pain and triggers unconscious processes related to homeostasis and reflexes, abnormal brain responses in IBS may reflect the sensory symptoms of rectal pain and hypersensitivity, visceromotor dysfunction, and abnormal interoceptive processing.PMID: 16247056Pain. 2005 Jun;115(3):398-409. Related Articles, Links Differences in brain responses to visceral pain between patients with irritable bowel syndrome and ulcerative colitis. Mayer EA, Berman S, Suyenobu B, Labus J, Mandelkern MA, Naliboff BD, Chang L. Center for Neurovisceral Sciences and Women's Health, David Geffen School of Medicine, University of California, Los Angeles, CA 90073, USA. emayer###ucla.edu Patients with mild chronic inflammation of the rectum or ileum have reduced perceptual responses to rectosigmoid distension compared to patients with irritable bowel syndrome (IBS). The current study sought to identify differences in regional cerebral blood flow (rCBF) during rectal distension, which might correspond to these perceptual differences. In 8 male ulcerative colitis (UC) patients with quiescent disease, 7 male IBS patients and 7 healthy male controls, rCBF was assessed using 15O-water positron emission tomography at baseline and during actual and anticipated but undelivered rectal distensions. No group differences were seen in anterior insula and dorsal anterior cingulate cortex (dACC), two regions consistently activated by painful intestinal stimuli. However, IBS patients showed greater activation of the amygdala, rostroventral ACC, and dorsomedial frontal cortical regions. In contrast, no significant differences were observed between UC and controls. When these two non-IBS groups were combined, functional connectivity analyses showed that right lateral frontal cortex (RLFC) activation positively correlated with activation of the dorsal pons/periaqueductal gray, a key region involved in endogenous pain inhibition. According to the connectivity analysis, this effect was mediated by inhibition of medial frontal cortex by the RLFC. Chronic colonic inflammation is not necessarily associated with increased visceral afferent input to the brain during rectal distension. In the sample studied, the primary difference between functional and quiescent inflammatory disease of the colon was in terms of greater activation of limbic/paralimbic circuits in IBS, and inhibition of these circuits in UC and controls by the RLFC. PMID: 15911167


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## eric (Jul 8, 1999)

"Dr. Gershon, too, theorizes that physiology is the original culprit in brain-gut dysfunctions. "We have identified molecular defects in the gut of everyone who has irritable bowel syndrome," he said."http://ibsgroup.org/eve/forums/a/tpc/f/71210261/m/369100861


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## Guest (Dec 7, 2005)

I dunno know about any of this but my god do I ever believe that childhood stress and bullying are a MAJOR factor in my illness. Sorry, have to get this off my chest.I was regularly beaten by my dad as a child. We have/had a very very complex relationship, I believe that he really does love me but as a product of a horrendous upbringing himself, had no idea how to show love, me and my sister were bound by endless rules and regs, spent huge amounts of time either on our own or with a horrible strict grandmother.At 11, I was packed off to a boarding school in Wales, because it was the "right thing to do", I was bullied regularly for about 4 years, I can't even begin to speak about some of these things.Things got better, much better and I have a reasonable, though distant relationship with my dad, try to understand why and how he did the things he did to me, I married the most wonderful supportive and caring man and he's still hanging in there after 18 years.Oh god, sorry, can't really believe I'm pouring this all out now but I really do think sometimes having the courage to face your past in the only way to resolve things now.Thanks for hearing me out.Sue


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## eric (Jul 8, 1999)

Suev, I am sorry to hear you had these troubles growing up.







Emotional Abuse and IBSStudy found link to severity -- but not causality By: Douglas A. Drossman, M.D., Co-Director, Center for Functional GI & Motility Disorders Center; Professor of Medicine and Psychiatry, University of North Carolina, Chapel Hill http://www.aboutibs.org/Publications/abuse.html


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## Talissa (Apr 10, 2004)

> quote:RECENT FINDINGS: Recent studies have overthrown the dogma that irritable bowel syndrome is characterized by no abnormality of structure by demonstrating low-grade lymphocytic infiltration in the gut mucosa, increased permeability and increases in other inflammatory components including enterochromaffin and mast cells. Furthermore, increased inflammatory cytokines in both mucosa and blood have been demonstrated in irritable bowel syndrome. While steroid treatment has proved ineffective, preliminary studies with probiotics exerting an anti-inflammatory effect have shown benefit. SUMMARY: *The study of post-infectious irritable bowel syndrome has revealed the importance of low-grade inflammation in causing irritable bowel syndrome symptoms.* It has suggested novel approaches to irritable bowel syndrome including studies of serotonin and histamine metabolism which may be relevant to other subtypes of of the disease.


Knew this would happen some day Eric...think of how many arguments could've been avoided had you been able to see into the future...Glad I was here to see this...I'd like to think you & I are on better terms now, but can I just say, with the utmost humility & respect for all you do here on this bb...I was right! I told you so!!







Your pal Tal


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## eric (Jul 8, 1999)

Tal, LOL"I'd like to think you & I are on better terms now"I never thought we were on bad terms. Just diagreeing on some points.







They have known about inflammation in IBS for over five years or so now through PI IBS studies, however the study I posted there by Spiller one of the leaders if not the leader in Post infectious IBS.That is on PI IBS which is at the moment considered a subgroup, people who develop IBS after an enteric infection. Which is why at the end of the study it says "serotonin and histamine metabolism which may be relevant to other subtypes of of the disease."However, notice he is calling it a disease! Very importantly."Several studies have suggested that infection and inflammation in the GI tract cause changes in the intestinal physiology that can persist after the infection and inflammation have resolved. The altered intestinal lining that is left after the inflammation has resolved is believed to trigger a neuroimmune interaction that may be implemented in the pathogenesis of some IBS patients (Yehuda et al. 2002). "http://www.lef.org/protocols/prtcl-157.shtmlAs I have mentioned before, the term neurogenic inflammation.The infection has resolved and chronic stressors physical and mental can reactivate specific cells in the gi tract lining. Specificly and very importantly one of them being mast cells.The other important part he wrote recentlyRobin C. Spiller, MD IntroductionClinical Features of Irritable Bowel Syndrome"Evidence of Abnormal Serotonin Metabolism in IBSAnimal studies have indicated that acute inflammation increases EC cell numbers,[50] enhances 5-HT release,[41] and depresses the serotonin transporter.[51] Studies of 5-HT availability in humans have been limited so far to measurements of peripheral 5-HT in platelet-poor plasma following a test meal. This is a very indirect measure of intestinal 5-HT because most 5-HT released is taken up locally or by the liver or lung and metabolized. However, 4 studies have reported increased postprandial 5-HT in patients with IBS-D.[52-55] In one of these studies, the patients had PI-IBS, whereas in the other investigations, the mode of onset of IBS was not specified. Two studies agreed that in patients with IBS-C, the release of serotonin is abnormally depressed.[53,54] Dunlop and colleagues[53] reported reduction in the 5HIAA (5-hydroxyindoleacetic acid [metabolite of 5-HT])/5-HT ratio, an indication of impaired serotonin turnover compatible with the reduced blood levels noted postprandially. This study also showed that constipated IBS patients have more 5-HT per EC cell, in keeping with the idea of impaired release."http://www.medscape.com/viewarticle/514413"What's happening now is that there is an increasing recognition that IBS is a problem that is occurring in both the central nervous system and the gut and the interplay between the two. "They know now there are molecular defects in EC cells that store serotonin. The 5ht3 receptor is malfunctioning. I am still not sure how important that is to you. its is the chemical that signals sensations to the brain from the GI tract for one, but also explains altered motility in IBS. Yet, they don't know exactly why its malfunctioning yet. They are studying if this contributes to neurogenic inflammation on the bottom up and top down model. There is increasing evidence on top of evidence they have alredy now that this to happening in both animal studies and humans.There are also still some extremely important issues with brain function in IBS that need to be figured out in regards to the ACC or anterior cingulate cortex and pain.The last chat with the experts. Dr Drossman,"GI Disorders of function."symptoms are generated by abnormalities in motility (movement of the muscles), sensation (a lower pain threshold) or perception (how the brain interprets and modifies the nerve input from the bowel).To varying degrees, these disorders are characterized physiologically by any of 3 components. The first as shown here for IBS is that of increased motility or muscle contractions. In this slide, after eating a meal, the pressure generated in the lower bowel (sigmoid motility index) is similar to but greater in intensity for IBS (shown in yellow) compared to normal subjects. The second physiological component, is that of visceral hypersensitivity or a lower pain threshold. Here with IBS, after progressive rectal distension using a balloon, there is a predictable rise in the number of people reporting pain with greater distension.Drossman: The 3rd component is that of brain-gut dysfunction or difficulties with the brain controlling gut function or painful sensation. This slide shows that there is a 2-way connection between brain and gut. Pain in the intestines goes up the spinal cord to the brain where it is experienced as painDrossman: But what we see in IBS and other functional GI disorders (e.g., functional esophageal pain, functional dyspepsia, functional abdominal pain) is that the brain is not working well enough to â€œturn downâ€ the pain. "The importantance of mast cells contributing to pain in IBS is important. There connected to allergic reactions, the bodies stress system and to help in fighting infection and contributing to pain in IBS by the release of histimine onto the smooth muscle. That is not the whole picture however, but shows a covergence for infection and stress and mast cells, as well as neurogenic inflammation.I have been saying this for a couple years now, EC cells and mast cells are extremely important in IBS research.Distinctive Features of Postinfective Irritable Bowel Syndrome PI IBS have "greater increase in serotonin-containing enterochromaffin (EC)" http://www.medscape.com/viewarticle/459230and IBSers without a history of infection, have altered serotonin dysregulation from the ec cells and a molecular defect in its functioning.The macroscopic inflammation in IBS are specific cells, like mast cells embedded in the gi tract lining.So" By defining different 'key players' such as mast cells, lymphocytes, and EC cells, they suggest new specific pharmacological targets for therapy. They also suggest new objective measures such as plasma serotonin or serum tryptase with which we can seek to subclassify IBS and to identify those individuals who will respond to specific therapies." http://www.medscape.com/viewarticle/459230so basically, all the sites saying "we don't find anything" is not entirely accurate anymore, They are starting to see structural and biochemical reasons for the symotms, through the brain gut axis system. Both of which are operational to cause the symptoms.


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## eric (Jul 8, 1999)

By the way, pay close attension to the word "neuroimmune" and its meaning. Because its extremely important.


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## eric (Jul 8, 1999)

This is importantAlthough this doesn't mention IBS it is how stress stress and inflammation"Neurogenic Inflammation in Chronic Pain Conditions "We usually associate inflammation with the response of the body to tissue injury or invasion by hostile microorganisms. The central and autonomic nervous systems play an essential role in the initiation and modulation of this process. Although tissue trauma or infectious agents may be initiating factors in neurogenic inflammation, neither of them are required. The inflammation may be initiated and maintained by the central and peripheral nervous systems in response to psychological stress[1]" http://216.109.125.130/search/cache?p=hpa+...&icp=1&.intl=usYou here about "Macroscopic inflammation" in IBS and this is part of the picture.It is believed the mast cells in the gut are effected by stressors in IBS and they degrandulate from stressors without a pathogen.They then release histimine onto the smooth muscles of the gut (toxic), which can contribute to pain in IBS along with the problems they already see in the serotonin system in IBS.Inflammatory Changes Seen in Irritable Bowel Chronic Pelvic PainA DGReview of :"Neurogenic inflammation and chronic pelvic pain"World Journal of Urologyhttp://www.docguide.com/news/content.nsf/n...ritable%2CbowelLecture: Neurophysiology of Brain-Gut Interactions During Stress Presenter: Jack Wood, PhD "Jack Wood, PhDProfessor of Physiology and Internal MedicineChairman Emeritus, Department of PhysiologyThe Ohio State University College of Medicine Dr. Wood was the first to use microelectrodes to record the electrical and synaptic behavior of neurons in the enteric nervous system. He coined the term "brain-in-the-gut" in view of emerging evidence that the enteric nervous system had neurophysiological properties like the brain and spinal cord. In recent years he has focused on signaling interactions between the enteric immune system and the brain-in-the-gut during infectious enteritis and food allergy. In this lecture he shows how the central nervous system, enteric nervous system and intestinal immune system are integrated during physical and emotional stress to produce irritable bowel symptoms of diarrhea and abdominal pain and discomfort. "http://www.conference-cast.com/ibs/Lecture...cfm?LectureID=7"Irritable bowel syndrome (IBS) is a functional intestinal disorder characterised by changes in bowel habits, which range from constipation to diarrhoea, associated with abdominal discomfort or overt pain (Drossman et al., 2002; Talley & Spiller, 2002). These symptoms can be attributed to modifications of the sensory-motor function of the intestine, where the substrate(s) involved could reside within the intestinal wall, in extrinsic ganglia, or in the central nervous system (Camilleri, 2001). As has recently been pointed out (Drossman et al., 2003), psychological distress, affective disorders, and narcotic abuse have to be considered as important ethiopathogenetic factors for IBS; however, there is little doubt that such factors also trigger peripheral changes. In accordance with this concept, stress can reactivate a previous peripheral inflammation (Collins, 2001), thus establishing a link between psychological factors and post-infectious (or post-dysenteric) IBS (Spiller et al., 2000). Current pharmacological treatments are aimed at controlling specific symptoms (e.g., tricyclic antidepressants for pain, 5-HT3 antagonists or spasmolytics for diarrhoea, 5-HT4 agonists for constipation) and the improvement obtained is relatively modest (Mertz, 2003). Therefore, a single drug that could potentially affect all of these symptoms would represent an important therapeutic achievement (Kirkup et al., 2001)."More information here on IBS and inflammation and neurogenic inflammation.Critical role of mast cells in inflammatory diseases and the effect of acute stresshttp://ibsgroup.org/eve/forums/a/tpc/f/43110261/m/957107871Stress reduction in IBS is even important for inflammation.


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## Guest (Dec 7, 2005)

Thanks Eric - sorry, re-reading this now, sounds a little over-dramatic but I think you have to face these demons. Yeah, I'm not totally blaming all this on my dodgey colon but I do think stress is the looming factor in my life and my symptoms.Thanks for all the helpful articles too.Sue


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## eric (Jul 8, 1999)

No Problem Suev.







Stress can be a contributing factor in developing IBS. Something for you to think about."Every time you are tempted to react in the same old ways, ask if you want to be a prisoner of the past or a pioneer of the future. The past is closed and limited; the future is open and free."


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## eric (Jul 8, 1999)

PI IBS development to IBSNeurogastroenterol Motil. 2005 Dec;17(6):863-870. Links Enterochromaffin cell hyperplasia and decreased serotonin transporter in a mouse model of postinfectious bowel dysfunction.Wheatcroft J, Wakelin D, Smith A, Mahoney CR, Mawe G, Spiller R.Wolfson Digestive Diseases Centre, University Hospital, Nottingham, UK.Abstract Patients with postinfective irritable bowel syndrome and Trichinella spiralis-infected mice share many features including visceral hypersensitivity and disordered motility. We assessed enterochromaffin (EC) numbers and serotonin transporter (SERT) using National Institute of Health (NIH) female mice studied for up to 56 days post-T. spiralis infection. The effects of steroid treatment and the T-cell dependence of the observed responses were assessed by infection of hydrocortisone-treated or T-cell receptor knock out [TCR (betaxdelta) KO] animals. Enterochromaffin cell density in uninfected animals increased from duodenum 10.0 cells mm(-2) (5.9-41.0) to colon 61.8. (46.3-162) cells mm(-2)P < 0.0001. Infection increased duodenal and jejunal counts which rose to 37.3 (22-57.7) cells mm(-2) and 50.6 (7-110.8) cells mm(-2), respectively, at day 14. Infection significantly reduced jejunal SERT expression, with luminance values falling from 61.0 (45.1-98.3) to a nadir of 11.6 (0-36.0) units at day 9, P < 0.001. Specific deficiencies in all T cells reduced EC hyperplasia and abrogated infection-induced mastocytosis. Thus infection induced inflammation increases EC numbers, as has been reported in PI-IBS, and reduces SERT. This may increase mucosal 5HT availability and contribute to the clinical presentation of PI-IBS.PMID: 16336502


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## eric (Jul 8, 1999)

Dr Lin ChangIrritable Bowel Syndromepdf formathttp://www.ibs.med.ucla.edu/PDFs/IBSReviewArticle.pdfStress and the Gastrointestinal TractIV. Modulation of intestinal inflammation by stress: basic mechanisms and clinical relevance Stephen M. Collins McMaster University Medical Centre, Hamilton, Ontario L8N 3Z5, Canada "In a recent study in healthy volunteers and patients with food allergy, a cold pressor test increased luminal release of mast cell mediators and jejunal water secretion in both groups (16). Although stress-induced release of tryptase and histamine was greater in food-allergic patients, the study does link stress and mast cell degranulation in the gut in the absence of other inflammatory or immunological stimuli. This is in keeping with the demonstration of Pavlovian conditioning of mast cell degranulation in the rat (11). Together, these findings indicate that neuroendocrine brain-gut circuitry can be activated to stimulate immune cells in the absence of preexisting disease."http://ajpgi.physiology.org/cgi/content/full/280/3/G315


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## eric (Jul 8, 1999)

Medscape"Review Article: The Role of Serotonergic Agents in the Treatment of Patients With Primary Chronic ConstipationPosted 12/08/2005B.D. Cash; W.D. Chey SummaryChronic constipation is a highly prevalent disorder that is associated with significant direct and indirect costs and has substantial impact on patient quality of life. It is more common among women and non-white populations and is evenly distributed across adult age groups. Constipation is a heterogeneous disorder associated with multiple symptoms and aetiologies.Recent research has increased our understanding of the pathogenesis of this disorder and the central role of the neurotransmitter serotonin in mediating gastrointestinal motility, secretion and sensation. Abnormal serotonin signalling and reuptake appear to play central roles in the symptoms of a subset of patients with chronic constipation. This observation provides a rationale for the use of targeted serotonergic agents for the treatment of chronic constipation. As the role of serotonin in gastrointestinal function is further elucidated and additional candidate drugs are developed, it is likely that serotonergic agents will afford additional treatment options for patients with chronic constipation.This article provides a concise review of the evidence supporting a role for serotonin in the pathogenesis of chronic constipation and a summary of the currently available evidence supporting the use of serotonergic agents for this disorder."SummaryOverview of Chronic ConstipationThe Brain-Gut Axis and the Role of Serotonin in Gastrointestinal FunctionSerotonergic Agents and Chronic ConstipationConclusionhttp://www.medscape.com/viewarticle/518324?src=mp


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## eric (Jul 8, 1999)

This is medscape also an an excellent article."Post-infectious Irritable Bowel SyndromePosted 12/08/2005Robin Spiller; Eugene Campbell Abstract and IntroductionAbstractPurpose of Review: Irritable bowel syndrome patients form a heterogeneous group with a variable contribution of central and peripheral components. The peripheral component is prominent in irritable bowel syndrome developing after infection (post-infectious irritable bowel syndrome) and this has proved a profitable area of research.Recent Findings: Recent studies have overthrown the dogma that irritable bowel syndrome is characterized by no abnormality of structure by demonstrating low-grade lymphocytic infiltration in the gut mucosa, increased permeability and increases in other inflammatory components including enterochromaffin and mast cells. Furthermore, increased inflammatory cytokines in both mucosa and blood have been demonstrated in irritable bowel syndrome. While steroid treatment has proved ineffective, preliminary studies with probiotics exerting an anti-inflammatory effect have shown benefit.Summary: The study of post-infectious irritable bowel syndrome has revealed the importance of low-grade inflammation in causing irritable bowel syndrome symptoms. It has suggested novel approaches to irritable bowel syndrome including studies of serotonin and histamine metabolism which may be relevant to other subtypes of of the disease.IntroductionAlthough the idea of irritable bowel syndrome (IBS) developing after infection is not new, being first clearly described in 1962,[1] scientific study of mechanisms is relatively recent. The demonstration of mucosal abnormalities, overthrowing years of dogma that IBS is characterized by no abnormality of structure, has stimulated others to re-examine the IBS gut. Post-infective IBS (PI-IBS) develops in 3-30% of individuals with bacterial gastroenteritis. Known risk factors include female sex, severity of initial illness, bacterial toxigenicity and adverse psychological factors, including neuroticism, hypochondriasis, anxiety and depression, as reviewed in 2003.[2] The purpose of the current review is to update the literature since 2003, during which time there has been an explosion of interest and many productive new approaches with implications for novel treatments."Abstract and IntroductionClinical FeaturesImportance of Psychiatric FeaturesRole of SerotoninRole of Inflammatory CytokinesRole of Mast CellsEvidence of Chronic Inflammation in Irritable Bowel SyndromeAnimal Models of Post-infective Irritable Bowel SyndromeAnti-inflammatory Effect of ProbioticsAnti-inflammatory Treatments in Irritable Bowel SyndromeConclusionInteresting on probiotics."Anti-inflammatory Effect of ProbioticsNumerous studies have shown an anti-inflammatory effect but the study by McCarthy et al.[30] is of particular interest since it showed a benefit in the interleukin-10-knockout mouse model of colitis using two probiotic bacteria, Lactobillus salivaris and Bifidobacterium infantis, which have since been used in IBS patients (see below). The same group also demonstrated that bacteria did not need to be living to be effective. Nor did they need to be administered orally but could be effective when given subcutaneously,[31] showing that the anti-inflammatory effect is systemic with a generalized decrease in proinflammatory cytokines." http://www.medscape.com/viewarticle/518355?src=mp


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## Blair (Dec 15, 1998)

My cause was a herniated disk in the low back. How many years did it take me to figure that out? 6 years. It took a year to get a IBS diagnosis ( 1997 ) and once I got it it stuck. Anyway I finally figured it out. Kind of explains why I had pain AFTER a Bowel movment. pretty important symptom completly missed by all doctors if thay even bothered to ask. Also why I was sicker at work and better when off work. I sit at work and that is really bad for a low back, another symptom brushed off as stress by doctors, of course this is assuming they even asked what makes it worse? So I never had IBS, at least not the real bad pain kind I was getting off and on for 6 years. Oh that and leg pain traveling to foot, duh. Anyway I had surgery on back. 1cm herniated disk straight back and bent down, old injury I was told. I still get some pain and phantom urges to go to bathroom but I eat what I want and put heat on low back, etc. Anyways thats my story, pretty werid huh? I was at nerologist and he also didn't know what to make of it. my story. So I assume I am a very rare case or I have been to over 6 very stupid doctors, kinda hard to say? Merry Christmas, etc to all.


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## eric (Jul 8, 1999)

New Updates in Chronic Constipation and Irritable Bowel Syndrome CME/CELin Chang, MD http://www.medscape.com/viewarticle/517739


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## eric (Jul 8, 1999)

Scand J Gastroenterol. 2006 Jan;41(1):54-9. Detection of inflammatory markers in stools from patients with irritable bowel syndrome and collagenous colitis.Lettesjo H, Hansson T, Peterson C, Ung KA, Ringstrom G, Abrahamsson H, Simren M.Department of Gastrointestinal Research, Pharmacia Diagnostics, Uppsala, Sweden.Objective. Irritable bowel syndrome (IBS) and collagenous colitis (CC) share chronically recurring symptoms of altered bowel habits associated with abdominal pain or discomfort. The aims of the present study were to investigate whether inflammatory markers could be detected in faeces from patients with IBS and CC, and to elucidate whether such analyses could be used as non-invasive tools to distinguish between these disorders. Material and methods. Stool samples were obtained from 18 patients with CC, 46 patients with IBS and 20 healthy controls (HC). Eosinophil protein X (EPX), myeloperoxidase (MPO), tryptase, interleukin-1 beta (IL-1beta) and tumour necrosis factor alpha (TNFalpha) were measured in supernatants from processed faeces using immunoassays. Results. EPX levels were enhanced in faeces from CC patients (median 3.8 microg/g (0.47-16.2)) compared to patients with IBS (0.44 microg/g (0.25-1.8)), p<0.001, and HC (0.46 microg/g (0.21-1.3)), p<0.001. In addition, MPO was increased in CC patients (11.7 microg/g (2.0-124)) compared to IBS patients (1.7 microg/g (0.81-5.2)), p<0.01, and HC (2.5 microg/g (1.1-6.3)), p<0.05. Tryptase was found in 9/18 patients with CC, 6/46 with IBS and 1/19 HC. IL-1beta was only enhanced in 2/11 CC patients and TNFalpha was not detected in any sample. Conclusions. Increased levels of EPX, MPO and tryptase were observed in stools from collagenous colitis patients, whereas the levels in IBS patients did not differ from healthy controls. Our data suggest that faecal markers could be used as part of the clinical work-up to determine which patients should be biopsied and evaluated for collagenous colitis.PMID: 16373277


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## eric (Jul 8, 1999)

Neurogastroenterol Motil. 2006 Jan;18(1):6-17. Related Articles, Links Functional gastrointestinal disorders and mast cells: implications for therapy.Barbara G, Stanghellini V, de Giorgio R, Corinaldesi R.Department of Internal Medicine and Gastroenterology, University of Bologna, Bologna, Italy.The pathophysiology of functional gastrointestinal disorders is poorly understood. Accepted common mechanisms include psychosocial factors, abnormal gastrointestinal motility and disturbed visceral sensory perception, but the underlying causes remain unclear. Mast cells (MCs) are immunocytes widely distributed throughout the gastrointestinal tract. Several stimuli (e.g. allergens, neuropeptides and stress) lead to MC activation with consequent mediator release (e.g. histamine, tryptase and prostanoids). The MC mediators interact with nerves supplying the gut leading to altered gut physiology and increased sensory perception. The intestinal mucosa of irritable bowel syndrome patients contains on average an increased number of MCs. These cells release an increased amount of mediators in close vicinity to mucosal innervation. The MC activation and their close proximity to nerve fibres is correlated with the severity of perceived abdominal painful sensations. These data provide a strong basis for considering MCs as important participants in visceral hypersensitivity and pain perception in irritable bowel syndrome. Inhibition of MC function may ameliorate irritable bowel symptoms. Novel drugs with an increased potential in the control of MC function (e.g., anti-IgE antibodies, the intracellular protein tyrosine kinase inhibitor Syk) and mediator release (e.g., second generation antihistamines, proteinase-activated receptor antagonists) may be useful pharmacological tools for these common disorders.PMID: 16371078"Why some people feel the burden of stress in their gutâ€"and not for instance, in their heartâ€"can also be explained by the close communication between the brain and the gut. When the big brain consciously perceives a stressful situation, it calls on its fraternal twin through specialized cellsâ€"called mast cellsâ€"embedded in the gut's lining. These mast cells secrete a chemical called histamine, which activates the nerves controlling the gut, telling the muscles to contract. Hence, the cramps and bathroom trips so often associated with bouts of stress. " http://faculty.frostburg.edu/psyc/bristow/386/newarticle.htm


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## eric (Jul 8, 1999)

Eur J Gastroenterol Hepatol. 2006 Feb;18(2):151-158. Links Rectal afferent hypersensitivity and compliance in irritable bowel syndrome: differences between diarrhoea-predominant and constipation-predominant subgroups.Zar S, Benson MJ, Kumar D.aSt Helier Hospital, Carshalton, Surrey, UK bSt George's Hospital Medical School, London, UK.OBJECTIVES: To evaluate the differences in rectal compliance and sensory thresholds for the urge to defecate and discomfort between irritable bowel syndrome (IBS) subgroups and controls, and to correlate these parameters with rectal symptoms. METHODS: A total of 38 IBS patients [Rome II criteria; 19 diarrhoea-predominant IBS (D-IBS), 16 constipation-predominant IBS (C-IBS), three with alternating diarrhoea and constipation IBS (Alt-IBS)] and 10 controls were studied. A barostat was used to measure rectal compliance and sensory thresholds, in the 'unprepared' rectum. The thresholds for the urge to defecate and discomfort were determined using phasic rectal balloon distension in a double random staircase sequence. RESULTS: D-IBS had significantly lower rectal compliance and threshold for the urge to defecate compared with controls [4 ml/mmHg interquartile range (IQR) 3.99 versus 8.4 ml/mmHg IQR 5.69; P=0.001; 8 mmHg IQR 6 versus 20 mmHg IQR 4; P=0.003]. D-IBS also had significantly lower rectal compliance and threshold for the urge to defecate compared with the C-IBS group (5.8 ml/mmHg IQR 4.61; P=0.027; 16 mmHg IQR 12; P=0.003). The volume at the threshold for discomfort was significantly lower in D-IBS compared with controls (163 ml IQR 99.5 versus 212 ml IQR 147.25; P=0.016). The severity of abdominal pain and rectal symptoms showed a significantly negative correlation with rectal sensory thresholds. CONCLUSION: This study shows that the sensory threshold for the urge to defecate and rectal compliance is significantly lower in D-IBS compared with C-IBS and controls. The consequent inability to tolerate rectal faecal loading may account for the symptoms of the passage of frequent, small-volume stools in D-IBS patients.PMID: 16394796 Aliment Pharmacol Ther. 2006 Jan;23(2):265-74. Links Influence of acute serotonin reuptake inhibition on colonic sensorimotor function in man.Tack J, Broekaert D, Corsetti M, Fischler B, Janssens J.Department of Internal Medicine, Division of Gastroenterology, University Hospital Gasthuisberg, University of Leuven, Leuven, Belgium.Summary Background It is unclear whether decreased serotonin transporter function contributes to sensorimotor abnormalities in irritable bowel syndrome. Aim To study the influence of acute serotonin transporter inhibition on colonic sensorimotor function in man. Methods Ten healthy subjects (five men, aged 20-29 years) underwent a combined manometry/barostat study of the descending colon on two occasions. Stepwise distentions by 2 mmHg increments were performed until discomfort. Subsequently, placebo or citalopram 20 mg were administered i.v. over 20 min and distentions were repeated. Afterwards, isobaric tone measurements were performed 30 min before and 90 min after ingestion of a meal. High-amplitude propagated contractions, colonic motility index, colonic compliance, sensitivity and colonic response to a meal after placebo or citalopram were compared by t-test and two-way anova. Results Citalopram induced a significant increase in colonic motility index (5.6 +/- 0.9 to 0.8 +/- 1.9 mL*min, P < 0.005) and high-amplitude propagated contractions (32 after citalopram vs. 2 after placebo, P < 0.05), which were associated with abdominal cramping. Administration of citalopram increased colonic compliance (10.3 +/- 1.5 vs. 14.5 +/- 2.2 mL/mmHg, P < 0.01) and inhibited colonic response to a meal (volume decrease 48 +/- 12 vs. 16 +/- 12 mL, P < 0.01). Conclusions Acute serotonin transporter inhibition in man increases colonic phasic contractility and the occurrence of high-amplitude propagated contractions, increases colonic compliance and suppresses the colonic tonic response to a meal. These data suggest that both release and elimination of 5-hydroxytryptamine by serotonin transporter are involved in the control of colonic motility in man.PMID: 16393306


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