# Narcotics and IBS-D (percocet/codeine/oxycodone)



## JeffnSD (Sep 7, 2007)

Hey All,I've been suffering with chronic IBS-D now for nearly two years. Its been so debilitating I haven't been able to work or even go out. I've had all the tests (everything is always normal) and have even tried the psychiatrist route with no help. I'm on Klonopin which helps with nerves but not the diarrhea at all and have been on a variety of anti-depressants which dont help at all.I'm at a loss here so I'm grasping at anything. I heard that narcotics slow the gut motility and some have had success with Tylenol #3 (with codeine) and want to know if anyone has had any luck with slowing/stopping the diarrhea with codeine, morphine, oxycodone or Percocet or whatever else I might not know. All my doctors are baffled too to I'm sure they're open to anything too. I'm sick of going to the doctor and nothing working!!Thanks for your advice.ps: I've also started taking L-Glutamine and Peppermint Oil capsules cause I heard that helps. Anyone tried those?JeffnSD


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## Kathleen M. (Nov 16, 1999)

Narcotics (anything derived from opium) tends to slow the gut.Imodium (OTC) and Lomotil (prescription) have the gut slowing activity without the pain killing or mind numbing effects of narcotic pain killers.The problem with long term use of narcotics to control diarrhea is that some people will get Narcotic Bowel Syndrome which is more painful than IBS and it is hard to get off the narcotics to break the cycle of them causing additional abdominal pain.Have you tried Imodium or Lomotil?They don't hit the pain receptors the same way as the narcotics so usually aren't a risk for narcotic bowel syndrome.You might look at Calcium Carbonate (LNAPE's info OTC) or Questran (prescription) to control the diarrhea before risking the narcotics. Questran is in the list of things in a review of medications for IBS in the New England Journal of Medicine back about 2000 or 2001 I believe in June or July if they have a problem trying that and need a source of information about it.K.


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## code9 (Dec 3, 2007)

Yes, Kathleen is right. Codeine works, 120mg + Lomotil works for me. I've taken hydrocodone and morphine and just plain old codeine.From what I have found, after using Codeine for many years, is that I believe it affects my memory. Long term memory specific to the times I was on it. Also, it will be damn hard for you to get codeine that doesn't have tylenol or ibuprofen. I had a prescription for a while and had a hard time find a pharmacy that could even fill it. Tylenol #3s have a lot of tylenol for not much codeine. I think they tend to hurt the gut as much as they help. Depending on your genetics, it's possible to become addicted as well. (Some people have no problem with opiates while others will be nearly hopelessly addicted, it's not something doctors like to chance. I don't really agree with them or the DEA on that, but such is the country we live in, or at least I live in anyway.)They do work, but they are far from ideal, I gained weight, had memory problems, and they would only work for 8-10 hours, as soon as they wear off the D is back. For me Lomotil and Zofran work much better, all things considered. If lomotil doesn't work on it's own, opiates also have a tranquilizing/calming effect, but you can get that from librax or klonopin, or even valium.I have read Lomotil has a much less powerful effect on the brain than other opiates, although I think you slowly gain tolerance to it, like you would an opiate. But I've taken it for years.Overall, considering how hard it will be to get an opiate that's not full of a gut harming adulterant (tylenol, ibuprofen), I would try Lomotil first, see if you can stop it with that, maybe add one of the new drugs. I'm trying to move to lotronex if possible


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## JeffnSD (Sep 7, 2007)

Yes....I use Imodium all the time. Its the only thing that stops me up...but I've noticed I'm growing immune to it effectiveness. I've also tried both Lomotil and Questran and they did nothing for me.I've been doing that Calcium Carbonate thing for quite awhile too. It might somewhat form the stool cause my diarrhea is never water but more of a sludge or loosely formed. But I question whether the Calcium is doing it for me. I even switched from the Caltrate brand that has the evil magnesium in it to a pure Calcium carbonate 1000mg gelcap and take that after every meal.I'm still at a loss here. I asked the doctors about the narcotics and none of them would even consider treating me with that. Right now I'm back to the Klonopin and slowing increasing that to 3x a day and just started the anti-depressant desipramine. But so far no results. My GI doctor, which is apparently one of the best, is now considering me a candidate for Lotronox. The one that killed all those women and the FDA pulled it but recently put it back on the market for only a select few doctors to prescribe. I'm just hesitant to even go there. That frightens me.


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## Kathleen M. (Nov 16, 1999)

There was a handful of women, and it isn't even clear if Lotronex was the cause. Some people get Ischemic Colitis anyway (and it has been associated with a lot of medications over the years, some that are available over the counter) and there is some thought it may trigger it if you are prone to it. Just some people prone to it anyway may show up as potentially having IBS (and it was also being prescribed to people with IBS-C because doctors weren't paying attention to the "only for diarrhea" thing, which probably didn't help).In any case the percentage of people that get IC taking Lotronex is extremely low. If you catch it early it is a very treatable condition. First sign of bloodiness in the stool stop taking it and go to the doctor or ER to be checked.It isn't significantly more lethal than anything else. Lots of drugs everyone thinks are "safe" kill way more people. They didn't pull it because it is too deadly to be on the market (and it was pulled by the company voluntarily) They pulled it because the only thing every IBSer ever needs to be 100% better is to eat more fiber and anything riskier than eating a bowl of bran flakes in the morning was an unacceptable risk. A lot of people from this board were involved in educating the FDA that IBS is, in fact, a serious disease and the only way they could testify before them was in diapers because they didn't have the one drug that ever worked.The patient response to the removal of the drug was unprecedented because IBS is serious and there needs to be treatment and not having any treatment at all specifically for IBS was something the patients weren't going to put up with anymore.All treatments for all diseases have risks (and almost all of them can kill people). IBS was being held to a completely different standard of no risk at all is allowed because too many people want to believe the lie we'd all be right as rain if we'd just eat some fiber.Honestly, if Lotronex was treating acne it would have never been pulled for the very small number of deaths, it would have just gotten a rewrite of the warnings with a strong see your doctor if in the instructions..K.


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## celestin (May 20, 2004)

Kathleen M. said:


> A lot of people from this board were involved in educating the FDA that IBS is, in fact, a serious disease


Really? When, how, officially? Could you give some details?Thanks..


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## Kathleen M. (Nov 16, 1999)

If you look at the Diarrhea specific medication part of the board: http://www.ibsgroup.org/forums/index.php?showforum=30Back around 2001-2002 you will find a lot of the discussion going on back then about the voluntary withdrawl and the fight to get it back on the market.Jeff, the owner of the board, also started the Lotronex Action Group. Here is the webpage with that with information about the struggle.http://www.geocities.com/lotronexactiongroup/mission.htmlThe one thing I remember most was when the FDA said how many complaint letters they got. Usually if something is withdrawn (either by the FDA or by the company that makes it) they get a handful of letters of complaing. However, usually there are several other treatments people can try. With the removal of Lotronex they got over a thousand which was like 1% of all people who had used the drug. K.


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## celestin (May 20, 2004)

Thanks, but this is mainly related to Lotronex. I had understood IBS-D and FDA.


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## code9 (Dec 3, 2007)

JeffnSD,Knowing what I do now, I would try Lotronex. (Still waiting on mine). Or you could try Zofran and see if it works, it would be an indicator I believe, since they work in a similar manner, only I'm told Lotronex is much better.You'll basically never get narcotics out of a GI. I mean, sure if you visited 300 of them, one might consider it. But the general rule is that they'll never give you narcotics. One did for me for 6mos, un-adulterated codeine. I printed out reams of info on codeine, ibs and diarrhea and got into a shouting match with him over whether he should even read the info or not. It is basically never going to happen long term.There are other sources of opiates, if all else fails, pain clinics, online doctors/pharmacies in the US. (Although all the ones I know of have been shut down.) And these places are not particularly cheap or reliable, they get shut down.How much lomotil did you try in the past? I take up to 9,10,11 a day at times, it's been cut down because the Zofran helps a lot, but it's a low dose, I still use lomotil to supplement it. I think you can basically take lomotil till the D stops. It's probably as close as you will get to an opiate, legally.But given all the stuff I've tried, i'd go for the lotronex. I'd be willing to bet acetaminophen has killed more people that lotronex ever will. I mean that seriously, i'd be willing to bet money on it, a lot. Anyway, if you can get lotronex, I would try, just follow the instructions, Kathleen laid out all the things to look out for. Most of the people who got ill, from what I have read, continued to take it long past when they should have stopped.There's an old saying, the only difference between a poison and a medicine is dosage. And that applies to pretty much any medicine, especially for IBS when they are throwing in atropine, and hysocyamine, things that come from the deadly nightshade, for instance. If it doesn't work, or seems to be making you ill, do what Kathleen says, stop and go to the ER.If you are still worried, I've been taking Zofran for a quite a while now, it doesn't last long, (6 hours) but it is fairly cheap, and would probably be an indicator, since it is a 5-ht3 antagonist as well. But it has stopped the D for me when combined with lomotil and klonopin. (Not sure the Klonopin plays much more than an ancillary role, there's no doubt in my mind : IBS causes anxiety; Anxiety does not cause IBS.)


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## Kathleen M. (Nov 16, 1999)

The conversations with FDA were primarily about Lotronex, but the point was that IBS requires treatment http://www.geocities.com/zelnormactiongroup/ is the sister group for Zelnorm.I'm not sure what else the question you are asking has to do about.This group, especially Jeff has worked hard to educate those that make the decisions about what medications are allowed on the market (the FDA in the USA) that IBS deserves to be treated and not just blown off as something so insignificant that there should not be any drugs at all ever available for it.http://health.groups.yahoo.com/group/ibspag/ is the yahoo group (they were combined into the IBS patient action group awhile go) is still a resource people can use.If this isn't answering your question (people here are involved with the FDA about decisions concerning medication, which to me is in part educating them that fiber alone is not nearly enough) can you tell me more about what you are looking for.K.


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## celestin (May 20, 2004)

Kathleen M. said:


> can you tell me more about what you are looking for.


First of all I am looking for a good treatment..







Actually it was more a surprise than a question. I did not know that patients (groups of) had contacts with the FDA at a high level. Good thing of course.But if it is so, why are the gastroenterologists so negative with IBS/D ? In my country with an IBSD sufferer they do the usual tests (usually forgetting the Giardia...) and after it's done. When you come back -still complaining- they look at you 2 minutes and they give anything. And as soon as you are out they start laughing with the nurse (or the student) : 'hé hé again one of those patients with psychological problems..". And Belgium is supposed to have a (very?) good level in medicine.Do you know how many gastroenterologists read -regularly- this board?And yes, fiber alone is not nearly enough...!!!Thanks


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## eric (Jul 8, 1999)

FYINarcotic Bowel article in GI & Hepatology News NEWhttp://www.gastro.org/user-assets/document.../GIHEP_0108.pdfCelestin"Fibromyalgia and irritable bowel syndrome: How real must they be?http://www.aboutibs.org/site/news-events/n...commentary#Realhttp://www.ibsgroup.org/forums/index.php?showtopic=92806http://www.aboutibs.org/site/about-iffgd/advocacy/http://www.aboutibs.org/site/learning-center/video-corner/http://www.med.unc.edu/wrkunits/2depts/med...n_materials.htmhttp://hopkins-gi.nts.jhu.edu/pages/latin/...3&lang_id=1


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## Kathleen M. (Nov 16, 1999)

Unfortunately even with our efforts (which took finding the right people to talk to who will listen) and the efforts of other organizations (like the IFFGD http://www.iffgd.org and the doctors on the Rome Committee, which is a group of researchers who are experts in Functional GI disease) a lot of doctors are at least 10-30 years behind in their understanding of IBS and other functional GI diseases.Hopefully more doctors will finally see the light, but it is a slow process and the "IBS is no big deal" idea can be very hard to change. I think why the patients got the attention of the FDA here in the USA is that there were so many people and a lot of hard work by those who were ready to fight for the cause that they really couldn't ignore us anymore.Unfortunately it seems doctors aren't even keeping up well with the medical literature (some are, a lot are not) much less reading boards for patients.K.


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## code9 (Dec 3, 2007)

Celestin, They do the same thing in this country, believe me. It's very hard to get IBS-D treatment, there just isn't that much they can do really. Unfortunately. I've mentioned it several times before, but Michael Gershon's book, "The Second Brain", holds quite a bit of information about IBS and the malfunction of the large intestine.Eric,I have taken codeine and various opiates for years, every day for years. I have never experienced narcotic bowel. The point is to maintain regular bowel function. The amount of opiates it would take to cause severe long-term constipation would be quite large, and as far as I know, is seen amongst addicts attempting to achieve a high in the brain, not normality in the gut.


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## Kathleen M. (Nov 16, 1999)

The problem with narcotic bowel isn't that you take doses so high you severely constipate yourself on some sort of long term, post drug time frame.The problem is that for SOME people (not every single person, but more than just a few) the narcotics after some period of continued use change something in the nerves of the GI tract so that you have much more pain, and much more difficult to control pain than the IBS-pain you had before you started taking narcotics regularly.Now some people will never get this, but you don't have to be an addict on extreme doses for decades. It happens to some people in the sorts of doses and time frames you see after an injury. The problem is then they are given more narcotics for the additional pain which just increases the problem and it escalates. Once a doctor finally realizes what is going on it takes time and the right treatment to break the cycle of sensitization and get someone back to the levels of pain they would have (and treat that pain) if they had never taken narcotics.The pain sensitization problem is why they sometimes don't even want to use them "just" for severe diarrhea unless there is no other way to treat it. Making the problem much worse in the long run isn't helpful.Hopefully you are one of the ones that this never happens to. From what I've heard it can be extremely painful.K.


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## JeffnSD (Sep 7, 2007)

After reading all the posts in response to my question...the fact comes down it all depends on your doctor/GI specialist or whomever to write a prescription for you if they understand or not. I saw a GI doctor for 7 months and he basically shoved me to a psychiatrist and then he sent me back to a GI doctor. I followed up with my old GI doctor (since I had this long relationship with him...and he basically said there isn't anything he can do anymore). Just shows you he doesn't understand or keeps up to date with the latest and how debilitating it is. So onto the next doctor.I checked with my insurance and I'm not even covered under Lotronox since its a brand name unless I want to pay hundreds of dollars. Just isn't an option for me.I think right now I will do my best and revisit the Lomotil and maybe try higher quantities and toggle back and forth between that and Imodium. (My old GI doctor said to take 1 lomotil a day) Now I'm understading what a moron he was so maybe a higher dose can help. I recently read about Motofen (which is apparently now out of stock until 1/09) but I live in a major city and called a few pharmacies and they still have it on their shelf. So I might attempt that and see if I can manage. I do agree with the previous poster that anxiety doesn't cause IBS...IBS causes anxiety. So the Klonopin I take helps ease my worries..but it doesn't help the diarrhea, urgency or knowing where every bathroom is or the fact I rarely leave me house. Its sad when you're a single 37 year old guy who cant even go on a date. How do you explain that to a potential mate? Hello...baggage and their onto the next one. LOLThanks for everyones comments!!!JeffnSD


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## eric (Jul 8, 1999)

IN IBS there is pain because of a lowered threshold to pain from specific cells in the gut. Narcotics also effect those receptors and lower the pain even further, it is a big problem although as mentioned not every single person perhaps, but even some people may go from discomfort to mild pain or to sever pain on long term narcotics on top of the pain already generated with IBS."IBS causes anxiety; Anxiety does not cause IBS"Its extremely important here to understand this more fully which some of the posts above do and although just anxiety by itself if you don't have IBS will not cause IBS anxiety on top of IBS is a big part of the picture in triggering symptoms. Its important to step back and look at this from the bigger picture as well as the fine details. Anxiety can trigger the hpa axis and the fight or flight and directly effect mast cells in the gut that can contribute to the symptoms. They are an extremely important area of IBS research as well as enterochromaffin cells. The brain and the gut are in constant bidirectional communication with each other constantly. This is really important.This helps explains things"Brain-gut - The brain plays a role as well. The brain and the gut are connected. Thinking and feeling can have affects, influencing release of proteins that interact with the nervous system (neuropeptides), which can affect motility, secretion, blood flow, and inflammation. Stress may influence inflammatory pathways causing a dysregulation that can lead to emotional conditions and more stress - a vicious cycle. It is not a question as to whether this cycle begins in the gut or in the brain. The problem is that both systems are effected concurrently thus producing a disturbance of the regulation between the brain and gut; a "vicious cycle" with no beginning or end. Understanding this will open the door to more specific treatments. We can see examples of brain-gut interactions by looking at post-infectious IBS (PI-IBS) or dyspepsia. A study done after a salmonella infection outbreak showed that 10-15% of patients continued with their symptoms of either dyspepsia or IBS after the initial infection subsided. Some recent studies show that this is associated with greater levels of immune cell activity. In IBS, the subgroup of patients with diarrhea as the predominant bowel symptom is the group where more of this inflammatory response is seen; there is also increased psychologic distress occurring at the time of the initial infection, which may be enabling the post-infectious response. In the gut we see infection followed by an inflammatory response, altered motility, and increased sensitivity. But these factors alone are not enough - the brain has a role in regulating these factors. If there is psychological distress around the time of the initial infection, it can result in the expression of the post-infectious symptoms. Thus, the brain and the gut are interacting so with this disorder the brain can influence the inflammation in the bowel while the bowel inflammation can produce psychosocial - emotional and social - distress. Similarly the pain experienced may occur more when there is psychological distress. Both factors are predictive of post-infectious IBS. Since post-infectious IBS has inflammation in the intestine, it challenges the concept of functional vs. structural, since there are features here of both. "http://www.ibsgroup.org/forums/index.php?showtopic=92806Both the brain and gut brain are operational to cause the symptoms of IBS. The systems that are connected to the mast cells and enterochromaffin cells and the cells themselves are very important players in the puzzle of IBS both of which can basically cause all the symptoms of IBS although it is not all completely and fully understood yet.A persons emotions effect their gut function and gut function effects peoples emotions. But its a lot more complicated.


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## code9 (Dec 3, 2007)

JeffsND,Yes, 1 lomotil will probably not be enough. I think the max recommended daily dose is 8, I'd talk to a different doctor. You might try to find another source of Lotronex, but I'm not sure how you might get it w/o insurance. I'm still not positive mine will cover it. But you might try Zofran, it just went generic, it is normally for nausea, chemotherapy nausea specifically, but you could probably get it if you tried. It's considerably cheaper, and it works better than codeine for me. Still not perfect, but it's alright.How much Klonopin do you take? If you are still that anxious, you may need to up the dose. Valium was incredibly effective for anxiety in me, but it made me too tired, so I am sticking with Klonopin. Of course, when I feel well, anxiety disappears completely. It's all related to how I feel in the gut. If I feel fine in the gut, a situation that would normally be filled with anxiety is completely fine. I know the brain and gut are in constant communication, but it seems to me that the gut is causing anxiety. A very real fear of defecating ones self will probably cause anxiety in anyone, and probably should. Anxiety when you feel well is a problem. Anxiety when you are anxious about something completely normal is not.


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## code9 (Dec 3, 2007)

Kathleen and Eric,Are you serious in that, say, 120mg of Codeine or 12mg of Morphine for just a few weeks, even if it doesn't cause constipation, can in some people severely lower their pain threshold? I have never heard of this. I've heard of narcotic bowel in long term addicts or high doses of opiates, but never heard of any cases on such a low dose of opiates. How often does this occur? Is it a valid reason for not using Codeine?In my experience, Codeine has just as much gut slowing effect has Morphine or other more powerful opiates. So, a low dose of Codeine can be very useful in the treatment of IBS. I always assumed it was the fear of addicts running around and fear of losing their license to the DEA that stopped doctors from prescribing this.I'd be interested to know if there is any real threat from narcotic bowel at these doses in IBS.I'd also be interested to see some information showing that opiates affect pain tolerance in relation to 5-HT3 receptors or whatever other receptors may be involved in IBS.Thanks.


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## Kathleen M. (Nov 16, 1999)

There is some recent articles in the medical literature, prior to the last year or so there wasn't a lot written about it in detail.http://www.ibsgroup.org/forums/index.php?s...=narcotic+bowel is one that I posted about.It can happen to people who are not addicts using 10X what anyone else would use for long periods of time. That sort of abuse of drugs can cause all sorts of problemsBut like _any_ side effect it only happens to some people.You may be one of the ones that would never have a problem and won't get it from the doses you are taking. High short term doses (like after some surgeries/injuries) or chronic uses for IBS/functional pain can trigger this in some people. This is at doses your doctor would prescribe you.I'm not sure what the incidence is, but it seems higher than most people believe in people taking pain medications at doses that are typically prescribed.That is one of the reasons it is a "last resort" sort of treatment rather than something you try first.However, you may be perfectly safe at the doses you take, but if you notice escalating pain it may be a sign you need to do something different, not just take stronger narcotics or a higher dose.K.


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## JeffnSD (Sep 7, 2007)

Hey Code9,The funny thing is I dont feel anxious at all. All the docs just assume I'm anxious which is causing the diarrhea. Sure...if I'm having a bad day and I'm driving somewhere where I know bathrooms aren't easily accessible..then I rush or speed to my destination. Once I'm there...I"m ok usually. I'm taking .5mg of Klonopin 3 times a day now. Cant say i see any difference really.I understand about the brain-gut connection. That's why I've tried so many anti-depressants but I'm so sensitive to these drugs I feel the side effects bad and cant get through them. I'm right now on Norpramin which I'm tolerating well, but I still see no difference in my bowel habits. the only side effects I see so far are sexual ones (which isn't good for a single guy which causes anxiety more if you cant perform) and some mild chest heart palpitations. They say constipation is a side effect which I welcome...but eventually most side effects wear off so I'll be back to square 1.Anyways...I'll look into the Zofran med. Will probably ask for a larger dose of Lomotil and continue using Imodium and inquire about Motofen. I just dont see the point in the anti-depressant or even the klonopin if the imodium or lomotil is doing the job ya know? Cause if I dont have an urge to go...then I'm fine.I'm just so sick of dealing with this and trying drug after drug. I'm losing what's left of my youth!!! and I'm not even young anymore. haha.


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## code9 (Dec 3, 2007)

I know what you mean, I've been sick since I was 18, so it's been a long slog, several years of not working, being flat broke, with nowhere to really live, now I feel like I'm hanging by a thread. It really makes me wish I could mirror this pain onto someone who says this illness isn't important enough that we should be able to get the medicine that will help us.If public citizen or the top people at the FDA knew they had to go through this for decades, they'd be pretty quick to authorize things I think. We wouldn't be sitting around waiting for approvals, or have people telling us what risks we should be allowed to take.


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## eric (Jul 8, 1999)

FYI and this might take a bitBy the way I ask Dr Drossman who worte the Narcotic bowel article and he said that is was relatively common and I think more common then some realize. Can't say in your exact case though.There is the fight or flight which will go off faster then you can think about it.http://www.ahealthyme.com/article/primer/101186767Look up mast cells and IBS and ec or enterochromaffin cells, the ec cells store the gut serotonin.This Dr is an expert on IBS, the enteric nervous system and food allergies, he is international recognized and has done a lot of work in understanding IBS.FYI"You have two brains: one in your head and another in your gut. Dr. Jackie D. Wood is a renowned physiologist at The Ohio State University. He calls the second brain, "the-little-brain-in-the-gut." This enteric nervous system is part of the autonomic nervous system and contains over one hundred million neurons, which is as many as are in the spinal cord. This complex network of nerves lines the walls of the digestive tract form the esophagus all the way down to the colon. This little brain in the gut is connected to the big brain by the vagus nerves, bundles of nerve fibers running from the GI tract to the head. All neurotransmitters, such as serotonin that are found in the brain are also present in the gut.Dr Wood has discovered that this little-brain-in-the-gut has programs that are designed for our protection and which are very much like computer programs. They respond to perceived threats in the same way that the limbic system or the emotional brain does. So the threat of a gastrointestinal infection can activate the program that increases gut contractions in order to get rid of the infection. The symptoms are abdominal cramping and diarrhea. Dr. Wood has determined that a type of cell found in the body and the gut, called the mast cell, is a key to understanding the connection of the big brain in the head with the little-brain-in-the-gut. Mast cells are involved in defense of the body. In response to certain threats or triggers, such as pollen or infection, mast cells release chemicals, such as histamine, that help to fight off the invader. Histamine is one of the chemicals that causes the symptoms of an allergy or a cold. When an infection of the gut occurs, such as food poisoning or gastroenteritis, the mast cells of the gut release histamine. The little-brain-in-the-gut interprets the mast cell signal of histamine release as a threat and calls up a protective program designed to remove the threat at the expense of symptoms: abdominal pain and diarrhea. The brain to mast cell connection has a direct clinical relevance for irritable bowel syndrome and other functional gastrointestinal syndromes. It implies a mechanism for linking allostasis and the good stress response to irritable states (e.g., abdominal pain and diarrhea) of the gut.* Mast cells can be activated to release histamine in response to perceived psychological stress, whether the stressor or trigger is consciously perceived or not. So the end result is the same as if an infection activated the program in the-little-brain-in-the-gut: abdominal pain and diarrhea."*http://www.parkviewpub.com/nuggets/n5.html Then go back and read the 2007 report againIts the altered serotonin signaling that they are seeing in regards to the d and c and d/c, but its connected to the entire body and the symptoms. Serotonin is also the neurotramsitter that sends signal of sensation to the brain and is involed in sending the pain signalsaltered serotonin signaling and ibs compilationhttp://www.ibsgroup.org/forums/index.php?showtopic=80198This is one of the top PI IBS experts if not the top guy.Neurogastroenterol Motil. 2007 Aug;19 Suppl 2:25-31. LinksRecent advances in understanding the role of serotonin in gastrointestinal motility in functional bowel disorders: alterations in 5-HT signalling and metabolism in human disease.Spiller R.Professor of Gastroenterology, Wolfson Digestive Diseases Centre, Nottingham, UK. [email protected] (5-hydroxytryptamine, 5-HT) is present in abundance within the gut, most stored in enterochromaffin cell granules. It is released by a range of stimuli, most potently by mucosal stroking. Released 5-HT stimulates local enteric nervous reflexes to initiate secretion and propulsive motility. It also acts on vagal afferents altering motility and in large amounts induces nausea. Rapid reuptake by a specific transporter (serotonin transporter, SERT) limits its diffusion and actions. *Abnormally increased 5-HT is found in a range of gastrointestinal disorders including chemotherapy-induced nausea and vomiting, carcinoid syndrome, coeliac disease, inflammatory bowel disease and irritable bowel syndrome (IBS) with diarrhoea (IBS-D), especially that developing following enteric infection. Impaired SERT has been described in IBS-D and might account for some of the increase in mucosal 5-HT availability. 5-HT(3) receptor antagonists inhibit chemotherapy-induced nausea and diarrhoea associated with both carcinoid syndrome and IBS. While IBS-D is associated with increased 5-HT postprandially, IBS with constipation (IBS-C) is associated with impaired 5-HT response and responds to 5-HT(4) agonists such as Prucalopride and 5-HT(4) partial agonists such as Tegaserod.*PMID: 1762008J Pediatr Gastroenterol Nutr. 2007 Dec;45 Suppl 2:S115-9. LinksSerotonin, inflammation, and IBS: fitting the jigsaw together?Spiller R.Department of Gastroenterology, Wolfson Digestive Diseases Centre, Nottingham, UK. [email protected] diarrhoea is a frequent indication for gastroenterologic referral, and after full investigation the most common final diagnosis is irritable bowel syndrome (IBS). Some patients with IBS describe an acute onset of symptoms following infective gastroenteritis. Postinfective IBS affects 7% to 31% of individuals infected, and appears to be a nonspecific response to injury which has been reported following Salmonella-, Campylobacter-, and Shigella-related IBS. The strongest risk factor for developing postinfective IBS is severity of the initial diarrhoea illness, but toxigenicity of the infected bacteria, age <60 years, and female sex also are important risk factors. Adverse life events, hypochondriasis, and depression are also important, as is increased enteroendocrine cell and lymphocyte numbers in rectal biopsies. *Postinfective IBS and IBS with diarrhoea without an infectious onset both show increased postprandial release of serotonin, whilst constipated patients show a depressed release. Several studies suggest impairment of the serotonin transporter in IBS, which in animal studies has been shown to occur following a range of inflammatory insults. Clinical conditions with an inflammatory basis, such as coeliac and Crohn disease, also are characterised by excess postprandial serotonin release. Several studies report evidence of low-grade inflammation in IBS with diarrhoea. However, reliable markers of low-grade inflammation that may predict response to serotonin antagonists or other anti-inflammatory agents remain a goal for future research.*PMID: 18185071Those two cells can explain a lot of IBS symptoms as well as some non gi symptoms associated with IBS, although as we know the whole picture is not figured out yet. It is all so complex.Part of the inflammation seen in post infectious IBS has to do with stress at the time of infection and mast cells, they are connected to the stress system and also help fight infection and are involved in homeostasis. So it can contribute to the development of IBS in PI IBS.


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## code9 (Dec 3, 2007)

Eric,I don't want to get into a "thing" about it, I mean, we all know that anxiety in the head can cause GI disruption. But it's acute, in normal people, and in myself. It's short lived, and you can recognize it.I don't think it's the same problem that happens at 5am, or just sitting at my desk and bam, feel sick. I think that is the reverse, the gut sending bad signals up to the brain. I've read about the mast cells, inflammation, serotonin and histamine. It seems to me that the neurotransmitters and receivers are the problem.If I take an SSRI, I will have virtually unstoppable D within a matter of days. What should be relieving depression and anxiety has a terrible effect on the neurotransmitter serotonin. Other drugs, like wellbutrin, do not affect my stomach but make anxiety much, much worse, because they do not change serotonin.Zofran, which specifically blocks serotonin doesn't "fix" me enough to feel normal, but it does stop D on a nearly permanent basis. There's still urgency and various other problems.But all my trial and error, in myself, seems to point to a malfunction in the gut itself, sending signals to the brain, not vice-versa. I was on a large dose of valium, 30-40mg a day for a month, anxiety was gone, but I still felt sick (as well as exhausted all the time.)Relieving stress and anxiety will probably help in those acute moments, but I can guarantee you it's not going to help me on a daily long-term basis. There is something else very wrong.Like I said, I don't want to get into a thing, but when people start saying it's the head not the gut, I think they are perpetuating a stereotype that has bogged down research and treatment for everyone. I'm not saying ignore facts, but I believe the fact that the brain can signal the gut is being over-emphasized. Most doctors know nothing of the enteric nervous system, or how it communicates with the brain. They assume anxiety and depression cause illness.I know in myself, when I wake up, and my stomach feels good, I feel good mentally. When it feels sick, I feel sick mentally. And all my trial and error points to that causation, not vice versa. It's the overemphasis that begins to annoy me.EDIT : As an addendum, I've had the 5HIAA test several times, it has never shown elevated serotonin. But elevating it with an SSRI or SNRI causes me extreme discomfort.


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## Kathleen M. (Nov 16, 1999)

Typically SSRI's are somewhat prone to cause diarrhea as a side effect. Tricyclics tend to cause constipation as a side effect. (both increase serotonin in certain locations, but by different mechanisms)The nerves in the gut use all the same neurotransmitters as the ones in the brain, it depends on how they twig them. Now some people get constipated on SSRI, and some get diarrhea from tricyclics because the responses are that idiosyncratic, but the usual pattern seems to be SSRI's tend to speed up the gut, if they effect speed, and Tricyclics slow it down, if they effect speed.Antidepressants are usually prescribed for pain more than speed changes, but they can effect speed in some people.Almost all drugs either block or enhance a specific receptor for a naturally occurring compound. Zofran primarily hits a different serotonin receptor than SSRI's (although there can be cross-reactions so sometimes things hit more than one). The amount of serotonin in your blood usually isn't the main concern for SSRI's it is how much is in between specific neurons. SSRI's increase that by blocking the serotonin from a recycling receptor that puts it back in the cell.


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## code9 (Dec 3, 2007)

Yes, I agree, I was just responding to Eric's information about increased serotonin levels and the brain/gut reaction. But you are right, that makes sense to me, I guess the real question is : What is the source of the problem?I believe it could be the 5-HT3 receptors themselves, rather than 5-HT3 just being collateral damage in a bigger mast cell reaction to stress. For instance, it seems possible to me that a serious infection, or over use of NSAIDs could damage the nerves themselves?I just think the ideas he is putting forth focus to much on the brain, not enough on something physically being broken in the intestines. As Gershon demonstrated in many different ways, the ultimate source of the problem appears to be the intestines. Even when they are fully separated from the brain they can still function normally or malfunction. He points to alzheimer's affecting the nerves in the gut and causing these functional diseases as well as damage in the brain. He also showed that you can completely remove the intestines, suspend them in an organ bath and change their function to simulate IBS with the application of neurotransmitters and neurotransmitter blockers.Although he says it's hard to figure these things out, because by the time someone dies, there is usually too much damage to make a definitive conclusion about the source of the problem. I guess if I die from head trauma in a car accident or something similar, I should donate my intestines for testing, perhaps they can figure out why they have pained me for so long. =)


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## Kathleen M. (Nov 16, 1999)

I don't think it is the "gut" itself that is broken, but the nerves controlling the gut (which is not the same as the brain).The Enteric Nervous system is diffuse, but complex.There were studies quite awhile ago that shows that inflammation of the gut wall can damage the nerves in the gut wall. That is the mechanism believe to be why GI infections (and sometimes inflammatory bowel disease) trigger IBS/Functional Bowel problems.I don't think anything suddenly changes your DNA so you now have different receptors than you had before IBS (and protiens are turned over so often that even if something got in your body that could selectively kill every receptor of a specific type you'd regenerate new undamaged ones)That IBS is a disruption of the nerves controlling/sensing the gut is why most drugs for IBS effect nerves. They aren't effecting the muscles or the lining as those work just fine. Just like your engine may be fine, it won't run right if the sensors telling the computer are mis-reading things or if the computer has died, that is how I see IBS. The "engine"/intestines aren't broken but the sensory and control aspects are what is broken (either in the ENS or in the CNS, the brain).Since the ENS and the CNS talk to each other you can effect the ENS either directly (like with drugs) or indirectly (by the feedback it gets from the brain).Doesn't matter much which you use to normalize its function, IMO. Whatever works for someone is what they should do.I was shocked and amazed that the CBT study I did (cognitive behavioral therapy) did so much for my IBS. I really wanted to be in the antidepressant side of the study because I like the direct route rather than the indirect one, but you get put where you are put and so I made the best of it.Looking back I see how it is like when I cut my finger deep enough I severed the nerve. For awhile it was numb, but when the nerve healed it went nuts. Everything that touched the finger hurt like hell for about 72 hours. Now for that the feedback from the brain/rest of the nervous system was automatic (there were other fingers right there for it to check in with) and the nerves "learned" what was appropriate and what wasn't.Now if you translate that to damaged ENS nerves. I just didn't have the right feedback to get the healed/remaining nerves to behave properly so they did whatever they were doing. Now through the CBT I think I figured out how to get my brain to send the signals the ENS needed so it could function better. What I was doing before either wasn't doing anything, or may have been saying "good job, keep it up, make more pain, more more more" rather than "sit down and shut up there isn't any reason to be going off right now"With the finger it happened automatically. With the gut I needed help to get things to be better.So, anyway. I see how the indirect can work (from direct experience) AND I don't believe it was in anyway "all in my head" because in some part my brain was part of the dysfunction.I don't think my healing is any less valid because I learned to do it by the indirect method rather than always needing a medication to force things to behave regardless of anything that would encourage them to misbehave.


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## code9 (Dec 3, 2007)

Well, it's clear that pain is felt in the brain. I wouldn't disagree with that, training your brain to re-interpret signals from the body is fine, if it works for you.But that doesn't negate the gut being broken. And by gut, I mean the enteric nervous system. There is nerve damage that is irreversible, I could find a million examples of that which do not require a change in DNA.It's quite possible the receptors in the gut, the nerves, have been damaged and are overly sensitive. The research seems to point there, as do the drugs that normalize the condition. Regeneration of nerves is a sketchy subject, cut your finger off and reattach it and you may or may not ever regain 100% mobility in it. Who knows how that compares to damaged nerves in the gut.I think we are essentially agreeing, if you want to separate the ENS from the gut as a whole, it's just a matter of terminology. The gut cannot and will not function without the ENS. It can, however, function completely normally without any CNS input at all.Again, I am primarily responding to Eric's posts that the CNS is just as guilty as the ENS, it is clearly not. ENS is the problem, at least in a specific sub-type of IBS. And again, we're back to terminology, I wasn't separating nerves from the physical being of the gut, it's all one thing, each is inoperable without the other.But I think it stands to reason that if you removed the CNS completely, and IBS symptoms persist, that the problem is unrelated to the CNS, and cannot be treated with CNS affecting drugs. (i.e. reducing anxiety and stress in the CNS does not cure IBS, it may improve acute situations, but does not fix the hypersensitivity of the ENS.)What you have described in regards to your CNS/ENS relationship is a low-level (sub-concious?) way you process the incorrect signals from the ENS to the CNS. Just as someone who might be able to not feel pain at will. But how do you know if anything is possibly wrong with your 5-HT3 receptors? Have you ever taken a 5-HT3 antagonist? That would have shown a dramatic change if so.What I'm trying to say, is we all accept there are a myriad of problems that can result in IBS. One of them being a nerve disorder (which you are not necessarily born with, there a plenty that develop over a lifetime, again, no DNA change required to develop a nervous system condition)... yours may be a misinterpretation of signals causing CNS discomfort, but how does that repair your ENS?Your experience would seem to say the CNS is required to send bad signals to the ENS in order for IBS to occur, but this is not the case, the ENS can malfunction completely on it's own, without any input from the CNS. You may be saying that CNS malfunction was the cause of your IBS, which I'm not going to try to refute, it's a possibility. BUT, just because you retrained your CNS to ignore ENS signals, and not go into fight or flight mode (I can do that with a big enough dose of valium and opiates) it still doesn't change the function of a broken ENS.I guess the question is, if the CNS is responsible in your case, do your 5-HT3 receptors show the same reaction to a 5-HT3 antagonist as people who are helped by them.If they do, then you are saying the problem is CNS based, and can be cured by treating the CNS and ignoring the ENS.If they don't react the same way, we are talking about two different types of IBS.There is also the possibility that you have retrained your ENS to respond different without the use of medication, which I think would be extremely rare, if not impossible?There is also the possibility of pure coincidence, IBS is known to disappear in some people, there is the possibility your body recovered around the same time you did the CBT.


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## Kathleen M. (Nov 16, 1999)

Well I didn't have severe enough diarrhea to be someone that would take a 5-HT3 drug.No point stopping up the little bit of loose stool I had.Pain was my major symptom, stool consistency and the urgency I had would have been mild enough to not bother with much of any treatment at all if that was all I had. It was the stop in my tracks and drop to the ground pain that was my biggest issue. I didn't mind an occasional gee I really need to go now thing if it had been painless.That mild a diarrhea is not in anyway an indication of needing a 5-HT3 drug.I tend to think the measurable changes you see in the brain (which all the research says are there) may come from improper signals coming up the brain-gut axis. What we don't know is if the brains were different before IBS (which might play into who is likely to get IBS and who isn't in some way). We've only looked at the after.I don't think you can just say none of that research is real at all and it can't be a part of the problem in any person because the research is very real.Now how you interpret that will vary. None of the doctors I know that do that research says it means IBS is all in your head and nothing at all is wrong in the ENS and it is just your brain and only your brain.What I am saying is my ENS was messed upStop. read that again.I AM SAYING MY ENS WAS MESSED UP. (actually, I believe it still is, at least a little bit)have I made my point?However the ENS doesn't just do what it does in complete and total isolation from everything else. It is supposed to be connected to and get feedback from the brain/CNS (which includes the spinal cord). My guess is if you severed the connection with the brain you could get problems because you severed the connection it needs to behave 100% normally.Which is actually one theory of functional diseases (of any kind) that the problem is often the feedback mechanisms are screwed up and the body part is doing all the right things, it just does them at the wrong time or at the wrong intensity because it isn't getting all the information it needs. Like you would do if you were driving blindfolded, you might work the pedals and steer just fine, but you aren't quite getting all the information you need to really drive well.But whatever.I know that changing how I interacted with my ENS by using my brain (via what I can do with the mind, and the mind and the brain are two different things IMO) allowed it to work better. Started off about 50-75% better and has gotten to where I am about 98% better.The damage still seems to be there, a bit, but it now has what it needs to function nearly normal almost all the time.With medication (which I took before the CBT study) I could reduce the pain about 25-50%. It was enough to make me functional, but not enough to really make me comfortable.About 1/2 way through the CBT study I needed a lot less medication to feel really good, not just be barely able to trudge through my day.Now I took Buspar (effects the 5-HT2 receptor) and Levbid (Levsin during the study so we could count how many pills I took) to take the edge off the pain.I went from 7 Levsin a day to 0-1 a day and 2 doses of Buspar to 1 a day during the study.As is common for people who do CBT I continued to improve over time and now I take about 5 Levsin a year and no Buspar.I could take the Buspar and have no symptoms at all, but I choose not to because I don't need that extra 2% control over the IBS. The amount of pain I get is manageable and infrequent. My stool consistency is a bit more variable then I remember pre-IBS (or when I was still taking 0.5 doses of Buspar a day) and my frequency is usually 2-4 times a day, but that isn't enough to risk the side effects of medications. The frequency of pain and the slight issues with stool consistency/frequency are really too mild to actually have a current diagnosis of IBS. I may not be completely 100% totally normal, but I'm doing pretty good.I never expected that. I expected the CBT would do not one thing at all. However, I was willing to give it a shot, especially since it was free.I may be placebo, but it was part of a clinical study where 70% of all the CBT-treated people in a pretty large study did better during the CBT and even better than that 1 year later.The medication arm was less successful and much closer to the placebo control (for the CBT side there was a come in once a week to get information about IBS sessions, so they controlled for the whole the Clinical Trial people are nice to you so you stick around for 3 months thing).CBT and Hypnotherapy usually do much better in clinical trials percentage wise than any of the medications that are tested. Even the 5-HT3 studies with Lotronex only helped like 40-50% of patients.But you aren't going to believe me, so I probably will just exit the thread as I've said what I need to, and I'm sure nothing I say will change your mind.


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## code9 (Dec 3, 2007)

"*However the ENS doesn't just do what it does in complete and total isolation from everything else. It is supposed to be connected to and get feedback from the brain/CNS (which includes the spinal cord).*"That has been proven untrue. Look at a brain dead patient. You put a tube in their stomach, and they digest food properly. The ENS begins at the throat and ends at the rectum. It controls everything in between without any necessary intervention from the brain. This has been proven, as I said, intestines will function fine in an organ bath.Also, since you've not taken any drug that would affect the ENS in isolation, you don't know how the ENS would react, so there's no way to definitively say your ENS is acting improperly. A 5-HT3 antagonist would fill in that gap."*But you aren't going to believe me, so I probably will just exit the thread as I've said what I need to, and I'm sure nothing I say will change your mind.*"I'm not sure what you think I need to change my mind about. You feel better, I don't doubt that you do, or how you got there. I'm just wondering if by changing the ENS/CNS response, can you really fix damaged nerves in the ENS. That puts CNS in control of the ENS, when everything I have read that is backed up by scientific experiments says it is not.If CBT and hypnotherapy work, that's fine. I think there are a wide variety of causes for IBS, some may be CNS, some may be ENS.But I think you are jumping the gun, and not being scientific, and perhaps detrimental to the rest of us, to say that ENS problems can be solved by re-training the CNS with CBT and hypnotherapy. You have to know that won't work for everyone, and is the problem. Just like a 5-HT3 antagonist won't work for EVERYONE.What works for you is fine, but I don't think you have presented any evidence that the ENS was affected in your case. If it was a CNS problem and you fixed it, I'm not saying that's untrue or incorrect.Let me be clear : *I'm saying, I believe one cause of IBS is ENS nerve damage, and I doubt CNS therapy in the form of CNS medication, hypno, or CBT will fix that physical problem. If you want to refute that, be my guest.*


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## Kathleen M. (Nov 16, 1999)

ENS doesn't really change you digest food. The enzymes and lining work just fine on their own.IBS doesn't change how you digest food.I thought paralyzed or brain dead people often had problems with constipation, etc. and didn't always have one perfectly formed stool every morning like clockwork.*shrug*Oh I kinda feel like you did doubt that I felt better, and that any research that involves anything to do with the brain is completely totally wrong, and maybe even hurtful for patients and should be abandoned completely.My IBS appears to be infection related.PI-IBS is likely caused by damage to the ENS.I don't think there is any test to PROVE TO YOU that is what happened.I know things aren't 100% right even now, but they aren't nearly as wrong as they were.What makes most sense based on all the research is there was damage down there and by using the gut-brain axis I was able to compensate for that. I don't have a better answer, and I don't think science is going to find something substantially different from that based on my understanding (I could be wrong, but I'd have to see the data before completely abandoning everything in the scientific literature to date)I don't understand why it is completely and totally unacceptable and "DETRIMENTAL" for me to have my own damn opinion.I'm not saying you have to change your mind either. But that this is at the "agree to disagree" stage of conversation, and I'm not going to be "detrimental" to the board with endless disagreement with you. We have plenty of feedback that pages and pages of endless back and forth between people who cannot agree is a problem for a lot of people who are here trying to get help.*I NEVER EVER CLAIMED CBT or HT* would fix every single person or that there was one and only one answer.*sigh*They work for 70-80% of people in clinical trials.*I NEVER EVER SAID THE ENS IS TOTALLY CONTROLLED BY THE CNS* Just that they "talk" and that interaction can be used to benefit some patients.*I NEVER EVER SAID I FIXED THE NERVES*I still think they are messed up, they just get enough of the right "talk" to work better than they were,*5-HT3 drugs* I'm not going to look it up for this thread but I was pretty sure these receptors are not solely in the GI tract nerves, and like I said I am not a candidate for those drugs because I do not have diarrhea severe enough to take them.You don't like anything I have to say and you seem to think I am only here to hurt people which is so totally wrong, but, whatever.I will leave this thread with this.It is the study I was in, interpret it however you want. http://www.ncbi.nlm.nih.gov/pubmed/1285186...Pubmed_RVDocSums.K.


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## code9 (Dec 3, 2007)

"*ENS doesn't really change you digest food. The enzymes and lining work just fine on their own.*"Since ENS controls motility, it does change how the large intestine works. Brain dead people do not just constantly leak D because their CNS is inactive."*Oh I kinda feel like you did doubt that I felt better, and that any research that involves anything to do with the brain is completely totally wrong, and maybe even hurtful for patients and should be abandoned completely.*"That is completely your spin on what I am saying. I'm saying the history of IBS has very little involved the ENS, and even today the standard treatments are CNS based. As if anxiety and a little stress management are all a person needs. Maybe a little willpower, and they will be all better. That is a COMMONLY held belief by much of the medical community.I would suggest Gershon's book, "The Second Brain" if you have not read it. It's first hand research on the GI tract."*We have plenty of feedback that pages and pages of endless back and forth between people who cannot agree is a problem for a lot of people who are here trying to get help.*"Part of helping people is making sure they get all the information. As I said, I was responding to Eric's post when you, apparently, decided to take my opinion personally. Whatever you did to get better is great. I do not doubt you feel better. I'll say it again, CBT and hypno works for you, then good, it works for you.But I'm trying to look at this scientifically, from a logic standpoint. I'm trying to understand how CBT changes how the ENS functions. Given that the ENS is comprised of millions of nerves with a minute, MINISCULE fraction of those even connected to the CNS, I'm not sure you positively say that CBT and CNS therapy fixed any ENS problem. Changing your ENS responses would be at least some scrap of evidence that there was an ENS problem to begin with.I don't dispute that anxiety and stress can cause GI disruption. No one on the planet would dispute that, we've all felt it. However, most people would not say that stress and anxiety made them have D 20x a day for a decade. When it gets that extreme, there is something else wrong, *in my opinion.*When it comes to that level, I believe there is an organic ENS cause, Gershon proves this to my satisfaction in his book. That the ENS can sustain the same nerve damage as the brain tissue in various nerve diseases, means it's just as susceptible to damage as any other nerve. Even you are saying PI-IBS causes nerve damage to the ENS.All I am saying, is that if the ENS is permanently damaged (and you can test that, at least indirectly with drugs that affect the ENS directly), I think it would be extremely rare to treat the CNS and fix and/or compensate for that damage.The issue at hand, is does the CNS control the ENS, or do they just communicate, and how do they communicate. I don't think anyone knows for certain, but given the very few nerves connecting the brain to the ENS and the ENS's ability to function on it's own with no communication to or from the CNS, it seems to me that the CNS may play a much smaller role than is pushed by nearly ever practicing doctor in the country.I think the CNS's role in IBS is more an acute reaction, I don't think it wakes you up in your sleep because of the pain, I don't think it causes you to wake in pain every day. I think it is receiving errant signals from the ENS. Even compensating for these signals, and blocking the pain, does not stop the ENS from malfunctioning.As I said, I can put myself on enough valium/klonopin that I feel no anxiety or stress, I can be about to #### myself and not worry about it. But that's the point, removing stress/anxiety, severely numbing the CNS does not change how the ENS functions.That is the part I find hard to believe.I believe you did CBT and got better. I'm just not sure it's scientifically causal. And as I said, there's no way to know if you even had ENS damage. Logically and scientifically, I think we can look at other possibilities. 5-HT3 antagonism is causal, that has been tested over and over, you can even take slices of individual nerves and see how they react. That can be proven. Saying you can will your brain/gut axis to cause your ENS to act properly is a different animal. I believe you can teach your CNS to ignore the pain coming from your ENS, but you cannot repair your ENS with hypnotism. No more than someone with Cerebral Palsy can force their nerves to operate properly once they are damaged.*Read this very carefully before you take this personally --> I'm not doubting your story. I'm not doubting that you did CBT and improved. I'm not doubting that a good percentage of people did CBT improved. I'm not doubting that a large group of people who did acupuncture improved. I'm not even doubting that people on the placebo improved.*I'm doubting the science and causality of it, which I believe I am allowed to do. And that does not constitute any attack on you. I'm am simply questioning Eric's information, and the ability to will your nerves back to operating correctly.


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## eric (Jul 8, 1999)

I had to quickly look through the thread, but will go back and read this more throughly.However for a start here and then I will come back and clarify somethings.But first, yes dr gersho is huge in all this and so is Dr Mayer, Dr wood and Dr Drossman and DR Spiller, Dr Whitehead all major experts working on the problem.You know who Dr Drossman is though yes?*Back in the 1990's they realized abnormal motility alone was not enough to explain pain in IBS.*also*"Neuroimaging has provided evidence of physiological differences between normal individualsand those suffering from IBS in the way a visceral stimulus (ie, rectal distention) is processed inthe brain.[*14,15] Initial data from positron emission tomography (PET) scans demonstratedincreased activation of the anterior cingulate cortex (ACC) among normal individuals, comparedto IBS patients. The ACC is a cerebral cortical area that is rich in opiate receptors and is thoughtto be a major component of cognitive circuits relating to perception as well as descending spinalpathways involving pain. More recently, fMRI was used to demonstrate increased activity in theACC, prefrontal (PF), and insular cortex areas, and in the thalamus of* IBS patients compared tonormal individuals."*using both fmri and pet scans














They have already shown now IBS and post infectious IBS are brain gut axis disorders.History of Functional Disorders"While abnormal motility plays a vital role in understanding many of the functional GI disorders and their symptoms, it is not sufficient to explain reports of chronic or recurrent abdominal pain. ""The UNC Center for Functional GI& Motility Disorders5BRAIN-GUT AXISThe concept of brain-gut interactions brings together observations relating to motility and visceral hypersensitivity and their modulation by psychosocial factors. By integrating intestinal and CNS central nervous system activity, the brain-gut axis explains the symptoms relating to functional GI disorders. In other words, senses such as vision and smell, as well as enteroceptive information (i.e. emotion and thought) have the capability to affect gastrointestinal sensation, motility, secretion, and inflammation. Conversely, viscerotopic effects reciprocally affect central pain perception, mood, and behavior. For example, spontaneously induced contractions of the colon in rats leads to activation of the locus coeruleus in the pons, an area closely connected to pain and emotional centers in the brain. Jointly, the increased arousal or anxiety is associated with a decrease in the frequency of MMC activity of the small bowel possibly mediated by stress hormones in the brain. *Based on these observations, it is no longer rational to try to discriminate whether physiological or psychological factors produce pain or other bowel symptoms. Instead, the Functional GI disorders are understood in terms of dysregulation of brain-gut function, and the task is to determine to what degree each is remediable. Therefore, a treatment approach consistent with the concept of brain-gut dysfunction may focus on the neuropeptides and receptors that are present in both enteric and central nervous systems. "*http://66.218.69.11/search/cache?ei=UTF-8&...=1&.intl=usI am going to post even more and it will become even clearer and there is still some extremely important info still here to go.The thing is its not a competition between what causes the symptoms between the brain and the gut, both cause the symptoms. You still have to remember also this is not all completely figured out yet, but they are making substanstial progress and brain gut interactios are the keys to the puzzle.


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## code9 (Dec 3, 2007)

First of all, I'm not sure what to make of Dr. Drossman. Some of his articles seem to walk a fine line. Appears anti-opiates to me and my friend. Drossman is the only one who makes claims of narcotic bowel, so that makes me quite suspicious. I've known a lot of people who have and take opiates, and I've never heard of one of them mention narcotic bowel. A small sampling to be sure, but why is he the only one publishing papers on it? Secondly, I've seen those PET scans. And they don't prove any causality. If anything, they back the idea that ENS is sending bad signals to the brain, which are learned.If you have PI-IBS, and learn a negative behavior due to an acute illness, you would show this as well. CBT would probably help you with the negative learned behavior, but that doesn't mean you had permanent or long-term ENS damage.I believe permanent or very long-term ENS damage can occur with varying severities. And that 5-HT3 antagonists work but quelling the signals from over-sensitive nerves.Hypnotherapy cannot treat a broken foot. Nor can it treat a broken neurotransmitter receptor in the large intestine, in my opinion.


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## eric (Jul 8, 1999)

First of all your way ahead of yourself and still are missing some really important things here.*Drossman is the chairman for the rome committee *to diagnose functional disorders. He is also a gastroenterolgoy teacher on functional disorders and all of the doctors I just mentioned above work together on all this and share research.The reason why drossman wrote the narcotic bowel syndrome article or talks about it, is because its important and is very real, but all of the above doctors know about it.So first let me post who these guys really are.Douglas A. Drossman, MDhttp://www.med.unc.edu/medicine/fgidc/drossman.htmThe article I posted before is all of there research combined. Read this again carefully"Brain-gut - The brain plays a role as well. The brain and the gut are connected. Thinking and feeling can have affects, influencing release of proteins that interact with the nervous system (neuropeptides), which can affect motility, secretion, blood flow, and inflammation. Stress may influence inflammatory pathways causing a dysregulation that can lead to emotional conditions and more stress - a vicious cycle. It is not a question as to whether this cycle begins in the gut or in the brain. *The problem is that both systems are effected concurrently thus producing a disturbance of the regulation between the brain and gut; a "vicious cycle" with no beginning or end. Understanding this will open the door to more specific treatments. We can see examples of brain-gut interactions by looking at post-infectious IBS (PI-IBS) or dyspepsia. A study done after a salmonella infection outbreak showed that 10-15% of patients continued with their symptoms of either dyspepsia or IBS after the initial infection subsided. Some recent studies show that this is associated with greater levels of immune cell activity. In IBS, the subgroup of patients with diarrhea as the predominant bowel symptom is the group where more of this inflammatory response is seen; there is also increased psychologic distress occurring at the time of the initial infection, which may be enabling the post-infectious response. In the gut we see infection followed by an inflammatoryresponse, altered motility, and increased sensitivity. But these factors alone are not enough - the brain has a role in regulating these factors. If there is psychological distress around the time of the initial infection, it can result in the expression of the post-infectious symptoms. Thus, the brain and the gut are interacting so with this disorder the brain can influence the inflammation in the bowel while the bowel inflammation can produce psychosocial - emotional and social - distress.*http://www.ibsgroup.org/forums/index.php?showtopic=92806ON PI IBS the bodies stress system helps fight infections by the release of chemicals in the gut, one being histimine. Do you know this aspect?There is also some very important aspects of the brain and gut functioning here being left out. One of the things your leaving out here is the BIOLOGICAL stress responce. Its this stress reponce that matters for one and I don't think its what you think. Stress and Irritable Bowel Syndrome: Unraveling the CodeBy: Yvette Taché, Ph.D., Center for Neurovisceral Sciences and Women Health, Digestive Diseases Center, Department of Medicine,Digestive Diseases Division, University of California at Los Angeles and VA Greater Los Angeles Health Care System, CaliforniaDr. Taché was the recipient of the IFFGD 2005 ResearchAward to Senior Investigator, Basic Science. Her earlypublications put the "brain-gut axis" on the map. Since then,she has been one of the pioneers in this field. In many ways,it has been her energy and enthusiasm that has ensured thecontinued vibrancy of the field. Her identification of the roleof corticotrophin-releasing factor (CRF) signaling pathwaysin stress-related alterations of gut motor function andvisceral pain are of major and lasting importance.http://www.ibsgroup.org/forums/index.php?s...veling+the+codeDr Mayer a top neurogastroenterologist studying IBS"The Neurobiology of Stress and EmotionsBy: Emeran A. Mayer, M.D.UCLA Collaborative Centers for Integrative Medicine, UCLA School of Medicine, California "Stress is an adaptive response that is not unusual or unique to only certain individuals. In humans and animals, internal mechanisms have developed throughout evolution, which allow the individual to maximize their chances of survival when confronted with a stressor. *A stressor in this context is any situation that represents an actual or perceived threat to the balance (homeostasis) of the organism."*http://66.218.69.11/search/cache?ei=UTF-8&...=1&.intl=usMast cell and cellularity of the colonic mucosa correlated with fatigue and depression in the irritable bowel syndrome.http://www.ibsgroup.org/forums/index.php?showtopic=93117There is something called neurogenic inflammation, the brain can re inflamme cells in the gut as well as the fight or flight can activate the mast cells in the gut, via the HPA axis which releases hitimine unto the smooth muscle of the gut, which can contribute to pain and d. It might also be the brain senses problems in the gut and keeps activating systems to correct it, when it should not, kind of like, but not quite an autoimmune disease, because the body is trying to get back to homeostasis. However the brain is very inovled in everything, I am still not done yet."The 'brain-gut axis' helps to explain the influence that thoughts, emotions, and psychological or social stress have on the function of the gut."http://www.merck.com/yourhealthnow/volume2-2/braingut.htmlThey also now from treating IBSers from research treating the whole person and not just the gut is more effective then just treating the gut.However"Hypnotherapy cannot treat a broken foot. Nor can it treat a broken neurotransmitter receptor in the large intestine, in my opinion."It can change pain nerve pathways, it can modify pain to the brain, it can calmed down the brain gut communication, it can relax muscles, relieve anxiety and stress, it can boost the immune system, it can modify rectal hypersensivity without changing anything, it can help the altered gastro colonic responce in IBS and has been shown to be a long term effective treatment after you stop doing it, so it is cahnging some very important aspects of IBS. No it won't cure a broken foot, nor is is touted as a "cure" for IBS, just an effective tool. This is another discussion though.They also use HT to study IBS itself.Stilll there is more to come, because there is stil a lot more to it all.You should also read this threadEric,anything new on distention sensitivity?http://www.ibsgroup.org/forums/index.php?showtopic=90110


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## code9 (Dec 3, 2007)

I just got done reading several of Dr. Drossman's "wean them off opiates because they are doing more harm than good, and be sure to judge their 'genuineness'" articles. I am not impressed. I'm not impressed with any doctor who is so against opiates because "they do more harm than good" when they have absolutely NOTHING else to offer someone with long-term intractable chronic pain, except for some useless anti-depressants and stress management.That theory is so biased and clearly based on some misguided moral principles, that it's really disgusting. I refuse to talk about this joke "narcotic bowel syndrome" of which the only examples outside of 1 or 2 in Drossman's documentss, are as I said, very long term addicts, who experience short term hyperalgesia. If such a thing even exists beyond withdrawal, it's no reason to NOT give someone opiates when there are so few options available.And as I said before Eric... And by the way you can stop pasting pages and pages, I can read them, and I know they mean as little or as much as you want them to mean. As I said, there are several different types of IBS, your brain/gut axis theories do not explain people who take SSRIs Trycyclics, Benzos... etc etc... eliminate anxiety, yet still have the same exact IBS symptoms, if not worse.The brain/gut axis does not explain the people who spent money on hypno and CBT and are no better for it.The brain/gut axis does not explain hyperalgesia.The brain/gut axis does not explain why opiates have helped many, many IBS sufferers past and present.The brain/gut axis does not explain why 5-HT3 antagonists work so well in some people.The brain/gut axis does not explain how the ENS functions completely independently when the FEW nerves that connect it to the brain are severed.It may well be that some people can be helped by these things, but I see people presenting themselves as authorities, telling every new person on this board their theories, and berating anyone who points out another WELL DOCUMENTED (there's a whole entire book about it) and SCIENTIFIC theory of why 5-HT3 antagonist work for some people, and SSRIs and Hypno and Levsin and Phenobarbitol and Valium are worthless to them.Kathleen has so emotionally, and accusingly presented her side.You have pasted a book about your brain/gut axis.*I am now stating my final word on this : There are some people that NONE of those things work for, and the theories do not apply to. I'm sorry that upsets you both so much that you feel the need to argue the point and take it personally, but that is the truth of it. There is a physical problem, identified by much MUCH research, at least in some people. If you stopped re-posting the same brain/gut articles and looked around for some newer stuff on the ENS, you would be aware of this.End of story, take it or leave it. But I'm tired of repeating myself. They won't work for everyone, so let other people have a word.*


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## eric (Jul 8, 1999)

All I have to say is wow you are really confused about a lot and not seeing this very clearly. So because yu don't get it, your not happy for others who have been helped by a lot of those treatments and they are recommened by the rome experts and yes they do know more about the ENS then you do.Wow that is cold.I also personally know of two people on the bb here that had it and it was really bad, then they had IBS pain and naroctoc blowel syndrome on top of it and they didn't have a lot of options then to treat pain. They have come a long ways in understanding and treating chronic pain as well.also all the doctors we have posted here ALL view IBS now as a brain gut axis disorder and you don't and that is odd to say the least. They also recomnmend the treatments your mentioning, CBT and HT and antidepressants ect.. So I have no idea where you coming from on all this, because your arguing against all the research that has shown why these things help IBS. They are very aware for the need for better IBS treatments. also because you have never seen it narcotic bowel syndrome doesn't exist? That article is for other doctors really who already know about it and need to treat people with it and it is not rare. Narcotic bowel syndrome is an opitate induced functional disorder. It can make pain receptors in the gut have a lower tolerence to pain and in IBS where there is already a lower tolerence for pain, then that is probably not a good idea, *especially in a chronic disease* with NO CURE. Were not talking about addition which is another issue. There should be other methods tried first, but you would tell people to go straight for the narcotics. and that all these top IBS researcher don't know what there doing, aren't all working together and want to harm you or give you bad advise. Wow I know a lot of them personally and you could not be father from the truth. A lot of the research you have posted comes from these same doctos, so you can believe what you want. They are figuring it all out and unless your a researcher your not.Some 80 percent of narctoic use is just in the US. I am in no way against drugs for specific reasons."Narcotic. Narcotic analgesic drugs are usually not prescribed for continuous treatment because of possible development of physical dependency or addiction and unwanted side effects, such as drowsiness and interference with clear thinking. *Furthermore, continuous narcotic use can actually increase pain sensitivity and also alter gut motility, leading to severe constipation. This is called the "narcotic bowel syndrome" (Annals of Internal Medicine, 1984;101:331-334). Keeping these cautions in mind, narcotic analgesic drugs are occasionally used to relieve intermittent attacks of more severe pain. "*http://www.grandtimes.com/Treatment_of_Irritable.html"The latter can produce narcotic bowel syndrome, *which is usually observed in patients who abuse opiates for chronic pain."*http://www.emedicine.com/med/byname/intest...y-disorders.htm"Narcotic bowel syndrome is a form of intestinal pseudo-obstruction characterized by chronic opiate use leading to ileus, vomiting, and abdominal pain."http://www.medscape.com/viewarticle/469586_2There is also Functional Abdominal Pain Syndrome which is "poorly related to gut function"http://66.218.69.11/search/cache?ei=UTF-8&...=1&.intl=usThe Experts SpeakAbout IFFGD Learn about IFFGD on video Go »At IFFGD's 7th International Symposium on Functional Gastrointestinal Disorders in April 2007, we had the opportunity to talk to some of the international experts in functional GI disorders. Our discussions covered some of the most recent developments in this field.http://www.aboutibs.org/site/learning-center/video-corner/Brain Imaging: CNS Abnormalities in Patients with IBS"ConclusionBrain imaging and other studies of IBS pathophysiology indicate that the perception of gut stimuli and altered autonomic responses to these stimuli are affected by activation of various parts of the brain, resulting in increased attention to these stimuli, greater unpleasantness of the subjective experience, greater threat appraisal, and greater arousal in response to visceral sensations. Further study may lead to new developments in treatment for persons with IBS. "http://www.cmecorner.com/macmcm/pcp/pcp2000_01.htmNeuromuscular Dysfunction and IBS: Clinical Implications"Classically, the pathophysiology of IBS has been thought to involve an interplay between psychosocial stressors and abnormalities in gut motility and visceral sensation. A variety of motility abnormalities have been described in IBS, including more frequent and prominent colonic contractions in response to meals in patients with IBS and diarrhea (IBS-D), and delayed colonic motility or abnormal colonic propulsive activity in patients with IBS and constipation (IBS-C).[1] Additionally, disorders of evacuation, as seen with puborectalis dysfunction or a rectocele, may also play a role, either alone or in conjunction with abnormal motility, in some IBS patients.Visceral hypersensitivity has long been accepted as an important feature in a subset of IBS patients and has even been suggested by some to be a biological marker of the condition.[2] *Until recently, the concept of visceral hypersensitivity was based largely upon studies that identified differences in patient pain response or cortical activation measured by brain imaging techniques following painful visceral distention. An interesting recent study using functional magnetic resonance imaging (fMRI) found that subliminal rectal distention resulted in a greater volume of cortical activation in IBS patients than in controls. By eliminating the effects of stimulus-related cognitive processes through the use of subliminal stimuli, this study more definitively established the hypersensitivity of neural circuitry involved in visceral sensation in IBS patients.[3]*http://www.ibsgroup.org/forums/index.php?showtopic=48036Neurogenic Inflammation in Chronic Pain Conditions"We usually associate inflammation with the responseof the body to tissue injury or invasion by hostilemicroorganisms. The central and autonomic nervoussystems play an essential role in the initiation andmodulation of this process. Although tissue trauma orinfectious agents may be initiating factors in neurogenicinflammation, neither of them are required. Theinflammation may be initiated and maintained by thecentral and peripheral nervous systems in response topsychological stress. The severity of neurogenicinflammation is usually modulated by the psychologicalstress throughout its course. There are several definitionsof Neurogenic Inflammation."http://66.218.69.11/search/cache?ei=UTF-8&...=1&.intl=usIn order though to fully undertsand why this is not just a gut problem you need to understand some other aspects of the way the brain and the gut work. The brain has eveolved mechanism to keep chornic viceral sensations from the gut to reaching the brain and that is lost in IBS.Visceral Sensations and Brain-Gut Mechanisms http://www.aboutibs.org/store/viewproduct/127


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## eric (Jul 8, 1999)

I had to come back to this really.The point here is to understand things really, although they get heated.The article was for doctors to recognized and treat their patients who have narcotic bowel syndrome and code 9 I hope your never in that position you need that advise, but if you ever do there it will be.Was your first reaction a "gut feeling" on this? Or a visceral reaction? Emotions can cause anger and that can effect the gut and pain.You don't understand fully chronic pain treatment if you don't understand why stress reduction is important or the mind body. I can tell you for sure it will go further then taking narcotics on a regular bais for chronic pain the rest of your life and it has no side effects. To think stress is not an important factor in IBS is clearly off, not just IBS but any pain condition, but even more so with IBS.HT and CBT are tool against IBS. HT hasan 80% success rate from clinical studies and is 80% effective on pain and can be long term. So your saying this without the facts about it and its just YOU don't personally care. We differ there.Hypnotherapy for Functional Gastrointestinal Disorders By: Peter J. Whorwell, M.D., University Hospital of South Manchester, EnglandWe have also undertaken some research in an attempt to ascertain how hypnosis might lead to benefit. There is no doubt that it can improve anxiety and coping capacities as might be expected. However, of far more interest, was the observation that motility and visceral sensitivity could also be modified in the desired direction. Thus, this approach to treatment appears to offer symptomatic, psychological, and physiological benefit and this presumably explains why it appears to be so effective. However, hypnosis should not be regarded as a panacea as up to 25% of patients fail to respond. Even when patients do improve, conventional approaches to treatment should not necessarily be ignored. Therefore it is still important that lifestyle factors such as diet are also taken into account. In addition, some patients may find that an occasional loperamide or laxative, depending on the bowel habit abnormality, maybe required. One concern over the use of hypnotherapy is the possibility that patients might relapse once a course of treatment has been completed. We have recently addressed this question with a study on the long-term follow up of patients attending the unit. This has shown that after a period of between one and five years, 83% of responders remained well with 59% requiring no further medication at all. Patients also took much less time off work and consulted the medical profession less often. Following the success in patients with IBS, we have recently looked at the use of hypnotherapy in functional dyspepsia, which is a closely related condition resulting in primarily upper gastrointestinal symptoms. Again, compared with controls, the hypnotherapy patients showed substantial improvements in both symptoms and quality of life. One of the most striking outcomes of this particular study was that, after a follow up of one year, not one patient in the hypnotherapy group required any further medication compared with 82% and 90% of subjects in the 2 control groups. Similar trends to those observed in the IBS studies were seen for a reduction in medical consultations and time off work. http://aboutibs.org/site/about-ibs/management/hypnosisSo what are you talking about here, were the above people helped with IBS? It looks like it to me and long term, after treatment, I hope you understand that part, because you stop a drug and the symptoms are right back.Modulation of the Brain-Gut Axis as a Therapeutic Approach in Gastrointestinal DiseaseMedscape"IntroductionBi-directional brain-gut interactions play an important role in the regulation of many vital functions in health and disease. In health, brain-gut interactions play a crucial role in the regulation of digestive processes (including appetite and food intake), in the modulation of the gut-associated immune system, and in the co-ordination of the overall physical and emotional state of the organism with activity in the gastrointestinal (GI) tract. In disease, altered brain-gut interactions are likely to underlie the symptom generation in functional GI disorders (FGIDs),[1] and may be involved in the modulation of immune activity in irritable bowel syndrome (IBS),[2] and in the pathophysiology of various eating disorders.[3] In this current review article, we will focus on evolving pharmacological strategies aimed at various targets within the brain-gut axis, which may yield novel therapies for IBS and related FGIDs. Even though the gut itself is one component of the brain-gut axis, the review will not deal with targets restricted to peripheral mechanisms in the gut and the reader is referred to other recent reviews.[4,5]While research over the past few years has provided significant advances in the understanding of IBS pathophysiology, the precise mechanisms underlying the symptom generation remains incompletely understood. *However, the various aspects of IBS symptomatology can best be viewed as a dysregulation in the complex interplay between events occurring in the gut lumen, the mucosa, the enteric nervous system (ENS) and the central nervous system (CNS) leading to alterations in sensation, motility and immune function.[6] A schematic of the afferent component of the brain-gut axis is shown in Figure 1."*http://www.medscape.com/viewarticle/545103"As I said, there are several different types of IBS, your brain/gut axis theories do not explain people who take SSRIs Trycyclics, Benzos... etc etc... eliminate anxiety, yet still have the same exact IBS symptoms, if not worse.The brain/gut axis does not explain the people who spent money on hypno and CBT and are no better for it.The brain/gut axis does not explain hyperalgesia.The brain/gut axis does not explain why opiates have helped many, many IBS sufferers past and present.The brain/gut axis does not explain why 5-HT3 antagonists work so well in some people."People themselves explain this, genetics and not all people are going to have the exact same PI IBS or IBS, even though similarites in all IBSers. That is why the research is being done and that is why they had to take into account brain gut axis. This is the only thing there studying."The brain/gut axis does not explain how the ENS functions completely independently when the FEW nerves that connect it to the brain are severed."You mean the Vagus nerve? If the brain is severed and not controlling blood flow, breathing and other body functions the gut isn't gonna work. But I do understand this really.This is the way it evolved to run on its own for specific reasons, but the brain is still the boss and there is CONSTANT back and forth communication. but Are You a Gut Responder? Hints on Coping with an Irritable Bowel"The gut and the brain develop from the same part of the human embryo. So it is not surprising that the intestinal tract has such a rich nerve supply that it is sometimes referred to as "the little brain." The gut shares many of the same kinds of nerve endings and chemical transmitters as the brain to which it remains linked through a large nucleus (the locus ceruleus). This collection of nerve cells is partly responsible for controlling anxiety and fear, which explains why these emotions can sometimes be associated with bowel function."http://www.aboutibs.org/store/viewproduct/1082007 Enteric Nervous Systemhttp://www.medscape.com/viewarticle/551794_print"*The cause of IBS is yet to be determined. However, modern research understands IBS as a disorder of increased reactivity of the bowel, visceral hypersensitivity and dysfunction of the brain-gut axis. There are subgroups being defined as well, including post-infectious IBS which can lead to IBS symptoms. Other work using brain imaging shows that the pain regulation center of the brain (cingulate cortex) can be impaired, as well as good evidence for there being abnormalities in motility which can at least in part explain the diarrhea and constipation. So finding a specific "cause" of IBS has grown out of general interest in place of understanding physiological subgroups that may become amenable to more specific treatments. Hope that helps."Doug Drossman*http://www.ibsgroup.org/forums/index.php?showtopic=94055This is BRAND new*"Central regulation of visceral sensitivity: pain perception - A number of factors lead to the experience of pain. These involve mostly areas of the brain. When a pain signal is generated in the intestines,there is an ability of the brain to regulate this signal. We are learning that there are areas of the brain that stimulate or potentially cause more pain, which seem to be more associated with hypervigilance and attention. Alternatively, there are areas of the brain that turn down the pain signal. This can be viewed on brain imaging. We are moving toward an understanding that patients with greater pain severity have a dysregulation not so much at the level of the gut, but at the level of the brain."*http://www.ibsgroup.org/forums/index.php?showtopic=94055"Second is the concept that these disorders are "nebulous" or poorly defined. *Over the last two decades there has been an explosion in research in brain-body science, neurotransmitter function, and brain imaging that is precisely defining the location and mechanisms that explain these symptoms. This is probably the most exciting area in modern medical investigation, and many new drugs are being targeted to treat these mechanisms. "*http://www.aboutibs.org/site/news-events/n...commentary#Realand here you go brand new on Functional GI disorders: from animal models to drug developmenthttp://gut.bmj.com/cgi/content/full/57/3/384You might noticed all the doctors names drossman and mayer, chang, whitehead, Gershon, Camerilli, spiller, dr wood and many more on on all of these articles and are working together and what I have been posting is state of the art on IBS and functional disorders.and you might notice"*There has been reported a correlation of abdominal pain with the number of mucosal mast cells in close proximity to nerve endings,13 14 but this finding will need to be reproduced by other laboratories before it can be considered a true biomarker of IBS symptoms.* Potential biomarkers for which correlation with IBS symptoms have not been published include recently reported abnormalities in stool microflora7 and in stool proteases.15 "and go back to how the fight or flight can trigger those mast cells to degradulate. So yes it does matter. What your missing is the people side of things and instead of them looking at one abnormalitiy they are looking at the whole person holistically and all the systems, which work together and infleunce each other based on our own makeups for exactly the reasons you mentioned.Not everyone is getting better and that is why they call it research, but your missing some of the basic science here on things first. In the mean time people need help and things that work.


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## cookies4marilyn (Jun 30, 2000)

* As a Moderator, I have been asked by Jeff and the others to gently do the moderator bit. Please kindly refrain from long long posts with lots of cut and pastes to prove your point - this has been mentioned to posters over and over - please just put a statement or two, the link and move on. Please refrain from personal attacks. You are all well-intentioned, and want to get the information out to help others. Long long posts and confrontation wont do it.If this continues, the thread will be closed.Thank you kindly for your cooperation. *


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## eric (Jul 8, 1999)

By the way"The Brain Gut Axis "In normal people, distension of the gut will trigger nerve fibres lining the gut to transmit signals to higher centres in the brain that register pain. In IBS sufferers, it has been proved that pain is perceived at much lower levels of distension. This is known as the 'hypersensitive gut' or in scientific terms visceral hyperalgesia."http://www.ibs-research-update.org.uk/ibs/brain1ie4.htmlanother term is viceral hypersensivity, although there are some different meanings in the two.Dr Whitehead from chat with the experts"Whitehead: Eric, Dr. Gershon's research on serotonin is an important part of the story in IBS. There is evidence that differences between people in how their body clears serotonin from the synapses can *affect both mood and gut motility*. The newer drugs such as alosetron and tegaserod work on serotonin. "This is important especially in IBS d.*Everytime* someone is afraid to get in their car or rushes to find a restroom or fears an accident in their pants, or is afraid to go out because of fear the fight or flight is activated via the HPA axis.What is the "fight or flight response?"*This fundamental physiologic response forms the foundation of modern day stress medicine. The "fight or flight response" is our body's primitive, automatic, inborn response that prepares the body to "fight" or "flee" from perceived attack, harm or threat to our survival.* http://www.thebodysoulconnection.com/Educa...nter/fight.htmlWhich by itself has the potential to make you throw up or ###### your pants itself if the fear is strong enough. In IBS its compounded and here the brain can trigger the gut which will then trigger the brain, its part of the viscious cycle. This in turn can stimulated mast cells to release histimine unto the smooth muscle of the gut and contribute to pain and d, calm the fight or flight responce and what happens then?So we have the CNS connected and constantly communicating with the ANS wich communicates with parasympathetic and sympathetic nervous systems and the enteric nervous system which then communicates back to the brain.The organs (the "viscera") of our body, such as the heart, stomach and intestines, are regulated by a part of the nervous system called the autonomic nervous system (ANS). The ANS is part of the peripheral nervous system and it controls many organs and muscles within the body. In most situations, we are unaware of the workings of the ANS because it functions in an involuntary, reflexive manner. For example, we do not notice when blood vessels change size or when our heart beats faster. However, some people can be trained to control some functions of the ANS such as heart rate or blood pressure. The ANS is most important in two situations:In emergencies that cause stress and require us to"fight" or take "flight" (run away) andIn nonemergencies that allow us to "rest" and "digest."The Cri$i$ in Academic Medicine"Because one cannot explain illness adequately by exclusive focus on disease processes,this failure to know the patient results too often in "efficiently" delivered care, which is, however, unsatisfying to both patient and physician and is sometimes totally inadequate or even incorrect.One must know and understand the person with the disease in order to fully understand and treat theillness (13). Almost all universities claim to know this and insert scattered courses aimed at teachinghumanistic approaches to patients and their personal concerns. However, most give only lip serviceto teaching comprehensive medicine that is truly patient centered and that takes psychosocialissues into consideration as significant factors in determining health and disease.http://www.cmj.hr/2005/46/1/15726669.pdfYou might want to also read this from dr drossman before your too quick to judge him. He was the editor of gastroenterology as well as the chairman of ROME committee to diagnose functional disorders.Research GroupMedicine Has Become A Business: But What is the Cost? Douglas A. Drossman, MD, EditorEditor's Column -- Douglas A. http://66.218.69.11/search/cache?ei=UTF-8&...=1&.intl=usI am done here.


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