# IBS brain versus heathy brain?



## LoriAnn (Jan 31, 2002)

I recently saw comparison MRI scans of a healthy brain versus the brain of FM. I was wondering if there was an internet site where a comparison is done between the IBS brain / healthy brain and also wondered how the IBS image differs from the FM image.I would appreciate any direction.ThanksLori


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## Guest (Feb 23, 2003)

Eric might be able to help you with that, Lori Ann.I've seen some pictures of both from the outside and the inside.......







Evie


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## eric (Jul 8, 1999)

Loriann, there are differences in IBS then normals.Here is a bunch of information.breathroughs in IBS research http://www.med.ucla.edu/ndp/Newsletters/Spring97Break.htm looking to the brain for answers http://www.med.ucla.edu/ndp/Newsletters/Spring97Look.htm Brains responce to pain http://fmcfsadvocacy.healthyplace2.com/custom.html Fibro and IBS http://www.med.ucla.edu/ndp/Newsletters/Spring98Fibro.htm A pet scan of IBS







Irritable Bowel SyndromeClinical IssuesAdapted from a radio interview conducted by Bob Enteen, host of Living Without Limits, with Douglas Drossman, MD, UNC Center for Functional GI and Motility Disorders at Chapel Hill North Carolina "What would be an example of new understanding?Well one example is that we're starting to understand how the brain is responding to the pain in IBS. There have been some studies done where they've artificially created a kind of an irritable bowel by placing a balloon to stretch the bowel, and that produces pain. Then they've compared people with IBS to non-IBS, or "normal" individuals. And what they've found is that when you stretch the bowel-and use PET scans to monitor the response-in normal individuals, certain areas of the brain that register pain respond and release chemicals called neurotransmitters that suppress and lower the pain. But it seems that doesn't happen as well in people with IBS. In fact, in people with IBS another area of the brain responds that is associated with anxiety. So what we find is that people with IBS, aside from having a bowel problem, may have some difficulty in terms of the way their brain is regulating the pain." http://www.aboutibs.org/Publications/clinicalIssues.html webmdMind-Body-Pain Connection: How Does ItWork?Pain experts Brenda Bursh, Ph.D., Michael Joseph, M.D.,and Lonnie Zeltzer, M.D., discuss the way that the mindand body affect, and are affected by, pain. http://my.webmd.com/content/article/1700.50465 Hope this helps.


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## trbell (Nov 1, 2000)

the pictures can be misleadingsince they show activity levels rather than the brain itsef as i understand it. To use a gross example ifthey took pictures of the colon what yu would be seeing is the rate at which things move through. This actually might be something UNC might be interested in doing a 'chat' on?tom


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## eric (Jul 8, 1999)

They show increased blood flow to the prefrontal cortex and hence activation, that is higher then in normals.The brain does not seem to be getting the signals and processing them right.


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## trbell (Nov 1, 2000)

I like that way of describing it. It's a process and as a poet i think sometims readers might not get the message I send and sometimes might not understand the medium. this is not a question of my fault or theirs. It;s the process.i think that's also the problem thatcomes up on the bb all the time. There's a tendency to say it's in the gut or in the brain when neither one is at fault. it's the communication system that's fawlty.tom


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## eric (Jul 8, 1999)

Loriann, an important connection to IBS and to fibro and cfs, is the HPA axis."hypothalamic-pituitary-adrenal cortex HPA axis which produces the hormone cortisol. The HPA axis interacts with other brain areas which are concerned with the responses to pain and in the autonomic nervous system function of the bowel during stress. There is a growing body of evidence that suggests that altered HPA responses in IBS and other chronic pain syndromes, such as fibromyalgia, play a role in the body's increased sensitivity to painful and non-painful stimuli resulting in chronic pain and other symptoms of discomfort and distress." http://www.med.ucla.edu/ndp/Newsletters/Wi...teredStress.htm


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## Guest (Feb 24, 2003)

Rats... one of these days we're gonna have to figure out how to harnass those slippery little neurochemical critters ........







In the meantime...."We get by with a little help from our friends.............."  Evie


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## LoriAnn (Jan 31, 2002)

Thank you for the input everyone.Thanks for the picture & links, as soon as hubby if off to work tomorrow I'll get reading. I wonder, if the IBS patient pictured suffered from IBS C or D, (or both) and if there would be a different picture between them.Would the picture be the same in all IBS sufferers? Or are there variations?Lori


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## trbell (Nov 1, 2000)

i think I remember some research published by one of the docs at Vanderbilt on the difference but I don't know if there were pictures. tom


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## eric (Jul 8, 1999)

The picture was taken of an IBSer who had a ballon inflated in their bum







These have been confirmed. This isn't the only one. they are going to be majorally studying this,it is very important to IBS, especially pain but also symptoms in a very complex intereaction.The problem partly with the c or d is that is in the gut where part of the problem is in how serotonin effects the colon.These are studies on pain in IBS and bowel sensitvity and too see what parts of the brain are effected. http://www.mindbodydigestive.com/brain.html Fibro has differencesNormals are differentIBD is differentI have a lot of information on this all if you want more.Oddly enough pet scans of HT subjects in pain studies basically show the opposite of IBS.


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## mikeralph (Jan 27, 2003)

so you are saying the immune system is not involved


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## eric (Jul 8, 1999)

Mike I have told you numerous times yes.


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## trbell (Nov 1, 2000)

eric, i have to ask whatn medical qualifications you have to interpret pet scans?tom


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## eric (Jul 8, 1999)

Tom, what interprtation are you reffering to?


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## eric (Jul 8, 1999)

Lori anne, this is more that explains it some more.Pain in the brain and IBS. http://ibs.med.ucla.edu/Newsletters/Fall97Brain.htm


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## eric (Jul 8, 1999)

Tom, are you talking about the fact I said there were differences?"To determine if an alteration in how the brain processes visceral and somatic pain information in IBS and FM, the investigators at the UCLA Neuroenteric Disease Program are comparing the brain responses to visceral and somatic stimuli in patients with IBS alone, IBS + FM, and FM alone. Brain responses are assessed by positron emission tomography PET which can measure blood flow to brain areas in response to a particular stimulus. During this study, a visceral stimulus balloon inflation in the rectum and a somatic stimulus pressure applied to a somatic tender point are given. Results have shown that in response to a rectal balloon inflation, IBS patients exhibit activation in a portion of the brain which is called the prefrontal cortex. This brain area is involved in the attention and arousal to a particular stimulus and also in memory retrieval of past pain experiences. Patients with IBS + FM have activation in this same brain region to a somatic stimulus but not to a rectal stimulus. Most of the IBS + FM patients reported greater muscular pain due to FM than abdominal pain from IBS at the time of the PET study. These findings suggests that brainï¿½s mechanisms of attention/arousal are activated in response to visceral pain in IBS, but in response to somatic pain in patients with coexistent FM.In summary, clinical characteristics and a significant overlap of symptoms suggest that the functional syndromes IBS and FM may have a common etiology. Visceral and somatic perception studies and PET imaging have demonstrated that each of these conditions have specific responses to painful stimuli and that patients with both IBS and FM may have responses to somatic and visceral stimuli that are uniquely different from that of IBS alone and FM alone. Further studies including PET, visceral perception tests, and sleep studies are being completed in patients with IBS and/or FM. Hopefully, these studies will improve the understanding of chronic visceral and somatic pain conditions and lead to more effective treatment. " http://ibs.med.ucla.edu/Newsletters/Spring98Fibro.htm "Visceral and somatic perception studies and PET imaging have demonstrated that each of these conditions have specific responses to painful stimuli and that patients with both IBS and FM may have responses to somatic and visceral stimuli that are uniquely different from that of IBS alone and FM alone."On the IBD and IBS scnas that is on a different site and I would have to find it.


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## trbell (Nov 1, 2000)

I suggest you check with a radiologist on what is considered a medical opinion in this area. I'm not an expert and I don't think you are either.tom


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## eric (Jul 8, 1999)

Tell me what interpretation tom, and enough with the cryptic message already. Just flat out say what interpretation.Nothing here is any kind of interpretation. They are facts. It was a ballon up the rectum to measure what happens in the brain and a lot of the pet scan studies measure pain.The other conditions are different, I posted and backed that up, so what.And please don't post another flippin cryptic stabbing message at me again, I am more then tired of it.


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## trbell (Nov 1, 2000)

"And please don't post another flippin cryptic stabbing message at me again, I am more then tired of it."I'll try not to be cryptic. If you want to be an expert then be an expert. Being an expert involves admitting that you are not perfect. tom


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## trbell (Nov 1, 2000)

sorry about that last eric. i guess that if I feel I'm being attacked personally sometimes I respond because I have IBS?time for jeff o move this into the kindergarten, I guess.tom


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## trbell (Nov 1, 2000)

apol;ogies to you as well Lori. you got hijacked and i'm not going to get into the IBS fingerpointing but you might want to ask your question again?tom


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## LoriAnn (Jan 31, 2002)

ok, I'm finally here, with the time to research some of these links.I'll be back to post some questions in a bit.Thanks Lori


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## Guest (Feb 25, 2003)

Eric,I'm confused. At one point, did you not post information linking IBS to the immune system?Didn't we watch the graphics and listen to Dr. Drossman discuss how the autoimmune system was connected to IBS?If IBS is just one of many dysfunctions that I have... that's fine.... but from what I ascertained from the UNC chats, everything including limbic system was connected.Clarification?Evie


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## LoriAnn (Jan 31, 2002)

I was wondering the same thing evie.Tom,I'm sorry my use of the word "normal" bothers you, but I can't escape the fact that things are not "normal" for me.It isn't "normal" that every day has to be an exercise in pain.It isn't normal to plan every outting based on bathrooms.It isn't normal to have to starve yourself for 24 hours before you can leave your house.It isn't normal when you can't hold a job because your bowel won't let you.It isn't normal to look at food with fear.etc etcI have seen "normal", thats what I want, what we all want. I understand the screwed up signals, but I also understand that my life is not "normal". I struggled for so long to achieve "normal" that it had devastating consequences for my emotional health. This is my life. ABNORMAL. Accepting it makes it easier to go forward instead of always grasping for something I can't quite reach.Just call me abby


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## trbell (Nov 1, 2000)

LoriAnn, Sorry for the confusion, but I was referring to 'normal' in the general everyday diagnostic and iften pejorative sense of normal and abnormal. i prefer to think of everyone as normal and some are normal people with problems. it has to do with whether you talk about the personas a whole or just attributes. I know there is often a way of thinking that I am an IBS person but I'd rather think of myself as person that happens to have IBS, or pains, etc.tom


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## LoriAnn (Jan 31, 2002)

OK......I've read everything you suggested Eric, and as usual I have more questions







and a couple of observationsI often see the phrase "mind/gut connection" and I think it immediately sets people on the defensive. The reasoning is fairly simple. When doctors think you are making it up they say "its all in your mind", when they suspect you have a tumour for example they say its in your brain. If they said it was in your mind, that would imply imagination. The perceptions may or may not be accurate but they have been ingrained in most people over a lifetime so getting people to be willing to look at the info and accept a connection might be as simple as always saying "brain/gut" connection, as the use of the word mind implies imagination. That's just IMO, but I wonder if others felt the same.This has given me a LOT to think about.Eric I thought on another post that you said there was no biological marker for IBS, but I read on the first site that there was, I could be wrong...I mean that it wasn't you who said that.According to what I read, I don't fit into the ROME criteria. While I was told many years ago that I had IBS, "learn to live with it", my experiences this past year did not occure previously, bloody stool, debilitating pain, 35lb weightloss, vomiting. This may explain why, while they may shrug and be unable to explain why this is happening, they have not said IBS was the cause. In fact, it now occures to me that by adding the IBS symptoms into the mix it has hindered their diagnosis, it may have been helpful not to do a history on me and just deal with the problems at hand because there may not be a connection.Now........I can relate to having a hyper-active everything, I have often thought my body was over reacting to many things, for example, if I bump my hand, I will develope a scab, as though my brain or immune system preceived the injury to be more severe than it really was, and the fact that pregnancy was a serious problem for me, in all 4 pregnancies, my body treated the fetus as an invader and tried to rid itself of the fetus. That is the way it was explained to me by the doctors. But I can't really comment further on that until I read the clarification on the immune system.The other area I need to address is seritonin, as there didn't seem to be a lot of info on that particular item in the sites you gave me, so I would really appreciate if you could send me in that direction Eric, I am trying to get a grasp on the connection, with some info on how & why they believe SSRI's are helpful. (though I must admit, they haven't seemed very effective in my case, at least not yet.)I cannot deny that the SSRI is having an effect on my perceptions, and altering my thought processes, but it has done nothing for my pain levels from either the IBS or FM. It has also had the negative effect of lowering my IQ, my ability to think clearly, to make connections and even follow conversations, this part bothers me most, as I considered a bright and intelligent mind gods way of making up for a dysfunctional body, now I have neither a mind or body that functions well.Thanks for all your help, I really appreciate it.Lori


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## eric (Jul 8, 1999)

Okay this is going to take me just a bit and I will post things and you can absorb them and then I will post some more, because it is very complex and you can't learn it all at once, however that your taking the time, is a very good thing.I know there is a high posiblitiy the thread could be hijacked so bare with me. LOLThe gut is the enteric nervous system and the brain is the central nervous system. The gut can work on its own basically, but it is hardwired to the brain. They communicate to each other and one of very important chemicals in this is serotonin. This will explain a lot the enteric nervous system consists of millions of nerve fiber perhaps as many as the spinal cord. This was really valuable to me the first time I read it, although there is a lot more on all this. http://www.ibsgroup.org/other/usnews000403.htm I am gonna go slow so you know.First 95 percent of the serotonin in the body is created in the gut and is located through out the gi tract. It has a very important role in the Peristaltic Reflex and gut function. I will post more and say more about this next, but first the immune system. Many things can trigger the immune system at the gut level, but other things can also trigger the immune systtem, it can even be triggered without a pathogen, via the brain and chemicals. This is very important in IBS.The system invovled in IBS is the limbic system and the The hypothalamic-pituitary-adrenal or HPA axis. This system is involved for one in the fight or flight responce but also to fight infections. This is another really complex system. This is also a system that seems to be involved and connected to IBS in Fibro and CFS and other things.Its important to understand this system and the fight or flight responce in IBS. There also seems to be some biological differences in men and women they are investigating. But the premise is still accurate for this discussion. Another aspect of this is homeostasis. But it will help to read this. http://www.mindbodymed.com/EducationCenter/ The serotonin issue I will go over to, but this is a brief thing on it, although its a question someone asked it explains it pretty good, but I will add to it, there are two very important cells in IBS and I will also talk about that store serotonin in the gut. Skip the 5htp question for know.This is from Harvards website."General Medical Questions.Q: I have suffered from irritable-bowel syndrome for many years. I get diarrhea. The doctors I've seen have offered little help. Recently, my daughter suggested I try an over-the-counter medicine called "5-Hydroxy-tryptophan," made by a company called Natrol Inc. My daughter says it is a mild antidepressant. It seems to have helped quite a bit, but it also seems to slow me down and make me feel tired. Can you give me any information on this? What is it, exactly, and are there any serious side effects? The only other medicine I take is Synthroid....The Trusted Source..Harold J. DeMonaco, M.S.Harold J. DeMonaco, M.S., is senior analyst, Innovative Diagnostics and Therapeutics, and the chair of the Human Research Committee at the Massachusetts General Hospital. He is author of over 20 publications in the pharmacy and medical literature and routinely reviews manuscript submissions for eight medical journals...June 19, 2001.A:Irritable bowel syndrome is now recognized as a disorder of serotonin activity. Serotonin is a neurotransmitter in the brain that regulates sleep, mood depression, anxiety, aggression, appetite, temperature, sexual behavior and pain sensation. Serotonin also acts as a neurotransmitter in the gastrointestinal tract.Excessive serotonin activity in the gastrointestinal system enteric nervous system is thought to cause the diarrhea of irritable-bowel syndrome. The enteric nervous system detects bowel distension expansion on the basis of pressure-sensitive cells in the bowel lumen opening. Once activated, these pressure-sensitive cells promote the release of serotonin, which in turn promotes both secretory function and peristaltic function the contractions of the intestines that force the contents outward. At least four serotonergic receptors have been identified to be participants in the secretory and peristaltic response.Patients with diarrhea-predominant IBS may have higher levels of serotonin after eating than do people without the disorder. This recognition led to the development of the first drug used specifically to treat diarrheal symptoms of IBS, alosetron also known as Lotronex. Alosetron blocked the specific serotonin receptors responsible for recognizing bowel distention. In doing so, it blocked the effects of serotonin and reduced both bowel secretions and peristalsis. Constipation was the most common side effect seen. Note: Alosetron was removed from the market by the manufacturer after repeated reports of a dangerous condition known as ischemic colitis became known. Tegaserod Zelmac is another drug under development and under review by the U.S. Food and Drug Administration for approval. Tegaserod is indicated for the treatment of constipation-predominant IBS and works to increase enteric nervous system serotonin activity.So, increasing serotonin activity in the enteric nervous system produces increased bowel secretions and peristalsis and potentially diarrhea, whereas depressing serotonin activity produces reduced secretions and reduce peristalsis and potentially constipation. Increasing serotonin activity in the brain would increase awareness and, in higher doses, produce anxiety, insomnia and restlessness. So I would have expected exactly the opposite effects of those that you experienced.I am unable to identify any possible drug interactions between 5-HTP and Synthroid levothyroxine but the symptoms described suggest a check with your doctor may be in order. Persistent feelings of tiredness and constipation may be signs of an underactive thyroid hypothyroidism.June 19, 2001" http://www.intelihealth.com/IH/ihtIH/WSIHW...438/325205.html On the serotonin issue, don't think of it as an amount is to low in the body or to high really, ect, but that There seems to be a problem in cells in the gut that store and release it and that it is also a player in communicating to the brain and back and it is in how all the systems dysregulates chemicla signals to the brain and back, not an amount in the brain say that can be fixed easily it more complex then just taking the 5htp.


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## eric (Jul 8, 1999)

Sorry also I missed this,"my experiences this past year did not occure previously, bloody stool, debilitating pain, 35lb weightloss, vomiting."These are red flags and you should have a doctor check you out if you haven't, these are not IBS symptoms!!!This is going to be and sound complicated and even though all this is complicated there is hope for many people and actually some easy natural things to do to counteract a lot of IBS symptoms.Also keep in mind many people can have more then IBS going on. Also, I forgot to answer the biological marker, the pets scan were high as a marker in the 80 percent and rectal sensitivity also some 80 percent, but as of yet no marker, but they have found problems.Keep this in mind as you read all this, because this is the big picture at the moment.Ringel Y, Drossman DA.Division of Digestive Diseases and Nutrition, Department of Medicine, University of North Carolina at Chapel Hill, 778 Burnett-Womack, CB# 7080, Chapel Hill, NC 27599-7080, USA. ringel###med.unc.eduThe irritable bowel syndrome is one of a group of functional gastrointestinal disorders within the Rome classification system that is characterized by abdominal discomfort or pain associated with a change in stool habit. It is a multidetermined biopsychosocial disorder in which physiological, psychological, behavioral, and environmental factors may contribute to the clinical expression of the disorder. These can include: 1 early life e.g., genetic or environmental factors; 2 physiological factors including increased motor reactivity, visceral hypersensitivity, which may be enabled by postinfectious events, and dysregulation of brain-gut communication e.g., altered central pain control mechanisms. In addition, psychosocial factors including psychiatric co-morbidity, major trauma e.g., abuse history, and maladaptive coping may amplify the clinical expression of the disorder and its outcome. Currently, clinical outcome has become understood in terms of global symptom relief and health-related quality of life.Publication Types: * Review * Review, TutorialPMID: 12184143


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## Guest (Feb 25, 2003)

Appreciate your taking time to post the above clarificationk Eric.Thanx







Evie


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## Mike NoLomotil (Jun 6, 2000)

The thread reflects just how difficult it is for IBS sufferers, and even physicians managing IBS patients, to gain a broad perspective on this difficult-to-understand area in IBS investigation and Interpretation of IBS pathogenesisï¿½especially since the range of variables is soooo vast and the investigation sooooo earlyï¿½.and the perspectives of investigators and clinicians can be soooo divergentï¿½.Not possible to address the whole thread but some key comments are jumping-off (on?) points:_______________trbell:ï¿½ï¿½the pictures can be misleadingsince they show activity levels rather than the brain itsef as i understand it. To use a gross example ifthey took pictures of the colon what yu would be seeing is the rate at which things move through.ï¿½Eric response:ï¿½They show increased blood flow to the prefrontal cortex and hence activation, that is higher then in normalsï¿½.ï¿½The brain does not seem to be getting the signals and processing them rightï¿½ï¿½__________________Toms point is well putï¿½if we approach specific tests based on exactly what they tell us and exactly what they do NOT tell us.For example in an asthmatic a pulmonary function test will show airway obstruction because we know that obstruction reduces flowrates therefore measuring reduced fliowrates means obstruction. F you know nothing else (no other parameters and you do not understand the biochemistry of asthma yet, as medicine one time did NOT) you can interpet the flowrate reduction and obstruction causes widely.Clinicians know, for example, that asthma victims present clinically with a lot of apparent stress. And that tracking episodes by clinical presentation showed stressed people with worsening bronchospasm. ERGO for many years asthma was considered a psychosomatic condition (stress induced)ï¿½late of course whenmore physiologic measurements were possible including invasive studies, allergy studies, immunochemisry et al and understaninding of intrinsic and extrinsic asthma evolved to the point that today asthma pathogenesis is understood so well that even lay people have a basic understanding of why asthmatics ï¿½do what they doï¿½In this case, Ericï¿½s response is very important to grasp in its exact phraselologyï¿½.iPET scanning as performed shows increased blood flow to specific areas of the brain. Thatï¿½s all it shows. Now, from a general understanding of neurovascular physiology one then can postulate and presume, when those findings are placed in the context of other measurements, WHAT that means. You can isolate a peripheral stimulus ï¿½balloon in the bumï¿½) which shows a consequent increase in blood flow to a specific area, and then postulate what that means.If you understand and consider and measure EVERY SINGLE PARAMETER at the same time that can produce this cause-effect relationship then you can state unequivocally what that event means.However, at this time, since this is yet to be done (take into account every single mechanism which may be occurring which can cause this event to be observed) what we are left with is ï¿½this suggestsï¿½ï¿½followed by the investigators supposition based on his or her interpretation of the data formed from his or her perspective depending upon training, credentials, experience and specialty bias.Which leaves the correct response, which was given: ï¿½ï¿½The brain does not seem to be getting the signals and processing them rightï¿½ï¿½ï¿½then again it may not be the processing at all it may be the afferent signal itself is alteredï¿½.or the brain may NOT be ï¿½processingï¿½ it right so we have to determine WHY. What are ALL the neurobiochemical variables which can cause this part of the brain to show increased bloodflow and what variables effect the patients self-reported experiences.So ï¿½seemï¿½ and ï¿½processing them rightï¿½ are just one grouping of the many phrases which taken in total mean ï¿½we donï¿½t know yet what that means ONLY that it happensï¿½.Which is what I think TR is trying to clarify for the readers.________________________ERICï¿½There is a growing body of evidence that suggests that altered HPA responses in IBS and other chronic pain syndromes, such as fibromyalgia, play a role in the body's increased sensitivity to painful and non-painful stimuli resulting in chronic pain and other symptoms of discomfort and distress."_________________Indeed, that is a correct statement. However, one must take into account the integration of the so called HPA in the grand scheme of neuroimmunoendocrine regulation of the brain-gut axis and its function.ï¿½Activation ofï¿½ the ï¿½HPAï¿½ can occur from a group of possible different precursor events which lead to ï¿½activationï¿½ of the HPA. To oversimplify, so-called ï¿½stressï¿½ ( much overused and poorly explained term) events will activate the HPA and thus the end organs and systems affected thereby. But the ï¿½stressï¿½ event can be top-down (ie: some psychoneural event) or bottom up (some immunologic event). Once ï¿½activeï¿½ the opposing potential origin of the stimulus be3cimes the affected system, and vice versa. A primary event such as a psychoneural ï¿½stressï¿½ event then can result in a multitude of upregulating activities which include activation of the HPA and increased activity o the cell-mediated and humoral immune response.CONVERSELY any primary immunologic event (immune response or hypersensitivity response) will activate the HPA and upregulate the CNS and ENS and other systems in kind. This fact cannot be overlooked, though it often is.This tutorial, which I will post the link rather than bury everyone under the entire thing for effect, is useful in better understanding the intricate nature of the interaction of the organ systems and how not all stimuli are sourced to either system aloneï¿½.thus it is, when taken in context of studies done elsewhere which tested other data points than just CNS blood flow, for example, it becomes clear that there is no single clear definitive explanation fro these events as of yet.From the American College of NeuropsychopharmacologyInteractions Between the Nervous System and the Immune System http://www.acnp.org/G4/GN401000069/CH069.html ______________Trbellï¿½There's a tendency to say it's in the gut or in the brain when neither one is at fault. it's the communication system that's fawlty.ï¿½_______Ah, a fan of Fawlty Towers perhaps?In a sense saying it is the communication system is at fault may be correctï¿½.but the communication systems that exist between the gut and the brain represent connectivity, and there is as yet no proof that the primary dysfunction is ion the connectivity itself. The behaviour of the connective systems (neuroimmunoendocrine systems all have means of communicating between the brain and gut) is what we can observe as apparently alteredï¿½.but we can see that in people with allergic reactions in the lungs as well, for example. So if you took that out of the context of knowing an IgE mediated reaction to an inhlant was the primary dysfunction (as WAS done for many years before the IgE-mast cell-antigen reacton was understood) then you would interpret what you see literally.Since we know that some people have been able to isolate mechanisms of IBS symptom generation provoked by psychological stress events, as well as IBS symptoms precipitated clearly by immunolgic events which occur in the guts anatomic structuresï¿½ (various), it is not only premature but probably fawlty when one tries to make a forcible case that IBS is a singular ï¿½functional disorderï¿½ linked solely to a pathogenesis of psychoneuro conseqeuences. You have to ignore to many other things observed by other investigators to state that. OR you have to inerpret EVERYTHING YOU OBSERVE solely in the context that the CNS can alter the function of other bodily systems, and disregard the fact that those same systems can alter CNS function. For example, a recent investigation in 2002 on people who present with GI symptoms that any doc would diagnose as ï¿½diarrheic IBSï¿½, and which symptoms were provoked by proven dietary challenge (double blind oral challenge) and who tested negative for any IgE allergy, found , In summary, "Significant increases in numbers of MBP+ eosinophils, IgE-bearing cells, and T cells were found in the duodenal mucosa of the patients when they were symptomatic in comparison with when they were asymptomatic and in comparison with healthy controls. Numbers of IL-4+ cells were increased and numbers of IFN-gamma+ cells were reduced in the patients when they were symptomatic in comparison with when they were asymptomatic and in comparison with the controls. There were no differences in total s-IgE levels between any of the groups."Remembering that the subjects responses measured occurred via food provocation and they manifest with typical pain, gas, diarrhea, etc. which was episodic, how do you interpret such findings? Well an allergist/immunologist might say that he has observed some revelation about intrdudodenal IgE arming mast cells in the absence of circulating IgE and say that this is some heretofore unobserved allergic phenomenon. While another, from a behavioral perspective, might assert that, since stresa can alter immune function, then what you may have is activation of the humoral and cellular immune system in response to stressï¿½.and then a tortuous explanation of how this is possible. Then the two camps can debate their perspectives as to which insult is primaryu and which is secondary until cows come home.Meanwhile, however, having isolated these people we can send them home with treatment instructions which will eliminate their symptoms quickly while the investigators and their minions debate the possibilitiesï¿½.or try to find the specific drug which will attenuate either the immunologic response (maybe cromolyn sodium) or the neurologic response (pick the antidiarrheal du jour). Or you can try to put them in behavioral therapy so as to try to alter blunt the response, or try to hypnotize them out of their diarrhea.Or, if you are practical, and have isolated what provokes the reactions seen thus the symptoms, tell them not to eat the foods which provoked the mediator release.For these subjects, if we are talking about helping sick people, which makes the most sense?________________ericThe problem partly with the c or d is that is in the gut where part of the problem is in how serotonin effects the colon.andï¿½Mikeralphso you are saying the immune system is not involvedericMike I have told you numerous times yes.______________One can keep saying something that is incorrect as often as one likes. This does not make it correct.Its pretty simple if one reads the literature inclusively. IBS symptoms can be provoked (precipitated) a number of ways, and reaction of mucosal and cellular immunocytes within the bowel mucosal and wall and circulation are one of the mechanisms. And they will respond to extrinsic factors (dietary provocation, including specific foods or chemicals to which a specific patient has lost oral tolerance) or intrinisic factors (the brain-gut-psychosocial models of IBS symptom generation). There is evidence to suggest that in some cases the immune system may be ï¿½armedï¿½ by an aberrant CNS/HPA mediated stimulus as a consequence of persistent psychosocial DISstress, and in the opposite extreme there is evidence which suggest that the immnocytes may be armed by a primary immune hypersensitivity mechanism (or more than one, as mast cells and T cells and NK cells and other aberrant reactions are observed) heretofore unseen prior to invasive studies of immunohistochemistry being done.In either case it makes little difference in the meantime, while the entire pathogenesis is researched further, in the clinical treatment of these patients. If you isolate the precipitating events and eliminate them, or blunt response to them, you can reduce or eliminate symptoms._______________Eric:Brain responses are assessed by positron emission tomography PET which can measure blood flow to brain areas in response to a particular stimulusï¿½.________Indeed you can see what happens, and a precursor physicoal event. You cannot quantify WHY it happens without testing quite a few other parameters inclusivelyï¿½every single thing which could account for what is observed and then ruling out those which come up negative. This has ywet to be done, so hypothesis is the rule of the day. All the discussion that follows, and descriptions of findings, are subject to the exact same footnote. Thatï¿½s why the investigators always qualify what they say with language like ï¿½suggestsï¿½, ï¿½may lead one to concludeï¿½, etc.For example:ï¿½ï¿½.suggests that brainï¿½s mechanisms of attention/arousal are activated ï¿½.ï¿½We have a suggestion of a mechanism being ï¿½activatedï¿½, then we have to dissect what ï¿½activatedï¿½ entails and then every biochemical event which can result in this ï¿½activationï¿½. There remains much work to be done to separate possibility from actuality.ï¿½.further onVisceral and somatic perception studies and PET imaging have demonstrated that each of these conditions have specific responses to painful stimuli and that patients with both IBS and FM may have responses to somatic and visceral stimuli that are uniquely different from that of IBS alone and FM alone."Eric in response to tom:ï¿½Nothing here is any kind of interpretation. They are factsï¿½On the contrary the cited literature and tutorials are consistently rife with, and based upon, possibility, supposition, conjecture, and probability analysis. That is a fact. The part that is fact is the part that is factï¿½.the quantified-action-response relationships (blow up balloon see blodd flow increase). That part is fact. Descriptions of known physiology which CAN result in the observed response is factï¿½but no one has concluded that any given mechanism IS FACTUALLY the mechanismï¿½only suggests or possible. That is the stage of investigations from both the psychobiological models of IBS as well as the perspective from the other divergent perspectives. There is an abundance of quantitative analysis of eventsï¿½not just intracranial blood flow eventï¿½.and all that is act is that quantitative analysis. Everything else is, so far, basically conjecture. Objectivity makes that self evident wherever objectivity exists._____________Essence:Eric,I'm confused. At one point, did you not post information linking IBS to the immune system?Didn't we watch the graphics and listen to Dr. Drossman discuss how the autoimmune system was connected to IBS?If IBS is just one of many dysfunctions that I have... that's fine.... but from what I ascertained from the UNC chats, everything including limbic system was connected.Clarification?_____________Hopefullly some of what I referenced above will help you put it in proper context. If you want to study the functions of the immune system and how it affects the functions of other organs including the bowel and the brain here is a good place to start:Online from Western Kentucky University:Immune Cells http://bioweb.wku.edu/courses/Biol328/Cells.htm Immunology, Inflammation, Mediatros tutorials http://bioweb.wku.edu/courses/Biol328/default.html The thing that confuses patients sometimes is that we do not really comprehend the perspective of different doctorsï¿½where they are coming from and why this determines how they approach certain diseases.For example the mission statement below makes it very clear WHAT the mission of the UNC Center under discussion here actually is:ï¿½Mission:To advance the biopsychosocial understanding and care of patients withFunctional GI &Motility Disorders through research, training, and education.ï¿½The MISSION of the center is to expand upon the biopsychosocial model of the possible pathogenesis of IBSï¿½its NOT to investigate any possible aberrant immunologic or hypersensitivity dysfunctions (food provoked or otherwise) in any IBS population so we do not look to them to study that nor will you find it. It is not their schtick. You look to them for information on this specific approach.This is the approach as the center leaders have background in psychology and psychiatry integrated with gastroenterology. The perspective will be different than a team with an approach from immunology/allergy board certification combined with gastroeneterology. This is not bad or goodï¿½it is just a factï¿½everyone exists to fulfill a specific purpose, and it is good in the sense that it adds diversity to the approach to the syndrome, increasing the odds of coming to a full understanding of all the possible mechanisms.On the flipside if you want people who are looking into the symptoms for aberrations in primary immune function and the provoking mechanisms you would, for one example, go to Sweden and see what the immunologists/allergists approach is at several centers there. They do not even start with the supposition that people who present with the symptoms of so called IBS have any mystery disease for which there is no physiologic basis. They rule out other pathology like everyone else, but then also rule out (through testing) all possible known hypersensitivity responses which could provoke the symptoms seen then go probing into the plumbing of the small bowel and its local immune respsone. So they are collecting and looking at cells, cell reactions, mediators and markers and finding all kinds of fun stuff too.Now if you could put them alllll together you would have a broad view of the IBS population when it is defined by symptom-based criteria, then start deciding which quantitative analysis should be used to exclude someone hence forth from being diagnosed with IBS, and who do you leave IN.Or someone somewhere has to do ALL the procedures on the same patients at the same time and it will be easier to understand. I do not see this funded anywhere yetï¿½though there are those trying to find a way to fund such an investigationï¿½.total top down integrative investigation of the provoking events, mechanisms, and all possible physioloigc markers.All the discussion that followed therafter, with the focus on 5HT[x] and suggesting that there are no physiologic markers seen in IBS patients is just myopiaï¿½.there a re a multitude of neuro and endocrine mediators of CNS, ENS and other giut related functions which may be ï¿½activeï¿½ in IBS patientsï¿½in fact may even at times represent precurosor events to any 5HT involvement.Gotta reun but here is a quickie example of what we cannot forget about gastroneuroimmunocontrol mechanismsThere are multitudes of possibilities, and they come from both directionsï¿½top down and bottom up models of IBS pathogenesisï¿½and there is as yet no fully integrated picture of which parts are actually involved and which are notï¿½plenty of good theory to go on though.Gastroenterology 1996 Dec;111(6):1683-99	The immunomodulation of enteric neuromuscular function: implications for motility and inflammatory disorders.Collins SM.Intestinal Diseases Research Unit, McMaster University Health Sciences Centre, Hamilton, Ontario, Canada.Gastrointestinal motility and sensory perception are altered in a variety of mucosal inflammatory conditions of the gut, ranging from peptic esophagitis to ulcerative colitis. Studies in animal models now clearly indicate a causal relationship between the presence of mucosal inflammation and altered sensory-motor function. In many instances, these changes occur in the absence of any discernible encroachment of the deeper neuromuscular layers by the inflammatory infiltrate, which remains largely within the lamina propria. Accordingly, attention has focused on local sources of mediators, and recent studies indicate that smooth muscle cells and enteroglia are sources of and targets for cytokines such as interleukin 1 beta and interleukin 6. In several instances, neuromuscular dysfunction persists after mucosal inflammation has subsided; this state may be maintained by locally produced mediators. Studies also show the ability of enteric muscle to modulate lymphocyte function via major histocompatibility complex II-restricted antigen presentation. Clinical observation and experimental data also suggest that nerves modulate intestinal inflammation via local release of proinflammatory neuropeptides (substance P) and via the activation of extensive circuits that may involve the brain. Taken together, these findings provide plausible explanations for a variety of clinical scenarios ranging from inflammatory bowel disease to pseudo-obstruction syndromes and subgroups of functional bowel disorders.Vet Res 1996;27(4-5):427-42Integrative neuroimmunology of the digestive tract. Theodorou V, Fioramonti J, Bueno L Ecole superieure d'agriculture de Purpan, Toulouse, France.The epithelium of the gastrointestinal tract is continuously exposed to the external environment containing food antigens, microbes and other pathogens. Immunologic and nonimmunologic mechanisms contribute to the neutralization and elimination of these foreign antigens. The immune system of the intestine is the most extensive in the organism and involves diffuse populations of immune cells, lymphoid aggregates and intraepithelial lymphocytes. On the other hand, the functions of the digestive tract contribute to the overall host defense (mucus secretion, gastric acid secretion, water and electrolyte secretion and peristaltism). These functions are regulated by intrinsic and extrinsic nervous systems. It is currently recognized that the physiological and pathological responses of the intestine require an integrate neuroimmune network. Such neuroimmune regulation is based on anatomical and biochemical supports. Indeed, there are membrane-to-membrane contacts between axonal varicosities and the immune cells. Specific receptors for neurotransmitters such as substance P, vasoactive intestinal polypeptide and somatostatin have been identified in many immune cells. Nerve profile change has been described under pathological conditions such as parasitic infections and acute phase of inflammation. In addition to supporting the growth and survival of several populations of nerves the classical nerve growth factor (NGF) has been shown to affect an immune cell population by inducing mast cell hyperplasia. Furthermore the NGF can induce mast cell degranulation, acting directly on mast cell membrane NGF receptors or indirectly by NGF-mediated release of substance P by peripheral extrinsic or intrinsic nerves. Moreover, non-immune cells such as epithelial and smooth muscle cells can produce immunologic messengers under pathological conditions such as infectious diseases or inflammation. Besides the local regulation of gut functions, neuroimmune control can be exerted at extra-intestinal sites. During physiological and pathological conditions, gastrointestinal secretions and motor events are strongly regulated by the central nervous system. Moreover, infectious agents can induce cytokine and particularly interleukin-1 release by the brain astrocytes and microglial cells which have been shown to play a pivotal role in fever induction and modifications of the gastrointestinal functions. Visceral afferent fibers play a pivotal role in 'cross-communication' between central sites and immune response. Recent studies evoke, more specifically, the role of vagus as a key modulatory participant in the close relationship between the extraintestinal nerves and the immune system. Future work in this field will clarify the role of the different participants in the intimate communication between the gastrointestinal tract, immune system and central nervous system.: Reprod Nutr Dev 1994;34(6):513-25	Neurohormonal control of intestinal transit.Bueno L, Fioramonti J.INRA, Department of Pharmacology, Toulouse, France.This review shows that numerous neuropeptides and hormones are involved in the regulation of intestinal transit. Many gastrointestinal hormones known to act on smooth muscle to influence muscle contractility also play a role in the genesis of abrupt changes associated with alimentary behaviour. In many monogastrics and ruminants, the cyclic occurrence of the migrating motor complex (MMC) is linked to peripheral hormonal factors only slightly influenced by the nature of food. Motilin is the major hormone involved in triggering the gastric migrating motor complex while somatostatine and enkephalins are implicated in the propagation along the small intestine. Other hormones, like CCK8, insulin, gastrin, and neurotensin, trigger the development of an intestinal feed pattern but CCK released at the central nervous system ventromedial hypothalamus is involved in maintaining the postprandial type of activity. Gastrointestinal transit may be altered in physiopathological situations in which CRF, TRH and some cytokines (IL1 beta, TNF alpha) play an important role.Can J Gastroenterol 1999 Mar;13 Suppl A:42A-46AEffects of inflammatory mediators on gut sensitivity. Bueno L, Fioramonti J Department of Pharmacology, INRA, Toulouse, France. lbueno###toulouse.inra.frOver the past decade, attention has been paid to the role of visceral sensitivity in the pathophysiology of functional bowel disorders, especially irritable bowel syndrome, and visceral hypersensitivity is the most widely accepted mechanism responsible for both motor alterations and abdominal pain. Inflammatory mediators sensitize primary afferents, especially C-fibre polymodal nociceptors, favouring the recruitment of silent nociceptors that give rise to secondary spinal sensitization. After local tissue injury, the release of chemical mediators such as potassium ions, ATP, bradykinin and prostaglandin E2 directly activate nerve endings and indirectly trigger the release of algesic mediators such as histamine, 5-hydroxytryptamine and nerve growth factor from other cells, which, in turn, stimulate proximal afferent nerve endings and silent nociceptors. Among the intermediary structures activated by inflammatory mediators and susceptible to the release of proalgesic substances, mast cells and platelets play a crucial role; however, immunocytes such as macrophages and neutrophils or sympathetic nerve terminals are also candidates. Moreover, events likely to activate synthesis of mediators by mast cells, such as stress and septic shock, also trigger colonic hypersensitivity. Prolonged visceral hyperalgesia may also depend on spinal sensitization. A number of substances are candidates to play a role at the spinal cord level in mediating painful and nonpainful sensations. Among them, substance P, dynorphins and glutamate play a pivotal role in postsynaptic sensitization, particularly during and after gut inflammation. Finally, despite the complexity of the relationship between inflammatory mediators and gut hypersensitivity, numerous results strongly suggest that alteration in neuroimmune communications at the gut level may trigger a series of events that give rise to chronic changes in visceral sensitivity.___And on and on it can go to make the point....integrated ot "holistic" approaches which are inclusive, not exclusive, gibve rise to a broader view of the possibilities.MNL


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## Mike NoLomotil (Jun 6, 2000)

OOPS...twitchy finger twitched twice....







SorryMNL


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## trbell (Nov 1, 2000)

Mike, Why don't you wite a book like eric did here on a thread? it might make it easier to follow.tom


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## eric (Jul 8, 1999)

Some comments and sorry Lorianne. I knew this was coming. And I knew this would basically turn all off and hijack the thread to try to put the focus on foods with Mike. Which makes it harder to talk about any other aspects, or get anything across, except by Mike that foods cause D IBS, all I a trying to say it is a complex brain gut interaction processes. This has been going on for years now.First you have to understand that Mike, is involved in a company that does food testing. He is not an IBS research center like the extremely well respected around the world center on IBS and other functional disorders UNC is, which is also a school on nurtrition and a lot of other focuses in health.You have to ask yourself at that point do you want your info from Mayo, UCLA and UNC or the leap website. Where do you look for accurate info. This has nothing to do with if your personal doc is bad or not or explain IBS to you well or not. This is to expand the horizons and treatment options. While I am being told I have to narrow of a focus.That was also a really low shot at HT there Mike. Good for you take a shot at what they now from tenty years of IBS research works on global symptoms, not just think your d away. Comments like that show me how much you really want to help people in the big scheme of things.maybe this is what he meant." The experience to date may be outlined as follows: * Reported success rates range from approximately 70-95% in all studies with any significant number of patients for example, in the work of the Manchester group in England 4,5,13 and our studies 6,7. * The improvement enjoyed from this treatment often lasts at least two years after the end of treatment 5. * All major IBS symptoms improve from this kind of treatment abdominal pain, diarrhea/constipation, and bloating. * There are some indications that individuals with certain characteristics are somewhat less likely to benefit from this kind of treatment5,7,13: People with very little hypnotizability perhaps 15-25 % of all people, persons with psychiatric disorders, and maybe according to one report males with diarrhea-predominant type of IBS. * This treatment can be effective also when people are treated in groups14. * In addition to effects on physical symptoms, the treatment commonly improves psychological well-being and life functioning substantially 6,7,13,15 and can have long-term positive effects in reducing disability and health care costs and improving the quality of life of IBS patients 15.From an actual IBS research center and not just one. This is not because IBS is "all in your head" either.To highlight"All major IBS symptoms improve" http://www.aboutibs.org/Publications/HypnosisPalsson.html - It is one of the most successful treatment approaches for chronic IBS. The response rate to treatment is 80% and better in most published studies to date.- The treatment often helps individuals who have failed to get improvements with other methods see for example: Whorwell et al., 1984, 1987; Palsson et al., 1997, 2000.- It is a uniquely comfortable form of treatment; relaxing, easy and generally enjoyable.- It utilizes the healing power of the person's own mind, and is generally completely without negative side effects.- The treatment sometimes results in improvement in other symptoms or problems such as migraine or tension headaches, along with the improvement in IBS symptoms.- The beneficial effects of the treatment last long after the end of the course of treatment. According to research, individuals who improve from hypnosis treatment for IBS can generally look forward to years of reduced bowel symptoms. After treatment still improve. That says a lot of what it is doing on IBS!!!!! http://www.ibshypnosis.com/whyhypnosis.html He constantly makes comments I for one and other IBSers are not looking at the whole picture or even worse the researchers. meanwhile he constantly focuses on one problem, foods. This is simplistic approach in IBS, everyone in the world knows foods are a problem in IBS FOR MANY REASONS not just immunology, that is one part in IBS and people can have other conditions and there is a lot of over lapp of functional conditions, is that from foods? There are also very real food problems. Like Celiac or fructose malabsorbtion ect.. that some people have along with IBS and its well known some of the reasons foods trigger symptoms, like mast cells for one, but mast cells can be triggered for a lot of reasons, not just foods. Because of this single focus on foods its harder to present all of the other aspects in IBS, not food related. he says I don't focus on foods and only stress, I am trying to point out their is a much bigger picture that is important to have in mind with all this. Taking into account the what things effect the gut.He also makes comments that immunologists are not working with the UNC center and other well respected IBS centers around the world like UCLA and Mayo for example, among may others.Some of the most respected leaders in the field of neurogastroenterology, immunology, gastroenterology and other diciples are looking at it constantly.He also mentioned the prefrontal corrtex without mentioning the acc, an important player in IBS, these centers are not making this stuff up, they are basing a lot on what they have found already through years and years of research and combine heads from centers around the world and their is more then what Mike is saying here and models that may help to explain complex systems. there is a lot to learn, but they are not totally clueless as some would like others to believe. Mike's model does not expalin why they developed sertonin gut drugs because they found their was a problem in the release of serotonin in the gut, not by foods, although it can be also triggered by foods, but not solely. Nor does he explain the role of other mechanism in IBS they have found altered, so they have found an altered stress responce and an altered gastro reflex responce. The later is a big player in D predominate IBS and has to do with calorie content and signals from the stomach to the lower intestines. The colon responce is altered to the signal and hence d.Nor does he explain the hypersensitivity of nerves that line the gi tract in IBS, only that foods are the cause of d predominate IBS. Well from the post above the act of eating releases serotonin and causes d or c.I will point this out again and again.


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## trbell (Nov 1, 2000)

LoriAnn, You are normal. All this stuff is really confusing. As eric said somewhere in the posts above the prefrontal cortex is a ig player in ibs. That means that some of us with ibs have probllems with civil social interaction and the finger I'm pointing is pointing at me today.I think I wrote a poem here?tom


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## LoriAnn (Jan 31, 2002)

There is an enormous amount of information to take in. I need to digest it more before I comment. I am keeping a completely open mind on all points of view, as it improves my understanding. I deeply appreciate all the efforts made to contribute to this topic.I will be back tonight to read through it again.Lori


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## LoriAnn (Jan 31, 2002)

Wow, where to start?I spent the day thinking about what I have read and making notes to myself, the best way to start I suppose is to explain my situation without turing it into a huge life story.I have had bowel problems from the time I was put on solid food. Had my first upper GI when I was 2, as well as some other tests. All fine. Mom took me off wheat for a couple of years and I improved but never was a really healthy kid.Had a fairly bland diet growing upAround 16 I developed a host of more serious problems, asthma, ovarian cysts, breast cysts etc, rashes etc. D was still a problem but I was use to that, everyone in the family had a problem so I thought it was normal. At 23 I was told I had severe PMS, at 24 after a bad time with D and bleeding I was told I had IBS and my gallbladder was removed(no tests were done). At 25 I was fairly crippled with body pain, told I have FM and Levator syndrom. Placed on elavil for 8 years, this did a lot to help with both pain & IBS, but gradually it stopped working, even with increases. No replacement was tried. In Oct 2001 I began the worst D attack of my life with bleeding(it was also a very stressful time) I ran to the bathroom upwards of 20 times a day, I could not even drink water without running, the doctor said it was gastritis and prescribed Nexium, it didn't get better, he continued to try various similar drugs, no effect. By Jan the stresses were resolved but I wasn't getting better and dropped 20 lbs. In Feb I began to have the most vicious attacks of abdominal pain, I was given more pills and drinks, had an endoscopy done and Upper GI. My heart began to go wild from the malnutrition.I stopped trying to eat and lived on Jello, gradually adding things to my diet very slowly, first chicken broth, then plain rice. I got better on my own, stayed on a strict gluten free diet, avoiding anything that was a known irritant, coffee, tea, chocolate, peanuts, citrus etc, vinegar, alcohol etc., after 6 weeks my heart was back to normal, after 2 months I felt better than ever before and started to regain the weight I had lost.Suddenly in June, without warning it struck again, and again and again. By August it was decided that a complete hysterectomy might help me, this was immediately done. They suspected Endo in the diaphagm. No lap was done, no investigation, just immediate surgery. I developed a host of complications including infections & bloodclots. But my problems with these "attacks" did not improve, I have lost 35 lbs and I was never big to begin with, I am now 5'9" at around 104lbs. I have seen 13 doctors in the last year, 8 of them in the ER and each one for no more than 15 minutes. I have been hosiptalized 6 times, totalling 6 weeks. I have never had a colonoscopy done, or a stool sample taken in all this time. The first time I saw a GI doctor was after my mother flew into a rage at my GP for allowing this to go on so long, 10 months after it started. I met with him once, he told me to go back to a normal diet and he ordered an abdominal MRI, prescribed Levsin, Reglan and Domperidone over the phone, I have not heard from him since.The only test I had done DURING one of these attacks was an upper GI that showed the small bowel was inflamed, the radiologist wrote "appears to be the result of an allergic or intolerant reaction", my GP said "he was only guessing" and this was dismissed. I begged for allergy tests which were finally done last week, it appears I have no allergies, not even to dust or dust mite. The allergist told me that tests for intolerance are not available in our province, and all I could do was an elimination diet (been there, done that)I have grasped at every straw held out to me, I have done everything I was told, and tried everything that was even suggested to me. The D attacks have subsided to just several times a week, but the attacks of unbearable pain have continued, I have seriously considered suicide to escape the pain. Thank God it isn't constant or I no doubt would have ended it all by now. Most of the attacks happen at night while I am sleeping and I wake up in terrible pain. I understand this is unusual, that abdominal pain will rarely wake someone.In Dec I told my GP this and he prescribed Paxil as well as morphine. I rarely touch the morphine, but it provides me a small measure of comfort to know that it is here, if I can't take the pain anymore.Paxil has done very little for me in terms of reducing pain or helping with the bowel problems, but I believe it has helped me cope with the frustration and self pity, or perhaps I am too numb at this point to care.So, based on everything I have read, it would seem I have 2 seperate problems going on. No doubt one is affecting the other. To be perfectly honest I have some doubts about the IBS diagnosis based on the fact that some very important testing was neglected and because I do not seem to fit the criteria for IBS, but having FMS.....well the 2 do seem to go hand in hand in many cases.It is certainly true that bowel function can be affected by what we eat, thats true of most people with IBS, but considering how many changes I made to my diet, (and I did improve for a period of 4 months) but it wasn't enough to resolve my problems.It is also true that how we think and feel can effect bowel problems which I witnessed every time I had a stressful moment. It is also true that stress will effect most medical conditions, parkinsons, MS, heart disease etc. So most people with chronic health conditions would benefit from some type of CBT, not just people with IBS.Now...........The FMS PET scan I saw showed differences in the brain even without painful stimuli........so how does the pain induced IBS PET scan differ from an IBS patient who is not experiencing pain.....is it still different or does it appear "normal"?What about when I have diarrhea without cramps?Does that mean my brain isn't receiving any pain signals? Is is normal to have D without pain?Would the picture be different in naturally occuring pain rather than induced pain? Have any PET scans been done during actual IBS attacks?Vigorous exercise stimulates endorphin & seritonin production? If so why are people with FM told to engage in gentle exercise....obviously it would make the pain worse in simple terms, but I mean that in the case of people with IBS/FM increasing endorphins seems to fail to have the desired effects.If each group has different PET scans then it would seem people with combined FM/IBS are in a class by themselves. Its been my experience that people with FM feel that IBS is a symptom of that condition, yet I know in my case the IBS came long, long before the FM, so is FM the consequence of prolonged and untreated IBS?If elavil helped for a time, why doesn't the paxil? I realized they are different drugs but they are advertised as having similar effects. I understand better now HOW they work, but I'm not sure why they stop eventually? Does the brain become tolerant to them?Seems like I have a million more questions, but this is getting really long, I will keep reading and keep making notes on points I want to address.Thanks again for all the info.Lori


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## Guest (Feb 26, 2003)

I can identify with much of what you are writing, Lori, as I developed IBS before the FMS as well. Do you also have CFS?In the past few years I've also progressively lost more weight, although not as wispy as what you described yourself at 5'9" and 104 pounds.Regarding endorphins, I go for them whenever I can because for me they do help... a lot.I can also identify with the allergies which are becoming worse also as time goes by.The IBS diagnosis would need to come from your doctor.I have also considered suicide more than once, but loving people in my life have intervened.I've gotten to a point in my life where I don't trust most doctors/meds/treatments anymore and I do what I have to do to survive... one of which includes avoiding most G.I. tests because they almost always make me worse.I've also gotten myself to a point now where how I view what is happening to me is more of a "so what?" attitude.... because if I dwell on it, the anxiety perilizes me. I wouldn't classify it as denial... I'm long since past that..... just that the more I make out of it, the harder it seems to be for me to get past it all, if that makes sense?I used to awaken with abdominal pain on a regular basis, but since the self-hypno, that has improved significantly.I have also sometimes had D without pain.There IS a connection among all of the symptoms.At this time in my life, most of my relief appears to be coming from redeveloping a link with my spirituality. If I think about all that is wrong with me, I can't handle it.... so I am giving it to God and doing the best that I can no matter what.Hope this helps, Evie


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## Mike NoLomotil (Jun 6, 2000)

Short return.....__________________________TR:Mike,Why don't you wite a book like eric did here on a thread? it might make it easier to follow._____________________LOL well 3 reasons1.	Not enough time2.	There are already enough books and papers to read without me adding to the soup3.	The whole subject is intrinsically hard to follow as it is very very hard to form an all-encompassing viewpoint, and take in all the possible anglesï¿½so conveying such a viewpoint is even harder, especially when recipients have fallen into the selective thinking habit. This is not something that can be changed easily, so one has to just accet that this is how it is and put information out as one best knows it to exist and can best expound on it and hope for the best.Hey ï¿½I yam what I yamï¿½ (Popeye, Sailor Man)--------Ah we are OFF to the races again!!!--------"Some comments and sorry Lorianne. I knew this was coming. And I knew this would basically turn all off and hijack the thread to try to put the focus on foods with Mike."-----LOL. Anytime someone (present company included) adds to any thread in any fashion which is ï¿½inclusiveï¿½ of all aspects of the conditon when certain aspects are being either ignored or misstated, you cry foul, and shout that they ï¿½:hijackedï¿½ the thread or that someone has somehow victimized someone.Pointing out that material is being ignored, or morphed from ï¿½postulateï¿½ into ï¿½factï¿½ and material is even being selectively deleted when holding forth to sick people who suffer the condition and look for guidance is not hijacking. Adding it back in is ï¿½inclusivismï¿½. ----ahh just getting cranked up for another ï¿½White Hat: Black Hatï¿½ and ï¿½victimï¿½ scenario I seeï¿½..----ï¿½First you have to understand that Mike, is involved in a company that does food testing.ï¿½-----ï¿½Actually this is not wholly correct. Let us make sure we are clear when we describe someoneï¿½s present affiliations. I am ï¿½involvedï¿½ as a shareholder, Board Member, Patient Care Committee member, and the Chief Operating Officer of a licensed medical laboratory and Disease Management company (Signet Diagnostic Corporation). This is common knowledge. See the link posted below my name and the several times I posted my bio in the past and the thousands of posts I have made on the subject. I wuld post the threads of a few but you know exactly what I mean and the links would serve no purpose but to add clutter.Now, let's be very clear since you want to discuss it as if to imply that it is somehow unsavory.The companyï¿½s focus on detecting non IgE mediated (cell mediated) reactions to food and chemical provocation is driven by the known biological realities and facts as regards these types of aberrant immune functions, and their applicability to IBS, as it is set forth in the literature for a period of 20 years now. It is summarized succinctly in the Merck Manual , which resides on every doctors shelf from the time he became a medical student until today, as follows: ----------------------Page 1051 of the hard copy of the 17th edition of the Merck Manual, and online Merck Manual at http://www.merck.com/pubs/mmanual/section1...ter148/148b.htm "Recently Food Intolerance was found to be responsible for symptoms of some patients with the IRRITABLE BOWEL SYNDROME, confirmed by double-blind food challenge. An increase in rectal prostaglandin levels was noted when a reaction occurred.Preliminary information suggests the same phenomenon may take place in patients with chronic ulcerative colitis.ï¿½ ----------------------------The research immunologist led group who developed Signets patented (2000) and medical insurance-reimbursed testing methodology to accurately isolate, within this population, ï¿½food intoleranceï¿½ reactions and then treat (them) effectively, also included a team comprised of numerous consulting researchers and clinicians. First an foremost is the worldï¿½s leading authority on the subject of food allergy and intolerance has been Signet's leading independent consultant for a number of years. His most recent medical text published is:FOOD ALLERGY AND INTOLERANCE, Professor Jonathan Brostoff, MD, Stephen Challacombe, MD (NEW 2002) http://www.amazon.com/exec/obidos/ASIN/070...product-details Other Books by: Professor Brostoff http://www.greenleaves.com/bookcat/by_brostoff_jonathan.html [EDIT: OOPS THE LINK IS DEAD...WHEN I FIND THE NEW ONE WILL JUST POSY IT. THIS IS WHAT USED TO BE THERE:Asthma: The Complete Guide to Integrative Therapies- by Jonathan Brostoff, Linda GamlinThe Complete Guide to Food Allergy and Intolerance- by Jonathan Brostoff, Linda GamlinFood Allergies and Food Intolerance : The Complete Guide to Their Identification and Treatment- by Jonathan Brostoff, Linda GamlinImmunology- by Ivan Roitt(Editor), et alThe Allergy Bible : Understanding, Diagnosing, Treating, Allergies and Intolerances- by Reader's Digest(Editor), et alAutoimmune Disease : Aetiopathogenesis, Diagnosis and Treatment : Essays in Honour of the Retirement of Professor Ivan Roitt Frs- by Peter M. Lydyard(Editor), Jonathan Brostoff(Editor)Case Studies in Immunology- by Jonathan Brostoff, et alCase Studies in Immunology: Companion to Immunology, Fifth Edition- by Jonathan Brostoff, et alClinical Immunology- by Jonathan BrostoffClinical Immunology : An Illustrated Outline- by Jonathan Brostoff, David K. MaleImmunology- by Ivan M. Roitt, et alImmunology : Interactive 2.1- by David Male, et alThe Complete Guide to Hay Fever : The Latest Research & Techniques for Coping With Hayfever- by Jonathan BrostoffFood Allergy and Intolerance- by Jonathan Brostoff, Stephen J. ChallacombeImmunology- by Ivan Maurice Roitt, et alInmunologia Clinica- by Jonathan Brostoff, et alIntroducing Immunology- by Norman A. Staines, et al -----------------------------------The team also included a diverse group of physicians and registered dieticians who worked with the technology seeking the best applications clinically, for a period of (3) years, in a private clinic operated by the company in Boca raton, Florida. They worked with refractory IBS patients (IBS sufferers who were unable to gain relief from any of their existing doctors or treatments) and then developed a Disease Management Protocol for those patients whose IBS (and Migraine as well) are provoked by food and chemical intolerance (this is the diarrheic-component populationï¿½c-types rarely show evidence of cell mediated reactions to oral challenge). The resulting program was first shown to a few clinicians about (2) years ago, and is being adopted by more each day as the information is disseminated and the program is shown to physicians, tried out, and then adopted as they get good results (most based on symptom surveys and QOL assessment by SF36 reports).The protocol, called LEAP, (www.nowleap.com again as it always shows below my name every time I say anything anywhere) is in compliance with the content standards for Disease Management Programs set forth by the Disease Mangement Association of America (DMAA, of which I am a member http://www.dmaa.org ) . The program consists of a method of patient selection (predetermine who can be helped and who cannot), outcome assessment tools, MRT testing (the companies proprietary method of blood testing for food intolerances in ISB, Migraine and othersï¿½now paid for by over 300 insurance plans nationwide and growing), a patient-specific oligoantigenic phased diet followed by a patient specific rotation diet, a Stress Reduction (Hypnotherapy) Program on CD (developed by these doctors here www.ibstherapy.com Dr. Leonard Weinstock, Board certified in Gastroenterology and Internal Medicine, Barnes Jewish Hospital, St. Louis and Washington University medical School, and Dr. Thomas Lipsitz, Board Certified in Psychology), and a complete program of implementation set forth for the physician and patient to follow.-----ï¿½ He is not an IBS research centerï¿½-----Uh, yeah, I do not ever recall claiming to be a research center, or researcher. Rather I incessantly declare myself to be a mere student of those who do research and clinical treatment of patients who suffer allergic and non-allergic chemical and food hypersensitivity reactions, their symptoms, and their consequences. I have said numerous times that I am what I amï¿½a retired Registered Respiratory Therapist with 30 years experience in patient care and education, medical technology development, and who is a lifelong sufferer of diarrheic IBS. I was, by the age of 40, a GI cripple barely able to run my AMA accredited private training schools for RTï¿½s at that time. I have said I was brought to remission by the work of the research and clinical immunologists and allergists I later came to work with (in 1995).Their dietary therapy instructions (oligoantigenic dietary therapy based on early methods of cell mediated testing) put me in remission in about 1993 I recall. As an IBS victim and healthcare professional, bound by the ethics of my profession, I came to work with these doctors so as to perpetuate their knowledge and its application to the betterment of the lives of those who suffer from food and chemical intolerance symptoms. This includes, as says the standard manual of diagnostics and therapeutics and bountiful literature (which I also made certain to become at least a dedicated student of before speaking to any sick person about it), specific IBS patients, Migraine patients, and several other conditions where food and chemical sensitivities are comorbities which worsen the underlying condition (such as IBD as the Merck Manual states, and certain FMS and CFS victims).------ï¿½ï¿½. like the extremely well respected around the world center on IBS and other functional disorders UNC is, which is also a school on nurtrition and a lot of other focuses in health.ï¿½-----I guess the reader is supposed to infer that this is stated in juxtaposition so as to imply that I have somehow "dissed" UNC. On the contrary, if one reads everything I ever write objectively, I have not only never expressed any such disrespect for any of the physicians or the institution, rather I recall I have pointed out that what they do and their approach is valuable. I think saying ï¿½this is a good thingï¿½ is, well, no simpler way to express ones opinion with precision.Pointing out a mission statement for any clinical and research center is done so as to keep in mind what that centers self-declared perspective is, and their goals are, relative to their reason for existence. Contrasting it with the mission of others of different credential and perspective is merely stating fact. Why someone would suggest otherwise must be explored by that person examining their own motives for morphing someone elseï¿½s actions into something they are not.------ï¿½You have to ask yourself at that point do you want your info from Mayo, UCLA and UNC or the leap website.o ask yourself at that point do you want your info from Mayo, UCLA and UNC or the leap website. Where do you look for accurate info. This has nothing to do with if your personal doc is bad or not or explain IBS to you well or not. This is to expand the horizons and treatment options. While I am being told I have to narrow of a focus.ï¿½-------I am perpetually puzzled and bemused as to how anyone can state that I have suggested that these are mutually exclusive activities? When in fact this is my exact pointï¿½to be Inclusiveï¿½to look at OTHER PERSPECTIVES as there is valid information there as well.I cannot express it better than to quote physicians with expertise in this areaï¿½This is the perspective that many other doctors and researchers expressï¿½which contrasts in some ways with the perspectives of the physicians that Eric works with. So my point is not that they are mutually exclusive. Nor have I ever said ï¿½get your info from the LEAP website instead of UNC UCLA etcï¿½. Thatï¿½s simply false.Rather I suggest that IBS victims also consider this contrasting perspective... -----------------------ï¿½Considerable confusion is now arising over the relationship between food intolerance and the Irritable Bowel Syndrome (IBS). Although the name has been hallowed by long usage, IBS is not a distinct entity but merely a collection of disorders which are characterized by abdominal symptoms but no obvious organic pathology. G.W. Thompson forecast in 1985: ï¿½the IBS is organic; that is all sufferers will eventually be found to have measurable, unique pathologic defects.ï¿½When that happy day arrives, the term ï¿½IBSï¿½ will no longer be used, and each patient will receive a more precise diagnosis. Until then it is sufficient to appreciate that food intolerance represents an important proportion of the conditions which together make up IBS.ï¿½John Hunter, MD, FCRPDirector or Gastroenterology and Consultant PhysicianAddenbrookeï¿½s HospitalCambridge, United KingdomFromï¿½Food Allergy and Food Intoleranceï¿½ Second Edition 2002J. Brostoff, MDS. Challacombe, MDSaunders --------------------------IF this makes sense to you, then I always suggest the patient learns more by reading these booksï¿½IBS: A DOCTORS PLAN FOR CHRONIC DIGESTIVE TROUBLESBy Gerard Guillory, M.D.; Vanessa Ameen, M.D.; Paul Donovan, M.D.; Jack Martin, Ph.D. http://www.amazon.com/exec/obidos/ASIN/088...3369143-6824157 ï¿½FOOD ALLERGIES AND FOOD INTOLERANCE: THE COMPLETE GUIDE TO THEIR IDENTIFICTION AND TREATMENTï¿½, Professor Jonathan Brostoff , M.D.. Allergy, Immunology and Environmental Medicine, Kingsï¿½ College, London http://www.amazon.com/exec/obidos/ASIN/089...6487508-3420903 FOOD ALLERGY AND INTOLERANCE, Professor Jonathan Brostoff, MD, Stephen Challacombe, MD (NEW 2002) http://www.amazon.com/exec/obidos/ASIN/070...product-details ------------------------In fact I do not recall ever, in thousands of posts, ever telling anyone to even GO to the LEAP website for informationï¿½except perhaps if a person asked about their symptoms and I suggested they complete the private Symptom Survey which is then reviewed by a respected Registered Dietician (respected within the ADA I mean..)---------------------ï¿½That was also a really low shot at HT there Mike. Good for you take a shot at what they now from tenty years of IBS research works on global symptoms, not just think your d away. Comments like that show me how much you really want to help people in the big scheme of things.--------Sorry, but you cannot try to morph what I posted into a ï¿½Shotï¿½ at HT. Ask yourself, why would (MNL) take ï¿½shotsï¿½ at HT when HT is part of the LEAP Disease Management Program? Duh. The problem is a bit of victim-mentality. This I cannot help you with. But you are in a place surrounded by people were they can if you want it.Again, my point, as it always is, that the current standards of care for IBS are that a multi-modality approach produces the best overall outcomes. This is the whole point of any medical care of chronic or acute illnessï¿½If Modality A gets A degree of relief, and Modality B brings about B degree of relief, if you can combine A + B and make them as patient-specific as possible your patients will overall receive the combined benefits and the remission rates will be higher. To try to pursuade people that a therapist stating this is damning a modality is simple again selective (or biased) reasoning.-----ï¿½Comments like that show me how much you really want to help people in the big scheme of things.ï¿½-----I once again am impressed with the degree, or lack thereof, of insightfulness into my personal motivations. To quote Washington Irving again ï¿½A tart temper never mellows with age and a sharp tongue is the only edged instrument which grows keener with constant use.ï¿½As I read further in your post, I am again overwhelmed by your inability to quote OR interpret and reiterate what I write with accuracy, objectivity or inclusiveness. Further pursuit would be folly. While I would LOVE to banter with you further, I would If I thought that it would serve any good purpose.But consuming time better spent answering questions for sick people who will actually consider the answers exactly as written (as verbose and dense as they may be at times due to the nature of the material and the communication medium) would be would be foolish, as time is the only thing we have in limited quantity.Adieu! Parting is such sweet sorrowï¿½.MNL


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## ohnometo (Sep 20, 2001)

EricYou are not being very nice...Now you know some of the top notch hospitals may understand IBS very well but they still dont have answers or solutions for everyone with IBS....I have been to some of the best hospitals in the US and they never was able to help me....with my IBS not CVS..and if you happen to go to the conference in Milwaulke I am going to be the person that Dr Fleischer will be talking about on Friday..Aduldts with CVS !!! I wish I could go but I cannot...5th International Symposium on Functional Gastrointestinal Disorders April 4-7, 2003The Pfister Hotel, Milwaukee WisconsinI know one day you and Mike will be working together on IBS








and dont you say no way







I appreciate so much what both of you guys do for everyone here.....and you'll have helped me when nobody else could...


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## trbell (Nov 1, 2000)

LoriAnn, It sounds like you are caught in the maze of names like many others of us. One thing that might help is to stop looking for a label and single easy treatment.tom


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## trbell (Nov 1, 2000)

MNL, what i meant by a book was a thread like eric put together that you could just refer to each time rather than typing outthe info.tom


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## eric (Jul 8, 1999)

Lorianne, regarless of the discussion here, I am personally most concerned at the lack of treatment and help you have gotten for what appears to be in your case mulitpy conditions and that you are presenting with some red flag symptoms, that a colonscopy wasn't done and stool sample is of great concern. I would start there with having a doctor order the tests for you, they are really important and I believe neccesary at this time for you to see if you have IBS or not, perhaps microscopic colitus for example.This is ten question to take with you. These can be very helpful. http://www.medicinenet.com/script/main/art...rticlekey=13683 I am sure you don't want to ever see another doc again perhaps, but if I were you I would get the tests done.The symptoms for IBS can wax and wane sometimes for months even years for some people, that is also a clue to foods roles in IBS. Who knows at anyone time, how well neurotransmitters are regulating throuh the body or what other influnces maybe effecting them, sleep for example. Also antidepresssants can stop working for some people as the receptors can become desensitized. Everyone is different with them and it may be trial and error on them.also there is confusion on d IBS and they know their is a release of serotonin in IBS d patients after a meal. Which has come much further then this study.Gut 1998 Jan;42 1:42-6 Related Articles, LinksPostprandial plasma 5-hydroxytryptamine in diarrhoea predominant irritable bowel syndrome: a pilot study.mental states aslo effect how we feel and manage pain, as you seem to be all to aware of.This is something in regards to IBS and the pet scans."The Mind-Body Connection in IBS.Perceptions of colonic activityPatients with IBS may perceive colonic sensations in a way that is different. For example, they may have a feeling of incomplete evacuation even though the rectum is empty. They also may feel that they are distended with gas though there is no sign of increased gas when it is measured.A number of studies have shown that IBS patients have a limited tolerance to distension of a balloon inserted into the rectum. They feel pain at a lower degree of distension of the balloon and also feel greater pain at the same degree of distension as normals. This may relate to a heightened sensitivity of the nerves that go from the colon to the spinal cord, known as visceral hypersensitivity.In one interesting experiment, balloon distension of the small intestine in IBS patients caused pain. However, if the patients were mentally distracted during the balloon distension, they did not feel pain. This illustrates a typical brain-gut relationship. ExampleIn addition to pain sensation, motility of the colon has been measured. IBS patients have an abnormal muscular response to a number of stimuli including stress and eating a fatty meal. This is important in terms of diarrhea and constipation patterns in IBS.Brain scanning in IBSOne study used a functional scanning technique called Positron Emission Tomography PET scan comparing IBS patients to controls. Using this method, it is possible to map certain areas of the brain that respond to specific stimuli elsewhere in the body.When this technique was applied to IBS patients during balloon distension in the rectum, the pre-frontal cortex was activated. This area of the brain is part of the limbic system, involved in emotional feelings. In contrast, a different area of the brain, possibly more involved in pain control, was activated in controls.Even more interesting was the observation that anticipation of rectal stimulation in IBS also activated the pre-frontal cortex. The last finding indicates a direct connection between emotional stimuli and colonic function." http://mindbodydigestive.com/ Mike quoted a top physcian in IBS from 1985 which by the way Drossman has written the science on IBS with above and this is a much more recent abstrat from him. from 2002. Aliment Pharmacol Ther 2002 Aug;16 8:1395-406 The treatment of irritable bowel syndrome. Thompson WG. University of Ottawa, Ottawa, Ontario, Canada. wgthomson###rogers.com The efforts of clinical researchers, lay organizations and pharmaceutical companies have increased the public profile of irritable bowel syndrome and made it a respectable diagnosis. Diagnostic symptom criteria encourage a firm clinical diagnosis, which is the foundation of a logical management strategy. This begins with education. Reassurance that no structural disease threatens should be tempered with the reality that symptoms are likely to recur over many years. Patients expect diet and lifestyle advice, even if this is not specific to irritable bowel syndrome. Only a few of those with irritable bowel syndrome see doctors, and even fewer see specialists. Therefore, the treating physician should ascertain the reason for the visit, the patient's fears and the presence of any comorbid illness, such as depression, that might require treatment in its own right. No drug treatment is useful for all of the symptoms of irritable bowel syndrome, and many patients require no drug at all. If used, drugs should target the predominant symptom. Alosetron, a 5-HT3 antagonist, is effective in treating women with irritable bowel syndrome who also have diarrhoea. Tegaserod, a 5-HT4 agonist, is useful for women with irritable bowel syndrome who are constipated. Most patients with irritable bowel syndrome need psychological support. Reassurance, discussion and relaxation techniques can be provided by the family doctor. Difficult psychopathology may require referral to a mental health professional, and the gastroenterologist can settle diagnostic uncertainties. In all cases, successful treatment depends on a confident diagnosis and the strength of the doctor-patient relationship. Publication Types: * Review * Review, TutorialPMID: 12182740 Lancet 1993 Jun 19;341 8860:1569-72 Related Articles, Links Comment in: * Lancet. 1993 Jul 31;342 8866:314.I really urge you to get some more testing done at this point.


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## BQ (May 22, 2000)

LoriAnne, The above posts notwithstanding:After reading your story I would offer you a few ideas. (mostly practical, I'm afraid...) The symptoms you describe are definitely screaming for further investigations. I'm sorry to tell ya this, but I'm thinking that if I were you, I'd find SOMEONE to give me a colonoscopy. No more beating around the bush...... flat out ask for one which will include the standard array of biopsies. Also, ask for stool cultures to be done. Flat out ask for them and keep asking til you find someone that will do them.******* Pain that wakes you up and your weightloss are RED Flags for other GI disorders that should be treated sooner rather than later.*******Yes, the info above is useful, once you can decipher it all from the he said/he said stuff.Pull the info out of the 'back & forth', because it is all good info.I know you obviously realize, from what you posted, that you know more than 1 thing can be going on simultaneously. And I am sure you know that you are missing some very important diagnostics. I'm just affirming that.And tellin ya, "Yup, get em done".







Practically speaking, relaxation has helped me manage my gut pain. ("My gut pain" is more than likely NOT IBS pain, if we all wanna get technical. It is probably functional dyspepsia pain. However, I care less about what my symptoms are ultimately called, and more about what helps me manage them.) So I thought you may benefit from using relaxation for the pain you are feeling. I hope so anyway. Here is an article on it: (forgive me if this has already been posted here.) http://www.med.unc.edu/medicine/fgidc/relax.htm The article refers to "functional" GI disorders and please know I am Not assuming that you have one. You may in fact have a dysfunctional disorder, but I think the only way you are going to find that out is via a colonoscopy and other diagnostics. I just thought you might get some respite from your pain via relaxation while you are awaiting said diagnostics.Here is a good relaxation technique that Eric found: http://www.noah-health.org/english/illness...y/progmusc.html So my hope for you is Lori, that you are able to get a colonoscopy, biopsies, and stool cultures soon.I hope this helped and please feel free to keep us updated on how you are doing.BQ


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## Feisty (Aug 14, 2000)

Hi Lori Ann







I agree with BQ. You need to insist that a colonoscopy be done along with stool cultures, etc. It's hard to understand why those tests have never been done.I know you, Lori Ann, so go in with "your guns loaded" and tell 'em you're not going anywhere until they listen up!







BTW--I've sent you numerous e-mails, including a PM from here the other day. Are you getting them? Was wondering because I haven't heard from you. Check in with me soon, okay?Take care, my friend.


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## Guest (Feb 27, 2003)

LoriAnn,I would go with Eric's and BQ's advice on this one.Mike,Hi.... you know I support your interests... but I really have to tell you that when you post these lengthy messages with all of those links, I become overwhelmed just reading them. And you may also have to translate some of the technical jargon from the links as well. I don't have enough time to peruse all of this in detail due to my hectic schedule... but I do try







Is there any way that you could devise to condense what you are saying and make it more understandable to the average lay person here?I am not pointing any fingers, but I also tire of the FP. Eric posts great information and he speaks to us on our level. And while I do enjoy your intelligence as well as your playful spirit, there are times when I both need and wish that you would come down to my level.....







I think that if you and Eric disagree so strongly on so many points that it is better if you do your jousting off-line. Many reasons for this:1) It puts off new members2) It annoys old members3) It confuses me (not alone in this)4) It overwhelms me (not alone in this)5) I really like both you and eric, but this pulls me at both ends.From my own experiences, I really DO believe that allergies play a very important role. My issue is with the system that controls allergic response. Why is it malfunctioning in the first place? I don't want to read the feud between you and eric or anyone else ...... And I also don't want you to write me a book or give me 14 links to technical sites....(I'm dense in that arena) just tell me here in plain English... what I need to do to get rid of all of these allergies that I have, inclusive of G.I. and respiratory and tactile. And I am sorry, but I don't have any money to pay you for your expertise at this time because an HMO is raking me over the coals.But I still luv ya... and luv your spirit....  Evie


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## ohnometo (Sep 20, 2001)

Food Intolerance and Food Allergy are 2 different things....I was tested for Food Allergy and it came back Negative...But when I learned about Food Intolerance and started to practice my eating habits my life changed...I have no food allergy but my body cannot tolerate certain thingsEveryone's system is different and for my hypnotherapy didnt work...


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## Mike NoLomotil (Jun 6, 2000)

Hi EvieIn answer to your question first... _____________________________________"My issue is with the system that controls allergic response. Why is it malfunctioning in the first place?" _____________________________________The answer, which may illuminate why all the other answers are so seemingly complex, is that WHY is far less well understood than WHAT. In other words it is not difficult to quantify WHAT, say, your immune system elements do and what they do it in repsonse to (the various stimuli).WHY they do not function as predicted is so hard to answer because it is rooted in the fundamental weakness of the study and state of the art of immunology, even in the 21st century...to quote a leading immunologist, alergist, pathologist who has dedicated decades to the pursuit of understanding of immune function "The sum of what we understand about the immune system is far exceeded by the sum of that which we do NOT understand, Michael."So as you have seen many people (present company included) can hold forth or post references at great length about all the possibilities...no one as yet can set forth any single solid answer to your question. NO body.Since that is the case, sometimes we do end up having to go to great lengths to make sure that we have set before the sick person (who must be viewed as a patient even in this forum) who is interested in these issues ALL THE KNOWN POSSIBLE ANSWERS, not merely those that may please us as individuals or those which we personally understand well. It is an obligation that one is burdened with if one is an actual healthcare practitioner of any sort. If one is not, one is not bound to go to great lengths to live up to your "oath" to the patients.In this case there is no way to set forth all the possibilities to your question...except to say that you have through your diligence here read them ALL at one time or another already. So I won't try to repeat only point out the quandary everyone faces as of this date. ________________________"what I need to do to get rid of all of these allergies that I have, inclusive of G.I. and respiratory and tactile. " _______________________IF you have actual "allergies", desensitization for inhalant allergies can be helpful and as a consequence any cross-reactions to foods may also be blunted (ther are specific foods to which environmentally can get cross reactions....one of the books I post frequently has a chart in it which lists them).However actual food allergy, and food intolerance mechanisms which are immunologic, do not seem to respond to desensitization treatment. Some fellas are experimenting with enzyme-potentiated desensitization but this remains equivocal. that leaves avoidance and pharmacotherapy.Behavioral therapies can blunt (attenuate) many body systems functions including neuroimmune function, and/or blunt the persons PERCEPTION and RESPONSE to insult, hence their place in an integrated therapeutic plan for disease management of many conditionsAs for your other remarks they are of course noted as they are well intended.However, I am compelled to simply point out that you have not and will not find me taking the point in such engagements (making declarative derogatory statements about others first) in any public forum. I am responsive not proactive. However, when people do take the point and I am the object of their attention (or someone or entity I am associated with), when they declare first, in an effort to derogate me or attribute motives or claims or statements to me personally which are not 100% in compliance with reality, I am compelled to respond so as to set the record straight and will do so in the future. I do not feel it is inappropriate. In fact it is mandatory to ensure that attributions are not falsely made in a public place. That attempts at defamation do not go unchalleged.If that does indeed bother someone, that I will speak up when challenged, misquoted or metamorphosed into something other than that which was, Please Do Not Read what I wrote in response. I have no intention of offending observers. Change the channel. But you know sometimes its like that car accident on the freeway....omigod...I cannot look it may be gross....omigod...yet we slow down to a crawl as we pass...anyway, alot of people do it is just human nature. then we cuss the guy i front of us for doing it.







To paraphrase George Carlin the highway is filled with idiots and maniacs. Everyone going slower then the collective "us" is an idiot, and everyone going faster is a maniac.Anyway I do fully agree with the complexity and comprehension problem. While there may be a way for me to try harder to make exceedingly complex issues more understandable, this is simply not always possible with the material in question.If in the process you dilute the information so much that it becomes non-factual or misleading you must tell it like it is and try to provide the person reference material which they can go to which can explain it in better detail at length.Sometimes the references are of necessity comples as they are the applicable references.I guess I would like to summarize that the main issue is analagous to this scenario.Let us say we are on an asthma discussionboard. A discussion of asthma symptoms and their causes is ongoing with asthamatics in attendance.Someone is discussing the mechanisms of asthma from the psychosocial perspective and explaining in great detail those mechanims. If this is the only aspect of their disease which is openly discussed with them, this can lead the asthmatics to conclude from the teaching being given that this is the primary mechanism by which their symptoms are invoked. This will compromise their ability to assess their own condition and care.Yet it remains a fact that they need to be aware of OTHER mechanisms of their disease. The subject needs to be introduced for them to enjoy maximum health, that there is an immunologic mechanism (IgE, Lymphocytes etc) which precipitates their symptoms as well. As a therapist I am on the sideline observing the discussion.So I enter and add to, not refute, add to, the present discussion information about the other mechanisms for the benefit of sick people present.In what way is this inappropriate and worthy of scorn? Also Has the discussion been hijacked? How CAN you "hijack" a disscussion which is supposed to be teaching sick people more about their condition and how they may be able to help themselves?My answer is that the question is rhetorical as it is never inappropriate unless the information added is not factual. Since it is, there is nothing to defend as there exists an ethical obligation to add the information if it is pertinent at that time to the benefit of the sick.Indeed it is not always easy to make some complicated things into easy things...I wish it was or perhaps I am simply not that good at it even after 30 years as a healthcare provider and educator. OOPS maybe that is what is wrong!!! Old habits die hard.








Anyway, "thats all I have to say about that"...promise.







I hope that the answer to your question was more understandable.MNGump







MNL


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## LaurieJ (Sep 3, 2002)

Mike,Writing from a science background, I find that your information is presented in the most valid format of anyone who tries to present information as science. I believe that emotional tones, derogatory statements and excessive grammatical / spelling errors detracts from the information given. You are so correct that interpretation of "facts" can be controversial - noone can see information from a strictly objective viewpoint - even scientists and MDs.You are right in that all bases of the syndrome must be considered and that biases are inherent to that field in which the researcher works. It can't be helped. Just like a MD will approach your diagnosis and treatment based on his / her specialty so will the PhD researchers. Most "lay" persons do not understand the scientific process / methodology. Especially in how experiments are designed, information gathered and data interpreted. In every one of these steps, bias, error and unknown factors can influence outcomes. The best scientifiic mind does not see experiments necessarily as confirmation of a hypothesis but rather as, what other processes are being implicated? Where could error have entered? What is the design flaw of this experiment? As we all know, reproducibilty does not ensure accuracy. Especially when we have no clue what we are measuring.An example of how my personal bias influences my behavior on this board: Because my background is in the "Hard" sciences I have a tendency to skim over or be highly sceptical of the "soft" sciences (e.g. psycho"babble"). I have to recognize this tendency and consciously force myself to consider that information in an objective manner.


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## trbell (Nov 1, 2000)

LaurieJ the voice of reason.great.tom


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## BQ (May 22, 2000)

Laurie, Excellent post, very well said.(I know, high praise from a lay person and a buck will get ya a cup of java. lol But I really liked how ya put it.)BQ


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## trbell (Nov 1, 2000)

I do have to comment that there is a difference between psycho-babble and psychology as a 'hard' science. there is sol;id scientic/medical research available now on some of the babble and there is a need to sort the wheat from he chaff.tom


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## eric (Jul 8, 1999)

FYIMike is explaining IBS, due to loss of oral tolerence to foods, but in very complicated terms. They have found many other problems in IBS and IBS cannot be explained by loss of tolerence to foods, they maybe a TRIGGER for some people though. However, "Abnormal visceral sensitivity/perceptionPatients with visceral hypersensitivity are thought to be abnormally sensitive to normal physiologic stimuli that arise from within the intestine during digestion. It appears that the mechanism within the brain that should filter out these stimuli does not function properly in IBS patients Figure 533. As a result, they may experience pain and bloating from NORMAL colonic contractions. Patients may also have a reduced threshold of sensitivity to abnormal events.""Contributory factors (ï¿½triggersï¿½)In patients with IBS, the potential for abnormal function is always present. However a ï¿½triggerï¿½ is often required for symptoms to develop. The intestine of IBS patients is more sensitive and reactive than normal to a wide range of factors (Table 1) and exaggerated reaction to these stimuli triggers pain or other symptoms.Dietary factorsMany IBS sufferers report that their symptoms are triggered or exacerbated by eating a meal. Eating normally leads to colonic contractions, which may result in an urge to defecate 30 to 60 minutes after a meal. In IBS patients the urge may occur more quickly and may be accompanied by abdominal cramps and diarrhea. Some foods, however, may trigger intestinal spasms, causing delayed defecation and constipation. The effect of a meal is often related to its total calorific value and especially to the number of calories derived from fat. This may be because fat, from either vegetable or animal sources, is a strong stimulus of colonic contractions.In some IBS patients the consumption of specific foods may trigger symptoms Figure 7. This is especially common in those patients with D-IBS, bloating and pain. Dairy products, chocolate, caffeine, alcohol and pulses such as lentils and beans which are known to be gas-forming are examples of specific dietary factors that may cause problems in some patients. Food allergy or sensitivity is sometimes misdiagnosed as IBS because both conditions can lead to abdominal pain and diarrhea. A food allergy can be identified, however, by the presence of symptoms outside the GI tract.Figure 7""Food allergy or sensitivity is sometimes misdiagnosed as IBS because both conditions can lead to abdominal pain and diarrhea." http://www.ibsandhealth.com/pro/health/04/04.html They cannot explain global symptoms in IBS or the connection to other functional GI conditions."There are three primary features to functional GI disorders: Motility, Sensation, and Brain-Gut Dysfunction.Motility is the muscular activity of the GI tract. Normal motility e.g., peristalsis is an orderly sequence of muscular contractions from top to bottom. In functional GI disorders, the motility is abnormal. There can be muscular spasms that can cause pain, and the contractions can be very rapid or very slow.Sensation is how the nerves of the GI tract respond to stimuli for example, digesting a meal. In functional GI disorders, the nerves are sometimes so sensitive that even normal contractions can bring on pain or discomfort.Brain-Gut Dysfunction relates to the disharmony in the way that the brain and gastrointestinal system communicate. With functional GI disorders, the regulatory conduit between brain and gut function may be impaired." http://www.med.unc.edu/medicine/fgidc/bkgrnd.htm There is another problem here as well." Increased gastro-colic reflex. This is an awakening of the childhood reflex where food in the stomach stimulates colonic activity, resulting in the need to open the bowels."" Daily meal pattern will have a direct effect on IBS symptoms. Eating causes contraction of the colon. Normally, this response may cause an urge to have a bowel movement within 30 to 60 minutes after a meal. In people with IBS, this reflex can be exaggerated and can lead to cramps and sometimes diarrhoea. The strength of this response is directly related to the calorie content of the meal and as already mentioned the fat content of the meal. "So the stomach sends a single to the lower colon that food is on the way and the lower colon overreacts and dumps its contents.Already there is a ton of eveidence on an over reaction of serotonin in D predominate IBS that speeds up peristalsis giving a person D.This is the info Mike does not want to talk about and regards to d predominate IBS.notice, he did not explain why the new serotonin drugs like lortronex work on this serotonin problem in the gut and what that has to do with loss of food intolerence. Not to mention the constant focus on foods, and not on the bigger picture and that facts that loss of oral toerlence does not cause viceral hyperrsenitivity they find in IBS patients. or rectal sensitivity? The nerves in the gi tract are sensitive to ALL stimuli!!!!!!Ask him about all this. Why the above picture of the lower colon is off the charts and wouuld be causing d 15 minutes after you eat a meal.


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## eric (Jul 8, 1999)

next time a person goes to the doctor ask them about the gastro colonic reflex and what it would have to do with IBS.


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## eric (Jul 8, 1999)

FYI95 percent of serotonin is in the gut."A:Irritable bowel syndrome is now recognized as a disorder of serotonin activity. Serotonin is a neurotransmitter in the brain that regulates sleep, mood depression, anxiety, aggression, appetite, temperature, sexual behavior and pain sensation. Serotonin also acts as a neurotransmitter in the gastrointestinal tract.Excessive serotonin activity in the gastrointestinal system enteric nervous system is thought to cause the diarrhea of irritable-bowel syndrome. The enteric nervous system detects bowel distension expansion on the basis of pressure-sensitive cells in the bowel lumen opening. Once activated, these pressure-sensitive cells promote the release of serotonin, which in turn promotes both secretory function and peristaltic function the contractions of the intestines that force the contents outward. At least four serotonergic receptors have been identified to be participants in the secretory and peristaltic response.Patients with diarrhea-predominant IBS may have higher levels of serotonin after eating than do people without the disorder. This recognition led to the development of the first drug used specifically to treat diarrheal symptoms of IBS, alosetron also known as Lotronex. Alosetron blocked the specific serotonin receptors responsible for recognizing bowel distention. In doing so, it blocked the effects of serotonin and reduced both bowel secretions and peristalsis. Constipation was the most common side effect seen. (Note: Alosetron was removed from the market by the manufacturer after repeated reports of a dangerous condition known as ischemic colitis became known. Tegaserod Zelmac is another drug under development and under review by the U.S. Food and Drug Administration for approval. Tegaserod is indicated for the treatment of constipation-predominant IBS and works to increase enteric nervous system serotonin activity.So, increasing serotonin activity in the enteric nervous system produces increased bowel secretions and peristalsis and potentially diarrhea, whereas depressing serotonin activity produces reduced secretions and reduce peristalsis and potentially constipation. Increasing serotonin activity in the brain would increase awareness and, in higher doses, produce anxiety, insomnia and restlessness. So I would have expected exactly the opposite effects of those that you experienced.I am unable to identify any possible drug interactions between 5-HTP and Synthroid levothyroxine but the symptoms described suggest a check with your doctor may be in order. Persistent feelings of tiredness and constipation may be signs of an underactive thyroid hypothyroidism.June 19, 2001 http://www.intelihealth.com/IH/ihtIH/WSIHW...438/325205.html The above is a recognized problem in IBS, although not the whole picture.


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## LaurieJ (Sep 3, 2002)

BQ,Thanks for the pat on the back. I appreciate the support and I do not differentiate qualitatively between praise from "lay" persons versus "peers". I believe that everyone has the right to their opinions and beliefs but that they have to realize that everything is looked at and incorporated into their life through the filter of personal bias. This is not wrong - it creates diversity. But in order to appreciate this diversity and to recognize the validity of others opinions one must learn and practice tolerance continuously - and be awed at the wonder of the human thought processes - whether it is mind inspired or brain controlled.Tom,I am sorry about the psycho-babble connotation. This is a good example of how a word choice elicits emotional response, whether intended or not. This is what I was talking about when I said that it is hard to present facts as facts when you link them with emotional evoking terms. Shame on me for violating my own standards on using neutral words to present facts.LaurieJ


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## eric (Jul 8, 1999)

Laurie, I do agree with what you said, I also seem to have dyslexsia when I am typing on the computer as well as loss of feelings on two of my figer tips so sorry for the typo's on my part. Besides despite I was an english major I still can't speel. LOL]Dr Whorewell is a senior gastroenterologist stduying IBS in the UK. He is the father of HT for IBS as well and used it some twenty years ago.Brain gut interactions using HT to STUDY IBS. I am pointing this out just on modulating symptoms via the brain.Gut 2002 Nov;51(5):701-4 Related Articles, Links Click here to read Visceral sensation and emotion: a study using hypnosis. Houghton LA, Calvert EL, Jackson NA, Cooper P, Whorwell PJ. Department of Medicine, University Hospital of South Manchester, Manchester M20 2LR, UK. lahoughton###man.ac.uk BACKGROUND AND OBJECTIVES: We have previously shown that hypnosis can be used to study the effect of different emotions on the motility of the gastrointestinal tract. These studies demonstrated that both anger and excitement increased colonic motility while happiness led to a reduction. The purpose of this study was to investigate the effect of hypnotically induced emotion on the visceral sensitivity of the gut. METHODS: Sensory responses to balloon distension of the rectum and compliance were assessed in 20 patients with irritable bowel syndrome IBS aged 17-64 years; 17 female diagnosed by the Rome I criteria. Patients were studied on four separate occasions in random order either awake control or in hypnosis, during which anger, happiness, or relaxation neutral emotion were induced. RESULTS: Hypnotic relaxation increased the distension volume required to induce discomfort p=0.05 while anger reduced this threshold compared with relaxation p<0.05, happiness p<0.01, and awake conditions p<0.001. Happiness did not further alter sensitivity from that observed during relaxation. There were no associated changes in rectal compliance or wall tension. CONCLUSIONS: Further to our previous observations on motility, this study shows that emotion can also affect an IBS patient's perception of rectal distension and demonstrates the critical role of the mind in modulating gastrointestinal physiology. These results emphasise how awareness of the emotional state of the patient is important when either measuring visceral sensitivity or treating IBS. Publication Types: * Clinical Trial * Randomized Controlled TrialPMID: 12377810Gut 1990 Aug;31 8:896-8 Related Articles,Links Changes in rectal sensitivity after hypnotherapy in patients with irritable bowel syndrome. Prior A, Colgan SM, Whorwell PJ. Department of Medicine, University Hospital of South Manchester. Fifteen patients with the irritable bowel syndrome were studied to assess the effect of hypnotherapy on anorectal physiology. In comparison with a control group of 15 patients who received no hypnotherapy significant changes in rectal sensitivity were found in patients with diarrhoea-predominant irritable bowel syndrome both after a course of hypnotherapy and during a session of hypnosis p less than 0.05. Although patient numbers were small, a trend towards normalisation of rectal sensitivity was also observed in patients with constipation-predominant irritable bowel syndrome. No changes in rectal compliance or distension-induced motor activity occurred in either subgroup nor were any changes in somatic pain thresholds observed. The results suggest that symptomatic improvement in irritable bowel syndrome after hypnotherapy may in part be due to changes in visceral sensitivity.PMID: 2387513AlsoIsr Med Assoc J 2001 Feb;3 2:104-10 Related Articles, Links Brain-gut interaction in irritable bowel syndrome: new findings of a multicomponent disease model. Schmulson MJ. Department of Gastroenterology, National Institute of Medical Sciences and Nutrition Salvador Zubiran, Panamerican University of Mexico, Mexico City, Mexico. maxjulio###quetzal.innsz.mx Knowledge on the pathophysiology of irritable bowel syndrome has evolved, beginning with disturbances in motility to visceral hypersensitivity, and ultimately to alterations in brain-gut bi-directional communication, where neurotransmitters such as serotonin play a key role. Recently, a multicomponent disease model that integrates all these alterations was proposed. This model is divided into physiological, cognitive, emotional and behavioral components that explain the gastrointestinal as well as the constitutional symptoms. In recent years there has been an explosion of research together with new developments in pharmacological treatments for IBS that support each component of this model. This review presents recent data in favor of these alterations in IBS. Publication Types: * Review * Review, TutorialPMID: 11347592That IBS reponds well to treatments targeted at the brain also helps in understanding the brain gut interactions and issues associated with IBS.


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## eric (Jul 8, 1999)

becaue so many factors can influnce IBS, is one reason why they are looking for treatments that effect global symptoms and use treatments targeted at the predominate symptom also at the same time. Best Pract Res Clin Gastroenterol 2002 Dec;166:869-83 Related Articles, Links Evolving concepts in functional gastrointestinal disorders: promising directions for novel pharmaceutical treatments. Hunt RH, Tougas G. Department of Medicine, Division of Gastroenterology, McMaster University Medical Centre, Hamilton, Ontario, Canada In recent years there has been an increasing appreciation of the complexity of functional gastrointestinal disorders. These represent a spectrum of conditions which may affect any part of the gastrointestinal tract in which there appears to be dysregulation of visceral function and afferent sensation and a strong association with emotional factors and stress. There is a clear psychological dimension, with up to 60% of irritable bowel syndrome IBS patients reported to have psychological co-morbidities and altered pain perception is also common in comparison with control populations.The role of the enteric nervous system, the sensory pathways and the brain as well as the influence of the latter on sympathetic and parasympathetic outflow have likewise attracted increasing interest and have led to exciting new methods to study their complex interactions. The concept of low-grade inflammation, such as might occur after infection, acting as a trigger for neuromuscular dysfunction has also led to the broad integrative hypotheses that help to explain the biopsychosocial dimensions seen in functional gastrointestinal disease. The multi-component model places a major emphasis on neurogastroenterology and enteric and neuro-immune interactions where new approaches to pharmacotherapy lie.Drugs may affect motility, visceral sensation and other aspects of gut function such as secretion or absorption. More particularly, however, has been the search for and attempts to influence important mediators of these primary gut functions. Such targets include serotonin and selected 5-HT receptors, which are involved in gut motility, visceral sensation and other aspects of gut function, CCK receptors which are involved in the mediation of pain in the gut and nociception in the CNS, opioid receptors involved in pain in the brain, spinal cord and periphery, muscarinic M 3-receptors, substance P and neurokinin A and B receptors which are involved in motor adaptation and pain transmission in association with inflammation, gabba receptors involved in nociception and cannabinoid receptors which are involved in the control of acetyl choline release in the gut.With a better understanding of the structures and pathways involved in visceral perception and hyperalgesia, in the CNS, spinal cord and the gut and new pharmacological tools we will be better able to elucidate the neuropharmacology of visceral perception and its relationship to gut dysfunction. It is likely that there will be multiple therapeutic options based on the spectrum of abnormalities capable of causing the spectrum of symptoms of functional gastrointestinal disorders in any individual patient.PMID: 12473296


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## trbell (Nov 1, 2000)

I didn't mean to be so gib about the psycho-babble thing as i do think it's important for a lot of people here aand I think you are correct in pointing out that it does cloud a lot of the conversations. There is unfortunately a long history of lack of respect for psychology in our society and psychologists do have to take some responsibilty for this. My difficulty is that I would like to be able to not be a psychologist here as I am also someone who suffers from IBS. At the same timeit's hard for me to ignore messages that I don't feel respect psychology as a 'hard' science, a status which it is starting to achieve as you'll se in Drossman's biopschosocial understanding of IBS.So this is part of why my posts might be confusing at times.tom


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## eric (Jul 8, 1999)

FYIDR Mayer is an extremely well respected neurogastroenterologist at UCLA. One of his specialities is understanding pet scans and IBS. He also recently opened a new Research center.If you live in LA this might be worth looking inot, as well as he already establisted center at ucla. UCLA Receives NIH Grant to Create First National Center for Neurovisceral Sciences and Women's Health Treatments for Damage, Disease http://www.npi.ucla.edu/news/neurovisceralsciences.html They have learned more since this was published in 98. Eur J Surg Suppl 1998;583:29-31 Related Articles,Links Intestinal and extraintestinal symptoms in functional gastrointestinal disorders. Mayer EA, Fass R, Fullerton S. UCLA/CURE Neuroenteric Disease Program, UCLA School of Medicine, Los Angeles, CA 90073, USA. emayer###ucla.edu Functional gastrointestinal disorders such as irritable bowel syndrome or functional dyspepsia have traditionally been regarded as syndromes limited to the digestive system. However, both clinical experience and published evidence show that patients with such disorders also report a series of other symptoms of physical distress, such as fibromyalgia and irritable bladder and alterations in vital functions, such as sleep, libido, appetite and energy level. Some of these extraintestinal symptoms can be explained in the context of an evolving comprehensive disease model which views functional gastrointestinal disorders as manifestations of alterations in the interactions between the nervous system, the viscera and the musculoskeletal system. Alterations in central circuits concerned with arousal, attention and fear, cognitions about bodily symptoms and possible alterations in the hypothalamic pituitary adrenal HPA axis may all contribute to the wide range of symptoms reported by affected patients.PMID: 1002766999'Am J Med 1999 Nov 8;107 5A:12S-19S Related Articles, Links Emerging disease model for functional gastrointestinal disorders. Mayer EA. Division of Digestive Diseases, University of California Los Angeles School of Medicine, USA. In response to perceived or experienced change that is considered threatening to the individual, the central nervous system mounts a stereotypic response that decreases the sensitivity to pain, modulates the autonomic nervous system outflow, and activates the hypothalamic-pituitary-adrenal HPA axis. This response of the "emotional motor system" may or may not be associated with the conscious experience of feelings of fear or anxiety. Alterations in these response systems either up- or downregulation may produce symptoms, such as viscero-somatic hypersensitivity, altered bowel habits, or increased anxiety. Publication Types: * Review * Review, TutorialPMID: 10588168Some technical stuff on this from Dr mayer.Brain Imaging: CNS Abnormalities in Patients with IBSThe lack of a clearcut pathophysiology and an often noted association between physical and psychological symptoms has led some clinicians to dismiss irritable bowel syndrome IBS as a condition that is "all in their head." However recent findings showing CNS abnormalities in patients with IBS may offer a new perspective on the etiology of this debilitating condition, characterized by abdominal discomfort and pain and altered bowel habits. Until recently, the presence and severity of IBS were measured only by gut function and the subjective perceptions of the patient. "Now, the use of functional brain imaging techniques is contributing to an increased under- standing of the pathophysiology of this disease and new target areas for treatment," said Emeran A. Mayer, MD, Professor of Medicine, Physiology, and Biobehavioral Sciences, and Director of the CURE Neuroenteric Disease Program at the University of California, Los Angeles.Pathophysiology of IBSIBS is a disease that develops as the result of an abnormally altered brain-gut interaction Table 1. One manifestation of this alteration consists of aberrant output patterns of the emotional motor system, a part of the limbic system in the brain, in response to external psychosocial or internal immune, nutrient stressors. Outputs from the limbic system in the form of autonomic, pain modulatory, and neuroendocrine responses can be modu- lated by cognitive factors, such as the beliefs, thoughts, and emotions of the patient. Aberrant output of the emotional motor system in large part accounts for the constellation of symptoms that makes up IBS. "A hyperresponsiveness of circuits in the brain may be one common link to both the abnormal responses to internal inflammatory stressors and external psychosocial stressors," Dr. Mayer explained. Treatment is chosen with consideration of altered motility, visceral hypersensitivity, and the brain's role in modulating these factors.The autonomic regulatory systems affect not only muscle cells in the gut, but also other cell types, such as mast cells, enterochromaffin cells, and nerve cells of the enteric nervous system. Responses of some of these cells to autonomic modulation, for example in the form of tryptase secretion by mast cells or serotonin secretion by enterochromaffin cells, may play a role in the modulation of visceral afferent sensitivity. According to Dr. Mayer, such mechanisms may play a role in the development of stress-induced visceral hyperalgesia. Another form of visceral hypersensitivity may be related to altered arousal or hypervigilance toward visceral sensations. Such hypervigilance can result in decreased tolerance to balloon distension and lower discomfort thresholds. A cognitive factor involved in the development of hypervigilance is an increased threat appraisal of visceral sensations.Functional Brain Imaging TechniquesRecently, functional brain imaging techniques have been used to assess directly the activation of certain regions of the brain in response to visceral stimulation. Today, these techniques, particularly functional magnetic resonance imaging, are being used to assess activation of brain circuits that process visceral afferent information from the gut.Dr. Mayer noted that there are distinct but overlapping brain circuits that relate to subjective perception of gut sensations, autonomic responses, and pain modulatory responses. Even in terms of subjective gut sensations, different overlapping circuits are present for intensity coding of the stimulus; threat appraisal of the stimulus; and attribution of primary affect, or "unpleasantness".Both serial and parallel pathways are involved in the processing of visceral sensory information and the control of descending modulatory systems. Input from the gut is derived from multiple channels, such as spinothalamic, vagal, and dorsal column pathways; different regions of the brain then code for intensity, appraise the threat of the stimulus, and determine the level of attention the brain attributes to the stimulus and the unpleasantness the patient experiences. These processes are modulated both by the stress- or arousal- activated system and by recollection of past experiences.Intensity Coding, Threat Appraisal, and UnpleasantnessIntensity coding. As visceral sensory information is delivered via the spinal cord, it is encoded for intensity in the anterior aspects of the insula, or visceral sensory cortex. PET scan studies of somatic and visceral experimental pain have shown that the insula most objectively and reliably encodes information. Interestingly, studies have also demonstrated a greater activation of the insula in male IBS patients, compared with female patients, when exposed to the same stimulus intensity.Threat appraisal and unpleasantness. The information that reaches the insula is "appraised" in the dorsal aspects of the anterior cingulate cortex. Blood flow changes in this part of the brain may also correlate with attentional processes and the subjective unpleasantness ratings in response to a somatic stimulus. The ventral perigenual cingulate cortex, which is rich in muopioid receptors, functions to encode the affective quality of the stimulus.In a study by Mayer and colleagues, rectal and sigmoid distension resulted in a lower activation of the ventral anterior cingulate cortex in patients with IBS compared with healthy controls, but an increased activation of the dorsal aspects of the anterior cingulate. Increased activation of an unspecified region of the anterior cingulate was also reported by Mertz and colleagues, in a functional MRI study.Modulatory factors. Finally, the CNS processing of sensory experience may be simultaneously modulated by two parallel pathways: memory-based modulation and stress- or arousal-induced modulation. The posterior parietal cortex, or sensory association cortex, forms a network with the hippocampus and the amygdala the brain's memory centers as well as with the lateral prefrontal cortex. Somatic pain studies have shown that, in response to a stimulus, the recall of a similar past event, along with subsequent interpretation of this memory in the lateral prefrontal cortex, plays a major role in the threat appraisal of a sensory experience. The second modulatory effect is the stress- or arousal-induced response. The pontine locus ceruleus is activated in response to potentially threatening experiences. This region then projects to nearly all other regions of the brain that receive visceral input, causing secretions of norepinephrine and arousal of these sections of the brain. When the secretion of norepinephrine is excessive, these target regions are inhibited. It is of interest that descending projections from the locus coeruleus complex to the sacral spinal cord appear to play a major role in the modulation of distal colonic motor and secretory function.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. Table 1. Clinical Relevance of Altered Brain-Gut InteractionAltered attentional mechanisms o Greater awareness of normally subliminal visceral afferent stimuliAltered affective stimulus processing o Greater unpleasantness of visceral sensations, including heartburn, bloating, fullness, abdominal pain, incomplete rectal evacuationAltered threat appraisal o Leads to fears such as not being close enough to a bathroom anything eaten may trigger abdominal painEnhanced arousal o Shared by clinical conditions frequently overlapping IBS, such as anxiety, panic disorder and PTSD o Arousal reduced by sedatives, anxiolytics, low-dose tricyclics o May respond to relaxation exercises http://www.macmcm.com/pcp/pcp2000_01.htm There is a big difference between focusing one problem just the loss of oral tolerence with foods in IBS -there are a lot of problems both iin the gut and the brain as one problem in the gut in IBS and the new model of IBS using the Biopsychosocial AssessmentImportant in Diagnosis and Managementfor Functional GI PatientsThe biopsychosocial model of chronic gastrointestinal disease may be a better approach to diagnosing and managing patients than the traditional biomedical model, say experts, at the International Symposium on Functional Gastrointestinal Disorders, which was held in Milwaukee, Wisconsin, March 31st through April 4th (2001)."The biopsychosocial model proposes that illness and disease result from interacting systems at the cellular, tissue, organismal, interpersonal and environmental levels, explained Douglas Drossman, MD," professor of Medicine and Psychiatry in the Division of Digestive Diseases and Co-director of the University of North Carolina Center for Functional GI & Motility Disorders in Chapel Hill. Physicians can integrate the biopsychosocial model into their practices by evaluating dietary and lifestyle factors, the role of stress, social support, life trauma e.g., abuse history and the patient's coping mechanisms. "For treatment one should look at the severity of the condition, the biological and psychosocial factors that may be influencing the nature and severity of the symptoms, and let one's treatments be guided by that," said Drossman. http://www.med.unc.edu/medicine/fgidc/biopsychosocial.htm For example how would one explain through the loss of oral tolernce to foods causing.ClinicalCentral fear circuits less activated in IBS patientsSAN DIEGO, CA, May 22 Reuters Health - The threat of visceral discomfort appears to evoke an emotional rather than fearful response in patients with irritable bowel syndrome IBS, researchers report at the annual Digestive Disease Week meetings held here.Dr. Bruce D. Naliboff, of UCLA Medical Center, in Los Angeles, with colleagues there and at UC Irvine Medical Center, performed a PET study of 12 IBS patients and 12 controls to examine the brain response associated with the fear of anticipated visceral discomfort.Brain scans were obtained on all subjects at baseline, during moderate rectal distension and during expected but undelivered noxious distension. "Although we know that IBS is exacerbated by stress, we conducted this study to learn more about the connection between the disease and brain function," Dr. Naliboff said in an interview with Reuters Health.Brain scans showed that controls had "greater baseline activity in mid anterior cingulate cortex ACC, and greater activation in the perigenual mid ACC, lateral prefrontal cortex, thalamus, periaqueductal grey and medullary regions" than did IBS patients.During visceral stimulation, "IBS patients showed greater activation in mid anterior cingulate cortex as well as posterior cingulate," compared with controls, the researchers note.They found that expected but undelivered rectal discomfort activated the central fear circuits in the controls. IBS patients showed "less activation of the fear circuits but greater activity in posterior cingulate cortex.""Our findings indicate that the parts of the brain that respond in IBS patients are the same parts of the brain involved in processing emotionally charged information," Dr. Naliboff said. "These data give us a better understanding of this stress-related disorder and may provide information about potential new medication targets," he explained."This brain imaging study is one of a series examining IBS, dyspepsia and fibromyalgia," Dr. Naliboff added.-Westport Newsroom 203 319 2700


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## PatSimp89 (Feb 26, 2003)

I believe that we need to hear from people who have indepth knowledge of how foods can trigger the immune sytem and the neurotransmitters into a hyperactive or disordered state.I have been told too many times that this problem is all in my head. The psychosocial aspect of this disorder is of little concern to me especially since my symptoms operate independantly of my social or psyche states.I seem to be doing much better when I avoid all of my trigger foods.


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## eric (Jul 8, 1999)

Its in part because stressors/ lke threat or worry are not always concious reactions or thoughts to the person effected, but happen on a subconcious level, with the person not aware even.The threat responce happens before a person is conciously aware of the threat.For example the fear of an attack, is a threat to the body and the body molbolizes on it, before you are conciously aware of it, it happens almost instantly, so the organism does not waste time thinking about the threat. The threat of pain or an attack of D and finding a bathroom, this can happen everyday day in and day out in IBS and sets up a chronic stress responce and overloads the system. This happens at the core of our beings, not what most peoope consider stress, stress is to broad really. homeostasis and the Allostasis http://www.parkviewpub.com/parksub/n1.html "Psychological Consequences of Having a Functional GI DisorderAny chronic illness, including one of the functional GI disorders, can have significant psychosocial consequences such as: * Reduced sense of health and well-being * Constant concerns related to cause of the symptoms and how to control them * Problems with activities of daily living o Problems with interpersonal relationships with family, friends, and co-workers * Disability with missed work days. Remember, irritable bowel syndrome is the second leading cause of industrial absenteeism in the United States."Irritable bowel syndrome and other functional GI disorders cause symptoms and discomfort ranging from mild and inconvenient to severe, resulting in incapacitation and disability. Current evidence shows that many people with irritable bowel syndrome lead restricted lives in multiple areas: diet, social activities, and energy level, without much relief from current health-care practices and medications." http://www.parkviewpub.com/ibs/ibs4.html THE MIND-BODY/BRAIN-GUT CONNECTION: THE VICIOUS CIRCLE OF STRESS, PSYCHOLOGY, AND SYMPTOMSThe "fight-or-flight" response by the body in response to perceived stress results in an increase in blood pressure, heart rate, breathing, and metabolism Chapter 5. With continued or unrelieved stress, the body can become unbalanced and unable to recover, leading to the physical symptoms listed. The emotional responses to these unexplained symptoms and fear of not knowing when the symptoms will start can actually make them worse. A vicious circle of stress, psychology, and symptoms can be established. http://www.parkviewpub.com/ibs/ibs6.html Stress is not the whole picture and foods are not the whole picture and IBS is "not all in the head" it is a physcial problem. It is in how the brain and the gut communicate or in the case of IBS miscommunicate. Other factors can also trigger symptoms, the weather even or meds or a host of other reasons.But stress does influcnce it in a very big way.Gut Feelings: The Surprising Link Between Mood and DigestionChris WoolstonCONSUMER HEALTH INTERACTIVEBelow: ï¿½ Listening to your gut ï¿½ The stress alarm ï¿½ Functional disease in a dysfunctional world ï¿½ Setting your mind on reliefIf you've ever felt your insides twist in knots before a big speech, you know the stomach listens carefully to the brain. In fact, the entire digestive system is closely tuned to a person's emotions and state of mind, says William E. Whitehead, PhD, a professor of medicine and an adjunct professor of psychology at the University of North Carolina. People with irritable bowel syndrome often suffer flare-ups during times of stress and anxiety, and even perfectly healthy people can worry their way to stomach pain, nausea, diarrhea, constipation, or other problems. Even if a doctor can't find anything physically wrong, the misery is real.In the past -- back when scientists believed the mind and the body operated as separate entities -- some physicians wrote off digestive distress with no sign of organic disease as being "all in the head." But in recent years, that wall has crumbled. Doctors now see intricate links between the nervous system and the digestive system. The two realms constantly exchange streams of chemical and electrical messages, and anything that affects one is likely to affect the other. The connections between the two systems are so tight that scientists often refer to them as one entity: the brain-gut axis. The brain-gut axis is a hot topic in medicine. In the summer of 2001, more than 100 researchers from around the world gathered in Los Angeles for a convention called "2001: A Brain-Gut Odyssey." For people suffering from persistent digestive troubles unconnected to disease, such research suggests that reducing stress, depression, and anxiety may go a long way toward calming the gut.- Listening to your gutIt may surprise many people to learn that the gut actually contains as many neurons nerve cells as the spinal cord. In an article in the medical journal Gut, author J. D. Woods and colleagues compare this network -- known as the enteric nervous system, or ENS -- to a "local mini-brain" storing a library of programs for different patterns of gut behavior." Woods and colleagues compare the ENS to a microcomputer with its own independent software, "whereas the brain is like a larger mainframe with extended memory and processing circuits that receive information from and issue commands to the enteric computer."With all these messages, the connection between the brain and the digestive system is a busy two-way street. The central nervous system releases chemicals acetylcholine and adrenaline that tell the stomach when to produce acid, when to churn, and when to rest. Similar signals help guide the movements of the intestines. The digestive system responds by sending electrical messages to the brain, creating such sensations as hunger, fullness, pain, nausea, discomfort, and possibly sadness and joy.As strange as it sounds, our guts just might help shape our moods, says Emeran Mayer, MD, a gastroenterologist and the chairman of the new Mind-Body Collaborative Research Center at the University of California at Los Angeles. Mayer points to the vagus nerve, essentially a large electrical cable that runs between the brain and the digestive system. "Doctors once believed the nerve's main job was controlling acid production in the stomach," Mayer says. "But 95 percent of the fibers go the other direction -- from the gut to the brain."Nobody knows exactly what messages travel along this cable, but scientists have found that stimulating the nerve at different frequencies can cause either anxiety or a strong sense of well being. Perhaps the term "gut feeling" isn't just a figure of speech after all.Mayer suggests another intriguing possibility: Prozac and similar antidepressants may actually work on the gut, not the brain. Drugs known as SSRIs short for selective serotonin reuptake inhibitors ease depression by enhancing levels of serotonin. Most experts assume it's the extra serotonin in the brain that helps improve mood. But 95 percent of the serotonin in the body actually lies within the digestive system. Perhaps, Mayer says, SSRIs do their job by boosting serotonin in the gut and changing the signals along the vagus nerve.- The stress alarmWhatever messages may be passing back and forth, they can easily become garbled in times of stress. When the brain senses a threat, real or imagined, it sounds the alarm by flooding the body with adrenaline and another hormone called CRF short for corticotropin-releasing factor. These hormones trigger the "fight or flight" response -- helpful back in the days when humans had to run from lions, but a potential liability when we lose a job or go through a divorce.If you suffer from frequent emotional distress -- perhaps because of extreme stress, depression, or anxiety -- the unrelenting flood of adrenaline and CRF will take a toll on your digestive system. For one thing, the hormones can make the cells in the stomach and intestines extra-sensitive to pain. As a result, normal contractions and movements can become excruciating. The new signals can also disrupt the motion of the intestines, causing bouts of constipation or diarrhea.- Functional disease in a dysfunctional worldBecause of the close connection between the brain and many abdominal disorders, a multinational team of investigators, specialists, and federal research agencies convened in the mid-1980s to develop criteria for diagnosing more than 20 digestive disorders known as "Functional Gastrointestinal Disorders," or FGIDs. A "functional" disease, in this case, means a disturbance in GI function that it isn't related to any injury, infection, or other obvious physical problem. These criteria, which include persistent constipation, diarrhea, bloating, abdominal pain, or irritable bowel syndrome unrelated to diagnosable physical disorder, was recently updated by an international team known as the Rome II Committee, which called for a classification system of these disorders based on clusters of common symptoms.Among the disorders the committee examined is irritable bowel syndrome IBS, a very common and perplexing malady often characterized by painful cramps, bloating, and constipation alternating with diarrhea. If you have "functional" IBS, you may feel that "dysfunctional" is a much more apt term.Emotional distress alone can't cause IBS -- the source of the disorder is still unknown -- but stress or a mood disorder may worsen the symptoms. In fact, few other conditions provide such a clear illustration of the link between the mind and the body. One recent Australian study found that chronic distress -- arising from such traumas as divorce, lawsuits, serious illnesses, or job troubles -- accounted for 97 percent of all changes in IBS symptoms. Interestingly, short-term swings in mood don't seem to have much effect on IBS, which explains why many people still suffer symptoms on relatively calm, relaxing days.In a similar manner, strange messages along the gut-brain axis also seem to be a major cause of "functional" dyspepsia, or indigestion. People with dyspepsia often experience the discomfort of constant ulcer pain without actually having ulcers. Stress definitely makes the symptoms worse, but the effect isn't nearly as dramatic as with irritable bowel syndrome. If adding stress to functional dyspepsia is like throwing woodchips on a fire, combining stress with IBS is like dousing a blaze with gasoline.The influence of the mind on the gut goes beyond functional diseases. For instance, people with Crohn's disease or ulcerative colitis -- two conditions with clearly physical origins -- often suffer flareups during times of emotional stress. And in a recent survey, 68 percent of people with basically healthy digestive systems said stress gives them stomachaches.- Setting your mind on reliefSo what can you do if your mind and your digestive system aren't getting along? One thing you shouldn't do is suffer silently. Ask your doctor if you would be a good candidate for cognitive behavioral therapy, interpersonal therapy, relaxation therapy, or another form of counseling. In several studies, these treatments have been shown to give IBS patients more relief than standard medical therapies. You might even consider hypnosis or self-hypnosis.While rarely used in the United States, hypnosis is a popular -- and apparently effective -- treatment for IBS in Europe, Whitehead says. Preliminary studies suggest it may also help ease functional dyspepsia.It's worth noting that Prozac and other SSRIs may help calm the stomach. Small doses of a tricyclic antidepressant -- too small to affect mood -- can lessen stomach pain, presumably by blocking pain messages.There's another reason to go to the doctor: Simply hearing you're not crazy or gravely ill may be a great source of comfort. "Reassurance from a physician is probably the most effective treatment for IBS," Mayer says.Supportive docs will never go out of style, but even better treatments for IBS and other functional disorders may soon be on the way. Researchers are currently studying medications designed to block the release of CRF, the hormone that helps translate stress into stomach trouble. Mayer says the medication may be available in a little more than a year.But you don't have to wait that long to get better. Do what you can to avoid stress and work closely with your doctor. With a little luck, your gut feelings will be much more pleasant.-- Chris Woolston, M.S., is a health and medical writer with a master's degree in biology. He is a contributing editor at Consumer Health Interactive, and was the staff writer at Hippocrates, a magazine for physicians. He has also covered science issues for Time Inc. Health, WebMD, and the Chronicle of Higher Education. His reporting on occupational health earned him an award from the northern California Society of Professional Journalists. http://www.ahealthyme.com/article/primer/101186767 These are no intended to me the answer for everyone and every condition, just on how complex this is and other treatments in IBS and other reasons foods are not the only picture in IBS. There is also a lot of food phobia in IBS that needs to be researched, because in IBS there is a tendency to associate food=pain for one or d for one, and its not always the food, but many other reasons, may be the problem or contribute.


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## eric (Jul 8, 1999)

Just for the record also.My problem with Mikke really is his focus on loss of oral tolrence and the serotonin issue causes d right out of the gate.It is not someone trying leap which maybe benefical to the person, it is in his information he presents to people on this on only loss of oral tolerence causing d, or lack there of on major food and physiological and phycological issues and also some HPA axis issues.I also recommend foods from Heathers perspective too. There are chemical problems with foods that are not loss of oral tolerence issues, but shear chemistry issues in food contents.Nutrition and IBS. http://www.ibsregister.com/nutrition.htm


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## LaurieJ (Sep 3, 2002)

Eric,I am sorry about the implied "attack" on your posts concerning spelling errors, etc. I didn't mean it as a personal attack, only as why some information may not be as "appealing" as others, based on a subconscious reaction to the presentation of the information or an inherent snobbery of the reader to only look at the "skin" as opposed to the meat of the post (think of the phrase "beauty is only skin deep') - and yes, I am talking about myself - I can be snobbish sometimes - and forget to consider other peoples limitations.I have great respect for you for all the time you spend dispersing information especially given your limitations (and being an English major is your greatest one - LOL). And I have learned to consider other, more ephemeral, relationships found in this disorder because of what you have written.I am sure that the mind / body connection will be found to play an important role in all of this, but am just as sure that it is not the only or even the main factor in the cause or treatment of IBS. Who knows, maybe that little vestigel organ, the appendix, will be the culprit (just a joke, a joke!!!!!! No-one seriously suggests this - I am just always trying to find a reason for the appendix to exist - this seems to be a good enough reason as anyothers - and what a joke on all of us if this is the reason, ha, ha).LaurieJ


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## eric (Jul 8, 1999)

LaurieJ , yes my english major has gotten me a cup of coffee and a chef job. LOLI noticed after you said that my spelling was worse. LOL sorryThis is information to digest that's all.







My girlfriend has IBS also and we were discussing perhaps penut butter and jelly sandwhiches are the cause of IBS. LOL perhaps everyone lost their oral tolerence to them as kids and this set up IBS. LOl







She also told me recently of one of the worst things I think I have ever heard in regards to a doctors comment. It was a sticks doctor and she was telling him how much it impaired her soocial life, dating going out ect.. His comment was, "That's why they have vidoes." What an *******. There are good and bad doctors in the world for sure, and so you know, there are excellent doctors on the research end of IBS. If you want to read two great books.This is on that and you can find the book in amazon. Both these people are involved in IBS.The Enteric Nervous System:A Second Brain http://www.hosppract.com/issues/1999/07/gershon.htm and The balance withinEsther M. Sternberg, M.D.Esther M. Sternberg, M.D., is Director of Integrative Neural Immune Program and Chief of the Section on Neuroendocrine Immunology and Behavior at the National Institute of Mental Health and National Institutes of Health. Prior to coming to NIH, she trained in rheumatology at McGill University, practiced medicine in Montreal, and continued her research career and teaching at Washington University in St. Louis. The winner of the Public Health Service Superior Service Award and recent President of the International Society for Neuroimmunomodulation, Dr. Sternberg has written over one hundred scientific papers, reviews, and book chapters on the subject of brain-immune connections, including articles in Scientific American and Nature Medicine. She has also co-directed an exhibition on Emotions and Disease at the National Library of Medicine and lectures nationally and internationally on emotions, health,and disease. "The Balance Within:The Science Connecting Health and Emotions by Esther M. SternbergThis textbook explores the mind-body connection and what it means for health. Esther Sternberg provides accounts of the experiments that reveal the physical mechanisms, the nerves, cells and hormones - used by the brain and immune system to communicate with each other. She describes just how stress can make us more susceptible to all types of illness, and how the immune system can alter moods." http://www.esthersternberg.com/ Both these people are on the top in their fields.You know I have had severe refractory IBS for thirty years although I have been in remission the last three years, based on things I have learned in all this, to keep balance for one and calm the brain gut axis down and also not focus on one thing and the problem as a whole, and also watch somethings I eat.I have also like everyone had it implied this was in was in my head.Now however, from my research its easy for me to see it is both and that's hard for some people after the intital "its all in the head."


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## eric (Jul 8, 1999)

This may not work for all.However, if you close your eyes and take a little bit of time and really picture sucking on something sour like a lemon drop, does your mouth salivate.


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## eric (Jul 8, 1999)

something in more layans terms for simplisity.With permission from Jackson GastroenterologyIrritable Bowel SyndromeWhat is an Irritable Bowel?Medically, irritable bowel syndrome IBS is known by a variety of other terms: spastic colon, spastic colitis, mucous colitis and nervous or functional bowel. Usually, it is a disorder of the large intestine colon, although other parts of the intestinal tract -- even up to the stomach -- can be affected.GI TrackThe colon, the last five feet of the intestine, serves two functions in the body. First, it dehydrates and stores the stool so that, normally, a well-formed soft stool occurs. Second, it quietly propels the stool from the right side over to the rectum, storing it there until it can be evacuated. This movement occurs by rhythmic contractions of the colon.When IBS occurs, the colon does not contract normally. instead, it seems to contract in a disorganized, at times violent, manner. The contractions may be terribly exaggerated and sustained, lasting for prolonged periods of time. One area of the colon may contract with no regard to another. At other times, there may be little bowel activity at all. These abnormal contractions result in changing bowel patterns with constipation being most common.A second major feature of IBS is abdominal discomfort or pain. This may move around the abdomen rather than remain localized in one area.These disorganized, exaggerated and painful contractions lead to certain problems. The pattern of bowel movements is often altered. Diarrhea may occur, especially after meals, as the entire colon contracts and moves liquid stool quickly into the rectum. Or, localized areas of the colon may remain contracted for a prolonged time. When this occurs, which often happens in the section of colon just above the rectum, the stool may be retained for a prolonged period and be squeezed into small pellets. Excessive water is removed from the stool and it becomes hard.Also, air may accumulate behind these localized contractions, causing the bowel to swell. So bloating and abdominal distress may occur.Some patients see gobs of mucous in the stool and become concerned. Mucous is a normal secretion of the bowel, although most of the time it cannot be seen. IBS patients sometimes produce large amounts of mucous, but this is not a serious problem.Spastic ColonThe cause of most IBS symptoms -- diarrhea, constipation, bloating, and abdominal pain -- are due to this abnormal physiology.IBS is not a diseaseAlthough the symptoms of IBS may be severe, the disorder itself is not a serious one. There is no actual disease present in the colon. In fact, an operation performed on the abdomen would reveal a perfectly normal appearing bowel.Rather, it is a problem of abnormal function. The condition usually begins in young people, usually below 40 and often in the teens. The symptoms may wax and wane, being particularly severe at some times and absent at others. Over the years, the symptoms tend to become less intense.IBS is extremely common and is present in perhaps half the patients that see a specialist in gastroenterology. It tends to run in families. The disorder does not lead to cancer. Prolonged contractions of the colon, however, may lead to diverticulosis, a disorder in which balloon-like pockets push out from the bowel wall because of excessive, prolonged contractions.CausesWhile our knowledge is still incomplete about the function and malfunction of the large bowel, some facts are well-known. Certain foods, such as coffee, alcohol, spices, raw fruits, vegetables, and even milk, can cause the colon to malfunction. In these instances avoidance of these substances is the simplest treatment.Flaccid Colon Infections, illnesses and even changes in the weather somehow can be associated with a flare-up in symptoms. So can the premenstrual cycle in the female.By far, the most common factor associated with the symptoms of IBS are the interactions between the brain and the gut. The bowel has a rich supply of nerves that are in communication with the brain. Virtually everyone has had, at one time or another, some alteration in bowel function when under intense stress, such as before an important athletic event, school examination, or a family conflict.People with IBS seem to have an overly sensitive bowel, and perhaps a super abundance of nerve impulses flowing to the gut, so that the ordinary stresses and strains of living somehow result in colon malfunction.These exaggerated contractions can be demonstrated experimentally by placing pressure- sensing devices in the colon. Even at rest, with no obvious stress, the pressures tend to be higher than normal. With the routine interactions of daily living, these pressures tend to rise dramatically. When an emotionally charged situation is discussed, they can reach extreme levels not attained in people without IBS. These symptoms are due to real physiologic changes in the gut -- a gut that tends to be inherently overly sensitive, and one that overreacts to the stresses and strains of ordinary living.DiagnosisThe diagnosis of IBS often can be suspected just by a review of the patient's medical history. In the end it is a diagnosis of exclusion; that is, other conditions of the bowel need to be ruled out before a firm diagnosis of IBS can be made.A number of diseases of the gut, such as inflammation, cancer, and infection, can mimic some or all of the IBS symptoms. Certain medical tests are helpful in making this diagnosis, including blood, urine and stool exams, x-rays of the intestinal tract and a lighted tube exam of the lower intestine. This exam is called endoscopy, sigmoidoscopy or colonoscopy.Additional tests often are required depending on the specific circumstances in each case. If the proper medical history is obtained and if other diseases are ruled out, a firm diagnosis of IBS then can usually be made.TreatmentThe treatment of IBS is directed to both the gut and the psyche. The diet requires review, with those foods that aggravate symptoms being avoided.Current medical thinking about diet has changed a great deal in recent years. There is good evidence to suggest that, where tolerated, a high roughage and bran diet is helpful. This diet can result in larger, softer stools which seem to reduce the pressures generated in the colon.Large amounts of beneficial fiber can be obtained by taking over-the-counter bulking agents such as psyllium mucilloid Metamucil, Konsyl or methylcellulose Citrucel.As many people have already discovered, the simple act of eating may, at times, activate the colon. This action is a normal reflex, although in IBS patients it tends to be exaggerated. It is sometimes helpful to eat smaller, more frequent meals to block this reflex.There are certain medications that help the colon by relaxing the muscles in the wall of the colon, thereby reducing the bowel pressure. These drugs are called antispasmodics. Since stress and anxiety may play a role in these symptoms, it can at times be helpful to use a mild sedative, often in combination with an antispasmodic.Physical exercise, too, is helpful. During exercise, the bowel typically quiets down. If exercise is used regularly and if physical fitness or conditioning develops, the bowel may tend to relax even during non-exercise periods. The invigorating effects of conditioning, of course, extend far beyond the intestine and can be recommended for general health maintenance.As important as anything else in controlling IBS is learning stress reduction, or at least how to control the body's response to stress. It certainly is well-known that the brain can exert controlling effects over many organs in the body, including the intestine.SummaryPatients with IBS can be assured that nothing serious is wrong with the bowel. Prevention and treatment may involve a simple change in certain daily habits, reduction of stressful situations, eating better and exercising regularly.Perhaps the most important aspect of treatment is reassurance. For most patients, just knowing that there is nothing seriously wrong is the best treatment of all, especially if they can learn to deal with their symptoms on their own. http://www.gicare.com/pated/ecdgs03.htm


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## eric (Jul 8, 1999)

Something elseIF you have any doubt about the importantance of ""fight-or-flight"in IBSAnd the Threat to the indivual organism and concious and subconcious aspects of this read the current issue of Discover Magazine, March issue cover story in regards to how deep this goes and how people are not aware of it at all, because it happens so fast.Faster then a person can even say loss of oral tolerence. LOL Just a joke I know this can be real. DISCOVER Vol. 24 No. 3 March 2003Table of ContentsCOVER STORYEmotions and the Brain: Fear By Steven JohnsonFew memories are as easily formed and as difficult to shake as those triggered by stark terror. Part one of a new Discover Learning Series explores recent efforts to lessen the impact of primal fear on the modern psyche.


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## trbell (Nov 1, 2000)

eric, you might want to read the Archives of Internal Medicine article before you blow MNL off competely. tom


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## LaurieJ (Sep 3, 2002)

It occurs to me that one way to process all of this information and become more of a team when discussing this is to create a visual model of all the components. This example is going to be controversial and humorus I hope, so do not get bogged down in the particulars, but look at it as a whole (I am NOT advocating any one person's point of view - as far as I am concerned they are all wrong or all right - for the sake of the illustration)Imagine that IBS is composed of 5 theoretical dysfunctions.1 part I will call Eric and deals with the mind / gut.2 part is Mike and deals with food intolerances3 part is Ralph and deals with the immune system / infections.4 part is Tom and deals with our environment / support system.5 part is Doc and involves medicine / treatment, etc.Now each of these parts are very complex and to thoroughly study one of these leaves no time to become an expert in any other area of IBS research. Therefore, Mike's researchers becomes an expert in food. Ralph's in immunology, etc.....Each of these researchers are well regarded and are creating valid hypotheses that stand up to challenge within their area of expertise. And none of the hypotheses worked on by any group is mutually exclusive! As a researcher when you support one part, it doesn't mean that you don't believe that the other part isn't important, it's just that you are leaving it up to the other person to mine that data while you exhaustively research your area.However, in order to thoroughly describe the condition, your goal as a researcher is to meld each part into one whole organism. How is this done? By arriving at solid conclusions within your specialty then sharing your data with the other researchers in the sub specialties (Mike talks to Ralph who talks to Eric....etc). The data are shared to see if there are common links across the divisions and new experiments are designed to look for these links. Eventually the five parts combine to give one comprehensive explanation for the syndrome - a Universal theory of IBS.But in order to do that, the five parts must be willing to acknowledge the other's area of expertise and realize that the whole is too complex to study in its entirety by any one research team. Suppression / ridicule of another's data will only hinder us from melding the parts together. However, healthy debate can lead to eureka moments - those unexpected AHA THAT"S IT discoveries. By turning these debates into turf wars, we create an atmosphere in which eurekas may never occur.The moral of the story? Everyone could be right, everyone could be wrong but in order to find out, the parts have to talk to one another and respect each others views and realize that the end point is most likely going to have a little bit of each part in it. And we must recognize that we are still in the stage of everyone becoming experts in the subspecialties and that inter-specialty discussion is young yet. Which is why there is so much confusion over "who is right". Because right now, no one person, hypothesis or research group has the all-encompassing answer.


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## trbell (Nov 1, 2000)

there are specialist for some of those areas already I think but I'm not sure how much time they have to answer questions.tom


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## Guest (Feb 28, 2003)

Hi again, Mike,Before I pour through the rest of this I wanted to comment that I've already been through desensitization and was unable to complete the program due to having systemic allergic reactions.... you know... the kind where you break out in hives all over your body and your nose starts to run and you sneeze and your throat constricts????No fun.... No fun....







And the nurse who used to give me the injections at one point stopped, looked intently at me, held that syringe high in her hand in the air... and said to me... "Evie... I'm not gonna touch you with a ten-foot pole." (Later I came to work for her brother who is the Human Resources Director at my hospital)I have taken note of your comment regarding how you never make derogatory statements... and that is, in fact, true. So point taken....







On the other hand, I also cannot discount the research and the factual scientific information brought to us by Eric and UNC.In addition, Tom has always brought up valid psychological points, has lived through a few himself... as have I.... and we both know that often psychology rules biology as well as the reverse.This is my own personal belief, but I think that there are many behavioral health implications (brought about by physical and psychological occurrences throughout our lives)... that have great impact on IBS and its sister components. I also believe that allergies are the result of the immune system being worn down by Cortisol.... the stress hormone.At this time in my life, I am in such a chronic stress-debilitated state that I often feel overwhelmed, stressed, anxious and am very recently having serious difficulty controlling my thoughts/emotions.... so please forgive me if I've in any way been harsh to you, Mike, because that is not my intent. I think you know me well enough to know that while I can be a royal pain in the butt..







.... my heart is in the right place.There are no easy answers to any of this. But at least we have this board, we have Jeff who created this board, we have you and Eric and Tom and others who are moderators of this board.... and we have all of us who are members of this board...... and together... we collectively make up a very large, supportive and "edge of discovery" self-help board that I think would lend itself better to understanding by both new and old members if information could be formatted to better meet our needs as lay people (this is my teacher background coming forth). I adjust all of my training courses to the level of my students.... while at the same time, not overwhelming them with unnecessary details until they ask me or they are ready to hear them. I find this to be the most productive way to allow them to retain as much from their studies as possible.I'll read more and post more if I feel it relavent.And Mike... I have no doubt that allergies are responsible for many woes..... just as my own behavioral health, FMS and CFS are responsible for many of my own personal woes....... but globally speaking..... IBS is a functional disorder that may or may not encompass any of the above. We don't know enough about it yet to be sure. But I certainly have my suspicions... based on what doctors have told me over the years, what I've read, and my own experiences for the past 40+ years.SUMMARY: This info is good guys..... can ya pare it down just a tad so that we pea brains can assimilate it just a little bit better? It's sorta like giving us applesauce until we're ready to crunch into the real thing......







OH... and Eric.... this might be a good place to identify the link on the CBT/Hypno Forum where you posted about the cover article in Discovery Magazine and I posted about the cover article in Newsweek Magazine. Both are related to how the brain manages fear and anxiety and we consider them both to be a MUST-READ. There is a very delicate connection between body and mind... science can now track fear and anxiety in the brain and throughout the body. Evie


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## trbell (Nov 1, 2000)

Oh, you Wisconsin women! I knew there was a reason for my divorces.tom


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## trbell (Nov 1, 2000)

Sorry for the hijack. tom


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## Guest (Feb 28, 2003)

Oh now Tom....







.... you're making me ...BLUSHTake a break, Tom... and have some Wisconsin cheese....and Wollerscheim Prairie Fume.(it was an adorable hijack)Evie


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## Guest (Feb 28, 2003)

Eric,I have a few choice words that would accurately describe your S.O.'s doctor, but if I were to unleash them here, Jeff would ban me forever, so suffice it to say that he reminds me of the north end of a horse that is headed south.Evie


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## eric (Jul 8, 1999)

So the model would look something like this, which takes into account everything above you mentioned.







And researchers, from all the different groups would get together here. Not just from one center. http://www.conference-cast.com/ibs/Lecture...dRegLecture.cfm


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## trbell (Nov 1, 2000)

I'm not sure how it could be adapted for this forum?tom


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## Guest (Feb 28, 2003)

This looks like one of the same pictures we saw at one of the recent UNC chats.Again... makes perfect sense.Thanx, Evie


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## Mike NoLomotil (Jun 6, 2000)

An intriguing series of responsesï¿½.At first I began preparing detailed tutorial responses to each specific challenge set forth specifically with my name as the challenged individual, a gauntlet for me to run it would seem, to try to continue debating something as if there is a debate when in fact there is not. In fact the nature of the questions speak for themselves as to the pointlessness of response as each and every one has been responded to over and over again to the point of futility. A scotoma to what someone says cannot be overcome. Indeed, again, what the message of the doctors I work with or whose work in this area is familiar to me, have found and practice is again metamorphosed into a) ï¿½MIKESï¿½ as if it were mine and







set forth as if it were mutually exclusive to the findings of othersï¿½the polar opposite of everything I seek to convey to those interested in the subject.Since I have explained many times the concept of the need to first INTEGRATE all the findings everyone has so farï¿½everyone, including invasive studies which have quantified specific primary abnormal immunologic events within the large and small bowel of people diagnosed with IBS and food allergy was ruled OUT ï¿½I pulled up short as the following old quote echoed through my head first, then another statement was seen further down the thread which basically made what my response needs to be very clear.First Thomas Hobbes once observed ï¿½True and False are attributes of ï¿½speechï¿½ NOT of ï¿½thingsï¿½. And where speech is NOT, neither is there truth or falsehood.ï¿½You see, by way of clear and concise example, it is a fact, a truth, that in each case of any investigation which was posted in this thread or elsewhere wherein events and cause-effect relationships where observed in people selected for study who were chosen by the investigators as IBS sufferers (based on their criteria applied for selection) and such events range from the gastroneural phenomenon of, say, distention provocation followed by bloodflow changes in specific areas of the CNS, it is a fact that these events occur. It is also a fact that the explanation of the possible reasons (mechanisms) of these events when discussed are qualified by those setting forth their explanations with ï¿½it is believedï¿½ or ï¿½it is feltï¿½ or ï¿½it is suggestedï¿½ or ï¿½Patients with visceral hypersensitivity are thought to beï¿½ï¿½ etc. This is because the investigator has quantified an event, but not quantified the mechanism. Only that there are several possible mechanisms and bsed on that investigators perspective, and what he ahs personally studied and observed, and based on his selection criteria, this explanation seems plausible. Do we see the distinction between ï¿½thingï¿½ and ï¿½speechï¿½ and wherein ï¿½truthï¿½ lies on those observations.By the same token it is just as ï¿½FACTUALï¿½ that there is a substantial body of literature which apparently must be wholly unfamiliar to some, wherein such things as ï¿½ï¿½we can show an allergy-like inflammation during [food] challenges with parameters like Il-4, IFN-gamma, CD3, CD4, CD8 and IgE.ï¿½ (Ulf Bengtsson,MD, et al, Sahlgrens Medical University Hospital) are ALSO factual quantified observations from within the GI tract of subjects who would be also diagnosed as having IBS and in whom allergy was ruled out. If you know what that finding means, then you know why the investigators who study such things observe that there is a population of peiople diagnosed with IBS whose symptoms are provoked by abnormal immune responses to food challenges which often have nothing to do with innate (intrinsic) chemicals within the reactive foods. So what do they report? The exact same style of this ï¿½suggestsï¿½ an heretofore unobserved abnormal ï¿½allergy-likeï¿½ response to dietary provocation in these subjects.This is just as old, wizened, and documented (maybe more so) than other observed events for which an INTEGRATED understanding needs to be achieved.Silly challenges of ï¿½ask Mike why he does not [fill in the blank] or how does he answer [fill in another blank]ï¿½ are simply rhetorical and argumentative because the information first is not MINE to explain, it is merely something I read or saw someone more qualified than I quantify, and it has ALL been posted before if you actually read the references or links which I posted and which contained the information supposedly withheld from the sick people hereï¿½by design I guess is the implication..There are AMPLE tutorials which make it very clear how and why each of the observed psychoneuroimmunoendoexocrine events we can quantify in the narly bowels of ISB patients can occurï¿½like duh what an astounding non-news piece that 95% of serotonin is in the gutï¿½do you know how much is in the platelets within the entire microvasculature of the gut a any momentï¿½and what should happen if platelets allow serotonin release within the microvasculatureï¿½and what mediators released by other immunocytes provokes platelet responsesï¿½and what cell mediated reactions have been quantified to occur in the bowels of these people which release the precursor mediators of platelet responseï¿½ad nauseumThis must be considered as part of the whole equationï¿½along with all the other mechanisms. All the so called things I do not take time to further drain peoples patience explaining I donï¿½t explain because I post the places where people who want to leatrn such things can go read about them..and those who do nt donï¿½t have to scroll down for 5 minutes to get to something helpful to them.Like, with rising tone and irritation and desire to again try to establish a debate where there is noneï¿½.ï¿½ask Mike about global symptomsï¿½ï¿½duh x2. Like if the questioner actually read ALL the material on the subject one can easily observe the multiple biochemical origins of various global symptoms, and that the accused has posted tutorials showing how these phenomena can occur repeatedly. Evie is rightï¿½you want to banter further go offline as it is one thing to engage in legitimate debate, but another to keep answering the same things and posting the same answers and sources over and over and to be declared that it was never answered. Scotomas simply cause this. Get the books I refer people to, read them then go to the bibliographies and read all the references, and read references that are based upon these two following SOUND comments. Read them and integrate them you have to have the objective view that is distilled herein: _______________________________________________ï¿½It occurs to me that one way to process all of this information and become more of a team when discussing this is to create a visual model of all the components.ï¿½ ________________________________________________Thereï¿½s a solid triple. I have posted what is so far probably the best such visual model countless times, and I know it is in the Judges own library. Study it carefullyï¿½as the diagram posted above is not complete, based upon all the mechanisms know so far to be mechanisms of symptom generation in IBS. It is correct indeed as far as it goes but there are physicians, both clinical and investigators, who would add substantially to that diagram. This is not to be taken, again, and repeated that I am insulting anyone or questioning. I am pointing out again a fact...that there are other perspectives on this, not only one, and collectively I beleive them to be correct not exclusively, as there is data to support each shown mechanism.The diagram lays out in very simple schematic form, the interdependent inetrractions between each of the body systems which can generate symptoms associated with IBS.That diagram is FIGURE ONE (1) in this tutorial:Alimentary Pharmacology and Therapeutics Vol. 15 Issue 4 Page 439 April 2001 Food hypersensitivity and irritable bowel syndrome S. Zar, D. Kumar, M. J. Benson http://www.blackwell-synergy.com/servlet/u...36.2001.00951.x One cannot obtain the whole tutorial and all the diagrams freeï¿½so I cannot POST the diagram here without risk. But anyone who wants to see the kind of diagram suggested by Laurie it is hereï¿½and probably worth the $10 price of admission to be able to see it.If one comprehends that diagram one will take a big step forward in understanding also a comment, posted ironically among the many innuendos: _________________________________________________ï¿½ï¿½"Food allergy or sensitivity is sometimes misdiagnosed as IBS because both conditions can lead to abdominal pain and diarrhea." _______________________________________________HOME-RUN!!!JEEZ this is the entire point of all investigators and clinicians who approach IBS NOT from the perspective that it should be diagnosed based solely on symptoms, but more work should be done to isolate a causal basis for the symptoms. It is the very heart of the perspective which resides 180 degrees in juxtapositionï¿½the symptom based criteria will indeed isolate the IBS population from ALLERGY (food) populations fairly well IF the practitioner ALSO does an allergy workup. That is a careful history and intake-symptom analysis (immunoassays are not really required if you are good at this). By some estimates as many as 10% of people diagnosed with IBS actually suffer from food allergy (immunglobulin specific hypersensitivity).There is another population diagnosed with IBS and walking around living and suffering from it needlessly who are THESE people: _________________________________________________ï¿½Page 1051 of the Merck Manual, and online Merck Manual at http://www.merck.com/pubs/mmanual/section1...ter148/148b.htm "Recently Food Intolerance was found to be responsible for symptoms of some patients with the IRRITABLE BOWEL SYNDROME, confirmed by double-blind food challenge.An increase in rectal prostaglandin levels was noted when a reaction occurred.ï¿½ _________________________________________________The exact size of this subpopulation is unclear but if you actually make a concerted effort to study the related literature it is clearly defined as being predominantly among the 2/3 who suffer from diarrheic or cyclic symptoms. They are also characterized by the fact that their symptoms are rarely limited to GI symptomsï¿½they manifest themselves with a wide array of systemic symptomsï¿½as was observed by _______________________________________________Quote from:Lancet 2000 Jul 29;356(9227):400-1Relation between food provocation and systemic immune activation in patients with food intolerance.Jacobsen MB, Aukrust P, Kittang E, Muller F, Ueland T, Bratlie J, Bjerkeli V, Vatn MH.Section of Gastroenterology, Rikshospitalet, University of Oslo, N-0027 Oslo, Norwayb Section of Clinical Immunology and Infectious Diseases, Rikshospitalet, University of Oslo, N-0027 Oslo, Norwayc Section of Endocrinology, Rikshospitalet, University of Oslo, N-0027 Oslo, Norwayd Medical Department and Research Institute of Internal Medicine, Rikshospitalet, University of Oslo, N-0027 Oslo, Norwaye Medical Department, Vestfold Sentral Hospital, Tï¿½nsberg, Norway ï¿½ We found that food provocation in food intolerant patients was characterised by a general and systemic immune activation accompanied by an increase in systemic symptoms.ï¿½ ________________________________________Check out what happens when cell-mediated immune responses occur in the systemic circulation. What the biochemical consequences areï¿½what organ systems are affected including the CNSï¿½a whole additional realm of possibilities opens that requires exploration to further understanding.And observed many times before, such as from: _______________________________________________Curr Opin Immunol 1998 Dec;10(6):620-7T cell immunity to oral allergens.MacDonald TT.Department of Paediatric Gastroenterology St Bartholomews and the Royal London School of Medicine and Dentistry St Bartholomews Hospital London EC1A 7BE UK. ï¿½Considerable light has been thrown on the mechanisms of oral tolerance (or, more correctly, orally-induced systemic tolerance) in the past 12-18 months. While it is very clear that T cell anergy and apoptosis can occur after being fed antigen, a major pathway that has been described in different models is the induction of regulatory T cells which secrete transforming growth factor beta. These cells have been designated Th3 cells but their relation to the in-vitro-generated Tr cells, which inhibit tissue-damaging T cell responses in the gut mucosa, is not known. An important discovery is that food antigens have major systemic effects on T cells, similar in many ways to those seen following intravenous injection of soluble antigens. This conceptually moves us away from the notion that there is something special about mucosal (compared to systemic) lymphoid tissue to the notion that it is the type of antigens seen in the gut (i.e. digested, soluble polypeptides) which dictates the types of response seen there. ï¿½ ________________________________________________This is all relevant to the key point articulated, again, so there is no mistaking the message, hereby: ____________________________________________ï¿½Considerable confusion is now arising over the relationship between food intolerance and the Irritable Bowel Syndrome (IBS). Although the name has been hallowed by long usage, IBS is not a distinct entity but merely a collection of disorders which are characterized by abdominal symptoms but no obvious organic pathology. G.W. Thompson forecast in 1985: ï¿½the IBS is organic; that is all sufferers will eventually be found to have measurable, unique pathologic defects.ï¿½ When that happy day arrives, the term ï¿½IBSï¿½ will no longer be used, and each patient will receive a more precise diagnosis. Until then it is sufficient to appreciate that food intolerance represents an important proportion of the conditions which together make up IBS.ï¿½John Hunter, MD, FCRPDirector or Gastroenterology and Consultant PhysicianAddenbrookeï¿½s HospitalCambridge, United KingdomFromï¿½Food Allergy and Food Intoleranceï¿½ Second Edition 2002J. Brostoff, MDS. Challacombe, MDSaunders _________________________________________________So long as patients who suffer symptoms provoked by mechanisms which are sourced to food or chemical intolerance continue to be diagnosed as suffering ï¿½IBSï¿½ based upon their symptoms, they will continue to view themselves as such. And so will their caregivers. Some migrate to forums like this...seeking answers.If these patients believe, or are treated, as if this is NOT the mechanism of symptom generation they will NOT recover as much as they could if they were able to be put on a Disease Management Regimen for their problem, and they will continue to use more mediation than they would need to, and we will continue to think that there are (pick number du jour) 15,000,000 or 20,000,000 so called ï¿½IBS Sufferersï¿½ in this country. When in fact the actual population may be substantially lessï¿½less than half that perhaps. No on will know until ALL the information is integrated from ALL sources and applied universally to the differential diagnosis of patient presenting with symptoms which fir the Rome criteria and in whom allergy is ruled, out, IBD is ruled out, enteritis is ruled out, etc.In fact this is how clinical medicine is supposed to progressï¿½not remain stuck on old dogma. I have watched it al my life, not just the 30 years ï¿½at the bedsideï¿½ but the 40 years I have myself suffered the self-same condition.So one must see, if any degree of objectivity can be displayed, that there IS no debateï¿½indeed the term ï¿½food intoleranceï¿½ itself only denotes a clinical manifestation of a set of mechanisms which are not limited to immunologic, enzymatic, dysbiotic, or other such primary biochemical problems. Indeed ï¿½loss of oral toleranceï¿½ can be the consequence of psychoneural trauma as wellï¿½or the oft used ï¿½stress responseï¿½. If this was not beleived one would not have been also working with local representatives of the Mind-Body Institute (Dr. Benson of Harvards ï¿½relaxation responseï¿½ programï¿½a local wellness center which used that protocol plus a dietary therapy protocol we provided with which some maybe familiar). Ample discussion of this pathway is also in the literature.As long as people who suffer symptoms which are provoked by these mechanisms continue to be diagnosed as having ï¿½IBSï¿½ then they must be addressed, approached, and educated in that context. One cannot have it both ways. Again, suggested reading which can help further integrate an understanding of this topic in the context of IBS and other conditions which may or may not be comorbid:IBS: A DOCTORS PLAN FOR CHRONIC DIGESTIVE TROUBLESBy Gerard Guillory, M.D.; Vanessa Ameen, M.D.; Paul Donovan, M.D.; Jack Martin, Ph.D. http://www.amazon.com/exec/obidos/ASIN/088...3369143-6824157 ï¿½FOOD ALLERGIES AND FOOD INTOLERANCE: THE COMPLETE GUIDE TO THEIR IDENTIFICTION AND TREATMENTï¿½, Professor Jonathan Brostoff , M.D.. Allergy, Immunology and Environmental Medicine, Kingsï¿½ College, London http://www.amazon.com/exec/obidos/ASIN/089...6487508-3420903 FOOD ALLERGY AND INTOLERANCE, Professor Jonathan Brostoff, MD, Stephen Challacombe, MD (NEW 2002) http://www.amazon.com/exec/obidos/ASIN/070...product-details have a DFD all who wish it







MNL


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## BQ (May 22, 2000)

Laurie J, Admittedly I can get easily intimated by some of the folks here. The vast scope of their knowledge leaves me, well, in plain English, stupefied at times. lolAnd I mean more stupefied than Levsin can leave me.







Eric, Kmottus, MNL, Tom, (I put ya all in Alpha order, ok?







)ETC all have my respect. But I can get awestruck at their talents. I am NOT a gifted student of science. And I am ashamed to tell ya, my hubby actually taught me Algebra in my early 20's. lol So forgive me if I sit with mouth agape and take a rather lengthy and ambling trail to actual understanding. And also forgive me for finding you all fairly awesome folks.Perception is what we live in. It is our vision. It is a good thing made even better when shared. However I believe you were saying, "Here, try on my glasses and I'll try on yours." Yes? I will also say, that I have found looking through someone else's glasses, or walking in their shoes, to only be a good thing for me. It is a decision that only tends to foster my own education. And it has served me well. Keeping an open mind is essential to me. And maybe easier??? Cause if I know one thing.... I know, with clarity, that I know very little. LOLSo yeah, I'm all ears and eyes guys. And just M(very)HO, I'm guessing, truly guessing (Not even close to a hypothesis, ok?







) IBS ultimately will not be a brain *VS* gut thing. But rather a brain *and* gut thing.For me though, at the moment, my presence here is more to learn how to manage my symptoms, live my life as well as I can, despite IBS. And I try to help others in any way I can. For instance, I'm concerned that LoriAnne can see our replies that she really needs further diagnostics. I'm not sure she will see them within this lengthy thread. lolI just assume, I'm not gonna figure IBS out, (and yeah that *IS* a good hypothesis, take it to the bank).







But I am more than willing to share what has worked for me. We are all different and sharing what we know can only help. I needed to know certain things before I truly accepted that I had IBS in the first place. And that info I got here. Not in my Doc's office. BUT, big one here, I certainly would never have gotten too far in symptom management if I did not retain said open mind.BQ


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## LaurieJ (Sep 3, 2002)

Mike,VERY WELL SAID!!! I am intrigued by the study showing system wide activation of the immune system following oral challenge and hope to read your references more thoroughly in the upcoming weeks.I am disappointed that I only hit a triple though. I guess the pitcher put "something" on the ball!BQ,don't be intimated by the information. This doesn't mean that anyone is smarter than anyone else, just that they have spent more time in one area of study than another. For example, you may not feel confident in algebra but I bet there is something that you do or can explain that Mike, Eric or I (et al) couldn't even begin to compete with. Again, we are all qualitatively different, not quantitavely.....No one is better or worse than another only differernt. I may have an understanding of immunology but that is because I spent the last 20 years of my life working with this concept, however when it comes to understanding physics or cooking a meal or expressing myself succintly - I STINK!!! Does that make me smarter or dumber than anyone else? NO! It just says that my life experiences are different. To borrow a phrase from Mr Spock (the valcon): Celebrate "Infinite Diversity in Infinite Combinations!"


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## trbell (Nov 1, 2000)

I have to confess I didn't make the high school basebal team because i didn't try out for it. tom


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## eric (Jul 8, 1999)

LaurieJ, couple things here in regards to IBS, the d is happening right out of the gate from the act of eating in IBS, not from loss of oral tolerence, this needs to be understood, the release is from the act of eating. This is how the new drugs work, the exceess speeds up the peristaltic function and cause d. In the act of eating. This has been confirmed since this was written. Hence why Mike, does not talk about this, or why the new drugs work on d and serotonin, like lotronex or Zelmac.This is something Mike never talks about here and keeps saying d patients have IBS from loss of oral tolernce, it can happen to people, but that is NOT IBS!!! YOU CANNOT EXPLAIN IBS as loss of food intllorence, its a trigger.I will post this again.A:Irritable bowel syndrome is now recognized as a disorder of serotonin activity. Serotonin is a neurotransmitter in the brain that regulates sleep, mood depression, anxiety, aggression, appetite, temperature, sexual behavior and pain sensation. Serotonin also acts as a neurotransmitter in the gastrointestinal tract.Excessive serotonin activity in the gastrointestinal system enteric nervous system is thought to cause the diarrhea of irritable-bowel syndrome. The enteric nervous system detects bowel distension expansion on the basis of pressure-sensitive cells in the bowel lumen opening. Once activated, these pressure-sensitive cells promote the release of serotonin, which in turn promotes both secretory function and peristaltic function the contractions of the intestines that force the contents outward. At least four serotonergic receptors have been identified to be participants in the secretory and peristaltic response.Patients with diarrhea-predominant IBS may have higher levels of serotonin after eating than do people without the disorder. This recognition led to the development of the first drug used specifically to treat diarrheal symptoms of IBS, alosetron also known as Lotronex. Alosetron blocked the specific serotonin receptors responsible for recognizing bowel distention. In doing so, it blocked the effects of serotonin and reduced both bowel secretions and peristalsis. Constipation was the most common side effect seen. (Note: Alosetron was removed from the market by the manufacturer after repeated reports of a dangerous condition known as ischemic colitis became known. Tegaserod Zelmac is another drug under development and under review by the U.S. Food and Drug Administration for approval. Tegaserod is indicated for the treatment of constipation-predominant IBS and works to increase enteric nervous system serotonin activity.So, increasing serotonin activity in the enteric nervous system produces increased bowel secretions and peristalsis and potentially diarrhea, whereas depressing serotonin activity produces reduced secretions and reduce peristalsis and potentially constipation. Increasing serotonin activity in the brain would increase awareness and, in higher doses, produce anxiety, insomnia and restlessness. So I would have expected exactly the opposite effects of those that you experienced.I am unable to identify any possible drug interactions between 5-HTP and Synthroid levothyroxine but the symptoms described suggest a check with your doctor may be in order. Persistent feelings of tiredness and constipation may be signs of an underactive thyroid hypothyroidism.June 19, 2001"Excessive serotonin activity in the gastrointestinal system enteric nervous system is thought to cause the diarrhea of irritable-bowel syndrome."Then there is the gastro colon reflex causing d in IBS patients based on the calorie content of the meal.These things happen before loss of oral tolernece right out of the gate.Mike does not and never talks about this as he presents loss of oral tolerence as why IBS pateints have d, when in fact you have d from the overreaction of serotonin in the gut and you have c in IBS because not enough serotonin going through the receptor. Then you have alternating because of alternating sertonin through the receptors.The imunne system in IBS is way more copmplex then the loss of oral tolerence Mike is presenting as well, as he is not discussing some impoortant aspects here on the immune system the HPA and the fight or flight reponce and chronic stressors.I would listen to these sinnce your interested in the immune system and how it applies to IBS.Jack Wood, PhDProfessor of Physiology and Internal MedicineChairman Emeritus, Department of PhysiologyThe Ohio State University College of MedicineDr. Wood was the first to use microelectrodes to record the electrical and synaptic behavior of neurons in the enteric nervous system. He coined the term "brain-in-the-gut" in view of emerging evidence that the enteric nervous system had neurophysiological properties like the brain and spinal cord. In recent years he has focused on signaling interactions between the enteric immune system and the brain-in-the-gut during infectious enteritis and food allergy. In this lecture he shows how the central nervous system, enteric nervous system and intestinal immune system are integrated during physical and emotional stress to produce irritable bowel symptoms of diarrhea and abdominal pain and discomfort. http://www.conference-cast.com/ibs/Lecture...cfm?LectureID=7 Nigel Bunnett, PhDUniversity of California School of MedicineDepartment of Surgery and PhysiologyAccumulating evidence indicates that sensory nerves play a major role in inflammation of multiple tissues, and that communication between the nervous system and mast cells is of particular importance. Dr. Bunnettï¿½s lecture will highlight recent experimental evidence that mast cell proteases signal to sensory nerves through novel receptors that couple to the release of proinflammatory peptides, and that defects in this mechanism result in uncontrolled inflammation and disease. Dr. Bunnett will present evidence that therapies designed to block signaling by neuropeptides and proteases are attractive treatments for inflammation. http://www.conference-cast.com/ibs/Lecture...dRegLecture.cfm Esther Sternberg, MDChief, Section on Neuroendocrine Immunology and BehaviorDirector, Molecular, Cellular and Behavioral Integrative Neuroscience ProgramNational Institute of Mental Health, National Institute of HealthA pioneer in the field of neural-immune interactions, Dr. Sternberg will present the scientific evidence proving molecular, neuroanatomical and hormonal links between the brain and immune system and will discuss the role that disruptions of such links play in inflammatory/autoimmune disease. http://www.conference-cast.com/ibs/Lecture...dRegLecture.cfm These are experts in immunology of the gi track and immunology in disease and experts in the enteric nervous system and experts in Neurogastroenterology and gastroenterology and more.Some body also should let the neurogastroenterologists know there is no Brain gut axis and connections between the gut and brain.Dr Sternberg, you should look into, she is probably the leading expert in the world on, A pioneer in the field of neural-immune interactions. So when sombody repeatly says, immunologists are not looking at IBS, it couldn't be further from the real truth.Take a look into pubmed on the loss of oral tolerence and foods and the relationship to IBS and view how many studies there are? Don't confuse loss of oral tolerence its own problem with IBS. They are only the same here as Mike try's to make them the same.Also who is Dr Drossman? Dr. Drossman is a Co-director of the Center and Professor of Medicine and Psychiatry at UNC-CH. He established a program of research in functional gastrointestinal disorders at UNC more than 15 years ago and has published more than 250 books, articles, and abstracts relating to epidemiology, psychosocial and quality of life assessment, design of treatment trials, and outcomes research in gastrointestinal disorders.He was responsible for organizing the Functional Brain Gut Research Group as a special interest section within the American Gastroenterological Association, is a past president of the American Psychosomatic Society. Dr. Drossman sits on the Board of Directors and is Chair of the Scientific the Advisory Board of the International Foundation for Functional Gastrointestinal Disorders. He also sits on the board for the medical website Medscape Gastroenterology . Dr. Drossman chaired the 1999 Digestive Health Initiative on Functional GI Disorders ï¿½ sponsored by the American Digestive Health Foundation. He was the recipient of the 1999 Janssen Award for Clinical Research in Digestive Disease, which was at Digestive Disease Week(DDW), the American Gastroenterological Association's international conference in Orlando.In 2001, Dr. Drossman was appointed Associate Editor of Gastroenterology, the official journal of the American Gastroenterological Association and appointed to the Nerve-Gut Council of the American Gastroenterological Association. He received the prestigious Research Scientist Award for Clinical Research presented by the Functional Brain-Gut Research Group at Digestive Disease Week in Atlanta. In addition, he is Chair of the IBS Program for the American Gastroenterological Association.Dr. Drossman has developed a series of videotapes to teach physicians and other health professionals how to administer an effective interview, carry out a psychosocial assessment, and enhance the patient-doctor relationship available through the Center. He has taught numerous US and European workshops on this topic, was the chair of the Physician-Patient Relations Committee of the American College of Gastroenterology from 1994 - 1996, and is a charter fellow of the American Academy on Physicians and Patients, a consortium of physicians which teaches these skills to medical school faculty.Dr. Drossman is also involved in teaching the evaluation and management of patients with complex GI problems or difficult-to-diagnose conditions. He completed the AGA Clinical Teaching Project on IBS unit 13, and is now completing the AGA GI Teaching Project on IBS-II to be released this summer. He is editor of the Manual of GI Procedures now in its third edition, and Rome II: The Functional Gastrointestinal Disorders, 2nd Edition and has been appointed Chair of the International Rome III Committees with the book, Rome III, to be published in 2006.In addition to seeing patients in the GI clinic, Dr. Drossman precepts GI fellows and visiting gastroenterologists in seeing clinic patients with functional GI disorders. He also supervises medical faculty, psychiatry residents, and medical students, working with them on how to provide psychological care to patients with functional GI disorders. A list of his publications, check them out. http://www.med.unc.edu/medicine/fgidc/biblio.htm This is something they put together on IBS for general MD's and gastroenterologists a teaching project for gastroenterologists. If you want more on IBS it costs 150 bucks I believe.Irritable Bowel SyndromeCTP 13Table of Contents 1. Title Slide Functional GI Disorders - Definition 2. Functional GI Disorders - Definition 3. Functional GI Disorders - Anatomic Regions 4. Esophageal Functional GI Disorders 5. Gastroduodenal Functional GI Disorders 6. Bowel Functional GI Disorders 7. Biliary Functional GI Disorders 8. Anorectal Functional GI Disorders 9. Definition of IBS IBS - Epidemiology 10. U.S. Prevalence 11. World Prevalences 12. Health Care Seeking 13. Doctor Visits by Gender 14. Prevalence of Diagnosis in Clinical Practice 15. Work and School Absences - U.S. Data 16. Physician Visits per Year - U.S. Data 17. Epidemiology Summary Gastrointestinal Physiology 18. Effects of Stress on GI Symptoms 19. Time Line of Physiologic Research in IBS 20. Normal Colonic Response to Stress - Almy, 1951. 21. Increased Meal-Stimulated Sigmoid Motility in IBS - Rogers, 1989 22. Effect of Anticholinergic on Meal-Stimulated Sigmoid Motility - Sullivan, 1978 23. Stress-induced Effects on Jejunal Activity - Kumar, 1985 24. Normal Migrating Motor Complex 25. Discrete Clustered Contractions in IBS - Kellow, 1987 26. Prolonged Propagated Contractions in IBS - Kellow, 1987 27. Pain Produced from Rectosigmoid Distension - Whitehead, 1980 28. Lower Pain Tolerance in IBS Occurs Primarily in the Bowel - Whitehead, 1990 Brain-Gut Physiology 29. Integration of CNS-Gastrointestinal Function 30. Ascending Pain Pathway #1 31. Ascending Pain Pathway #2 continued 32. Descending Pain Modulating System 33. The Enteric Nervous System 34. Enteric Nervous System Anatomy 35. Effect of CNS on ENS Activity 36. Visceral Hypersensitivity 37. Spinal Hyperexcitability - General Concept 38. Visceral Hypersensitivity - Normal Regulatory Activity 39. Visceral Hypersensitivity - Painful Event 40. Visceral Hypersensitivity - Sensitizing Event 41. Visceral Hypersensitivity - Regulatory Activity After Sensitization 42. Visceral Hypersensitivity - Summary slide 43. Molecular Mechanism for Visceral Hypersensitivity - I. Magnesium Block 44. Molecular Mechanism for Visceral Hypersensitivity - II. Ca2+ Entry and Binding 45. Molecular Mechanism for Visceral Hypersensitivity - III. Nitric Oxide Diffusion 46. Colonic Distension in Normals - Pain Reporting 47. Rectal Pain Threshold Post Distension - IBS vs. Normals 48. Change in Symptoms and Rectal Sensitivity Over Time 49. Sigmoid Distension - Fedotozine Effect 50. Effect of Octreotide on Pain Reporting in IBS 51. Regional Cerebral Activation - PET Scan 52. Correlation of Anterior Cingulate Activity with Rectal Pain Intensity 53. Increased REM Sleep in IBS 54. Pathophysiology Summary Psychosocial Factors 55. Dysmotility and Hyperalgesia, Symptoms and Health Care Seeking 56. Self-selection into Clinical Practice 57. Psychosocial Disturbances in Referral Practices 58. Frequency of Psychiatric Disorders in IBS - Referral Centers 59. Are Psychological Disturbances the Same? 60. Comparison of Psychologic Disturbance 61. Abnormal MMPI Scores Among IBS Patients and Non-patients and Normals 62. Conceptual Model of IBS 63. Psychosocial Factors Affecting Outcome in IBS 64. IBS and Abuse - Abuse Reporting Based on IBS Severity and Treatment Site 65. IBS and Abuse - Effects on Health Status 66. Severe IBS and Abuse - Possible Mechanisms 67. IBS and Abuse - Self-Selection 68. Psychosocial Summary Diagnosis 69. Timeline of Diagnostic Approaches 70. Diagnostic Approach - Overall Scheme 71. Establish Symptom-Based Diagnosis 72. Manning Criteria 73. Rome Criteria 74. Identify Dominant Symptom 75. Other Clinical Factors 76. Perform Diagnostic Tests 77. Initial Evaluation -Rome Recommendations 78. "Red Flags" 79. Differential Diagnosis 80. Initiate Treatment - Reassess in 3-6 Weeks 81. Additional Specialized Studies 82. Change in Diagnosis Unusual After Initial Evaluation 83. Symptoms Retained at Follow-up 84. Symptom Onset and Disappearance Treatment 85. Physician-Patient Relationship - Treatment Guidelines 86. Treatment Guidelines and M.D. Visits 87. Combined Slide - Listing of Treatment Guidelines and M.D. Visits 88. The Patient's Agenda 89. The Doctor's Agenda 90. Factors Affecting Treatment 91. Placebo Response Rate 92. Spectrum of Severity in IBS 93. Mild IBS - Routine Check-up with Primary Care Physician 94. Education and Reassurance 95. Dietary Modifications 96. Moderate IBS - Referral to a Gastroenterologist 97. Monitoring and Modification 98. Symptom Diary 99. Pharmacotherapy of Gut Symptoms 100. Pharmaceutical Agents 101. Psychological Treatments 102. Psychological Treatments - Definitions 103. Psychologic Interventions - Treatment Study Results 104. Psychotherapy - Interpersonal Treatment 105. Psychotherapy - Interpersonal Treatment cont. 106. Severe IBS - Sent to Referral Center 107. Set Realistic Goals 108. Focus on Health, not Illness 109. Antidepressants for Pain Control 110. Brain - Gut Inhibitory Pain Pathway "Gate" Control 111. Comparison of Tricyclic and SSRI Antidepressants 112. Referral for Symptom Management 113. Indications for Referral 114. Treatment Summary 115. Future Pharmacological AgentsI am sure all these doctors are well aware of the fact a person can have loss of oral tolerence to foods!!! I am also sure they are aawre of what that means in IBS in the gobal picture, foods can trigger symtpoms. Not just because of loss of oral tolerence either, but because some foods can irritate the gi track, just through chemical means, such as coffee as a stimulant for example.


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## trbell (Nov 1, 2000)

"Who's on first", Mike?tom


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## eric (Jul 8, 1999)

here we are focssuing on foods again.Ask Mike directly why people have receptors in their guts malfunctioning and improve taking lotronex for example in IBS and what that has to do with loss of oral tolerence in the first place. How this relates to the other 20 gi functional disorders, why functional d does not have pain and IBS does?Functional GI Disorders: Current State of Knowledge http://www.med.unc.edu/wrkunits/2depts/med...gidc/bkgrnd.htm He yells intergrated approach and then focuses on foods while I am focusing on the intergrated approach and Biopsychosocial which takes into account many factors.Inflammatory Mediators in Irritable Bowel Syndrome maria O'Sullivan, PhD http://www.med.unc.edu/wrkunits/2depts/med...rymediators.htm By the way Dr Wood is an expert on food allergies and the gi tract and immunology.let look at the history of them.History of Functional DisordersDouglas A. Drossman, MDCenter-Co-DirectorMelissa SwantkowskiNew York UniversityThe PastHISTORICAL PRECEDENTSHistorians and physicians have documented the presence of Functional GI disorders throughout recorded human history. However, until recently, limited attention has been granted to these disorders due to the lack of identifiable pathology and the absence of a conceptual framework to understand and categorize them. Systematic investigation of functional GI disorders did not begin until the middle of the 20th century, and prior to this time, only occasional reports of functional GI symptoms were published, the first appearing only 200 years agver the past 25 years, scientific attention to understanding and properly caring for patients with functional GI disorders has grown progressively. With the understanding comes the rationale for use of medications directed at intestinal receptors as well as psychopharmacological, behavioral, and psychological forms of treatment. Additionally, there has been an increase in the rate of scientific publications and greater media exposure to the public through television, radio, and Internet.To understand the historical classification of these disorders, two differing theories relating to the interaction between the mind and body should be considered. o Holism: a theory built upon the foundation that the mind and body are integrated and utterly inseparable. o Dualism: a theory that proposes a separation between the mind and the body.Greek philosophers Plato, Aristotle, and Hippocrates first proposed the principle of holism about 3,000 years ago, and later in the 12th century; Jewish physician and philosopher Maimonides reexamined this philosophy. Based on holism, the study of medical disease must take into account the whole person rather than merely the diseased part. However, societal concepts of illness and disease drastically shifted when European philosopher Rene Descartes offered the divergent theory of dualism in the 17th century. Prior to the notion of dualism, the church discouraged human dissection on the premise that the spirit resided in the body. The acceptance of dualism paved the way for the emergence of scientific investigation and new medical discoveries by lifting the prohibition of human dissection. This shift in medical thought was congruent with the societal changes of the 17th century: the shift towards a separation in church and state.IMPLICATIONS FOR FUNCTIONAL GI DISORDERSBased on the concept of dualism, disease was now understood in terms of structural abnormalities. Therefore, the validity of a disease rested with the observation of morphological abnormalities. Medical conditions occurring in the absence of such morphological abnormalities and symptoms were not considered legitimate, and were often viewed as psychiatric, consistent with the concept of dualism. The concept of dualism had other effects with regard to treatment. For example, this would include all the functional GI disorders and other somatic syndromes, such as fibromyalgia. Until the latter part of the 20th century, a medical illness was considered amenable to scientific inquiry and treatment. However, patients with psychiatric disorders were interred in insane asylums and considered to no longer be treatable by medical physicians.Unfortunately this concept leads to a clinical dilemma. Specific diseases explain only about 10% of medical illnesses seen by physicians. Furthermore, people with structural i.e. organic diagnosis such as inflammatory bowel disease or cancer show considerable variation in their symptom presentation and clinical behavior. Gastroenterologists as well as other health care practitioners are all too familiar with the poor correlation between structural findings on endoscopy and their patient's symptoms.Although efforts to find morphological or even motility etiologies for functional GI disorders in the latter part of the 20th century were unsuccessful, the assumption that functional GI disorders must be psychiatric has developed and has permeated current thinking. However, in the face of current scientific research, this is being seriously challenged. Studies have shown that persons with irritable bowel syndrome who do not seek health care are psychologically much like healthy subjects.The PresentCONCEPTUAL BASES FOR THE STUDY OF FUNCTIONAL GI DISORDERS  o The recent acceptance of functional GI disorders as legitimate medical entities is based on the following three developments: o The concept of the Biopsychosocial model of illness and disease o The development of new investigative methods for studying disease o The development of the Rome CriteriaBiopsychosocial ModelIn 1977, the publication of the concept of the Biopsychosocial model by George Engel, and its later demonstration specifically for gastrointestinal disorders, marked an important change in thinking. A biopsychosocial model of illness and disease provides the needed framework to understand, categorize, and treat common GI symptoms. These symptoms are the integrated product of altered motility, enhanced visceral sensitivity, and brain-gut dysregulation and often are influenced by psychosocial factors. Figure 1 illustrates the proposed relationship between psychosocial and physiological factors with functional GI symptoms and the clinical outcome. Early in life, genetics and environmental influences family attitudes toward bowel training or illness in general, major loss or abuse history or exposure to infection may affect one's psychosocial development (susceptibility to life stress, psychological state, coping skills, social support or the development of gut dysfunction abnormal motility or visceral hypersensitivity. Additionally, the presence and nature of a functional GI disorder is determined by the interaction of psychosocial factors and altered physiology via the brain-gut axis. In other words, one individual afflicted with a bowel disorder but with no psychosocial disturbances, good coping skills and adequate social support may have less severe symptoms and not seek medical care. Another having similar symptoms but with coexistent psychosocial disturbance, high life stress, or poor coping skills may frequent his physician's office and have generally poor outcome.Development of New Investigative MethodsThe second concurrent process has been the expansion and refinement of investigative methods that allow the study of functional GI disorders in terms of biological, cultural, and psychosocial i.e. brain influences. These developments include: 1. the improvement of motility assessment, 2. the standardization of the barostat to measure visceral sensitivity, 3. the enhancement of psychometric instruments to determine psychosocial influences, 4. the introduction of brain imaging PET, fMRI to determine CNS contribution to symptoms, and 5. the molecular investigation of brain-gut peptides, which provide insight into how these symptoms become manifest.In less than ten years, these methods have produced new knowledge of the underlying pathophysiological features that characterize the age-old symptoms we now define as functional GI disorders.Rome CriteriaThe Rome Criteria is an international effort to characterize and classify the functional GI disorders using a symptom-based classification system. This approach that has its precedents with classification systems in psychiatry and rheumatology. The rationale for such a system is based on the premise that patients with functional GI complaints consistently report symptoms that breed true in their clinical features, yet cannot be classified by any existing structural, physiological or biochemical substrate. The Rome Criteria was built upon the Manning Criteria, which was developed from discriminate function analysis of GI patients.The decision to develop diagnostic criteria by international consensus was introduced as part of a larger effort to address issues within gastroenterology that are not easily resolved by usual scientific inquiry or literary review. By 1992, several committees had met to discuss the criteria, which ultimately resulted in the publishing of many articles in Gastroenterology International and a book detailing the criteria titled "The Functional Gastrointestinal Disorders Rome I". Elaboration of the Rome I criteria led to a second edition of the Rome criteria titled Rome II) in 2000 as well as the publication of a supplement to the journal Gut in 1999. Recently the Rome Coordinating Committee has met to begin Rome III, expected to be published in 2006. To learn more about the Rome Committees and to see a summary of the Rome II book: go to www.romecriteria.com.PRESENT PATHOPHYSIOLOGICAL OBSERVATIONSDespite differences among the functional gastrointestinal disorders, in location and symptom features, common characteristics are shared with regard to: o motor and sensory physiology, o central nervous system relationships, o approach to patient care.What follows are the general observations and guidelines.MotilityIn healthy subjects, stress can increase motility in the esophagus, stomach, small and large intestine and colon. Abnormal motility can generate a variety of GI symptoms including vomiting, diarrhea, constipation, acute abdominal pain, and fecal incontinence. Functional GI patients have even greater increased motility in response to stressors in comparison to normal subjects. 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.Visceral HypersensitivityVisceral hypersensitivity helps to account for disorders associated with chronic or recurrent pain, which are not well correlated with changes in gastrointestinal motility, and in some cases, where motility disturbances do not exist. Patients suffering from visceral hypersensitivity have a lower pain threshold with balloon distension of the bowel or have increased sensitivity to even normal intestinal function. Additionally, there may be an increased or unusual area of somatic referral of visceral pain. Recently it has been concluded that visceral hypersensitivity may be induced in response to rectal or colonic distension in normal subjects, and to a greater degree, in persons with IBS. Therefore, it is possible that the pain of functional GI disorders may relate to sensitization resulting from chronic abnormal motor hyperactivity, GI infection, or trauma/injury to the viscera.Brain-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.The Role for Psychological FactorsAlthough psychological factors do not define these disorders and are not required for diagnosis, they are important modulators of the patient's experience and ultimately, the clinical outcome. Research on the psychosocial aspects of patients with functional GI disorders yields three general observations: o Psychological stress exacerbates gastrointestinal symptoms in patients with functional GI disorders and can even produce symptoms in healthy patients but to a lesser degree. o Psychological disturbances modify the experience of illness and illness behaviors such as health care seeking. For example, a history of major psychological trauma e.g. sexual or physical abuse is more common among patients seen in referral centers than in primary care and is associated with a more severe disorder and a poorer clinical outcome. Additionally, psychological trauma may increase pain-reporting tendency. o Having a functional GI disorder has psychological consequences in terms of one's general well-being, daily functional status, concerns relating to control over symptoms, and future implications of the illness e.g. functioning at work and home.APPROACH TO TREATMENTThe approach to treatment for all functional GI disorders is founded on a therapeutic physician-patient relationship. The basis for implementing a strong physician-patient relationship is supported by evidence that patients with functional GI disorders have anywhere from a 30 to 80% placebo response rate regardless of treatment.Because functional GI disorders are chronic, it is important to determine the immediate reasons behind each visit, after which treatment can be based on severity and nature of symptoms, physiological and psychosocial determinants of the patients illness behavior, and the degree of functional impairment.These factors can separate patients into mild, moderate, and severe categories.Patients with mild symptoms: o usually seen in primary care, o do not have major impairment in function or psychological disturbance and o can maintain normal activity.These patients have concerns about their condition but do not need to make many visits to their physician. Regarding treatment, these patients require education about their disorder and its symptoms as well as information regarding a proper diet and the kinds of medication that can have adverse effects.Patients with moderate symptoms: o seen in both primary and secondary care facilities and o experience intermittent disruptions in activity on account of their symptoms. o may identify a close relationship between symptoms and inciting events such as stress, travel, or dietary indiscretion.For these patients, symptom monitoring to record time, severity, and presence of associated factors can help to identify inciting factors and give the patient a sense of control over the disorder. Additionally, pharmacotherapy directed at specific symptoms, particularly those that impair daily function, can be helpful, as can psychological treatments (relaxation, hypnosis, cognitive-behavioral therapy, and combination treatments) in reducing anxiety and encouraging health promoting behaviors.Patients with severe symptoms: o have trouble functioning daily, o find their disorder to be disabling and debilitating in nearly every facet of life, o have a high frequency of associated psychological difficulties, o make frequent visits to their physicians , and o may hope for a magical cure.In these cases a long-term physician-patient relationship, which sets realistic treatment goals (such as improved quality of life rather than elimination of all pain) is necessary. The focus for these patients needs to shift from treating a disease to coping with a chronic disorder, where much of the responsibility is place on the patient, himself. Furthermore, antidepressants have proven useful to control pain and alleviate associated depressive symptoms.The FutureFuture studies will identify pathophysiological subgroups, each having its own set of determinants and treatment. Examples are as follows: o :Some patients will develop their disorders or exacerbate symptoms via sensitization of afferent transmission from infection, enhanced motility, or trauma to the gut. They may respond to the newly developing neurotransmitter blocking agents. o Patients with more painful and severe symptoms may prove to have "abnormal perception of normal gut function" rather than abnormal function. This dysfunction in the central regulation of incoming visceral signs may be remedied with a psychopharmacological treatment approach. o The symptoms of some patients could be attributed to genetic factors, which result in abnormalities in central reactivity to stress, in which case genetic manipulation strategies would prove beneficial. o Early learning within the familial structure and socio-cultural influences has been demonstrated to affect symptom perception and illness behavior. Future studies are also likely to identify psychological and behavioral interventions that are targeted for this subgroup.While it is likely that there are potent new treatments that will follow our growing pathphysiologic knowledge of these disorders, it is unlikely that they will replace some of the fundamental clinical principles: o active listening, o careful decision making, o an effective patient-physician relationship, and o patient centered biopsychosocial plan of care. http://www.med.unc.edu/wrkunits/2depts/med...aldisorders.htm Type in brain gut axis and IBS in the serch and read away or HPA and IBS and read away or serotonin and IBS and read away. OR mast cells or enterochromaffin cells two key players in IBS.People can have loss of tolerence to food and believe its IBS or be misdiagnosed if the doctor did not know IBS well to seperate the issues. Digestion 2001;63(2):108-15 Related Articles, Links Click here to read Food-related gastrointestinal symptoms in the irritable bowel syndrome. Simren M, Mansson A, Langkilde AM, Svedlund J, Abrahamsson H, Bengtsson U, Bjornsson ES. Department of Internal Medicine, Section of Gastroenterology and Hepatology, Sahlgrenska University Hospital, Goteborg, Sweden. magnus.simren###medicine.gu.se BACKGROUND/AIMS: Postprandial symptoms are common in patients with irritable bowel syndrome IBS. However, existing studies have come to different conclusions about the role of food in the pathophysiology of IBS. We explored the prevalence of subjective food-related gastrointestinal GI symptoms and its relationship to clinical characteristics and psychological factors in IBS. METHODS: 330 patients with IBS and 80 healthy volunteers completed a food questionnaire developed for this study. The subjects graded their subjective symptoms after 35 different foods and a food score was obtained by adding the item scores. The relationship between subjective food-related GI symptoms and referral status, IBS subgroup predominant bowel pattern, sex, anxiety, depression and body mass index BMI was estimated. RESULTS: In 209 63% of the patients the GI symptoms were related to meals. Gas problems and abdominal pain were the most frequently reported symptoms. Foods rich in carbohydrates, as well as fatty food, coffee, alcohol and hot spices were most frequently reported to cause symptoms. The food score was higher in patients than in controls (p < 0.0001). In the IBS group higher scores were observed in patients with anxiety p = 0.005, and females p < 0.001, but the results were unrelated to IBS subgroup, referral status or BMI. The BMI did not differ between groups. CONCLUSION: A majority of IBS patients consider their symptoms to be related to meals. Especially foods rich in carbohydrates and fat cause problems. Nevertheless, the majority of IBS patients are normal or overweight. Female sex and anxiety predict a high degree of food-related symptoms in IBS. Copyright 2001 S. Karger AG, BaselPMID: 11244249I am not arguing if a person should be tested they should be for a lot of food problems, celiac, malabsorbtion,fructose, lactose ect.. I am saying d happens regarless of loss of oral tolerence in IBS. After that its a trigger.


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## eric (Jul 8, 1999)

FYIAliment Pharmacol Ther 2003 Jan;17 1:43-51 Related Serotonergic modulators in the treatment of irritable bowel syndrome - influence on psychiatric and gastrointestinal symptoms. Kilkens TO, Honig A, Rozendaal N, Van Nieuwenhoven MA, Brummer RJ. Departments of Psychiatry and Gastroenterology, University Hospital Maastricht, The Netherlands. BACKGROUND: : Both central and peripheral serotonergic modulators are used in the treatment of irritable bowel syndrome. The majority of patients with irritable bowel syndrome presenting to a gastroenterologist demonstrate affective dysregulation. Serotonin may play a regulatory role in both gastrointestinal motility and sensitivity, as well as in affective dysregulation, in irritable bowel syndrome. AIM: : To analyse, systematically, randomized controlled trials studying the influence of serotonergic modulators on both gastrointestinal and psychiatric symptoms in irritable bowel syndrome, in order to elucidate baseline irritable bowel syndrome symptomatology and possible differential effects of serotonergic modulation on this symptomatology. METHODS: : A standardized qualitative analysis was performed of studies investigating the influence of serotonergic modulators on both gastrointestinal and psychiatric symptoms in irritable bowel syndrome using a blind review approach. The studies were ranked according to their total quality score maximum 100 points. RESULTS: : Eleven studies fulfilled the entry criteria, six of which scored above 55 points. An association between gastroenterological and psychiatric changes was present in five of the six studies. CONCLUSIONS: : The results strengthen the serotonergic association between gastroenterological and psychiatric symptoms. Adjusted guidelines for combined gastrointestinal and psychiatric assessments are recommended in order to further elucidate the serotonergic interaction between gastrointestinal and psychiatric symptoms.PMID: 12492731"Is there then a distinction between someone who is constipation-predominant, someone else who might be diarrhea-predominant, and people who alternate between the two?Traditionally there has been that distinction. But we're beginning to see that this is not a condition that causes constipation or diarrhea, but it's a disturbance in the regulation of the bowel function. It's a brain-gut condition, and triggering factors may variously cause symptoms of diarrhea at one time and constipation at another. We've found that about half of those affected have alternating diarrhea and constipation. About 30% will usually have only the diarrhea, and about 20% usually only the constipation.""What would be an example of new understanding?Well one example is that we're starting to understand how the brain is responding to the pain in IBS. There have been some studies done where they've artificially created a kind of an irritable bowel by placing a balloon to stretch the bowel, and that produces pain. Then they've compared people with IBS to non-IBS, or "normal" individuals. And what they've found is that when you stretch the bowel-and use PET scans to monitor the response-in normal individuals, certain areas of the brain that register pain respond and release chemicals called neurotransmitters that suppress and lower the pain. But it seems that doesn't happen as well in people with IBS. In fact, in people with IBS another area of the brain responds that is associated with anxiety. So what we find is that people with IBS, aside from having a bowel problem, may have some difficulty in terms of the way their brain is regulating the pain." http://www.aboutibs.org/Publications/clinicalIssues.html "In fact, in people with IBS another area of the brain responds that is associated with anxiety. So what we find is that people with IBS, aside from having a bowel problem, may have some difficulty in terms of the way their brain is regulating the pain."Chronic Functional Abdominal Pain http://www.aboutibs.org/Publications/CFAP.html FYI on IBSThe Neurobiology of Stress and EmotionsBy: Emeran A. Mayer, M.D., UCLA Mind Body Collaborative Research Center, UCLA School of Medicine, California http://www.aboutibs.org/Publications/stress.html "What does this have to do with IBSConverging evidence from different laboratories and research groups are consistent with the concept of an "enhanced stress responsiveness" as a major vulnerability factor in many IBS patients. As outlined above, such an enhanced stress responsiveness may not be obvious to the affected individual, until he or she is exposed to a period of sustained threatening stressors financial or employment problems, divorce, aftermath of a major disaster with consequences on daily life, repeated mild to moderate stressors, or a one time severe life threatening type stressor robbery or physical assault. Under these circumstances the mechanisms that normally turn off the stress response are overwhelmed, and attempts of the nervous system at adaptation or habituation fail. Many of the vulnerability factors for such enhanced stress responsiveness have been identified and many of them occur in a particular vulnerable period of the developing brain before age 10. Some of the best-studied factors include loss of the primary care giver, distant mother-child relationship, emotional neglect, and physical and verbal or sexual abuse.In order to understand how a chronically enhanced stress response can produce the cardinal symptoms of IBS abdominal pain and discomfort associated with altered bowel habits we have to go back to the earlier section on the emotional motor system: activation of the stress system will stimulate contractions and secretion in the sigmoid colon and rectum. Depending on the specific emotional context fear vs. anger, the upper GI tract will be either inhibited fear or stimulated anger. In addition, recent research in animals has demonstrated a phenomenon referred to as stress-induced visceral hyperalgesia. What this means is that in vulnerable animals, exposure to an acute moderate stressor will make the colon more sensitive to distension and the perception of discomfort or pain."Perceptions of pain, muscle tensions, and other somatic symptoms can cause stress levels to spiral upward. Self-regulation strategies that reduce unpleasant symptoms offer both physical and psychological relief."ï¿½R. SovikWhy do the symptoms go away after one stressful situation has resolved and persist in another? Amongst many factors, anxiety and fear generated by IBSsymptoms themselves are sufficient in many patients to maintain the stress responsiveness in a chronically enhanced state. Some of the more common symptom related anxieties include: Am I close enough to a bathroom when my symptoms come on? Will I be OK for the rest of the day, unless I completely empty my colon in the morning before leaving the house? What can IBS patients do to guard against the detrimental effects of allostatic load and enhanced stress responsivenessBased on our current state of knowledge, little can be done in the affected patients to reverse vulnerability factors that have been programmed into our genes or have been hardwired into our nervous system during the first few years in life. Nevertheless, a variety of cognitive and behavioral approaches may be useful in protecting ourselves against the effects of allostatic load, or the wear and tear, of stress. These include: 1 Developing effective coping styles towards life stress and IBS symptoms; 2 Learning to activate mechanisms in the body that oppose the stress response and induce what has been referred to as the "relaxation response" through various relaxation techniques e.g., breathing exercises, progressive relaxation, hypnosis, meditation; and 3 Moderate but sustained exercise. "


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## trbell (Nov 1, 2000)

take a look at the Archives of Internal Medicine article, eric. And then ask mike directly rather than all thse games.I apol;ogize if my last remark was cry[itc, appearently it was too cryptisc for some.tom


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## eric (Jul 8, 1999)

Tom, this is no game to me in the slightest, these are very, very important issues and people with IBS should be aware of these things.I actually went to the experts on this as I thought they could presented better then I am here. I personally understand alot of it already,but the answer is in simpler terms so I could relay the information back to the group here on this and will post the link to the info here.


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## trbell (Nov 1, 2000)

I think I understand what you are trying to do and i've said that i approve of your effort in general. I do have problems though when it seems like you are attacking Mike personally rather than arguing about the research.same applies to Mike of course and I know he may have said things in the past but at least lately he seems to be sticking to what the research shows.tom


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## eric (Jul 8, 1999)

Tom, Mike has been here for years telling people that IBS d is caused by loss of oral tolerence in IBS. There are many gastro specialists, neurogastro specialists among others studying immune reactions in IBS as well as the whole big picture neuro chemistry,ect ect ect and he like's to argue that IBS researchers do not study immunology in the big picture of IBS and that is far from the truth. Loss of oral tolerence to foods maybe comorbid in an indivual, but there is an underlying condition, that makes the gut sensitve to ALL stimuli and there is also very strong evidence on what cause d in IBS and it's NOT loss of oral tolerence. A person can have this, its understood by everyone, but it does not account for the underlying D predominate IBS patients mechanisms. Dr Drossman's comment's. The question I asked was is d IBS caused by the loss of oral tolerence to foods? What role do foods play in IBS? http://www.ibshealth.com/ibs_foods_2.htm


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## trbell (Nov 1, 2000)

so that the argument is really about what IBS is? You know that's impossible to settle - even the experts take sides as that's how science works. but the other way it works is by looking at research in detail. Maybe this example will helpL: A while mback I was at Vamderbilt for an opinion. Of course it didn't help. I asked the intern what he thought about the psychobiology stuff. He said Drossman and the braingut group are findong out some stuff and it looks like they are starting to be accepted. I think some of our faculty agree. i'm also going to have you see our immunologist and maybe some brainscans might help. Here's an article that might be interesting on the affective disorder syndrome you might find interesting. ____________ is a psychiatrist and she is going to present it at our next faculty meeting. You can come if you like.The point is that you and Mike might help people here understand more if you debated about the evidence in a single article that everybody can read rather than just piling up references to throw at each other?tom


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## trbell (Nov 1, 2000)

this might be of interest here. it costs $79 per year but my guess is that most medical libraries subscribe to it and many et patients use their computers?tom


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## LoriAnn (Jan 31, 2002)

I can't say I am terribly pleased with the way this post has turned out.I was attempting to get an understanding of IBS as it pertained to actual clinical findings. I tried to keep an open mind.But what I got was a competition between 2 opposing opinions and two people trying to drown each other out by the sheer number of words they could put into a single post or how often they could repeat themselves to "prove" their point.I regret that I asked the question.Lori


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## PatSimp89 (Feb 26, 2003)

well, on the bright side you can examine both viewpoints and choose which one better matches and your specific symptoms. also, which one seems to make the most sense with respect to everything that you have suffered through. from your description it sounds like your immune system has taken a beating.it will probably be a melding of the two.


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## trbell (Nov 1, 2000)

my experience with the bb is that it's a self-help bb and for the most part I don't get specific answers to specific questions. tom


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## eric (Jul 8, 1999)

LoriAnne, I appologize for this, but its actually very important.I am also really concerned you have red flag symptoms to an IBS diagnoses and have not had a colonoscopy or stools samples or proper testing it sounds like.


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## Guest (Mar 3, 2003)

If it helps, the information that Eric is presenting is the most up-to-date and offered by the world's leading and foremost authorities on IBS. Come to one of the UNC chats which I believe are held every second Tuesday evening of the month at 7:00 p.m. central time and 8:00 p.m. EST.Evie


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## eric (Jul 8, 1999)

FYIAmerican College of Gastroenterology 67th Annual Scientific Meeting | IBS/ Functional Dyspepsia & Pancreatic DiseaseNew and Important Insights Into IBS: From Epidemiology to Treatment"PathophysiologyAltered Serotonin Signaling?The pathogenesis of IBS remains obscure, and in particular, an explanation for alternating diarrhea and constipation has been elusive. In arguably one of the most important papers presented during this year's meeting, Moses and colleagues 21 studied potential deregulation of the gut's serotonin transporter in IBS.It is known that serotonin 5-hydroxytryptamine or 5HT is released from enteroendocrine or enterochromaffin cells in response to either chemical or mechanical stimulation of the gut mucosa. Serotonin in turn initiates peristalsis, and then the serotonin released is taken up in health by a highly selective serotonin transporter SERT. One potential mechanism that could explain altered bowel function in IBS is an abnormality in the serotonin transporter itself. The study authors evaluated this hypothesis in patients with IBS with constipation and IBS with diarrhea compared with patients with ulcerative colitis and healthy controls. They were able to convincing show on blinded review that SERT immunoreactivity was less intense in patients with IBS with constipation and patients with ulcerative colitis.If these findings are indeed correct, they represent a landmark observation. The findings suggest that patients with constipation and IBS may have a reduced capacity to reuptake serotonin, leading to excess free serotonin and then desensitization of these receptors, thus reducing motor function. In contrast, in the setting of diarrhea, serotonin uptake was normal. If the underlying abnormality in serotonin transporter function alternated, then this would in turn explain alternating constipation and diarrhea.These data strongly suggest that IBS is a "real" gut disease and a potential diagnostic disease marker. They also suggest that it is valid to subdivide IBS into constipation and diarrhea symptom subgroups. This study also provides additional rationale for the use of serotonin-modulating agents in IBS and provides a new target for drug modulation. Confirmation of these very exciting initial findings in larger patient samples is awaited with great interest.""Postenteritis IBSCurrently, another area of major interest in IBS is the prognosis of postenteritis IBS.19 It is now well recognized that up to 1 in 5 cases of IBS will occur after infection, and a low-grade inflammatory process has been documented in some of these cases, although histologically the colonic mucosa is normal.1,19In a study by Spears and colleagues,20 patients with acute infectious enteritis were administered standardized questionnaires 3 months after infection as part of a repeat evaluation. Although a small study, the investigators observed that 2 patients with IBS 3 months after infection also had depression. In contrast, the remaining 9 patients who did not develop postenteritis IBS were negative for depression on the patient health questionnaire. These results are consistent with the literature, which suggests that psychological factors may identify a vulnerability to the development of postinfectious IBS.1 The latter may in turn reflect disturbed central down-regulation of visceral afferent signals from the gut that may be genetically determined." http://www.medscape.com/viewarticle/444514


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## ohnometo (Sep 20, 2001)

All I have to say is that Dr's dont know everything including the Rome Criteria they wrote...I dont believe that Mike is saying IBS-D is caused only by loss of Oral Tolerance...Eric, you are always trying to say that Mike is saying something when he is not...What is the big deal here with Food ! He has never said this is the only reason that IBS-D patients have got IBS...You are turning his words around


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## Mike NoLomotil (Jun 6, 2000)

DONNA...Yep that is about it...and watch the ruckus if I respond in any detail or with similar length posts...anyway you and thousands like you walking around with your lives back know what I mean and mean to say, and what our mission is, and how it differs from what some say it is.Stay well...what is it 18 months now?Anyway I guess there are some things that one must respond to...not that the answers will be taken in context or with the correct intent, but one is compelled to make the efort when again it is a public forum.------------ï¿½Mike is explaining IBS, due to loss of oral tolerence to foods, but in very complicated terms."-----------------------I am not explaining IBSï¿½I am explaining one population within the IBS population in toto based upon how diagnosis is presently (and historically) made. And the terms are complicated because it is complicated. It is much much more complex than I am explaining it. If you studied the subject very thoroughly and objectively you would see what I mean. I am making it as simple as I can. You do not see me even going near the actual ï¿½mechanismsï¿½ of oral tolerance (I avoid even going near IgA for example like the plague as then we have to go down a road that would be very difficult for people to conceptualize), nor even the specific reactions (of which there are at least 8 distinct an exceedingly complex stepwise processes which lead to the end game of mediator release, much less the over 100 known mediators, and the multiple possible combinant reactions. Even in direct contact with immunologists and allergists expert in this field it seems to take more than one at a time to compile all the information known it is so vast. So I intentionally keep it as simple as possible yet it remains complicated because it is what it is).--------------------ï¿½They have found many other problems in IBS and IBS cannot be explained by loss of tolerence to foods, they maybe a TRIGGER for some people though.ï¿½---------------------Indeed, as I have repeated incessantly, there are multiple pathways, multiple pathogenesis, multiple mechanisms, not one. "THEY" must indeed know this whomever "they" are since I hev met a lot of "OTHERS" who know this and consider it self-evident.This population is one of severalï¿½and indeed some of those patients where investigators believe the food eaten is merely a ï¿½triggerï¿½ it is indeed trueï¿½.and sometimes it is not as the food ï¿½triggerï¿½ is a consewuence of the underlying inflammtogenic mechanismsï¿½if they were absent the food would not be a trigger. This is why Zars schematic of IBS mechanisms is so valuable that everyone should have a copy. I think there would be an audible ï¿½Ohhhhhhhï¿½.I seeï¿½.ï¿½ Heard across the land at that moment.--------------ï¿½They cannot explain global symptoms in IBS or the connection to other functional GI conditions.ï¿½-------------I am not sure who ï¿½theyï¿½ is in this context...which "they"...or would it be "them" over there...or even what this is supposed to suggest, since the origin of global symptoms seen in IBS patients is well documented and easily understood not only in a biopsychosial model of IBS but in an immunologic model driven by loss of oral tolerance as well. In fact this one is easier to understand since there are immediate systemic biochemical sources which are quantified which lead to the entire spectrum of physical , emotional and cognitive changes which can be measured or reportes. ______________________________________ï¿½Increased gastro-colic reflex. This is an awakening of the childhood reflex where food in the stomach stimulates colonic activity, resulting in the need to open the bowels." etcThis is the info Mike does not want to talk about and regards to d predominate IBS."---------------------That is just plain old down-home hogwash to even utter such foolishness. Does not want to talk about.







In fact the mechanism involved sourced to cell mediated or humoral or combinant food intolerance reactions is rudimentary, if you know what happens. For the readers niot attuned to the immune systems vagaries and how they effect nerves and muscle and vessels et al, here is an analogy.The simplest way to describe is an analogyï¿½..an asthmatic even 18 hours post-antigen exposure suffers a chronically upregulated airway responsiveness as a consequence of the mediators releasedï¿½such that even the simple act of taking to deep a breath or inhaling air too fast or air which is can provoke bronchospasm. This is explained to patients in simple terms they can understand as ï¿½twitchy airwaysï¿½. The postprandial response, the MMC, and other more specific local actions of the gut muscles, the myenteric plexus, and the afferent and efferent pathways to and from the CNS as well as the CNS itself (depending upon which systemic immune response occurs ) can each or collectively be upregulated and the similar response occurs. It is not mysterious at allï¿½in fact in some cases the pulmonary and GI immune response and structure is so similar that some have referred to IBS as ï¿½asthma of the gutï¿½.The problem is you have to quantify so many parameters to illustrate and link it out to the clinical picture, it is work that has not been done collectively on the same patients at the same time with the various imaging studies which are done. Each is studied separate from another on separate patients so if you look at it from ONE direction with one set of physiologic measurements you will see it one way. IF you look at it from the other direction with different assays you will see it another way.The mechanisms AND the pathogenesis of what we call IBS is like a diamondï¿½.multifacetedï¿½the failure to mention every facet anytime one mentions a diamond does not mean one is unaware of the other facets. To presume so, and then spread that conclusion to others, is ill advised. If need be I can post an endless set of abstracts and tutorial to show the depth of the integrated systems and biochemical basis of regulation of the B-G and HP axis but this would be even more difficult for the patients to follow.---------------ï¿½My problem with Mikke really is his focus on loss of oral tolrence and the serotonin issue causes d right out of the gate.ï¿½----------------Your first problem is that you have a problem with a person, rather than focusing on the information the person conveys from others who are well-qualified, the data, the teaching, the duty to convey to sick people objectively. No, your problem with me is that I present information which if considered compels people to expand their vision of IBS beyond the biopsychosocial model and this troubles you so you take what I say and try to make it into something else, as you just did here again. By persoanlizing one can demonize and thus justify a lack of objectivity and inclusivity and sustain selective reasoning.The other problem is that just because research has found information about the role of srotonin, and 5HT[x] receptors and their roles in both regulating the system and ï¿½dysregulatingï¿½ the system, myopia has set inï¿½there are dozens of other mediators sourced to immune response, hormones sourced to endocrine response, which have been observed to play a role in the normal and altered brain-gut function in IBS patients as they are diagnosed by symptomology. These are either disregarded or explained-into the presumed model so as to make the data fit the presumed model. The trouble is there is enough evidence to suggest that not all these evnts can be shoehorned into the presumed model that it is clear the presumed model is not the only modelï¿½one can simplify it as a top-down model and a bottom-up model. That would be abit more accurate.-----------ï¿½also recommend foods from Heathers perspective too. There are chemical problems with foods that are not loss of oral tolerence issues, but shear chemistry issues in food contents.ï¿½---------Wow. I am shocked! Really? "Chemistry Issues??" Maybe if we reread the tutorials I have posted many times in prior years, one called ï¿½FOODS THAT BITE YOUï¿½ and another ï¿½FOODS THAT MAKE YOU GO HMMMMMMMMï¿½ and if you read the books I recommend for reading you would know that this is not only not alien to me but is part of the patient education process on food intolerance and is part of the Disease Management Program and dietary protocol we espouse.If I had the links to those threads I would post them but I believe they can be found by those titles.---------ï¿½IBS is not a diseaseAlthough the symptoms of IBS may be severe, the disorder itself is not a serious one. There is no actual disease present in the colon. In fact, an operation performed on the abdomen would reveal a perfectly normal appearing bowel.ï¿½-------------Some authorities would differ and consider that statement to be a bit out of date. That is because the colon is not the shock organ it is generally an affected or target organ. The shock organ in the population wherein aberrant immunocyet responses to ingested agents is the symptom generating mechanism, is the small bowel.Although multiple researchers have recovered signs of ï¿½diseaseï¿½ in the colon via full thickness biopsy of the ileocecal area (inflow tract from the small bowel) and consistently found increased tissue mast cell density. Study how and why this happens and one will have an idea of what this means. Mast cells do not just migrate there for vacation, nor do lymphocytes aggregate at the root ganglia of the nerves of the myenteric plexus in the small bowel because they like being in proximity to nerve endingsï¿½just to hang with them.







---------EVIE;ï¿½On the other hand, I also cannot discount the research and the factual scientific information brought to us by Eric and UNC.ï¿½--------------I think and gently suggest that if you look back over my thousands of posts you will also see in retrospect that I do not either ever discount the work of anyone anywhere including the UNC center. When it is suggested by others that I do I am being misquoted or morphed into saying something I never said.I do beleive however that their work is not the sole source of all factual information on the Syndrome of IBS. Their mission is to develop a better understanding of IBS as a psychosocial-manifestation. This is valid and appropriate. I have said this many times and cited their findings many times. I do put them in context of other peoples work, though, which might alter the way it is viewed.It is to some authorities clear that, based upon the way IBS is diagnosed, this is not the only model for the IBS sufferer and how they got that why and stay that way. Their work needs to be integrated with the work of others to come to a clearer understanding of the entire IBS population. This IS what I espouse,a long with multimodal disease management to reduce the need for pharmacotherapy by developing optimal prophylaxis. Just cannot make it any clearer any than that. ;-) ________________________ï¿½please forgive me if I've in any way been harsh to you, Mike, because that is not my intentï¿½ ________________________I know. Nor mine! I know that, and even if you were, there is a distinct difference in how a healthcare provider must view and respond to harshness from someone who is a sick person (a patient) as opposed to how one responds to harshness from one who has proclaimed themselves a healthcare provider. This is (2) different situations entirely. ______________________ï¿½And Mike... I have no doubt that allergies are responsible for many woes..... just as my own behavioral health, FMS and CFS are responsible for many of my own personal woes....... but globally speaking..... IBS is a functional disorder that may or may not encompass any of the above.ï¿½ _______________________If you can try to get a copy of Zarsï¿½ paper so you can see the diagram or if you want email me and I will email you a copy of the diagram you can look at in your computer. Also take a peek at some material that explains not only what the many inflammatory mediators do to local tissues but what happens when they get into the bloodstream and it will be easier to understand the concept of systemic effects as well as local effects. Takes some work but heck if I can do it anyone can. And as always no matter what the perpsective we remain with any gibven patient still in the dark usually as to which is actually chciken and which is egg and which came first. Luckily we don't have to know that to cook the egg and chicken and eat them as long as we are not reactive to chicken or egg.







-----------LAURIE:ï¿½I am disappointed that I only hit a triple though. I guess the pitcher put "something" on the ball!ï¿½-----------LOL that is just because I know that not only is there no single model available which shows every single known interactive mechanism, but that when I refercne Zars model some other models will be posted and will probably be claimed to be THE MODELï¿½when it will be incompleteï¿½so we will not be able to clean the bases. But at least you put the ball WAY out there in deep center..---------------ï¿½LaurieJ, couple things here in regards to IBS, the d is happening right out of the gate from the act of eating in IBS, not from loss of oral tolerence, this needs to be understood, the release is from the act of eating.ï¿½---------------Again declarative statement of universal fact which is not.







Rather, sometimes yes sometimes no. If you do not consider or clearly understand what occurs in different types of local and systemic responses to mediator release on provocation then you will assume this position. It is not a defensible position based on current information. Once again absolutes applied where no absolutes can be applied.And_________________ï¿½This is something Mike never talks about here and keeps saying d patients have IBS from loss of oral tolernce, it can happen to people, but that is NOT IBS!!! YOU CANNOT EXPLAIN IBS as loss of food intllorence, its a trigger.ï¿½______________Shouting incorrect information will not make it any truer.







On the contrary there is a population, substantial, where their symptoms are generated by the mechanisms I have referred to or described in sufficient detail that objectivity allows one to see the subpopulation. The area where there is a lack of clarity is WHY loss of oral tolerance occurs. As I have explained before from others work there are multiple mechanisms thus multiple possible pathogenesisï¿½people who keep confusing pathogenesis with symptom generating mechanisms are bound to remain confused and use shrill rhetoric which will confuse others. But it is a free country and this is ones right if one chooses to do so. Oh my.....here we go again with the ï¿½Mike this and mike thatï¿½ and ï¿½best infoï¿½ and all the zealotryï¿½.Perhaps it is time to just go ahead and make another effort to make it clear that there are indeed broader perspectives on the subject and that this information surprisingly is included in ones integrative view of IBS theory if one does indeed possess such a viewï¿½I am not sure how to start to show a broader perspective than maybe to begin at the beginningï¿½.There remains this persistent insistence among increasingly shrill rhetoric posted whenever someone points out that the psychocosociobiological model of the pathogenesis of IBS is not applicable as the SOLE pathogenesis nor symptom generating mechanism of the population of patients diagnosed with IBS. This, in spite of the fact that when all the cumulative investigation of IBS symptom generating mechanisms, precursor or predictive events, and specific observable phyisiologic occurrences, that it is self evident to many investigators and clinicians that there are multiple mechanisms involved in the pathogenesis and multiple subpopulatins which can be defend by dissimilar biochemical findings even when the core symptom sets meet current ï¿½symptom based diagnosisï¿½ suggestions.SO as to try to deflect attention from this reality, what others have learned and try to convey is often misstated, misinterpreted, metamorphosed, or even claimed to be non-inclusive. That others than the author of a given postulate lack either understanding or interest in specific aspects of the underlying physiology simply because out of necessity not every single detail of the systems involved can be re-explained, repeated, reemphasized, re-tutored every time one posts a contrasting point of view, or shows another mechanism. The other readers are challenged to conclude that the one who sets forth any information which conflicts with the desired paradigm is doing so from a position of ignorance.Then, if the accused (presetn company included) responds and provides detail to not only show he is not ignorant of the information, rather is merely supplementing it with other information rather than repeatedly restating all the physiology, and then attempts to show that by refiling it publicly, he is then faced with livid accusations of being combative, confusing, giving information people cannot understand, hijacking the discussion, abusing the bandwidth with excessive incomprehensible information and all other manner of sins. This is fairly characteristic of the problem when one is trying to carry on objective interchanges with individuals who suffer from a messianic need to be the bearer of the truth and the light.When dealing with or responding to such people it is never possible to satisfy the real problem, which has actually nothing to do with what information is or is not included at any time rather it has to do with someone having the audacity to suggest alternative points of view have been set forth and have validity and must be included. One can either choose not to respond (and thus leave the readers who do not recognize what is actually going on to conclude that the accusations are in fact correct), or to respond in detail and thus be accused of a new sin against the online community. However, in doing so, if one does demonstrate to even one reader that the accusation not only is baseless but is the result of selective or biased thinking, and that readers perspective ad understanding is widened to their personal benefit, then it is worth the effort.For example, how does one convey briefly that indeed one has made a reasonable and determined effort to try to set before people seeking information that there is more than one mechanism by which the effected body systems are regulated, thus there are multiple targets for investigation and that those altered functions which can and do affect the gut, the brain, the immune system, the endocrine system, the exocrine system et al must always be taken into account when evaluating any so called ï¿½dysregulationï¿½ or derangement of system function.For example, while the role of 5HT[x] receptors and their effects on the system make interesting key and logical targets for investigation especially when seeking pharmacotherapeutic targets, and indeed this system is (to quote a meaningless phrase) ï¿½activeï¿½ in so called IBS, to suggest it is the only, or even primary, origin of dysfunction for the entire population is not rational. It requires the ability to set aside or disregard all manner of other influences and evidences of same for the sake of pursuit of proving a specific postulate.Evidence of this can be found even within literature which does not consider other mechanisms to be sources of alternatives to drug therapy, but even alternative targets for drug therapy in the blunting of IBS symptoms. For example, to begin, this brief summary can lay the groundwork upon which to build an understanding that indeed there are multiple integrated systems fro which multiple models of symptom generation can be and are based: ___________________________________________Best Pract Res Clin Gastroenterol 2002 Dec;16(6):869-83	Evolving concepts in functional gastrointestinal disorders: promising directions for novel pharmaceutical treatments.Hunt RH, Tougas G.Department of Medicine, Division of Gastroenterology, McMaster University Medical Centre, Hamilton, Ontario, CanadaIn recent years there has been an increasing appreciation of the complexity of functional gastrointestinal disorders. These represent a spectrum of conditions which may affect any part of the gastrointestinal tract in which there appears to be dysregulation of visceral function and afferent sensation and a strong association with emotional factors and stress. There is a clear psychological dimension, with up to 60% of irritable bowel syndrome (IBS) patients reported to have psychological co-morbidities and altered pain perception is also common in comparison with control populations.The role of the enteric nervous system, the sensory pathways and the brain as well as the influence of the latter on sympathetic and parasympathetic outflow have likewise attracted increasing interest and have led to exciting new methods to study their complex interactions. The concept of low-grade inflammation, such as might occur after infection, acting as a trigger for neuromuscular dysfunction has also led to the broad integrative hypotheses that help to explain the biopsychosocial dimensions seen in functional gastrointestinal disease. The multi-component model places a major emphasis on neurogastroenterology and enteric and neuro-immune interactions where new approaches to pharmacotherapy lie.Drugs may affect motility, visceral sensation and other aspects of gut function such as secretion or absorption. More particularly, however, has been the search for and attempts to influence important mediators of these primary gut functions. Such targets include serotonin and selected 5-HT receptors, which are involved in gut motility, visceral sensation and other aspects of gut function, CCK receptors which are involved in the mediation of pain in the gut and nociception in the CNS, opioid receptors involved in pain in the brain, spinal cord and periphery, muscarinic M(3)-receptors, substance P and neurokinin A and B receptors which are involved in motor adaptation and pain transmission in association with inflammation, gabba receptors involved in nociception and cannabinoid receptors which are involved in the control of acetyl choline release in the gut.With a better understanding of the structures and pathways involved in visceral perception and hyperalgesia, in the CNS, spinal cord and the gut and new pharmacological tools we will be better able to elucidate the neuropharmacology of visceral perception and its relationship to gut dysfunction. It is likely that there will be multiple therapeutic options based on the spectrum of abnormalities capable of causing the spectrum of symptoms of functional gastrointestinal disorders in any individual patient. _______________________________________________To wit as well, ï¿½up to 60% suffer psychological comorbiditiesï¿½ is hardly a declaration that all IBS victims suffer a condition whose pathogenesis is linked solely to mechanisms which are the result of psychosocial activity, either chronic or even a single precursor event. And comorbidity does not denote pathogenesis. There are other mechanisms by which symptoms are prvoked and manifest themselves and to date not a single one has been clearly and irrefutablt described in sufficient detail to make that mechanism even one irrefutable ï¿½causeï¿½ of IBS in any given population. Rather each is being explored ane the findings are used to form postulatesï¿½ï¿½seemsï¿½ and ï¿½suggestsï¿½ and ï¿½appearsï¿½ are the words of interpretation of findings not quantification of specific pathogenesis. To date, due to the complexity of the systems, there is very little in fact which can be ruled OUT as a possible pathogenesis of any given patients symptoms and much which can be ruled in as plausible.For example, the baffling reactionism to the mechanisms of Loss of Oral Tolerance. This phenomenon, quantified in a subpopulation of the IBS population which appears to exceed as much as 50% of the population as a symptom generating mechanism (some of whom also suffer psychological comorbidities and some of whom do not) can be a consequence of several precursor events known in IBS patients. Mechanistically is results in immunocyte activation inappropriately in the presence of previously safe foodsï¿½antigenic response to what should be non-antigenic things with the apparent absence of any allergic basis (Type I Gel & Coombs response). Whatever the mechanism involved the end event is release of proinflammatory mediators into the gut wall and circulatory system.THIS is the underlying biochemical source of the gut sensory and motor upregulation observed in these particular patients. Since the neuroimmune system is bidirectionally active, the immunocyte activation may be and can be sourced to both primary neurologic events as well as to primary immunologic and chemotoxic events as well. This is the point that some keep trying to bury, or exclude, from their theories even though it is quantified and accepted in mainstream literature since at least 1985 or earlier.Or to suggest that this mechanism is not fully acknowledged in spite explicit statements when explaining it to the contrary.A look back may help define the actual perspective compared to the alleged perspective. First some basic groundwork againï¿½once more into the breachï¿½ _________________________________________________Excerptsï¿½.Scand J Gastroenterol Suppl 1985;109:117-21 Food intolerance.Lessof MH.Food intolerant symptoms can have various causes, including enzyme deficiencies (of lactase or aldehyde dehydrogenase) and pharmacological effects (e.g., caffeine, salicylates). The irritable bowel syndrome can also be associated with intolerance to specific foods in some cases, but the mechanism is unclearï¿½.ï¿½Diagnosis of food intolerance depends on withdrawing the food concerned and assessing the response to a blind challenge. Objective ways of detecting subclinical reactions are also useful, including the detection of a mediator response involving prostaglandins, histamine or serotonin. ________________________________________________Page 1051 of the hard copy of the current Merck Manual of Diagnosis and Therapy, and online Merck Manual at http://www.merck.com/pubs/mmanual/section1...ter148/148b.htm "Recently Food Intolerance was found to be responsible for symptoms of some patients with the IRRITABLE BOWEL SYNDROME, confirmed by double-blind food challenge.An increase in rectal prostaglandin levels was noted when a reaction occurred.Preliminary information suggests the same phenomenon may take place in patients with chronic ulcerative colitis.ï¿½ _________________________________________________How recentlyï¿½.? First of note in 1980ï¿½23 years agnward...___________________________________Adv Prostaglandin Thromboxane Res 1980;8:1627-31	An approach to evaluation of local intestinal PG production and clinical assessment of its inhibition by indomethacin in chronic diarrhea. Bukhave K, Rask-Madsen J Summary of Findings:The connection between gut motility and prostaglandin release was studied. PGE2 levels in the jejunal secretions IBS patients were elevated in 10 of 17 with cyclic IBS (D & C) and in ï¿½gluten enteropathyï¿½. Six IBS patients treated with indomethacin (INDOCIN: non-steroidal analgesic anti-inflammatory which works by inhibiting prostaglandins, which are inflammatory and pain mediators of various types) had a 50% reduction in stool volume and frequency. And withdrawal of the indocin caused the symptoms to return.(Due to the absence of indicators of Type I inflammatory-allergic response, the authors state the findings suggest localized or gut-wall reactions .) ________________________________________________Futher on it was again confirmed that the reaction, whatever it is, is not ï¿½food allergyï¿½ as the things which link the symptoms to allergic response are absent in the confirmed reactive symptomatic IBS victimsï¿½to witï¿½one exampleï¿½from Lancet, hardly a journal of nominal credibility. _________________________________________________Lancet 1982 Nov 20;2(8308):1115-7	Food intolerance: a major factor in the pathogenesis of irritable bowel syndrome.Jones VA, McLaughlan P, Shorthouse M, Workman E, Hunter JO.Specific foods were found to provoke symptoms of irritable bowel syndrome (IBS) in 14 of 21 patients. In 6 patients who were challenged double blind the food intolerance was confirmed. No difference was detected in changes in plasma glucose, histamine, immune complexes, haematocrit, eosinophil count, or breath hydrogen excretion produced after challenge or control foods. Rectal prostaglandin E2 (PGE2), however, increased significantly, and in a further 5 patients rectal PGE2 correlated with wet faecal weight. Food intolerance associated with prostaglandin production is an important factor in the pathogenesis of IBS.Publication Types: ï¿½	Clinical Trial ï¿½	Randomized Controlled Trial ____________________Nobody, even 18 years ago when it was first confirmed and to this date, ever said, again, that ï¿½foods cause IBSï¿½. Anyone who claims that others are making this declaration is in error, and it is likely intentional since the language used is quite explicit. Intolerance to foods and chemicals causes immunocyte activation and this releases mediators which cause the clinical symptoms in this patient population. Excluding pseudoallergy and enzymatic intolerance, The mechanism can be sourced to primary immunologic (cellular and mucosal) and/or to neurologic events as well. It is often difficult to ascertain which came first as no one has ever tken a healthy human and induced either mechanims under controlled conditions. ALL examonation is retrospective, thus one must attempt to deduce the pathogenesis, and what perspective one possesses tends to color the postulate.At any given time, then, which event was primary it is CLINICALLY irrelevant to the immediate and effective treatment of the patient once a mechanims of symptom generation is confirmed which can be avoided prophylactically and thus avoid pharmacointervention after the horse is out of the barn. Which is the chicken and which is the egg need still be pursued to eventually arrive at the ultimate prophylaxis: prevention of the precipitating event of the disease, but immediate treatment ability is enhanced by addressing the active mechanism just as one would address some specific ï¿½neurorecptorï¿½. If you isolate the source of provocation and remove it, then symptoms subside as the biochemical mediators involved are not expressed. It is just too simple sometimes.The problem is that most dietary programs are not very good at isolating the majority of the provocations as they are mostly non-allergic mechanisms, thus are dose-dependent and delayed onset so they cannot be isolated with conventional tests and dietary methods. Thuis there is a history of cocnlcuidng that this mechanism does not exist. This is analogous to suggesting that if man were meant to fly God would have given him wings when the flight designs currently known result in plummeting to ones death. The end of the investigative path is not determined by a lack of technology when the specific event has already been quantified. This is why the MRT assay was developedï¿½to isolate the common end point of the non-mast cell reactive component so that dietary therapy COULD BE clinically effective. Technology and even simple clinical means of patient assessment has long existed which can already identify mast cell degranulation precursors both directly and indirectly since it is not a delayed onset reaction. True allergy is easily ruled outï¿½the other multiple mechanisms have not been so easily discerned. This is because allergies cooperate nicelyï¿½ It is quick, profound and repeatable. And it is but one comoribid source of the inflammatorymediators which are upregulating the so-called brain-gut axis, easily reuled out, thus leaving erroneously the impression that there is no further specificity to the reactivity thus no mechanism. As we know that was found to be a false conclusion many years ago.Here I will try to make it as overtly simple as possible using the words of others, to illustrate that this view is always considered within the context of EVERYTHING which can influence GI function up and down the brain-gut axis and al along the watchtowerï¿½..the gut neuroimmune system is bi-directional. Gut function can be modulated by primary activation of immunocytes via an immunologic mechanism, or by neural stimuli, either of which will result in the release of a toxic soup of mediators which have multiple effects on gut motor and sensory and endocrine and exocrine function.__________________Z Gastroenterol 1995 Apr;33(4):219-24Neuroimmune interactions in the gastrointestinal tractArticle in GermanFrieling T, Strohmeyer G.Abteilung fur Gastroenterologie, Heinrich-Heine-Universitat Dusseldorf.The enteric nervous system and immune system are integrated systems that play an important role in the regulation of gastrointestinal functions. Recent studies suggest a bidirectional interaction between both systems. The relationship is based on the synthesis and release of neuropeptides from immune cells and the receptor-mediated alteration of nervous and immune functions by neurotransmitters and inflammatory mediators. The activity of the enteric nervous and immune system can be modulated by the central nervous system. These psycho-neuro-immuno-interactions are involved in gut inflammation, in functional bowel diseases and in the physiological control of gastrointestinal functions.Publication Types: ï¿½	Review ï¿½	Review, Tutorial ______________________________Vet Res 1996;27(4-5):427-42Integrative neuroimmunology of the digestive tract. Theodorou V, Fioramonti J, Bueno L Ecole superieure d'agriculture de Purpan, Toulouse, France.The epithelium of the gastrointestinal tract is continuously exposed to the external environment containing food antigens, microbes and other pathogens. Immunologic and nonimmunologic mechanisms contribute to the neutralization and elimination of these foreign antigens. The immune system of the intestine is the most extensive in the organism and involves diffuse populations of immune cells, lymphoid aggregates and intraepithelial lymphocytes. On the other hand, the functions of the digestive tract contribute to the overall host defense (mucus secretion, gastric acid secretion, water and electrolyte secretion and peristaltism). These functions are regulated by intrinsic and extrinsic nervous systems. It is currently recognized that the physiological and pathological responses of the intestine require an integrated neuroimmune network. Such neuroimmune regulation is based on anatomical and biochemical supports. Indeed, there are membrane-to-membrane contacts between axonal varicosities and the immune cells. Specific receptors for neurotransmitters such as substance P, vasoactive intestinal polypeptide and somatostatin have been identified in many immune cells. Nerve profile change has been described under pathological conditions such as parasitic infections and acute phase of inflammation. In addition to supporting the growth and survival of several populations of nerves the classical nerve growth factor (NGF) has been shown to affect an immune cell population by inducing mast cell hyperplasia. Furthermore the NGF can induce mast cell degranulation, acting directly on mast cell membrane NGF receptors or indirectly by NGF-mediated release of substance P by peripheral extrinsic or intrinsic nerves. Moreover, non-immune cells such as epithelial and smooth muscle cells can produce immunologic messengers under pathological conditions such as infectious diseases or inflammation. Besides the local regulation of gut functions, neuroimmune control can be exerted at extra-intestinal sites. During physiological and pathological conditions, gastrointestinal secretions and motor events are strongly regulated by the central nervous system. Moreover, infectious agents can induce cytokine and particularly interleukin-1 release by the brain astrocytes and microglial cells which have been shown to play a pivotal role in fever induction and modifications of the gastrointestinal functions. Visceral afferent fibers play a pivotal role in 'cross-communication' between central sites and immune response. Recent studies evoke, more specifically, the role of vagus as a key modulatory participant in the close relationship between the extraintestinal nerves and the immune system. Future work in this field will clarify the role of the different participants in the intimate communication between the gastrointestinal tract, immune system and central nervous system.Publication Types: ï¿½	Review ï¿½	Review, academic ____________________________Again, as clear as a bell, the bidirectionality is of key importance. Anything which will provoke a response on either side of the system affects the entire system, and external sites as well (extraintestinal symptoms). These so-called ï¿½IBSï¿½ victims suffer from aberrations in the activity of this system. The system can be triggered locally by over 8 different known mechanisms which make immunocyte class activation primary, and the system can be activated from the CNS and even the ENS has mechanisms by which the system cannot onloy be modulated but activated.Dietary provocation, loss of oral tolerance, is the summation of all the possible immunocyte primary mechanisms which can be invoked through dietary means, thus generating symptoms by affecting specific gut functions. On the other hand as everyone knows the neural side primary source of activation is DIS-stress (not ï¿½eu-stress)ï¿½and an aberrant or amplified stress response. Being bi-directional whichever is primary amplifies the other. Remove that which is the primary provocation and the whole system is DOWNregulated. The key is since some patients one mat be primary, and some the other, the better a job you do of isolating every single possible source of dietary provocation, and the better you do at getting the patient to follow a program of stress-reduction, the better the outcomes compared to any single modality in the overall population. It cannot help but be the result of an integrated DM approach, as you explore the integrated physiologic concepts furtherAn online tutorial of neuroimmune interaction primarily from the ï¿½top downï¿½ or psychoneural side of the system is found here: http://www.acnp.org/G4/GN401000069/CH069.html ________________J Gastroenterol Hepatol 1998 Oct;13(10):980-9Mast cells: a possible link between psychological stress, enteric infection, food allergy and gut hypersensitivity in the irritable bowel syndrome.Gui XY.University of Sydney Department of Medicine, Royal North Shore Hospital, St Leonards, New South Wales, Australia.Intestinal mast cell activation (degranulation), which results from previous enteric infection and/or intestinal allergy, may play a central role in the gut hypersensitivity in both motor response and visceral perception in the Irritable Bowel syndrome. This occurs through various mediators acting on enteric neurons and smooth muscle cells. Psychological stress may trigger this sensitive alarm system via the brain-gut axis.Publication Types: ï¿½	Review ï¿½	Review, Tutorial _____________________Can one yet see this is not a single-modal mechanism, rather an either/or/both proposition?. There is no mutual exclusivity when trying to gain an integrated understanding of those patients currently grouped under the ï¿½IBS Diagnostic Umbrellaï¿½. In addition, while the mucosa is Kingï¿½ in gut immune response, the cell-mediated mechanisms sit at the right hand and are inextricably involved in the affected population whereby immune response is triggered by lost oral tolerance HENCE the ability to detect the response in vitro via cell mediated response assay.________________________________Can J Gastroenterol 1999 Mar;13 Suppl A:42A-46AEffects of inflammatory mediators on gut sensitivity. Bueno L, Fioramonti J Department of Pharmacology, INRA, Toulouse, France. lbueno###toulouse.inra.frOver the past decade, attention has been paid to the role of visceral sensitivity in the pathophysiology of functional bowel disorders, especially irritable bowel syndrome, and visceral hypersensitivity is the most widely accepted mechanism responsible for both motor alterations and abdominal pain. Inflammatory mediators sensitize primary afferents, especially C-fibre polymodal nociceptors, favouring the recruitment of silent nociceptors that give rise to secondary spinal sensitization. After local tissue injury, the release of chemical mediators such as potassium ions, ATP, bradykinin and prostaglandin E2 directly activate nerve endings and indirectly trigger the release of algesic mediators such as histamine, 5-hydroxytryptamine and nerve growth factor from other cells, which, in turn, stimulate proximal afferent nerve endings and silent nociceptors. Among the intermediary structures activated by inflammatory mediators and susceptible to the release of proalgesic substances, mast cells and platelets play a crucial role; however, immunocytes such as macrophages and neutrophils or sympathetic nerve terminals are also candidates. Moreover, events likely to activate synthesis of mediators by mast cells, such as stress and septic shock, also trigger colonic hypersensitivity. Prolonged visceral hyperalgesia may also depend on spinal sensitization. A number of substances are candidates to play a role at the spinal cord level in mediating painful and nonpainful sensations. Among them, substance P, dynorphins and glutamate play a pivotal role in postsynaptic sensitization, particularly during and after gut inflammation. Finally, despite the complexity of the relationship between inflammatory mediators and gut hypersensitivity, numerous results strongly suggest that alteration in neuroimmune communications at the gut level may trigger a series of events that give rise to chronic changes in visceral sensitivity.Publication Types: ï¿½	Review ï¿½	Review, tutorial ____________________________:Baillieres Best Pract Res Clin Gastroenterol 1999 Oct;13(3):429-36Putative inflammatory and immunological mechanisms in functional bowel disorders.Collins SM, Vallance B, Barbara G, Borgaonkar MIntestinal Diseases Research Unit, McMaster University Medical Center, Hamilton, Ontario, Canada.The observations that irritable bowel syndrome (IBS) may be precipitated by an acute enteric infection, or occurs commonly in patients in remission from inflammatory bowel disease (IBD) has prompted consideration of inflammation as a putative basis for symptom generation in IBS. In this regard, IBS may follow a pattern of pathogenesis that is similar to asthma--which was once considered a psychosomatic disease. This review examines the basic scientific evidence of a functional interface between the immune and sensory-motor systems of the gut and discusses how this may be relevant to a subgroup of IBS patients. In addition, review will examine the implications of this for the diagnosis and treatment of IBS.Publication Types: ï¿½	Review ï¿½	Review, tutorial ____________________________: J Neuroimmunol 1999 Dec;100(1-2):140-8	IL-10 as a mediator in the HPA axis and brain.Smith EM, Cadet P, Stefano GB, Opp MR, Hughes TK Jr.Department of Psychiatry and Behavioral Sciences, The University of Texas Medical Branch, Galveston 77555-0431, USA. esmith###utmb.eduCertain functional interactions between the nervous, endocrine, and immune systems are mediated by cytokines. The pro-inflammatory cytokines, interleukin-1 (IL-1) and tumor necrosis factor (TNF) were among the first to be recognized in this regard. A modulator of these cytokines, IL-10, has been shown to have a wide range of activities in the immune system; in this review, we describe its production and actions in the hypothalamic-pituitary-adrenal (HPA) axis. IL-10 is produced in pituitary, hypothalamic, and neural tissues in addition to lymphocytes. IL-10 enhances corticotropin releasing factor (CRF) and corticotropin (ACTH) production in hypothalamic and pituitary tissues, respectively. Further downstream in the HPA axis endogenous IL-10 has the potential to contribute to regulation of glucocorticosteroid production both tonically and following stressors. Our studies and those of others reviewed here indicate that IL-10 may be an important endogenous regulator in HPA axis activity and in CNS pathologies such as multiple sclerosis. Thus, in addition to its more widely recognized role in immunity, IL-10's neuroendocrine activities described here point to its role as an important regulator in communication between the immune and neuroendocrine systems.Publication Types: ï¿½	Review ï¿½	Review, Tutorial ________________________________________ : Braz J Med Biol Res 2000 Oct;33(10):1141-1148The neuroimmune-endocrine axis: pathophysiological implications for the central nervous system cytokines and hypothalamus-pituitary-adrenal hormone dynamics. Licinio J, Frost P Department of Psychiatry and Neuropsychiatric Institute, School of Medicine, University of California, os Angeles, CA, USA.Cytokines are molecules that were initially discovered in the immune system as mediators of communication between various types of immune cells. However, it soon became evident that cytokines exert profound effects on key functions of the central nervous system, such as food intake, fever, neuroendocrine regulation, long-term potentiation, and behavior. In the 80's and 90's our group and others discovered that the genes encoding various cytokines and their receptors are expressed in vascular, glial, and neuronal structures of the adult brain. Most cytokines act through cell surface receptors that have one transmembrane domain and which transduce a signal through the JAK/STAT pathway. Of particular physiological and pathophysiological relevance is the fact that cytokines are potent regulators of hypothalamic neuropeptidergic systems that maintain neuroendocrine homeostasis and which regulate the body's response to stress. The mechanisms by which cytokine signaling affects the function of stress-related neuroendocrine systems are reviewed in this article.____________________________An intriguing aspect of the jejunal isolation results by Bengtsson et al in food reactive IBS subjects ahs been the role of t cell activation. As we know the onset of IBS in a subset of patients


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## trbell (Nov 1, 2000)

eric and MNL, One of the reasons that what the two of you post is confusing to me and I suspect to others is that the information you post seems to come almost entirely from the internet and there is little information given on dates when things you post were actually said and most of it is opinions. For example, eric, you posted this from the 67th meeting of some organization:"If these findings are indeed correct, they represent a landmark observation. The findings suggest that patients with constipation and IBS may have a reduced capacity to reuptake serotonin, leading to excess free serotonin and then desensitization of these receptors, thus reducing motor function. In contrast, in the setting of diarrhea, serotonin uptake was normal. If the underlying abnormality in serotonin transporter function alternated, then this would in turn explain alternating constipation and diarrhea.These data strongly suggest that IBS is a "real" gut disease and a potential diagnostic disease marker. They also suggest that it is valid to subdivide IBS into constipation and diarrhea symptom subgroups. This study also provides additional rationale for the use of serotonin-modulating agents in IBS and provides a new target for drug modulation. Confirmation of these very exciting initial findings in larger patient samples is awaited with great interest."Dividing A-IBS into IBS-C and IBS-D seems to be important for both of your arguments but if one of you were to actually look at the most recent issue of some journal, like, _Gut_ you might find this basic distinction is not agreed on by all.You both know that somebody can 'prove' anything by using internet information but you also know that doctors try to keep up with the literature which means the LATEST issue of journals.tom


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## eric (Jul 8, 1999)

Tom, the information I posted was from medscape.American College of Gastroenterology 67th Annual Scientific Meeting | IBS/ Functional Dyspepsia & Pancreatic Disease 2002and I posted the link for it and its up to you to go read it.The UNC gets there information from investigators ALL OVER THE WORLD. Dr Drossman is chair for the Rome Criteria to diagnose IBS. So this continous there is only one center one idea is extremely misleading. If fact the truth its a concensus of all IBS research centers around the world, that lead to the most current observations. Also Dr Drossman is the Gastroentrologist who is head of the Merck Manual on Gastroenterology.Some of Mike's abstracts here are from the 80's and don't even have IBS in the title. So lets talk about IBS first and foremost, he just leans to food. Its more important first people understand the underlying dysregulation and the big picture.Immunology is a part of the Biophycosocial model.When Mike posts to people new with D what is the first thing he says to them, foods cause your d, not the underlying issues that are present from the beginging and how that causes D. That is a problem I seriously believe, although not sure if people undertand why I think that is a problem.If someone is not explained the conditon in more detail first, the new people will think and go on a long hunt for there d source from foods when in actuallity it is a functional problem.Reread Dr Drossman's comment here and think about it for a bit and understand who he is and what he is saying and then think about Mike and who he is and what he is saying."However, it is important to separate factors that worsen IBS e.g., foods as above, stress, hormonal changes, etc. from the cause or pathophysiology of IBS. Just like stress doesn't cause IBS, though it can make it worse, foods must be understood as aggravating rather than etiological in nature." http://www.ibshealth.com/ibs_foods_2.htm Dr. Drossman is a Co-director of the Center and Professor of Medicine and Psychiatry at UNC-CH. He established a program of research in functional gastrointestinal disorders at UNC more than 15 years ago and has published more than 250 books, articles, and abstracts relating to epidemiology, psychosocial and quality of life assessment, design of treatment trials, and outcomes research in gastrointestinal disorders.He was responsible for organizing the Functional Brain Gut Research Group as a special interest section within the American Gastroenterological Association, is a past president of the American Psychosomatic Society. Dr. Drossman sits on the Board of Directors and is Chair of the Scientific the Advisory Board of the International Foundation for Functional Gastrointestinal Disorders. He also sits on the board for the medical website Medscape Gastroenterology . Dr. Drossman chaired the 1999 Digestive Health Initiative on Functional GI Disorders ï¿½ sponsored by the American Digestive Health Foundation. He was the recipient of the 1999 Janssen Award for Clinical Research in Digestive Disease, which was at Digestive Disease Week DDW, the American Gastroenterological Association's international conference in Orlando.In 2001, Dr. Drossman was appointed Associate Editor of Gastroenterology, the official journal of the American Gastroenterological Association and appointed to the Nerve-Gut Council of the American Gastroenterological Association. He received the prestigious Research Scientist Award for Clinical Research presented by the Functional Brain-Gut Research Group at Digestive Disease Week in Atlanta. In addition, he is Chair of the IBS Program for the American Gastroenterological Association.Dr. Drossman has developed a series of videotapes to teach physicians and other health professionals how to administer an effective interview, carry out a psychosocial assessment, and enhance the patient-doctor relationship available through the Center. He has taught numerous US and European workshops on this topic, was the chair of the Physician-Patient Relations Committee of the American College of Gastroenterology from 1994 - 1996, and is a charter fellow of the American Academy on Physicians and Patients, a consortium of physicians which teaches these skills to medical school faculty.Dr. Drossman is also involved in teaching the evaluation and management of patients with complex GI problems or difficult-to-diagnose conditions. He completed the AGA Clinical Teaching Project on IBS unit 13, and is now completing the AGA GI Teaching Project on IBS-II to be released this summer. He is editor of the Manual of GI Procedures now in its third edition, and Rome II: The Functional Gastrointestinal Disorders, 2nd Edition and has been appointed Chair of the International Rome III Committees with the book, Rome III, to be published in 2006.In addition to seeing patients in the GI clinic, Dr. Drossman precepts GI fellows and visiting gastroenterologists in seeing clinic patients with functional GI disorders. He also supervises medical faculty, psychiatry residents, and medical students, working with them on how to provide psychological care to patients with functional GI disorders. This is also very important in regards to D."The "gastro-colonic" response to test meals or sham feeding in patients with IBS results in prolonged rectosigmoid motor activity compared to normals"Again d right out of the gate.First the serotonin issuethen possiblyThis is also very important in regards to D."The "gastro-colonic" response to test meals or sham feeding in patients with IBS results in prolonged rectosigmoid motor activity compared to normals"The stomach signals to the lower colon foods are on the way and the lower colon over reacts and dumps its contents. Then there are food problems.


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## ohnometo (Sep 20, 2001)

TomI have shared on this board before what has helped me and that was learning about foods playing a huge part as a trigger for my IBS..I was told one time that I didnt even have IBS by a member here on the board...because they couldnt believe that I got that much better by taking certain things out of my diet...I was even told about the placebo effect...BTY Mike does that effect last for 18 months ???????







Well, it really dont matter how we get better but as long as we do...They may be taking info off the internet and posting it here but I think the patients view on how they found relief is more important then any statistics from any clinc or Doctor...and we should honor others opinions !!


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## trbell (Nov 1, 2000)

Bravo, Donna!"Well, it really dont matter how we get better but as long as we do...They may be taking info off the internet and posting it here but I think the patients view on how they found relief is more important then any statistics from any clinc or Doctor...and we should honor others opinions."My last post here seems to have been misunderstood. I think it's great that people post and share information here as patients.I think though that difficul;ties and confusions arise for readers when peope claim expert status and disagree as experts. I've tried to clear this up in my recent posts about psychology, but the bb isn't really a pl;ace for an argument among experts and for some reason eric seems to want to make it one.tom


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## eric (Jul 8, 1999)

Donna, that is not accurate, no one told you foods do not have a role, nor is anyone saying that here, we told you a lot that all the apple juice you were drinking was a trigger and there is a lot of info on that.You have also argued in the past stress has nothing to do with any of this before. Then you email me quite a few time to know what stresss had to do with it. After a lot of time had gone by from you doing leap.The underlying condition is IMPORTANT, people need to know what they are up against and what they are treating first and foremost. people also need to know that there are diet restrictions that should be gone through first in IBS that have nothing to do with immune responces, since the gut is sensitive to ALL stimuli, stimulant, irritants ect..The same article on the serotonin, has this.Sugar IntoleranceAnother condition that can be confused with IBS is sugar intolerance; however, the role of fructose and sorbitol in the etiology of symptoms typical of IBS remains controversial. A high prevalence of sugar malabsorption has been observed in patients with IBS, although the benefits of restricting intake of the problematic sugars has been highly variable.14,15Gagliardi and colleagues 16 noted that the mean fructose intake in the United States is at least 37 g/d. They studied 15 healthy adult patients who consumed both 25 g and 50 g of fructose on separate days. Breath hydrogen testing was then conducted. The study authors observed that 50% of patients had hydrogen peak levels above 20 ppm with the 25-g dose of fructose, whereas 75% taking the 50-g dose had an abnormal hydrogen peak. This finding suggests that in the normal population a large number of individuals have fructose malabsorption. Furthermore, symptom scores were greater after both doses of fructose, although the higher dose did not increase the scores.Choi and associates 17 specifically assessed fructose intolerance in the setting of IBS. They studied 209 patients with unexplained bloating, altered bowel habit, and pain who were given either a 25-g or 50- g fructose challenge. It was observed that in patients receiving the higher fructose load, symptom scores were higher for diarrhea but not for other gastrointestinal symptoms. Overall, one third of patients with suspected IBS in this tertiary referral center appeared to have fructose intolerance. However, avoidance of fructose and symptom relief were not evaluated. Clinicians may wisely wish to consider prescribing a low-fructose diet as part of their initial management of IBS with diarrhea, but the benefits even among patients with coexistent fructose intolerance are as yet not established." American College of Gastroenterology 67th Annual Scientific Meeting | IBS/ Functional Dyspepsia & Pancreatic Disease http://www.medscape.com/viewarticle/444514


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## ohnometo (Sep 20, 2001)

EricI am going to search and find the post on what I am talking about...Yes, Stress did play HUGE part in my IBS-D because I lived in fear of not being able to go anywhere and wondering when the next attack would happen..I was scared to death to even go to the store and get groceries because the fear of having to leave my cart there and not making it home...For 40 years my life was run by fear and stress..and part of the reason was listening to the stupid Doctors that said I was just getting myself all worked up !!!! But it is funny when I got better the stress become less and less....I know that stress plays a part in IBS and for me when I was getting sick I would panic and make it ALOT worse because I knew what I was in for.....the horrible pain and D along with everything else....It took time for me to practice new ways of dealing with IBS and when my symptoms started to improve I would have more faith that I was going to be fine !!! I was at the point when even a little gas bubble would pass I would panic !!!! You have told me before that I have fructose intolerance and I dont because I can eat all fruit except apple with no problem so it wouldnt be fructose intolerance...I have also been told it might be the placebo effect ? Do you remember that ? I am going to search for the post and I will post it here...I dont know and I dont care how or why my body become intolerant to certain things ...It dont matter if it was stress causing my immune system to go whacky or not....I know what has improved not cured my IBS and CVS...Stress was a huge part of my daily living ...Who wouldnt have it after living with this ####


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## trbell (Nov 1, 2000)

eric,who is this 'we' you are talking about when you say "we told you a lot"? i ike to know who is signiing prescriptions when i get them from the doctor's office.tom


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## ohnometo (Sep 20, 2001)

FYIQUOTE.......I am gald Donna, you found your trigger to your IBS and CVS. To know what really happened in your case would take a lot of investigation. It could be the IRS activation, it could be you were frutose intolerant. ETC. and would take some testing to really know for sure.EricI have no problem saying that stress didnt play a part in my IBS because it did...But you know that you have always doubted what I have shared here...and thats ok ! I know Food can be a trigger in some people... http://www.ibsgroup.org/cgi-local/ubbcgi/u...c;f=45;t=001458 http://www.ibsgroup.org/cgi-local/ubbcgi/u...c;f=45;t=001764


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## eric (Jul 8, 1999)

Donna, something you don't undersstand is that the FEAR is a THREAT to the person and that causes d, WITHOUT A PATHOGEN through the immune system, your argued this stress thing so much and put so much in the foods you were blind to what I was telling you in how the HPA axis causes d via FEAR!They also have a tonm of research on this in IBS which Mike does not explain to people in regards to the immune system. he just focuses on food reactions.Back to a mechanism in the brain gut dysfunction in IBS!!!!!You also don't get that Mike is calling a differeent conditon IBS and even using intolerent to foods as a huge broad catergory, which includes malasorption, lactose intolerence ect.You don't say someone who has lactose intolerence IBS. They are not the same just as loss of oral tolerence is not the same as IBS, a person may have both but they are different conditions.The most important thing is to seperate them and figure them out. But not by calling one condition IBS, by another problem. This is a misdiagnoses!!!!!!!!!!Mike has to understand by now, not everyone has loss of oral tolerence and there are a high precentage of food phobias in IBS and people who have fears to foods in IBS.A. person has IBSB. person has IBS and some food problem, there are a ton of them and some like celiac should be checked out first, before someone convinces someone they have loss of oral tolerence causing their d or fructose malabsorbiton, or lactose malabsorbtion, or all the trigger foods like sorbitol first, to rule those things out first, not use big immunology words to convince the technically chalanged in IBS mechanisms to jump to something they alreay know is causing the symptoms of d and c in IBS and not even explain them first to a person.I have seen Mike take over most of the threads at one point on this bb to tell everyone their d in IBS is from loss of oral tolerence. IBS symptoms of d and c and alternating come from serotonin dysregulation and that is in part the future of IBS.They also have to research pre serotonin as there can be impurities in the manufacture of it that maybe important. They have known this for years now, just like the brain gut problems in IBS and the focus is on foods to much here. They are triggers to an underlying problem that makes the bowel sensitve to ALL STIMULI foods, stress, the weather ect., and cause symptoms of d or c or alternating and they have a ton of eveidence on all this.We should all be focusing on IBS and methods and means to help it, including what we eat, but its flat out wrong to say IBS is a loss of oral tolerence.By the way, its interesting toread how wrong people were on the Hypnotherapy for IBS from the past.Yes Donna, the relief you found your foods could have helped your fear factor and decreased your d, and also giving up apple juice, and also may be your on more fiber and also maybe you had a loss of oral tolerence to some foods. The placebo effect is also very very real in IBS, none of this can be ruled out in your case.Which is why I said this and still stick to it."I am gald Donna, you found your trigger to your IBS and CVS. To know what really happened in your case would take a lot of investigation. It could be the IRS activation, it could be you were frutose intolerant. ETC. and would take some testing to really know for sure."What if Mike just at first said don't drink so much apple juice its a trigger to gut function and hence IBS?


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## trbell (Nov 1, 2000)

eric, you need to stop focusing on attacking one person and helping them instead of prescribing what they should do.tom


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## trbell (Nov 1, 2000)

sorry for the double post. i meant to delete it.tom


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## eric (Jul 8, 1999)

Donna, fear is a threat or stressor to the body, it happens so fast in a person, they are not even conciously aware of it.When this goes on day in and day out for years it upsets the bodies homeostasis and the systems malfunction.You would think people would want to know about these things also and not just foods."Why some people feel the burden of stress in their gutï¿½and not for instance, in their heartï¿½can also be explained by the close communication between the brain and the gut. When the big brain consciously perceives a stressful situation, it calls on its fraternal twin through specialized cellsï¿½called mast cellsï¿½embedded in the gut's lining. These mast cells secrete a chemical called histamine, which activates the nerves controlling the gut, telling the muscles to contract. Hence, the cramps and bathroom trips so often associated with bouts of stress."


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## eric (Jul 8, 1999)

I forgot the link to the last paragraph http://www.ibsgroup.org/other/usnews000403.htm


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## Guest (Mar 4, 2003)

Mike,Thanks for offering... yes, please email me a copy of the diagram (Zars papers).I am really interested in getting more clarification."Cofberries###aol.com"Evie


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## Guest (Mar 4, 2003)

Donna,I respect your experiences and your opinions. I do have a question for you, though. Being female, is there any possibility that your "recovering" from IBS could in any way be related to a hormonal shift such as that produced during menopause? I am curious because I am now there.Evie


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## ohnometo (Sep 20, 2001)

EvieThat isnt the case because they did a complete hysderectomy on me when I was 26 years old and I have been on hormones since that time and I am now 45 years old...EricI understand your point of view...I really do and I dont believe everyone with IBS-D has a problem with food but my case does not need to be investigated....Since I have my life back I have alot of other things to do today ! I dont need to come here and take time out of my day to argue with you !! I am only here to share with other what has helped to *IMPROVE* not *CURE* my IBS and CVS..Like I said before maybe it was stress that caused my immune system to not tolerate certain foods...maybe it was the placeo effect...To me it dont matter as long as it works I am tired of trying to figure out why and how things work "They just do when you keep an open mind" and I thank God EVERY day for my life...and yes there is alot more to IBS then a problem with food and I dont believe anyone said just food is the problem


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## ohnometo (Sep 20, 2001)

To answer the question below...I was here along time ago when this BB started and I believe my number was 60 something...I was desperate when I come here to find answers and was willing to do what others suggested...People said it was milk and I stopped drinking milk and didnt get better. I tried therapy, medications, relaxation exercises and other methods and didnt get better..So why would I believe anyone when they said to stop eating apple, coconut, mustard and sodium benzonate...People has told me for many years to stop this or take this medicine and you will get better...Well, I tried and it didnt work..So why would you think by Mike telling me the results from my test my mind believed I was going to get better and I did ???? That is the most farout statement I have heard...All my life I was told to stop this and stop that and you will get better....NOTHING ever worked NOTHING..







and I couldnt relax when I was going through horrible bathroom trips where I use to lay on the floor and couldnt make it even out to the couch...I know what improved my IBS and yes I still have alot of stress in my life right now but I dont have to worry about finding the bathroom QUOTE.........What if Mike just at first said don't drink so much apple juice its a trigger to gut function and hence IBS?


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## Carl_has_IBS (Feb 5, 2003)

Eric,you are really starting to annoy me with this constant harping on the psychosocial aspect of IBS. If i want that then all i have to do is go back to any doctor and have him tell me that i need to make changes in my thinking or my life. also, that a lot of it is in my head.therefore, when i hear a a guy like Mike N. talk about foods and immune reactions it really excites me because that is the area that has helped me so much.i never had one doctor ever mention this method of attacking the problem. from this, i can possibly conclude that dr. drossman and his psychosocial approach may be barking up the wrong tree.it seems also that you have this dire need to convince everyone of your way of thinking. when in fact most people have had your way forced down their throat from day one. why do you feel so threatened by an alternative approach to IBS symptoms that are ruining so many of our lives?once again, i don't care how many books a doctor has published or how many titles he holds all i care about is that i get better, and i am getting better when i put the focus on the things i eat.i told you before that hypnosis did not work and CBT did not work, and a lot of others have stated the same thing, yet you continue to push it as such a valuable method of treatment. i am not knocking it, but that type of treatment needs to be put in context. all it can really do is give the person some temporary relief. for most of us it does not get to the root cause.quit being so one-sided.


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## Mike NoLomotil (Jun 6, 2000)

RE:The abstract on:ï¿½One potential mechanism that could explain altered bowel function in IBS is an abnormality in the serotonin transporter itself.ï¿½Etc This was posted elsewhere on the Diet Board, and I had commented on it there. So rather than repeat the post if interested here is the thread where that was discussed http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000559 _____________________________ï¿½Some of Mike's abstracts here are from the 80's and don't even have IBS in the title.ï¿½ ___________________________NOW you got me cackling buddy!!!







LMAO!!! 1.	Does one lack the ability to read in sequence and in context so one can see the purpose of the particular reference in the discussion it is posted in, and where in the discussion, so as to contribute to the eventual point? For example, A tutorial about neuroimmune regulation of the gut is not obsoleteï¿½unless of course we have eliminated all those other troublesome, pesky, and annoying little chemicals and receptors which also regulate bowel function from the BGA and HPA and now we only have to concern ourselves with the 5HT[x] receptors since this is the current target of new drug development.2.	ï¿½and don't even have IBS in the title.ï¿½ Again LMAO x 10!!!







A prize example of selective thinking and screening-out related data. One acknowledges that if the acronym IBS is not in the title it has nothing to do with IBS at all ergo is to be ignored. NO Wonder your perspective is so narrowï¿½there is a treasure trove of information never studied which is directkly pplicable to the mechanisms of manifestation of IBS symptoms which aco****s for a large part of the symptom-based diagnosed population. Rather innate bias has removed the data from consideration. Indeed it is now advocated for others so as to not confuse themselves with the facts.Just a little clueï¿½







.There are some very well respected investigators, widely regarded published and respected by their peers, who when presented with a patient with episodic diarrhea or cyclic symptoms of indeterminate origin select those patients to rule out organic disease and atopy and then study them to see what provokes the symptoms. When they isolate abnormal GI focused immune responses or non-immune mediated mechanisms to dietary provocation they publish their investigative finidings in articles about how food or additive sensitivity or intolerance caused the symptoms they presented with. They even often explain how placing them on an oligoantigenic diet brought about remission. These patients, if they had presented in clinic, or in perhaps another center approaching the symptoms from a symptom-based diagnostic perspective or psychocial perspective, would simply be called ï¿½IBSï¿½ victims not "food intolerance" victims. Since these guys took a causal approach to the patient they may not have assigned your deired and preferred titel to their symptoms...instead they linked them to what PROVOKED their symptoms. If they were not investigated in the same manner they would be reported in a wholly different format! This is a very common occurrence over the last 25 years or so with these symptom sets.This whole statement is symptomatic of why peoples understanding of IBS subpopulations is so inadequate: selective exclusion of directly related information, data and physiology. If you do not function in a center which does specific study into food intolerance then this work remains invisible or disregarded on the basis of the presence or lack thereof of specific nomenclature? Talk about innate bias. From then on the position taken so often before the august body of IBS victims in this forum speaks for itself. There is a whole world of information about people who present with IBS symptoms of this type who are in this country typically diagnosed with IBS and treated as such that has never been read, intentionally. So it is impossible for such a person to gain an integrative perspective. ________________________ï¿½When Mike posts to people new with D what is the first thing he says to them, foods cause your d, not the underlying issues that are present from the beginging and how that causes D.ï¿½ __________________________







No it is not and you know it. The first thing, in general, is to ask about history and physical findings, whether a GI doc has put them through proper differential dagnosis, and if not direct them to do stherwise the first thing is to suggest that they EDUCATE themselves more fully about all aspects of their condition by reading these books in this order:ï¿½IBS: A DOCTORS PLAN FOR CHRONIC DIGESTIVE TROUBLESBy Gerard Guillory, M.D.; Vanessa Ameen, M.D.; Paul Donovan, M.D.; Jack Martin, Ph.D. http://www.amazon.com/exec/obidos/ASIN/088...3369143-6824157 ï¿½FOOD ALLERGIES AND FOOD INTOLERANCE: THE COMPLETE GUIDE TO THEIR IDENTIFICTION AND TREATMENTï¿½, Professor Jonathan Brostoff , M.D.. Allergy, Immunology and Environmental Medicine, Kingsï¿½ College, London http://www.amazon.com/exec/obidos/ASIN/089...6487508-3420903 Sometimes, if the person seems to fit the clinical picture of a person who has been through proper differential diagnosis and therapy and has been unsuccessful, I will direct them to threads populated by people similar to them where what they did is discussed in detail and reported and the person will do as they please. _______________________________________________ï¿½So lets talk about IBS first and foremost, he just leans to food. Its more important first people understand the underlying dysregulation and the big picture.ï¿½ _______________________________________________First I think what is more important is nmot to drag sck people looking for help into the middle of the investigative debate over the pathogenesis of IBS subpopulations. This oath does not lead to relief of their symptoms it leads to immerson in technical and phsyiologic perspectives. This is a nice parallel course for the interested patient, bit many just want some help!Anyway, as soon as the supposed ï¿½underlying dysregulationï¿½ is actually understood, not postulated with no explanation of the supposed pathogenesis, rather hypotheses, and indeed IBS patients no longer respond to integrative therapy with remission, then indeed then maybe that would be a time to ignore sterring people tothings which can bring them rapid symptomatic relief without drugs (many of whom get no relief from the drugs anyway).In the interim I think the first place to go is understand the persosn problem, think about all the things which might help them get over their immediate problem, and show them where to finsd that information. Or if they ask direct questions answer them objectively with what one knows to be potentially effective. This is ratioale behind coming by here every day...not to draw the sick into observation of interplay as absurd as that seen in Dr. Strangelove!In the meantime, since the information and suggestions I set forth for people are as objective, factual and effective as I can strive to make them, I do not think I will restrain myself from answering peoples questions in a manner which can help them gain some measure of control over their symptoms simply because it clashes with someone elseï¿½s paradigm or belief-system.Indeed there is each day less and less value in this form of extended debate, especially know that I can understand clearly why there is such a degree of self-imposed naivete about certain sources of information about the people who suffer the symptoms of the syndrome and why.Better to follow the advice a wise man once imoparted to me:ï¿½A proud mind cannot learn anything beyond the bounds of that which it is proud to know.ï¿½. (P.Saraswati) ___________________________Oh gsh darn it!!!!You know you were almost rid of me, THIS CLOSE,







until you now try now to once again artificially set me against Dr. Drossman and then wax on and on about it from your pinnacle on high.Oh well then I guess I do now need to repost what I wrote on the other thread to ensure my exact actual perspective is set forth against this innuendo again, the exact truth of ehat I allegedly am or represent or beleive, not rhetoric and innuendo.Let it reside on record alongside the aforementioned foolishness._____________________Lited verabtum from the other thread...where a paragrph from Dr. Drossman giving a quick refercne to food intolerance in someones website was posted as evidence of the lack of veracity or relation between IBS as it is presently diagnsoed and "dietary" issues. ________________________________________The problem that a number of other physicians would point out with the nominal referecne to food intolerance within Dr. Drossman's posted tutorial on the website in question is that a. It is not wholly accurate based upon how IBS is presently diagnosed andb. It is not inclusive of a large body of knowledge as regards the physiologic mechanisms of food intolerance and hypersensitivity.There are other investigators and clinicians expert in this area who would respectfully expand upon some of the rudimentary concepts quickly set forth in the paragraph in question.Let us consider the perspective of immunologists and allergists whose life work is investigating this aspect of physioology, not psychoneurogastroenterology which is a distinctly different area of expertise. First, the premise of the work of others with a different approach, perspective, and board certification credentials can be summarized by one of them...______________________________ï¿½Considerable confusion is now arising over the relationship between food intolerance and the Irritable Bowel Syndrome (IBS). Although the name has been hallowed by long usage, IBS is not a distinct entity but merely a collection of disorders which are characterized by abdominal symptoms but no obvious organic pathology. G.W. Thompson forecast in 1985: ï¿½the IBS is organic; that is all sufferers will eventually be found to have measurable, unique pathologic defects.ï¿½ When that happy day arrives, the term ï¿½IBSï¿½ will no longer be used, and each patient will receive a more precise diagnosis. Until then it is sufficient to appreciate that food intolerance represents an important proportion of the conditions which together make up IBS.ï¿½John Hunter, MD, FCRPDirector or Gastroenterology and Consultant PhysicianAddenbrookeï¿½s HospitalCambridge, United KingdomFromï¿½Food Allergy and Food Intoleranceï¿½ Second Edition 2002J. Brostoff, MDS. Challacombe, MDSaunders ___________________________Indeed, the one specific statement set forth by Dr. Drossman in the post above which no one does or would disagree with, is that food intolerance is no more the causal basis of the pathogenesis of the group of conditions currently called 'IBS" than chronic stress is.It is, however, known by many and is the basis for effective treatment of many IBS patients, to be a major set of symptom-generating mechanisms among the subpopulation of diarrheic-prone people diagnosed with "IBS".There is ample evidence of this in the literature, sufficent even to result in inclusion of it in the Merck Manual of Diagnosis and Therapy:________________________________"Page 1051 of the hard copy of the Merck Manual, and online Merck Manual at http://www.merck.com/pubs/mmanual/section1...ter148/148b.htm "Recently Food Intolerance was found to be responsible for symptoms of some patients with the IRRITABLE BOWEL SYNDROME, confirmed by double-blind food challenge.An increase in rectal prostaglandin levels was noted when a reaction occurred.Preliminary information suggests the same phenomenon may take place in patients with chronic ulcerative colitis.ï¿½___________________________In actuality the discovery of this mechanism is not all that recent....it sates back over 23 years to when it was first obserevd nad has been studied in vivo with invasive jejunal segmantal isolation studies which quantifiy inflammatory mediator release in the isolated small bowel of patients with so called "IBS" per the Rome criterai (food allergy ruled out) since about 1994. It can also be duplicated in vitro since about 1997.If one is seeking the most experienced and qualified experts on pscyhophysiology as it mat realte to IBS one should look to UNC and their work.If one is seeking expertise in fod allergy and intolerance one must begin at the top of the order, with Professors Brostoff, Challacombe and perhaps the 100 authors whoc contributed to the following new medical text on the subject...and for in vivo assays of immune response in food intolerance induce GI and systemic symptoms Prof Ulf Bengtsson has donw the most work to date in that area...____________________________Books written edited or contributed by Professor Jonathan Brostoff:FOOD ALLERGY AND INTOLERANCE, Professor Jonathan Brostoff, MD, Stephen Challacombe, MD (NEW 2002) http://www.amazon.com/exec/obidos/ASIN/070...product-details http://www.greenleaves.com/bookcat/by_brostoff_jonathan.html Asthma: The Complete Guide to Integrative Therapies- by Jonathan Brostoff, Linda GamlinThe Complete Guide to Food Allergy and Intolerance- by Jonathan Brostoff, Linda GamlinFood Allergies and Food Intolerance : The Complete Guide to Their Identification and Treatment- by Jonathan Brostoff, Linda GamlinImmunology- by Ivan Roitt(Editor), Brostoff et alThe Allergy Bible : Understanding, Diagnosing, Treating, Allergies and Intolerances- by Reader's Digest(Editor), et alAutoimmune Disease : Aetiopathogenesis, Diagnosis and Treatment : Essays in Honour of the Retirement of Professor Ivan Roitt Frs- by Peter M. Lydyard(Editor), Jonathan Brostoff(Editor)Case Studies in Immunology- by Jonathan Brostoff, et alCase Studies in Immunology: Companion to Immunology, Fifth Edition- by Jonathan Brostoff, et alClinical Immunology- by Jonathan BrostoffClinical Immunology : An Illustrated Outline- by Jonathan Brostoff, David K. MaleImmunology- by Ivan M. Roitt, et alImmunology : Interactive 2.1- by David Male, et alThe Complete Guide to Hay Fever : The Latest Research & Techniques for Coping With Hayfever- by Jonathan BrostoffFood Allergy and Intolerance- by Jonathan Brostoff, Stephen J. ChallacombeImmunology- by Ivan Maurice Roitt, et alInmunologia Clinica- by Jonathan Brostoff, et alIntroducing Immunology- by Norman A. Staines, et al__________________________Also, a good tutorial on the mechanisms (multiple) of food reactivity and how they marshall IBS symptoms in the food intlerant patients would be this one:Alimentary Pharmacology and Therapeutics Vol. 15 Issue 4 Page 439 April 2001 Food hypersensitivity and irritable bowel syndrome S. Zar, D. Kumar, M. J. Benson http://www.blackwell-synergy.com/servlet/u...36.2001.00951.x To gain some eprspective into the effectiveness of isolating and prophylactically treating food and chemical intolerance in IBS and related conditions these discussions would also be useful: http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000407#000002 http://www.ibsgroup.org/ubb/ultimatebb.php...=4;t=000286;p=4 http://www.ibsgroup.org/cgi-local/ubbcgi/u...0286;p=3#000106 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000364 http://www.ibsgroup.org/cgi-local/ubbcgi/u...=4&DaysPrune=30 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000286 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000285 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000331#000001 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000302 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000287 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000364 http://www.ibsgroup.org/cgi-local/ubbcgi/u...f=5&t=000313&p= http://www.ibsgroup.org/cgi-local/ubbcgi/u...0293;p=2#000069 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000276 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=5;t=000073 http://www.ibsgroup.org/cgi-local/ubbcgi/u...f=5&t=000356&p= http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000320#000016 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000383#000010 http://www.ibsgroup.org/cgi-local/ubbcgi/u...f=5&t=000126&p= http://www.ibsgroup.org/ubb/ultimatebb.php...c;f=17;t=000033 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000363#000002 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=028290#000001 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000335#000009 http://www.ibsgroup.org/cgi-local/ubbcgi/u...f=1&t=028290&p= http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000353 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000389 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000427#000006 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000421 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=000427#000015 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=030178#000003 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000476 http://www.ibsgroup.org/cgi-local/ubbcgi/u...t=029840#000027 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000478 http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000488 (OHNOMETOO One year anniversary) http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=4;t=000478 In general this is like any other area of medicine...everyuone posesses some information in any given area, and the most specialzied information will be found among those whsoe specialty area is devoted to a particular area. There are many centers of excellence on the subject of food and chemical intolerance mechansism and therapy which go beyond the common boundaries simply due to the fact that it is their focus, so it is usually helpful to seek out specialized information at the acknoweldged source of the specialty.I do beleive that the 2002 edition of Brostoff 7 Challacome remains the ONLY medical textbook yet published on the subject of this particular thread.The more patient-specific one can make the assessment of any patients food and chemical tolerance, or lack thereof, the greater the degree of remission one can achieve. This is not easily done in most centers, as most centers do not make use of the most current methodologies in this specialized area, or do not approach the issue from the perspective that a specialist in that area would.But a study of broader information would make it apprant that there is broader informatio available upon which to base treatment.______and------Post script....on another IF-THEN hypothesis which we need be careful not to stretch into more than it is at present:____________________________"One potential mechanism that could explain altered bowel function in IBS is an abnormality in the serotonin transporter itself."____________________________Indeed among the myriad biochemical activities which govern overall gut function and motility this is indeed as the authors state ONE of the many and indeed COULD be ONE mechanism._____________________________"If the underlying abnormality in serotonin transporter function alternated, then this would in turn explain alternating constipation and diarrhea."__________________________IF-THEN, but of, of course, it would. But what we have at present is the careful presentation of a postulate. While a specific observed abnormality indeed is quantitifed, the basis for it (the pathogenesis and mechanism whereby the observed abnormality occurred in the patients selected) is not quantitifed and there are multiple mechanisms which can lead to the quntified activity. These needs to be further elucidated, and then of course one must show the mechanism "cycles" which again as yet is not shown. There are, however, mechanisms quantitied in specific IBS patients which do already account for the observed diarrheaic and constipation cycles seen in so called IBS victims, and while 5HT[x] receptors may be involved, other mediators and/or hormones with the same effects on gut function have already been quantified, and protocols which lead to the cessation of this cyclic phenomena are in clinical use.So inded this may end up being a mechanism but as yet it remains a postulatem while other mechanisms have already been quantified.Which of course the investigators make clear in the summary...as well as the fact that the objective,as is the objective of all investigations into the role of 5HT and 5HT[x} receptors in IBS is to try to find new drugs which can be used for treatment...hence the targeting of individual neurotransmitters among the many different types of receptors which affect gut function.So yes indeed, as it says this would, if it had been done, but it has not, yet there remain other biochemical markers which have been quantified and which can be addressed which already resut in cessation of cyclic diiarhea and constipation without the need for drug therapy._________________________________"These data strongly suggest that IBS is a "real" gut disease and a potential diagnostic disease marker."_______________________________There are many who would agree with this, and who have since about 1980, who also have observed other potential "markers" among gut mediatros which appear that they may characterize certain subpulations. This might be one more.________________________________"They also suggest that it is valid to subdivide IBS into constipation and diarrhea symptom subgroups."________________________________This would be a good step forward as physicians who are advocates of not stopping at symptom absed diagnosis, rather continuing the pursuit of the causal basis for the patients symptoms, have long contended that this is an appropriate protocol. Nice to see that view becoming more widely espoused. Anything which will move the practcie towards causal based investigation is a good thing.__________________________"This study also provides additional rationale for the use of serotonin-modulating agents in IBS and provides a new target for drug modulation."____________________________But of course, this is the basis of most such investigations...seeking modulatable targets for pharmaceutical intervention in a pill-therapy oriented society, not prophylactic solutions.___________________________"Confirmation of these very exciting initial findings in larger patient samples is awaited with great interest."_____________________________Indeed like many existing postulates, one more which has potential merit among many....all of which, if they were integrated, could help assemble the puzzle that is the multiple mechanism syndrome of IBS.Have a DFD!MNL


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## BQ (May 22, 2000)

Hey Mike, Got a question for you. When you read posts that describe a person's symptoms, is there ever a time when you say to yourself







'This person may indeed have intolerances'. Like is there some sort of marker that _you_ see that would indicate intolerances may be the bottom line for that person? Or is it still the time honored fashion of: 'Well, that didn't work for them, and that didn't work for them, ETC>>>>> Maybe they have intolerances?'I am not sure I even phrased that question very well. But I tried.







Hoping you can read or at least translate BQ-ese. lolBQ


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## eric (Jul 8, 1999)

carl, foods are a trigger!!!!!!!!!!!!!!!!!!!! Not one person here is arguing this!!! The thing is there are specific food problems a person can have with IBS.There is an underlying malfunctioning of the gut.Maybe the HT did not work for you, because you did not think it would address the IBS, maybe you were subconciously thinking it was gonna mask the problem, which would mean then it would not work. Why I know so much about all this and wanted to help you!!!!! Defending HT is IBS on the bb here is not easy, but the results speak for themselves over and over again for anyone seriously researching it for IBS.Maybe there are foods issues in your case carl that have not been addressed. This is very common in a lot of IBSers.There is however the huge amount of IBS research going on know and anecdotal eveidence of an individual getting better. They are very very different.The information I have put on this thread is not solely from UNC, but UNC, Mayo, UCLA, the best researchers in the country, in all fields, this needs to be understood.You can say whatever you want about me carl. I will not give up on this!!!!!Carl read this a couple times and if you really want to learn IBS watch these videos. The entire world of serious IBS researchers use the model on IBS now. http://www.conference-cast.com/ibs/Lecture...dRegLecture.cfm I don't think your grasping how the gut functions!!I also don't think you realize how closely connected the brain is to gut functioning and how each effect each other. There connected from Birth and they are connected by millions of nerve fiberrs, as many as are in the spinal cord. ITS a fact they talk to each other and efffect each other, one of the things I am trying to help people understand in IBS."Gut-Brain Connection -- The gut and the brain develop from the same part of the human embryo. So it is not surprising that the intestinal tract has such a rich nerve supply that it is sometimes referred to as "the little brain." The gut shares many of the same kinds of nerve endings and chemical transmitters as the brain to which it remains linked through a large nucleus. This collection of nerve cells is partly responsible for controlling anxiety and fear, which explains why these emotions can sometimes be associated with bowel function." http://www.aboutibs.org/Publications/gutResponder.html http://www.ibsgroup.org/other/usnews000403.htm There is also another immune system problem in IBS, that does not require a pathogen between the gut and the brain!!!!!!!!!I suggest Heathers book on foods all the time and have a ton of food information on my website.They are way farther along then most people realize on IBS!!!!!!!!!!!!Considering dr drossman is the chair of the Rome to diagnose IBS and the international gastroenterologist association and has people all over the world sharing information with their center, all this ONE approach is crapola, and the entire world medical proffesion for IBS,knows the UNC and their work.Carl why don't you come to a UNC chat and ask them your specific comments? On Foods and the why's.I also don't think you understand IBS is a brain gut dyregulation and both are operational to give you sysmptoms, this is a fact!!!!!!!!!!!!You also don't understand HT in regards to IBS!!If a person does it and gets better after the treatment for years, then it is getting to root issues in IBS!!!!!!!!!What does that mean carl, a person stops treatment and continues to improve for years after?????The model, involves foods and the immune system, but it also involves everything else for a MORE accurate understanding of everything."Adapted from Gastroenterology & Endoscopy News, May 2001The biopsychosocial model of chronic gastrointestinal disease may be a better approach to diagnosing and managing patients than the traditional biomedical model, say experts, at the International Symposium on Functional Gastrointestinal Disorders, which was held in Milwaukee, Wisconsin, March 31st through April 4th 2001."The biopsychosocial model proposes that illness and disease result from interacting systems at the cellular, tissue, organismal, interpersonal and environmental levels, explained Douglas Drossman, MD," professor of Medicine and Psychiatry in the Division of Digestive Diseases and Co-director of the University of North Carolina Center for Functional GI & Motility Disorders in Chapel Hill. Physicians can integrate the biopsychosocial model into their practices by evaluating dietary and lifestyle factors, the role of stress, social support, life trauma e.g., abuse history and the patient's coping mechanisms. "For treatment one should look at the severity of the condition, the biological and psychosocial factors that may be influencing the nature and severity of the symptoms, and let one's treatments be guided by that," said Drossman." http://www.med.unc.edu/medicine/fgidc/biopsychosocial.htm Read this thread a couple times, by using it they can MORE accurately diganos IBS!!!!!!!The UNC is also a school on Nutrition I am pretty sure they understand foods and food problems, funny no body mentions that!!!!!!!!!!!Some of the worlds leading immunologists work with the center in sharing information on IBS.You also don't understand HT in regards to IBS it seems at all, it does not mask the problem, this is totally inaccurate!!!!How effective it has shown, in real clinical studies and in the IBS population.Hypnotherapy does get to some of the root issues in IBS!!!! Does it work for everyone no. Just most. They are putting it in hospitals!!!!!! It is however confirmed it works on IBS an not just one symptom, but GLOBAL SYMPTOMS, Including boosting your immune system!!!"Hypnosis for IBSThe results of the first formal research study 4 on hypnosis treatment for IBS were published in the Lancet in 1984. The investigators, Dr. Peter Whorwell and his group in Manchester in England, reported remarkable success from a seven-session hypnosis treatment of 15 patients with severe IBS problems who had not responded to any other treatment. All 15 patients treated with seven sessions of hypnotherapy improved, with dramatic improvement seen in all the central symptoms of IBS. The researchers furthermore showed that this therapeutic impact was not merely due to belief or expectancy of improvement, because a comparison group of 15 IBS patients who were instead treated with the same number of psychotherapy sessions and also received placebo pills pills with no medication showed only slight improvement. This was a powerful demonstration of the impact hypnotherapy could have on IBS, and led to considerable subsequent interest in this approach to IBS treatment.Since this first report, more than a dozen other published research reports have confirmed that hypnosis treatment is effective in treating IBS. Generally, the treatment procedures reported in the literature consists of 4 to 12 sessions shorter treatment than 7 sessions may be a bit less effective. Hypnosis sessions are typically conducted weekly or once every other week, last 30-40 minutes and consist of induction of hypnosis followed by deep relaxation and the use of gut-directed imagery and suggestions. Patients are commonly given short audiotape hypnosis home exercises to use during the course of treatment in addition to the sessions with the clinicians.The experience to date may be outlined as follows: * Reported success rates range from approximately 70-95% in all studies with any significant number of patients for example, in the work of the Manchester group in England 4,5,13 and our studies 6,7. * The improvement enjoyed from this treatment often lasts at least two years after the end of treatment 5. * All major IBS symptoms improve from this kind of treatment abdominal pain, diarrhea/constipation, and bloating. * There are some indications that individuals with certain characteristics are somewhat less likely to benefit from this kind of treatment 5,7,13: People with very little hypnotizability perhaps 15-25 % of all people, persons with psychiatric disorders, and maybe according to one report males with diarrhea-predominant type of IBS. * This treatment can be effective also when people are treated in groups 14. * In addition to effects on physical symptoms, the treatment commonly improves psychological well-being and life functioning substantially6,7,13,15 and can have long-term positive effects in reducing disability and health care costs and improving the quality of life of IBS patients 15. http://www.aboutibs.org/Publications/HypnosisPalsson.html A study of 250 people long term in IBS!!!!"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.""Our success has been reproduced by others""We 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. " http://www.aboutibs.org/Publications/hypnosis.html with permissionThe Effects of Hypnosison Gastrointestinal ProblemsOlafur S. Palsson, Psy. D.Research Associate, UNC-CHAPEL HillDepartment of MedicinesHypnosis is a treatment method, which still carries an aura of mystery,that unfortunately continues to be promoted by misrepresentations in movies and stage shows for entertainment. In reality, there is little mysterious about hypnosis anymore. It is a well-researched clinical technique which was formally accepted as a treatment method by the American Medical Association and the American psychological Association over thirty years ago. Clinical hypnosis is currently used by thousands of clinicians in the U.S. to treat both psychological and medical problems.Until recently, the possibilities of using hypnosis to treat gastrointestinal problems had received little attention. In the last 15 years, however, research has shown that hypnosis can influence gastrointestinal functioning in powerful ways, and that in particular, it is effective in helping patients with irritable bowel syndrome and to control nausea and vomiting.How Hypnosis Works:Hypnosis is a special mental state in which a person's focus of attention becomes narrow and intense like the beam of a bright flashlight in a dark room. This state is usually created with the aid of a hypnotist,who guides the person systematically to relax, focus only on one thing, and to allow things to happen by themselves.Whatever the mind focuses on while in this special mental state of hypnosis holds the entire attention. Therefore, people tend to experience things they think of, imagine or remember, more vividly and clearly than under usual circumstances. This is why people can sometimes recall things from their distant past under hypnosis even though unable to do so in the normal waking state (research has shown, however, that such hypnotically enhanced recall can be highly contaminated by the person's imagination. The narrow hyperfocus of this mental state is also why therapists using hypnosis are frequently able to help people make strong positive changes in their emotions and physical functioning. Hypnosis can work like a magnifying glass on the mind's effects on the body and emotion.Clinical hypnosis relies on suggestions, imagery, and relaxation to produce its therapeutic effects. Hypnotic suggestions are things that the hypnotist verbally suggests may happen while the person is under hypnosis. Due to the focused and receptive state of the hypnotized person, these suggestions happen almost automatically and without conscious decision or effort. If you, for example, receive the suggestion under hypnosis that your arm may be getting heavy, you will very likely feel it becoming heavy, without trying to do anything to make it happen. This "automaticity", the feeling of things happening by themselves, is by some considered the hallmark of hypnosis, and is often surprising to people experiencing hypnosis for the first time.Hypnotic imagery consists of picturing mentally events or situation or place in a way that has a desired positive physical or mental effect. For example, patients undergoing surgical or dental procedures are sometimes taught to enter a hypnotic state and go to a pleasant place in their mind. When successfully applied, the person gets completely engrossed in the vivid enjoyable imagery and is therefore happily unaware of the unpleasantness of the procedure.The hypnotic state is naturally accompanied by relaxation, and the physical relaxing effects are often deliberately strengthened further by clinicians through suggestions and relaxing imagery. Some of the benefits that come from hypnosis treatment are likely to result partly or entirely from the fact that hypnosis is a powerful relaxation method.Over decades of research and clinical experience, hypnosis has proven to have many valuable therapeutic uses. In psychotherapy, hypnotic techniques can speed the therapy process in various ways - for example by facilitating patients' self-understanding, extinguishing unfortunate habits, uncovering repressed or forgotten memories, reducing anxiety and phobias, and helping people to adopt a new and more adaptive outlook. In medicine and health psychology, hypnosis is used to reduce pain and discomfort associated with medical procedures such as childbirth, treatment of burns, and surgery where chemical anesthesia cannot be used effectively. It is also used to treat chronic pain and psychosomatic problems and counter unhealthy habits that contribute to illness. In dentistry, hypnotic analgesia is an effective needle-less alternative to topical anesthetic drugs, reduces bleeding and discomfort in oral surgery, and is used to treat teeth grinding and temporomandibular disorder. In recent years, the effects of gastrointestinal functioning and GI symptoms have been studied extensively.The Effects of Hypnosis on Gastrointestinal Functioning:The hypnotic state itself, without any particular suggestions, seems to slow down the gut, and clear-cut and specific changes in GI functioning can be induced in individuals by directing thinking or inducing specific emotional states under hypnosis.For example, one study 1 found that when healthy volunteers were hypnotized and simply instructed to relax, the orocaecal transit time the time it takes material to pass through the GI tract from the mouth to the first part of the colon was lengthened from 93 to 133 minutes. Another study 2 found that being in a hypnotic state decreases muscle movements in the stomach. The same study demonstrated that the emotional state of happiness, created under hypnosis, suppresses gastric muscle activity but anger and excitement increase muscle movement in the stomach . A pair of other studies 3 showed that when volunteers were guided to use imagery of eating a delicious meal while they were under hypnosis, gastric acid secretion was increased by 89%, and that acid production of the stomach could also be deliberately decreased during hypnosis using hypnotic instructions.Close to fifty published studies have reported on the therapeutic effects of hypnosis on nausea and vomiting problems related to chemotherapy, after surgery, and during pregnancy. Overall, this substantial body of literature indicates that hypnosis can be a powerful aid in controlling nausea and vomiting.Hypnosis may also be helpful in preventing gastrointestinal problems from recurring after they have been treated with medication: One study 4 of thirty patients with relapsing duodenal ulcers who had been successfully treated with a course of medication, found that only 53% of the patients who received preventive hypnosis treatment had a relapse within one year. In contrast everybody 100% in a comparison group receiving no hypnosis relapsed in the same period of time.In 1984, researchers in Manchester in England published a study 5 report in the journal Lancet, showing that hypnosis treatment dramatically improved the symptoms of IBS patients who had failed to benefit from other treatment. The researchers had randomly divided patients with severe IBS problems into two groups. Fifteen patients were treated with seven hypnosis sessions. Fifteen comparison patients were treated with seven sessions of psychotherapy, and those patients also received placebo pills pills with no medically active ingredients which they were told were a new research medication for IBS symptoms. Every patient in the hypnosis group improved, and that group showed substantial improvement in all central symptoms of IBS. The control group showed only very modest improvement in symptoms.Partly due to these dramatic results with treatment-refractory patients, a dozen other studies have followed, including three U.S. studies. The general conclusions from most of these studies are that hypnosis seems to improve the symptoms of 80% or more of all treated patients who have well-defined "classic" IBS problems, especially if they do not have complicating factors such as psychiatric disorders. The improvement is in many cases maintained at least for a year after the end of treatment. What is particularly remarkable is that this high rate of positive treatment response is seen even in studies where the participating patients all have failed to improve from regular medical care.The dramatic response of IBS patients to hypnosis treatment raises the question of exactly how this kind of treatment influences the symptoms in such a beneficial way.Four studies to date, two in England and two in the U.S., have tried to discover how hypnosis treatment affects the body of IBS patients. Since it is well known that many people with IBS have unusual pain sensitivity in their intestines, which is thought to be related to the clinical pain they experience, much of the focus of these studies has been on assessing the impact of this kind of treatment on intestinal pain thresholds. The two English studies both measured intestinal pain sensitivity with balloon inflation tests. The second study also measured muscle tone, to see if hypnosis relaxes the smooth muscles of the GI tract. No overall changes in pain sensitivity were detected, and gut muscle tension was also unchanged after treatment except a subgroup of unusually pain-sensitive patients had lessened pain sensitivity in the second study 7.. In 1995-1996, during my post-doctoral fellowship in the Division of Digestive Diseases and Nutrition at UNC-Chapel Hill, we conducted the first U.S. study 8 on hypnosis for IBS under the direction of Dr. Whitehead. We evaluated the effects of a highly standardized treatment protocol, delivered verbatim following written scripts, on rectal pain thresholds and muscle tone. Seventeen out of the 18 patients we treated with hypnosis showed significant improvement in their clinical symptoms. However, we found, like the English researchers, that gut pain thresholds and muscle tension were unchanged after treatment. In a second study 9, which I conducted with co-investigators at the Eastern Virginia Medical School, we used the same treatment protocol but this time measured autonomic nervous system functioning and blood levels of a gut hormone called vasoactive intestinal peptide. These are regulators of GI functioning in the human body, and the aim was to see if they would change due to treatment. Again, we found no changes in our physical measures after treatment with the exception of reduction in sweat gland reactivity even though 21 out of 24 treated patients were clinically improved. It should be noted, though, that in both our studies, we found clear improvement in the psychological well-being of our patients after treatment.In summary, it is clear from our work and other research that hypnosis treatment substantially improves all the central symptoms of IBS in the majority of patients who receive such treatment see the effects of our two studies on clinical symptoms in the Figure. What happens in the body of these patients to cause such improvement, however, remains a mystery.Future prospects:In light of the many studies which have shown hypnosis treatment to be effective for such problems as IBS and nausea and vomiting, the question may be raised why this kind of treatment is not more widely available or generally offered to patients with such GI problems.One limitation is the fact that not everybody is equally hypnotizable. Research has consistently shown that at least 15% of people are practically non-hypnotizable, and even those who are able to enter a hypnotic state vary greatly in how well they respond. Interestingly, the ability to be hypnotized is a stable mental trait. In other word, if you are highly hypnotizable now, you will most likely be so also in thirty years. Fortunately, the majority of people are sufficiently hypnotizable to have a potential for enjoying at least some of the medical and psychological benefits of clinical hypnosis.Furthermore, the idea of being hypnotized does not agree with all people. Even individuals who are sufficiently hypnotizable, may not like the idea of "letting go", may have difficulty trusting a therapist to guide them in hypnosis, or may have other concerns about the hypnosis experience. Fortunately, other forms of psychological treatment for gastrointestinal problems - in the case of IBS especially cognitive-behavioral therapy -- have also been found to be effective and are good alternatives.Finally, an obstacle which has barred many patients from receiving help for gastrointestinal disorders with hypnosis is the fact that in the U.S. the technique is more commonly used by psychologists and other mental health professionals than by physicians. Many mental health professionals who use hypnosis are not accustomed to treating gastrointestinal disorders, and therefore reluctant to take on treatment of such problems.As the reliably beneficial effects of hypnosis on gastrointestinal functioning become better known both to health professionals and the general public, this benign and comfortable form of treatment will hopefully become a more popular treatment option for GI patients - especially for those who have not received much relief from standard medical management. As far as IBS is concerned, we have been making an effort in the last two years to encourage clinicians across the country who have adequate training in hypnosis to provide such treatment for IBS. We have done this by providing them, free of charge, with the complete standardized treatment protocol which has proven effective in our research. To date, more than eighty licensed health professionals, practicing in almost all states, are started using our protocol, making it a little bit easier for patients in many geographical locations to receive help with hypnosis. http://www.med.unc.edu/medicine/fgidc/hypnosis.htm These are from extremely well respected IBS researchers in the world of IBS research all over the world.It not only is effective in IBS but dyspepsia.Gastroenterology 2002 Dec;123 6:1778-85 Related * Gastroenterology. 2002 Dec;123 6:2132-5. Long-term improvement in functional dyspepsia using hypnotherapy. Calvert EL, Houghton LA, Cooper P, Morris J, Whorwell PJ. Department of Medicine, Wythenshawe Hospital, Southmoor Road, Manchester, United Kingdom. BACKGROUND & AIMS: We have shown hypnotherapy HT to be effective in irritable bowel syndrome, with long-term improvements in symptomatology and quality of life QOL. This study aimed to assess the efficacy of HT in functional dyspepsia FD. METHODS: A total of 126 FD patients were randomized to HT, supportive therapy plus placebo medication, or medical treatment for 16 weeks. Percentage change in symptomatology from baseline was assessed after the 16-week treatment phase short-term and after 56 weeks long-term with 26 HT, 24 supportive therapy, and 29 medical treatment patients completing all phases of the study. QOL was measured as a secondary outcome. RESULTS: Short-term symptom scores improved more in the HT group median, 59% than in the supportive 41%; P = 0.01 or medical treatment 33%; P = 0.057 groups. HT also benefited QOL 42% compared with either supportive therapy 10% [P < 0.001 or medical treatment 11% P < 0.001. Long-term, HT significantly improved symptoms 73% compared with supportive therapy 34% P < 0.02 or medical treatment 43% P < 0.01. QOL improved significantly more with HT 44% than with medical treatment 20% P < 0.001. QOL did improve in the supportive therapy 43% group, but 5 of these patients commenced taking antidepressants during follow-up. A total of 90% of the patients in the medical treatment group and 82% of the patients in the supportive therapy group commenced medication during follow-up, whereas none in the HT group did so P < 0.001. Those in the HT group visited their general practitioner or gastroenterologist significantly less median, 1 than did those in the supportive therapy median, 4 and medical treatment median, 4 groups during follow-up P < 0.001. CONCLUSIONS: HT is highly effective in the long-term management of FD. Furthermore, the dramatic reduction in medication use and consultation rate provide major economic advantages. Publication Types: * Clinical Trial * Randomized Controlled TrialPMID: 12454833And its certainly safer then drugs and very safe in general and most people can use it effectively!!!!! The side effects are usally improvements in other areas, back pain, insomnia ect..


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## eric (Jul 8, 1999)

A new study on the brain and IBS.Gastroenterology 2003 Mar;124 3:754-761 Alterations of brain activity associated with resolution of emotional distress and pain in a case of severe irritable bowel syndrome. Drossman DA, Ringel Y, Vogt BA, Leserman J, Lin W, Smith JK, Whitehead W. UNC Center for Functional GI and Motility Disorders, Division of Digestive Diseases and Department of Radiology and Biomedical Engineering, University of North Carolina, Chapel Hill, North Carolina; and Cingulum NeuroSciences Institute and Department of Neuroscience and Physiology, SUNY Upstate Medical Center, Syracuse, New York. Background & Aims: The association of psychosocial disturbances with more severe irritable bowel syndrome IBS is well recognized. However, there is no evidence as to how these associations might be mediated. Functional magnetic resonance imaging fMRI offers an opportunity to study whether activation of the cingulate cortex, an area involved with the affective and pain intensity coding might be linked to poorer clinical status with IBS. In this case report, we found an association between the severity of a patient's clinical symptoms and psychosocial state, with activation of the cingulate cortex. We also found that clinical and psychosocial improvement was associated with reduced cingulate activation. METHODS: Observational case report of a young woman observed for 16 years with a history of sexual abuse, psychosocial distress, and functional GI complaints. Psychosocial, clinical, and fMRI assessment was performed when the patient experienced severe symptoms and again 8 months later when clinically improved. RESULTS: During severe illness, the patient had major psychosocial impairment, high life stress, a low visceral pain threshold, and activation of the midcingulate cortex MCC, prefrontal area 6/44, and the somatosensory cortex, areas associated with pain intensity encoding. When clinically improved, there was resolution in activation of these 3 areas, and this was associated with psychosocial improvement and an increased threshold to rectal distention. CONCLUSIONS: Activation of the MCC and related areas involved with visceral pain encoding are associated with poor clinical status in patients with severe IBS and psychosocial distress and appear to be responsive to clinical improvement.PMID: 12612913This is showing how things like CBT and HT change physiological aspects of the brain and imporve IBS symptoms!!!


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## trbell (Nov 1, 2000)

eric, lighten up. i think carl has a point. the first thing i tell a patient is that therapy helps some, medicine helps some, changes in diet or exercise help some because that's what research shows. I also tell them that some people can benefit from therapy and some don't do as well with the method because that's what the research shows.biopschosocial means biological and/or psychological and/or socialit doesn't mean that a serotonin pill fizes everyone or that hypnosis cds fix everyonebut thinking about it the social or a goodbellylaugh might do it for all of us.tom


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## trbell (Nov 1, 2000)

eric, those are some good articles. cna you post some of them on the news thread or the evidence thread so they don't get lost in this thread, please? I might even get up from my computer and go to the library and read them.tom


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## ohnometo (Sep 20, 2001)

If the results speak for themselves on IBS and hypnosis why get so upset when someone shares that it didnt work for them







I should get a gallon of apple juice and a few mounds bars and bring lots of snacks with sodium benzonate and come to your house and stay with you about a week ! I am sure you would ask me Donna, isn't your week up yet







And again for what it is worth I do appreciate all information you share with everyone...







Defending HT is IBS on the bb here is not easy, but the results speak for themselves over and over again for anyone seriously researching it for IBS.


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## eric (Jul 8, 1999)

I have tried to help the fact it didn't work for him and have offered my assistance to further find out if it won't or if he was trying to hard or for whatever reason he may not have had success., for some it even takes twice, for you it may have been the one you did and not Mike's. Which is a much more involved program and much more gut specific to IBS and that can make a difference.You also helps to understand it is working on IBS and the why's because even that ,makes a difference.What I was defending is when people say it masks the symptoms or it does nothing for IBS physically, it does and its not masking the symptoms, its improving the brain gut communication and calming the brain gut axis for one, which is the enteric nervous system and the central nervous system communication.


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## eric (Jul 8, 1999)

Didn't I recently write a whole thread, which took me quite of bit of time, to help explain why these treatments help IBS??


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## eric (Jul 8, 1999)

FYIThe Fight or Flight in Irritable Bowel SyndromeOveractivation Linked To Predominance of Diarrhea SymptomsAn intense, powerful "fight-or-flight" response comes in handy when you're running away from a hungry tiger, but it could be the source of misery for people with certain digestive disorders.The chronic gastrointestinal distress of Irritable Bowel Syndrome IBS has been linked to "miscommunication" between the gut and the brain. Although it's still unclear just exactly how a glitch in gut-brain interaction sparks specific symptoms, a recent study has uncovered one important potential mechanism in a subgroup of patients.In patients with IBS who regularly experience diarrhea, pain, and other symptoms soon after eating, an "overdominant" sympathetic nervous system - signaled in part by the heightened release of the stress hormone cortisol after eating - may play a key role in triggering their symptoms. Researchers evaluated a group of 24 patients with IBS and a group of healthy controls, measuring their salivary cortisol levels, their heart rates, and their heart rate variabilities at different times of the day.Compared to the controls and to IBS patients with constipation, IBS patients with chronic food-induced diarrhea "demonstrated a significant increase in cortisol" soon after eating - with levels nearly doubling. This subset of patients also showed a more dominant sympathetic nervous system response, as evidenced by their heart rate variability ratios.The sympathetic nervous system tends to mobilize the body's stimulatory "fight-or-flight" response. Normally it's kept in check by the dampening effects of the parasympathetic nervous system. In patients with IBS with diarrhea, however, this muting response mediated by the vagus nerve appears weaker - a condition called "vagal withdrawal." "Notably, this vagal withdrawal was significantly associated with patients' reports of gastrointestinal symptoms," the researchers pointed out. These included bloating, abdominal pain, indigestion, and heartburn.A heightened, stimulatory stress response, characterized by overactivation of both the HPA-axis and sympathetic nervous system, may be triggered by "abnormal ascending feedback from the gut," the researchers speculated.Source: Elsenbruch S, Orr WC. Diarrhea- and constipation-predominant IBS patients differ in postprandial autonomic and cortisol responses Am J Gastroenterol 2001;96(2):460-466.


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## eric (Jul 8, 1999)

Donna, if you spent one week with me in person, you might completely view IBS differently.







That you have CVS also compounds the problem.Is the doctor giving you a transcript of what he is talking about with you at the IFFGD conference? I would be interested in seeing that if possible.


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## ohnometo (Sep 20, 2001)

I am hoping to get a transcript from Dr. Fleisher he is a wonderful person and I talk to him often. Eric, I can let you in on a little secret that you will see the words stress and anxiety in the transcript







and he does think on the same lines as you about stress !!! but he also said on my visit to missouri that that the dread of the next episode happening and knowing at one time there was no relief makes the tresh hold for the symptoms to intensify since I had no way out at that time and he will be more then happy to discuss my IBS and Cyclic Vomiting Syndrome with anyone who wants to call him...and I told him about the apple juice from the time I was 4 years old until now..I have my papers at home on my evaluation but I dont want to put them here on the board...but I do want to see some kind of information from the conference....See the information below says dietary and stress...Here is some food for thought...about Cyclic Vomiting SyndromeOf the 76% that can identify a trigger:47% psychological and 2/3rds of that group identify positive excitement asa trigger over negative stress. 31% infection 24% exhaustion 23% dietary22% menses (in mature females) 12% motion 6% Atopic (allergic reactions)Just in case you think he dont know about Gastro problems....and he knows Dr Drossman because I ask him...David R. Fleisher, MD David Fleisher was born in New York City in 1934 and qualified as a doctor at the State University of New York at Buffalo in 1961. After doing military service in the U.S. Navy, he became a Fellow in Pediatric Gastroenterology at the Childrenï¿½s Hospital in Philadelphia. He worked for many years in a number of hospitals in California, becoming Clinical Professor of Pediatrics at the University of California at Los Angeles between 1982. He moved to his present position as Associate Professor of Child Health and Director of the Division of Pediatric Gastroenterology at the University of Missouri School of Medicine in 1991. David Fleisher is a member of many professional organizations. He is a Primary Medical adviser of CVSA Canada/USA and together with Kathleen Adams and Dr. B Li, was a prime mover in getting CVSA established in 1993. He belongs to the Functional Brain Gut Research Group and is a member of the Working Team for the creation of diagnostic standards for Paediatric Functional Bowel Disorders, better known as the ï¿½Rome Criteriaï¿½. Among many honors he has received are the University of Buffalo School of Medicine ï¿½ Lamb Foundation Award: in recognition of the doctor-patient relationship and the University of California, Los Angeles Annual Paediatric House Staff Golden Apple Award, no less than five times, an award recognizing an exceptional teacher.


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## eric (Jul 8, 1999)

Donna, I know they don't understand that condition well.I am not sure, but those things you posted are probbaly triggers yes?On this,"the dread of the next episode happening and knowing at one time there was no relief makes the tresh hold for the symptoms to intensify "This is something in IBS big time also and something I have been trying to explain in IBS.Dread is fear is stress on the body, its a THREAT to the oragnisms bottom line and if you read the new march issue of discover magazine, on the cover story, can the brain conquer fear, then you will see how fast it happens without our conciously being aware of it and it can hapen day in day out for years and this throughs the sytems out of whack and then they don't function right and it becomes embedded in the brain and memory, so its easier and easier for the neuropathwways to take that route, like a stream deepening and becoming a river and also the memory of the past attacks which your brain remembers-even past events where a food set off your IBS- and calls up chemicals when there is a threat to the individual, this is all very important to IBS, and why I am posting information on the brain in a gut disorder IBS, which is a brain gut dysregulation, with the problem in the gut first. Why these things need to be address for everyone's information, not just food reactions! That's why its important to understand the underlying malfunctions in IBS. If you have d already, then d from foods is just a compounding issue or trigger.Emotions which are also connected to serotonin and pain and symptoms make a huge difference in IBS and the fight or flight and the immune system is all part of this without a pathogen.I would be interested in seeing it when you get it, if you want to show it to me.Carl, I also didn't mean to be to rough on you, so I applogize, this is just hard to post all this while people are yelling at you or arguing with the real experts, like DR Drossman, perhaps the most knowledgable person in the world on IBS and someone who gets help from around the world. Come to a UNC chat and ask away about anything, they are REAL experts on all this and can answer your questions, they are also really nice and can say things in layman terms so they are easier to understand about it all and take the time because they care like I do. I want people to have the big picture then they can decide for themselves. They may go hey I don't have IBS I have fructose malabsorbtionn or celiac, or they may go yes I have IBS and this fits what I am feeling based on my education on the problem.


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## eric (Jul 8, 1999)

Just a note, positve stress can exapperate IBS just as much as negative stress, but really this is so deep it would blow your mind really. Stress is to broad a term and turns people off, its emotions.


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## eric (Jul 8, 1999)

In a way the gut brain does a kind of thinking for you so it does not burden your conciousness and for a lot of other reasons that are very deep.Read that march discover issue.Most people have had gut feelings about something or another, and there is truth to that.


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## vogue777 (Jan 23, 2002)

Eric,Not to be a major downer or anything... but no one here is a doctor, and if they are, they are not actively researching IBS, afaik.So, while massive amounts of information are interesting, why post it daily? I mean, getting closer to the exact cause settles the mind, but these are not useful to anyone here, in a real way. Not until something is developed to take advantage of this information. Even then, knowing the mechanism doesn't improve the effectiveness of a drug.Knowing the mechanism does not improve any of our lives... afaik. I'm just curious as to what the debate is over, I think we need a static place on the board for your and MNL, and anyone else who has done substantial, concrete research in a field to post their information. What does the daily back and forth on the board help?


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## ohnometo (Sep 20, 2001)

I will get the magazine...I have been told by someone that my IBS is a trigger and that sets off my CVS caused by anxiety attacks and dietary...but I hate to say this I still don't believe it is about the anxiety attacks for me...anyway, if I was to ever get sick again here is the plan to stop the episode and I have a paper to just go to the ER and I have to be there one hour after the episode starts...This is alot of medication but here it is : Start IV 50 mg of Zantac, 24 mg. of Zofran and 2 mg of Ativan...If that dont stop the symptoms within one hour they are to add benadryl and thorazine to promote sleep. Sleep works on some part of the brain that produces nausea..For sure I hate the word thorazine !!!but I hope I never have to use this paper and I know I am never going to drink apple juice







but that is how they try to stop the episodes once they start...


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## trbell (Nov 1, 2000)

I agree vogue. I'm getting old and i get lost in these long threads. I tried to separate the information into the evidence and the opinions but apparentl;y that offended eric or he doesn't think there's much real evidence. i know he's put a lot of work in collecting information and don't mind if those threads have his name on them.i don't know what else to suggest that would be helpful for others. I've suggested that he and Mike have an experts go at it over some actual research article rather than just throw refences at each other.speaking of which I am curious about Mike's question to eric about a better book on the immune function than Brostoff's?I missed the answer in the flurry.tom


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## Mike NoLomotil (Jun 6, 2000)

BBQ:Not a marker per se, but the history they give, and physical symptoms they describe. There is a pattern of symptoms, starting with the bowel changes with a core symptom set whic evolves from the episodic diarrhea with or without ï¿½constipationï¿½ cycling, which is the first red flag of food or additive provoked symptoms. The reactions involved cause the release of mediators (leukotrienes cytokines, prostaglandins etc) which are associated with a classic immunoprotective response of the gutï¿½also the more prevalent the extra-intestinal symptoms as well (constitutional symptoms) then the higher the probability keeps rising when evaluating the persons presentation that there are one or more food or chemical elicited mechanism at work contributing to the symptoms. There is also a set of symptoms which can and do accompany their bowel symptoms which are also directly linked to the biochemical affects of variosu mediators on everthing from peripheral blood vessels and nerves up to and including some medtaors which penetrate the blod-brain barrier and can affect specific areas of the brain. foe example before an epsiode many people perceive such thigns as hot-cold flashes or clamminess, slight dizziness, cognitive affects (sometimes called "fog brain"), chills, mils muscle pain, even more pronounced things like nausea.So it s a picture or presentationï¿½and if other pathology which could also account for the symptoms is reported to have been ruled out by differential diagnosis already that raises the probability higher. This is why food allergy and intolerance are evaluated by multiple symptom assessment in context with history and physical presentationï¿½and the more dietary-symptom history you have the better. from that, you can selct te peson who has a high probability of tesing positive for cell mediated reactions or other mechanisms and whos thus can successfully have a patient-specific dietary plan constructed for them rather thn having to go through the massive guesswork and frustration mnay experience trying to figure out which of all the various possible dietary non-nos are THEIR no-nos.







Also this minimizes th chance of a patient or their insurance plan needlessly investing in any testing which will come back negative. Why pay for a screening assay if you can prescreen out the negatives and save people money?the whole point of disease management in modern medicine is to1. improve outcomes2. reduce overall cost.Since the cost per annum of IBS patients care has been reported to be even higher than annual care for asthma (ons study I recall reported ove $7,500 as the per annum cost of care for the average IBS patient)getting the cost down and the remisison rate up is the objective. So ruling out testing for people you know will not likely need it is all part of a proper patient selection process.While there are patients with such conditions as chrocnic functional abdmonal pain or cos called constipation-predominant IBS who may demonstrate a limited spectrum of chemical or food intolerance if evaluated the probbality is much lower and the benefit of addressing it is much less in the overall clinical outcomes.Just like assessing someone who is short of breath for airway-obstruction reversibility, so called IBS presentation can be assessed for probbaility of symptomatic reversibility by specific symptoms a person presents with, Thatï¿½s all.OH FOR DONNA MY DEAR:







What's really funny, and would really make a lively discussion, is how cytokine induction from these types of reactions (which can be chronically invoked a number of ways, as you know personally) results in behavioral changes up to and including excessive anxiety, stress, even depression and the other psychosocial consequences seen in IBS. That is, any primary dysfunction which results in chronic release of certain proinflmmatory mediators, including those seen in loss of oral tolerance, can lead to a sequence of biochemical events which, can result in depressed people with other cognitive and affective behavioral dysfunction as well. This happens just as surely as a model of a patient wherein psychosocial events and chronic stress can elicit a sequence of biochemical events which can result in (among othe things) loss of tolerance and a sick belly et al!But that's a chicken-egg discussion which often cannot be resolved with means available to us yet. We can quantify what is happening, but as yet do not have a means to clearly trace it back to which event led to the present condition...pathogenesis. So that lively debate I will leave for another place and time...cytokine induced cognitive and affective changes...HPA and CNS activation...all that stuff which can happen in both directions to make the IBS victim what she is...Suffice it to say that your case, from all the we saw of it, was very likely a primary pathogenesis which is traced back to the various multimechanism immune dysfunctions you suffer from, and the other symptoms were consequences of living with the pain and suffering all those years...not to mention the effects of some of thsoe chemicals on your nervous system. A doctor who knew your case in total would likely interpet it that way.At least you don't have to know for sure enough to swear to a jury to be able get rid of the major symptoms!







Anyways, Makee sense BBQ and Donna?














MNL


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## Guest (Mar 5, 2003)

Hi again everyone,Just what would a debate thread be without me anyway???







Mike... I sent you an email that I received your files and I successfully downloaded them and will spend some time reading them later this evening.Eric... as you know... I have achieved significant relief utilizing the self-hypnotherapy in terms of improving on the D and C. I still have a few issues, however, such as the gas and bloating which are still with me and so for my own benefit I need to look into what Mike is offering as well.Carl... Hi.... we haven't met yet I don't think... unless you're the one who sent me the nasty email but didn't identify himself.... hope you're not that person... but in any event... I still stand behind the information that Eric is providing us here. Keep in mind that he does this all on his own time... he receives no remuneration for it. He also sincerely cares about the people here who suffer with IBS.Eric, you are also correct that POSITIVE stress can also aggravate IBS in major ways... just the same as negative stress. A very good point.I think the ticket is in treatment/therapy integration. We're all different and we all have individual needs. My needs include behavioral health management... not everyone falls into that category.... but research now suggests that many also do. So I guess I wouldn't get upset if someone suggests there is a connection between brain #1 and brain #2 (the gut). Keep in mind that while sometimes behavioral health issues can aggravate IBS.... often the converse is true.... IBS can aggravate behavioral health issues as well.And I am just one very complicated mess... so I am looking to any and all treatments/therapies that offer a bit of hope.Mike... I will comment on the files you sent me after I've had a chance to peruse them in detail. Thanks again.Oh... and Donna... thanks for that hormone clarification....







And Tom... I am with you all the way on the bellylaugh....... helps every time... doesn't it?







Be well, everyone,Evie


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## eric (Jul 8, 1999)

UCLA Patient learning seriesIrritable Bowel Syndrome IBSWhat is it?Irritable Bowel Syndrome IBS is a chronic clinical problem which includes a combination of abdominal pain and altered bowel habits. Patients may also suffer from a range of associated problems such as the feeling of incomplete emptying of the bowel, peculiar shape of their stool, discharge of mucus, the sensation of bloating, excessive gas, and abdominal distension.IBS can manifest itself in different degrees of severity. In its most devastating form, symptoms are longstanding, incapacitating, nearly constant, and have little correlation with food intake or bowel movement. In its milder form, symptoms may have flared only within the last few years and are closely related to food intake or bowel movement. Regardless of its severity, IBS is a chronic, frequently lifelong disease.Who may be affected?IBS is an extremely common problem, affecting as many as 40 million Americans. Sufferers of IBS make up almost half the patients seen by gastroenterologists bowel specialists. Interestingly, about 8 million more Americans experience similar, less severe symptoms that do not interfere with their lives or prompt them to see a doctor.What causes it?It has long been thought that spasms of the colon or psychiatric factors were the cause of this syndrome. Even though such factors may be associated with IBS in certain patients, they don't seem to play a major role in causing IBS in the first place.In the past few years, scientists have identified a specific abnormality in the sigmoid colon and rectum that can explain most of the symptoms of IBS such as bloating, gas, fullness, or constipation.This abnormality is an increased sensitivity of sensors within the bowel wall. This internal hypersensitivity is comparable to what occurs when you have a sunburn; the slightest touch or even breeze can be painful while unburned skin will hardly feel the same stimulus. For someone with the hypersensitivity, normal contraction and expansion of the rectum or colon can result in intense sensations. It therefore appears that most of the symptoms of IBS are due to an excessive perception of internal sensations.Frequently, other symptoms of hyper-sensitivity are associated with IBS. A patient may experience headaches, lower back pain, or pain during intercourse. This may be related to the fact that whatever mechanisms cause the hypersensitivity in the colon can also have the same effect on other parts of the body.Why this hypersensitivity develops is not yet understood. There may be genetic factors that make an individual susceptible to this problem. However, once someone is susceptible, factors in that person's environment become the most important triggers and aggravating forces.What affects the problem?Even just drinking water can cause bloating in some patients. For others, specific food items may cause or be related to distension of the stomach. Spices, milk products, artificial sweeteners, acids, and fats all interact with the same nerve receptors in the gut that are affected by IBS.Unresolved emotional problems, interrupted sleep patterns, grieving, depression, and anxiety can also trigger symptoms. So can situations an individual may perceive consciously or unconsciously as stressful. Most often, symptoms are triggered by a combination of factors.What can be done?IBS cannot be cured, but it can be controlled in many cases. While scientists try to discover the causes of hypersensitivity and develop more effective medications, the goal of treatment is to reduce the severity of symptoms to a level where they do not interfere with the person's lifestyle.The first step is seeing a physician who can rule out other treatable conditions and establish a firm diagnosis of IBS. Some physical abnormalities can be corrected with surgery, while medications can relieve some diarrhea, constipation, and pain.For most IBS patients, the gastroenterologist will identify specific triggers dietary, behavioral, or psychological so that a "custom-tailored" treatment can be planned. Therapies may include medications, relaxation training, short- term psychotherapy, acupuncture, and dietary counseling. Usually a combination of therapies is most effective.In general, a good response to treatment is more likely when symptoms are related to specific dietary or behavioral triggers, when onset or worsening of the problem is relatively recent, and when the patient accepts the special nature of the disease.What can I do? * Should problems develop, seek a thorough evaluation and counseling from a physician familiar with the variety of causes and treatments for bowel disorders, such as a gastroenterologist. * Keeping a diary of foods eaten or circumstances that worsen the problem can help provide information to your physician.* And, since the problem is largely one of hypersensitivity, cooperate with your physician to understand your problem and follow recommendations.Related Article* UCLA Healthcare Vital Signs Hypersensitivity of the Bowel http://www.healthcare.ucla.edu/pls/ibs.htm UCLA/CURE NDP for IBS and Functional GI Disorders - UCLA/CURE Neuroenteric Disease Program is now part of the new UCLA CNS: Center for Neurovisceral Sciences & Women's Health! http://www.med.ucla.edu/ndp/NwsltrIndex.htm


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## vogue777 (Jan 23, 2002)

Let me rephrase my original post...I think certain members... need SEPARATE... STATIC places on the board to post their research. Because seriously... you post an article every day... it's gone off the front page in a week or less... and back you go.. post back and forth, until people like me just ignore your posts. And I sure as hell am not going to go back X months to read something... you guys need a static place... post your stuff... don't argue about it, just post it. Then come back to providing concrete, applicable information to people on the board.How about that? Worthy of a response this time?







(thank you for your acknowledgement Tom.)


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## trbell (Nov 1, 2000)

i don't really see how this is news, eric. you are confusing me. This is what the first doctor you diagnosed me 10 years ago said. "You have a sensitive gut" That's what a psychosomatic condition is?tom


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## ohnometo (Sep 20, 2001)

MikeAfter reading your post and thinking on the way to work this morning that I have never got one fever blister in over a year and I was getting those things every week all my life it seemed like and also my legs use to ache really bad before an attack would happen and that has never happened one time...Oh My God ! I am so glad that I dont live in all that fear today . I know that I could not have keep living like that







There was no way !!!! I still work on my fears and anxiety ever day because that was the way I lived for many years and sometimes it is easier for me to fall back in old patterns that is comfortable that I lived with for along time....


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## BQ (May 22, 2000)

Yes Mike, makes sense to me. I knew there had to be some sort of markers that would peak your concern about a person's potential to be suffering from intolerances rather than or in addition to, IBS or other stuff. The fact that these markers, however subtle or not, have been indentified is a major plus.When I re-read some of Donna's symptoms, I see that some of them are a bit off of the IBS symptom's beaten track. (And I'm glad Donna has found such relief.







)There is no question this is a subtle business of looking at the whole of a person's symptomatology & history. Some of the symptoms even seem to be not GI related, so may not come to a Doc's attention. Especially if they never become associated with the GI symptoms in a patient's mind. It almost seems like one of those lengthy new patient surveys that lists: "Have you or someone in your immed. family ever experienced diabetes, heart disease...(other big ticket diseases) should be expanded to include other more subtle symptoms. I mean, knowing a person's disease background is critical for a Doc. However I think they either should do a separate "Symptom History" or include it with the "disease history". I know I didn't fill out ANY patient survey when I was referred to a GI specialist. And, after the diagnostics, I got the "You have IBS-D. Vegetables contain fiber, so don't eat them." Well, that was productive.








In my case, there weren't many other symptoms, aside from upper ab pain, which I was in denial about at the time, LOL. Anyhoo....But I'm not everyone and surely a GI could benefit from at least giving a cursory glance at a person's symptom history. I think this kind of survey may allow a Doc to maybe take a different investigative approach and make, perhaps, a better, more accurate diagnosis. Well, my two cents...anyway. And may I say, I live in hope of someday, perhaps, coming even close to your run-on sentence construction talents.







Thanks Mike.BQ


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## Mike NoLomotil (Jun 6, 2000)

This opens an interesting topic which is not discussed enough in this forum of sick peopleï¿½and should be discussed more openly for patients to understand how to approach the medical literature overallï¿½and the ï¿½IBS literatureï¿½ in particular:_____________________ï¿½This abnormality is an increased sensitivity of sensors within the bowel wall. This internal hypersensitivity is comparable to what occurs when you have a sunburn; the slightest touch or even breeze can be painful while unburned skin will hardly feel the same stimulus. For someone with the hypersensitivity, normal contraction and expansion of the rectum or colon can result in intense sensations. It therefore appears that most of the symptoms of IBS are due to an excessive perception of internal sensations.ï¿½_______________________Two things are key in such intriguing discussions as this.Number one is that there is a hierarchy of possible mechanisms by which the observed upregulation of the various sensors (pressure, distention, pain, motorï¿½.) as well as many of the other physical phenomena observed when studying ï¿½IBS SUBJECTSï¿½ can occur. A biochemical hierarchy which leads back to multiple possible mechanisms. It remains to be elucidated whether there is one particular hierarchy which is ï¿½theï¿½ causal basisï¿½or linked to ï¿½theï¿½ pathogenesisï¿½or is it more than oneï¿½or does it vary from one subpopulation (as defined by symptom sets) to another.Number two I just led up toï¿½.patient selection for a given study.Much is made of findings from study A, or study B or C or D etc, but there is often not a consistent subject selection criterion applied. So not only are the findings in each study based upon limited parameters (not all the possible mechanisms which could lead to the observed event have been investigated at the same timeï¿½) but the patient selection varies from group to group when you try to assemble and integrate the findings from study A with B,C, D etc.This fact, combined with the tendency of investigators to set forth their interpretation of their findings within the spectrum of the parameters they applied to the patients they selected their own way AND in the context of either their area of specialization (inherent bias level one) and/or the theory they have set out to ï¿½proveï¿½ concerning what they believe so called IBS to be, makes it exceedingly difficult for even the most seasoned and expert investigator to make any definitive claims as of yet regarding causal basis of IBS or subgroups. So everything we read and study and consider must always be both integrated with other findings, BUT qualified by an understanding of the limitations I just explained so as to not jump too far beyond supposition or speculation when looking at study data or groups of study data.Especially in the context of IBS investigations, as with other syndromes in the early stages of understanding, if we torture the data enough we can make it say whatever we want. So people across the board, including not only lay people in environments like this, but those who are considered opinion leaders, need exercise a bit of restraint when ï¿½laying down the law about what IBS isï¿½. If you read what they say and how they say it, carefully, you will see that most do exercise this restraint. Some, in their enthusiasm over their findings or enthusiasm over wanting to be the one with ï¿½the big breakthroughï¿½ lose a bit of that restraint from time to time.As we see here, the author is careful to qualify his statementsï¿½.______________________________ï¿½Why this hypersensitivity develops is not yet understood.ï¿½______________________________And then goes on as most do with one or more postulatesï¿½______________________ï¿½There may beï¿½.ï¿½ Etc._______________________As science knows, there are many possibilities for the observed changes in sensitivity (upregulation) of all manner of nerves and the smooth muscle itself in some instances.One intriguing one, just as an example, from Sahlgrens Medical Universityï¿½s allergy center, where the allergists, immunologists, gastroenterologists, pathologists, the whole team have been doing for about 8 years now a unique type of invasive investigation into the immune function of the GI tract of people who have symptoms that would be diagnosed as IBS by the Rome criteria and who have had allergy ruled outï¿½._______________________ï¿½ï¿½we can show an allergy-like inflammation during [double blind placebo controlled direct food] challenges with parameters like Il-4, IFN-gamma, CD3, CD4, CD8 and IgE.ï¿½_______________________See, these patients, whose symptoms of IBS are provoked by food challenges and who have NO FOOD ALLERGY, IBD, or any other pathology, have quantifiable multi-cell-type reactions beginning within the small bowel after they eat and food is presented to the gut immune system for identification. The immune system misdidentifies it as ï¿½not safeï¿½ and they show lymphocyte activation and even mast cell activation (interleukins and inteferons such as those are released from the lymphocytyes found and reported by others accumulating in the myenteric plexus even at the root ganglia of the nerves in question)ï¿½CD[x] are classifications of specific T lymphocyte antigen receptors (they sort of resemble immunoglobulins and sort of serve a similar purpose). These patients have these chemicals and many other appear within the lumen of the small bowel and the plasma after provocationï¿½and of course if you do not present to provoking food they do not appear and the symptoms do not appear.Now what has happened, and these investigators of course are careful to separate what you have from what you theorize, is that they have quantified what would be termed an ï¿½food allergy likeï¿½ cascade of mediator release of mediators which will cause many of the other events that have been quantified by other investigators in their subjects but who did not use this procedure at the same time they did what they did.So you have another ï¿½possibilityï¿½. They have quantified an event which can account for what other events have been seenï¿½but no one knows why this happens. Why are the lymphocytes responding to safe substances in these subjects (whose doctors are diagnosing them correctly based on current standards) with IBS since there is no ï¿½jejunal isolation and challengeï¿½ specified in the differential diagnosis for IBS. Why is there antigen specific IgE apparently arming gut mast cells when there is NONE in the bloodstream. Hey, and even weirder, why doe some asymptomoatic people the controls) also sometimes have antigen specific IgE in their bowels but not in the blood streamï¿½and why do some become ï¿½activatedï¿½ or provocable and some not?From there postulates and theory and supposition begin from the perspective of, and specialty are of, those investigators.Hopefully this makes an very important point s I set forth aboveï¿½there is a large gulf that sepaates multiple specialists doing multiple investigations with multiple strategies from multiple perspectives upon multiple subjects selected by various criteria but all seemingly (supposedly) suffering so called ï¿½IBSï¿½.So each has to ultimately be done collectively at the same time on the same patients to even find the freakinï¿½ starting point of the PATHOGENESIS of IBS and the subpopulations. From there maybe science can construct a model upon which to test their integrated postulates of how normal people come to act in this terribly abnormal manner so as to be able to avoid the whle thing or things at its origins.Regardless of what anyone may claim, science is not even close to that end game yet.DONNA:Funny things happen when certain systemic immune activation occurs and remains ongoingï¿½.you mentioned fever blistersï¿½we know the virus involved and, well, before I was able to get on a pan that kept me form ingesting things which cause aberrant reactions and symptoms I had several painful ï¿½shinglesï¿½ emergences over the years. I have never had an episode again since I got into my remission from constant IBS symptoms.OH yeah arthralgic pain (muscle pain) os one of those things that is reported as an extraintestinal symptom in some patients who are confirmed to suffer immunocyte-ralted food intolerance reactions. If we went into the details of which cells contain what chemicals and if they are released in which ï¿½compartmentï¿½ they will result in ï¿½:these actions and thus symptomsï¿½ we be here all day, but that is why 100 doctors and dieticisn wrote a new book all about all the different and varyin aspects of the subject for doctors to refer to.FOOD ALLERGY AND INTOLERANCE, Professor Jonathan Brostoff, MD, Stephen Challacombe, MD (NEW 2002) http://www.amazon.com/exec/obidos/ASIN/070...product-details ï¿½	Hardcover: 1120 pages ï¿½	Publisher: W B Saunders Co; ISBN: 0702020389; 2nd edition (August 9, 2002) Too bad it ainï¿½t cheepï¿½but then again it is intended fro doctorsï¿½who have by nature a higher specific-purchasing capacity than the rest of us!MNL


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## eric (Jul 8, 1999)

They know that serotonin is involed in this also and is used to talk to the brain, they know the signal is not going to the right place in the brain the ACC is underactivated -pain-and this would normally releases endorphines back to the gut so people don't feel anything, but instead the nerve signal goes to the prefrontaal cortex and "turns up the volume so to speak" of anxiety and emotions.Since that last one was written the same person, who is an expert neurogastroneterologist studying IBS has written this."Brain Imaging: CNS Abnormalities in Patients with IBSThe lack of a clearcut pathophysiology and an often noted association between physical and psychological symptoms has led some clinicians to dismiss irritable bowel syndrome (IBS) as a condition that is "all in their head." However recent findings showing CNS abnormalities in patients with IBS may offer a new perspective on the etiology of this debilitating condition, characterized by abdominal discomfort and pain and altered bowel habits. Until recently, the presence and severity of IBS were measured only by gut function and the subjective perceptions of the patient. "Now, the use of functional brain imaging techniques is contributing to an increased under- standing of the pathophysiology of this disease and new target areas for treatment," said Emeran A. Mayer, MD, Professor of Medicine, Physiology, and Biobehavioral Sciences, and Director of the CURE Neuroenteric Disease Program at the University of California, Los Angeles.Pathophysiology of IBSIBS is a disease that develops as the result of an abnormally altered brain-gut interaction Table 1. One manifestation of this alteration consists of aberrant output patterns of the emotional motor system, a part of the limbic system in the brain, in response to external psychosocial or internal immune, nutrient stressors. Outputs from the limbic system in the form of autonomic, pain modulatory, and neuroendocrine responses can be modu- lated by cognitive factors, such as the beliefs, thoughts, and emotions of the patient. Aberrant output of the emotional motor system in large part accounts for the constellation of symptoms that makes up IBS. "A hyperresponsiveness of circuits in the brain may be one common link to both the abnormal responses to internal inflammatory stressors and external psychosocial stressors," Dr. Mayer explained. Treatment is chosen with consideration of altered motility, visceral hypersensitivity, and the brain's role in modulating these factors.The autonomic regulatory systems affect not only muscle cells in the gut, but also other cell types, such as mast cells, enterochromaffin cells, and nerve cells of the enteric nervous system. Responses of some of these cells to autonomic modulation, for example in the form of tryptase secretion by mast cells or serotonin secretion by enterochromaffin cells, may play a role in the modulation of visceral afferent sensitivity. According to Dr. Mayer, such mechanisms may play a role in the development of stress-induced visceral hyperalgesia. Another form of visceral hypersensitivity may be related to altered arousal or hypervigilance toward visceral sensations. Such hypervigilance can result in decreased tolerance to balloon distension and lower discomfort thresholds. A cognitive factor involved in the development of hypervigilance is an increased threat appraisal of visceral sensations.Functional Brain Imaging TechniquesRecently, functional brain imaging techniques have been used to assess directly the activation of certain regions of the brain in response to visceral stimulation. Today, these techniques, particularly functional magnetic resonance imaging, are being used to assess activation of brain circuits that process visceral afferent information from the gut.Dr. Mayer noted that there are distinct but overlapping brain circuits that relate to subjective perception of gut sensations, autonomic responses, and pain modulatory responses. Even in terms of subjective gut sensations, different overlapping circuits are present for intensity coding of the stimulus; threat appraisal of the stimulus; and attribution of primary affect, or "unpleasantness".Both serial and parallel pathways are involved in the processing of visceral sensory information and the control of descending modulatory systems. Input from the gut is derived from multiple channels, such as spinothalamic, vagal, and dorsal column pathways; different regions of the brain then code for intensity, appraise the threat of the stimulus, and determine the level of attention the brain attributes to the stimulus and the unpleasantness the patient experiences. These processes are modulated both by the stress- or arousal- activated system and by recollection of past experiences.Intensity Coding, Threat Appraisal, and UnpleasantnessIntensity coding. As visceral sensory information is delivered via the spinal cord, it is encoded for intensity in the anterior aspects of the insula, or visceral sensory cortex. PET scan studies of somatic and visceral experimental pain have shown that the insula most objectively and reliably encodes information. Interestingly, studies have also demonstrated a greater activation of the insula in male IBS patients, compared with female patients, when exposed to the same stimulus intensity.Threat appraisal and unpleasantness. The information that reaches the insula is "appraised" in the dorsal aspects of the anterior cingulate cortex. Blood flow changes in this part of the brain may also correlate with attentional processes and the subjective unpleasantness ratings in response to a somatic stimulus. The ventral perigenual cingulate cortex, which is rich in muopioid receptors, functions to encode the affective quality of the stimulus.In a study by Mayer and colleagues, rectal and sigmoid distension resulted in a lower activation of the ventral anterior cingulate cortex in patients with IBS compared with healthy controls, but an increased activation of the dorsal aspects of the anterior cingulate. Increased activation of an unspecified region of the anterior cingulate was also reported by Mertz and colleagues, in a functional MRI study.Modulatory factors. Finally, the CNS processing of sensory experience may be simultaneously modulated by two parallel pathways: memory-based modulation and stress- or arousal-induced modulation. The posterior parietal cortex, or sensory association cortex, forms a network with the hippocampus and the amygdala the brain's memory centers as well as with the lateral prefrontal cortex. Somatic pain studies have shown that, in response to a stimulus, the recall of a similar past event, along with subsequent interpretation of this memory in the lateral prefrontal cortex, plays a major role in the threat appraisal of a sensory experience. The second modulatory effect is the stress- or arousal-induced response. The pontine locus ceruleus is activated in response to potentially threatening experiences. This region then projects to nearly all other regions of the brain that receive visceral input, causing secretions of norepinephrine and arousal of these sections of the brain. When the secretion of norepinephrine is excessive, these target regions are inhibited. It is of interest that descending projections from the locus coeruleus complex to the sacral spinal cord appear to play a major role in the modulation of distal colonic motor and secretory function.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. Table 1. Clinical Relevance of Altered Brain-Gut InteractionAltered attentional mechanisms o Greater awareness of normally subliminal visceral afferent stimuliAltered affective stimulus processing o Greater unpleasantness of visceral sensations, including heartburn, bloating, fullness, abdominal pain, incomplete rectal evacuationAltered threat appraisal o Leads to fears such as not being close enough to a bathroom anything eaten may trigger abdominal painEnhanced arousal o Shared by clinical conditions frequently overlapping IBS, such as anxiety, panic disorder and PTSD o Arousal reduced by sedatives, anxiolytics, low-dose tricyclics o May respond to relaxation exercises http://www.macmcm.com/pcp/pcp2000_01.htm


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## PatSimp89 (Feb 26, 2003)

Mike,I have been reading your information and I would like to say thank you for posting it. I sort of knew what was happening to me a long time ago, and I have been successful at treating it by watching stress and most importantly avoiding the specific foods that casue such severe reactions in me like wheat, dairy, and yeast. However, no one has ever explained it in such detail.I can completely relate to the issues of serotonin. I used to take an antidepressant for 6 years, but the last 4 years i have been off of them. It seems that when i would eat a specific food that gave me all my cramping, D, C, pain and the other symptoms like fatigue ---- it seemed like that would also throw my serotonin levels off. I am convinced beyond a shadow of a doubt that foods were triggering my depression, anxiety and panic. I only get these symptoms when i eat the offending foods.I can personally vouch that serotonin is involved in this whole matter. For me, it is just a matter of getting my bowels to function correctly and then everything else settles down.


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## Carl_has_IBS (Feb 5, 2003)

> quote: That is, any primary dysfunction which results in chronic release of certain proinflmmatory mediators, including those seen in loss of oral tolerance, can lead to a sequence of biochemical events which, can result in depressed people with other cognitive and affective behavioral dysfunction as well. This happens just as surely as a model of a patient wherein psychosocial events and chronic stress can elicit a sequence of biochemical events which can result in (among othe things) loss of tolerance and a sick belly et al!


Now i understand it !!!!!!!!!!!!!!!!!!!!!!!!!It can work both ways!!!!!!!!!!!!!one patient can have tons and tons of stress and stressors dumped on her and eventually the body may break under that stress. whereas another patient may not have that much stress but instead may be reacting to foods like cow's milk and wheat from a very young age and eventually after 20 years of constant, non-stop aggravation (combined with some stressors) her body finally breaks primarily due to the food reactions.I FINALLY GET IT !!!!!!!!however, i think that the message that we keep getting from our doctors is the message that eric keeps feeding us. that is all well and good, but it has done very little to really get to the bottom of my problems. What has really helped me is pinpointing the "offending" foods. Eric, even though you admit that foods are a trigger -- you seem to downplay their role. I think that you over-rely on your sources such as UNC and the rest. I think that you could be one of the best sources of information that we have if you just expanded your approach. your approach is leaving too many of us outside of what you consider to be "IBS". You or Dr. drossman never even attempt to explain what causes the gut - brain dysregulation. neither do you attempt to give a credible explanation as to why there is such a disturbed serotonin problem. however, i think there is enough evidence from the other camp -- Brostoff-- that these issues clear up once the offending foods are located. don't you see that this kind of proves that they get to the heart of the matter whereas your approach fails far too many people. but don't get me wrong -- i still think that there is a very strong need for treatments like CBT, HT, and accupressure. in fact some people can actually get healed by these methods alone.bye


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