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Research on hypnotherapy with regard to IBS is practically amazing, improvements seen in 80%+ persons. At the same time, there are number of interesting observations. We know that the results of placebos themselves are amazing for IBS. That makes drug studies hard because it is hard to beat the sugar pill for treating it. So does this imply hypnosis is a potent placebo (whatever that really is)?Interestingly the more severe the IBS, the better it seems to respond to hypnotherapy. What exactly is meant by "severe" is not defined in the studies. Most IBSers have very mild symptoms to the point where they don't consider their "condition" to be abnormal. Some researchers seem to think that those severely affected only have modestly more severe symptoms that are being misinterpreted at a higher level to be much more severe and that hypnosis is helping with this (i.e, coping).At the time, people under hypnosis (whatever that really is) can alter their autonomic functions remarkably, probably to the point of slowing one's heart rate to the point of fainting.The gut is a bit different since it has its own nervous system that can turn off input from the brain and many researchers don't believe the gut is acting abnormally in IBS to begin with. However, they do believe it is telling the brain the wrong thing and that does go through autonomic pathways, so it is quite reasonable to believe hypnosis is altering these pathways along with coping behavior.
 

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Fascinating, subtle points. Finepoints, really. I never really understood most of this, i.e., the point that many researchers don't believe the gut is acting abnormally in IBS -- but that it may be telling the brain the "wrong" thing...and thus "altering the autonomic pathways along with coping behavior." I knew that there was a disconnect between the brain and the gut, but not how it happened. This is not easy to understand; it's quite complex. But it certainly makes a good argument against certain trained individuals who have told me that "any activity in which you get lost in or 'achieve a flow' would achieve the same -- there's nothing any more special about hypnosis."[This message has been edited by Persistance (edited 02-25-2000).]
 
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Discussion Starter · #9 ·
Flux: let me preface this by saying that i'm not being sarcastic - i'm sincerely interested. (sheesh! i feel like i have to be so defensive now)~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~The gut is a bit different since it has its own nervous system that can turn off input from the brain and many researchers don't believe the gut is acting abnormally in IBS to begin with. However, they do believe it is telling the brain the wrong thing and that does go through autonomic pathways, so it is quite reasonable to believe hypnosis is altering these pathways along with coping behavior.~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~are you hypothesizing that when i have a pain im my gut, it's not really hurting - it's acting normally, but it's telling my brain that it's hurting for some reason and therefore i feel pain? i find this a fascinating theory - if i'm understanding you correctly. it could explain sooooooo much! Would you please expand on this?
 

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Put - you don't have to worry about sounding defensive. We all have a right to our opinions.I don't want to put words in flux's "fingers," but I don't think he is saying that your gut really isn't hurting. He's saying that the nervous system is getting all confused. For example, phantom limb pain is VERY real, but the limb isn't there. But the brain senses and interprets that the limb is there - actually, the nerve ending from the amputated limb is sending an impulse to the brain, saying that the nerve from the limb is hurting, even though it isnt' there. (Am I making this more confusing?)Sounds like there may be some of that type of impulse mix-up here.... I too, find the hypnotherapy results interesting. I have used some self-hypnosis myself in pain situations (actually, that's what Lamaze really is, which I use when the cramps are really bad, and I do the dentist thing without novicain by using self-hypnosis)This is interesting info....------------------"Society honors its living conformists and its dead troublemakers." (Mignon McLaughlin)[This message has been edited by Lefty (edited 02-25-2000).]
 

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quote:are you hypothesizing that when i have a pain im my gut, it's not really hurting - it's acting normally, but it's telling my brain that it's hurting for some reason and therefore i feel pain?
This is pretty much right. Nerves in the gut and along the brain-gut axis send pain signals to the brain when they should not be. These pain signals are real signals. The gut also responds inappropriately (hence D and/or C).
quote:But the brain senses and interprets that the limb is there - actually, the nerve ending from the amputated limb is sending an impulse to the brain, saying that the nerve from the limb is hurting,
I think it is the opposite. Nerves in the limbs have a "heartbeat" and that goes away with no limb to produce it. So the brain becomes sort of confused by the lack of the hearbeat, and somehow generates pain.
 

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I can accept that this theory MIGHT have some validity regarding pain. (At any rate, I can't think of an argument to disprove it.) But what about those of us who don't experience pain as a significant part of our IBS symptoms? What pain I experience is immediately relieved by having a BM. Rather, my major IBS complaint is urgency (violent intestinal contractions), frequency (3-10 times a day) and consistency (watery D). Can this be possibly be normal?...Or explained as misinterpreted signals from the brain?
 
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Discussion Starter · #15 ·
Thanks Eric. i found some very interesting material there - and in the links i followed from there. but i'm still trying to make sense of the theory that Flux has put forth about the gut-brain/brain-gut signals. it seems to explain so much about my symptoms. my brain is responding correctly to incorrect signals from my gut, right? then the gut synapses are short-circuited somewhere. diet, meds, etc. arent going to solve the basic problem, only alleviate it temporarily. and autohypnosis is only a "bandaid". seems to me the solution would be to figure out how the gut got out of sync in the first place. i dont think it could be something as simple as an adverse reaction to antibiotics or "Montezuma's revenge". and if it's Candida Albicans, there are tests to show that. so how does the breakdown in communication happen (originate)? if we can find the answer to that, we could "begin at the beginning" to find a cure.
 

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Put, I hope you can make sense of this I would try to explain it but it would take mee a couple days. Advances in Basic Science Hold Promise for New Therapies in Gastrointestinal Dysmotility Eamonn M.M. Quigley, MD Introduction Symptoms and clinical syndromes associated with disturbances in gastrointestinal motor function continue to pose a major challenge for the clinician. These functional disorders remain poorly defined, are difficult to evaluate, and have proven particularly resistant to successful therapy. Indeed, therapy remains, for the most part, largely empiric and symptomatic. In contrast, there have been tremendous advances in the physiology, neuroanatomy, molecular biology, and pharmacology of gastrointestinal motor function. In a state-of-the-art lecture presented at the 7th United European Gastroenterology Week in Rome, Italy, Dr. Lionel Bueno from the Department of Pharmacology at the INRA Institute in Toulouse, France, described how these advances in basic science may translate into new therapeutic options for patients.[1] A Neurophysiologic Basis for Motility Therapeutics Professor Bueno introduced us to the broad concept of brain/gut communications as the template for any understanding of gut-motor dysfunction in disease. This relatively new concept, which has led some to propose that this entire field of effort should be referred to as "neuro-gastroenterology" rather than "motility," emphasizes the inclusion of all elements that may lead to gastrointestinal symptoms. These elements include the smooth muscle of the gut wall, the enteric and autonomic nervous systems, sensory receptors in the gut wall, afferent neurons, and those centers in the spinal cord and brain involved in the reception of stimuli from the gut and in the initiation or modulation of gut motor activity. In this manner, nerve-gut interactions may take place at any one of three levels -- in the central nervous system, at the prevertebral ganglia, and within the enteric nervous system. Professor Bueno subsequently discussed some experimental models of disease that have provided considerable insight into the pathophysiology and pharmacology of functional bowel disorders, namely altered intestinal reflexes, visceral hypersensitivity and hyperalgesia, immune-mediated gut/brain dysfunction, and abnormal central modulation. The models are not mutually exclusive; indeed, there is considerable evidence for extensive interaction between them. Abnormal Gut Reflexes in Functional Gastrointestinal Disease: A Basis for New Pharmacological Approaches? Evidence, primarily from animal models, but supported by some recent data in humans, suggests that dysfunction of gut reflexes may play a role in the pathogenesis of a variety of functional gastrointestinal disorders. The gastroesophageal reflex, initiated by gastric distention, mediated by a vagovagal pathway and leading to transient lower esophageal sphincter relaxation (TLESR), is now regarded as central to physiologic gastroesophageal reflux and gastroesophageal reflux disease (GERD). Nitric oxide (NO), cholecystokinin (CCK)A, and serotonin (5-HT)3 receptors have all been identified as being involved in either the afferent or efferent arms of this reflex. Indeed, the CCKA antagonist, devazepide, has been shown to inhibit TLESR. Given the prevalence of GERD, it is likely that the regulation of TLESR is going to be the subject of major interest in the coming years. Gastric emptying, tone, and motility are influenced by intestino- and duodeno-gastric reflexes, whose dysfunction has been proposed to play a role in the pathogenesis of symptoms in functional or nonulcer dyspepsia (FD and NUD, respectively). Receptors involved in this reflex include those for CCKA, dopamine (D)2, 5-HT1A, and gastrin-releasing peptide (GRP). A cologastric reflex can also modulate gastric motor function and has been proposed to play a role in both FD and irritable bowel syndrome (IBS). Opioid, substance P (SP), neurokinin (NK1), and peptide YY (PYY) receptors have been implicated in this reflex, and the kappa opioid agonist, fedotozine, has been shown to inhibit the cologastric reflex. Indeed, this drug has been investigated in clinical trials for a number of functional bowel disorders. The rectocolonic reflex has also been implicated in IBS, and has attracted considerable interest recently. Vasoactive intestinal peptide (VIP), SP1, NK1, NK3, and bradykinin (BK)2 receptors have been associated with this reflex, and NK1, NK3, CCKA, BK2 antagonists, calcium channel blockers, trimebutine, and alverine have all been shown to inhibit the rectocolonic reflex. While the role of the peritoneo-gastrointestinal reflex in functional disease is almost unknown, this reflex, whereby in experimental animals peritoneal stimulation leads to motor inhibition, has provided considerable insight into the pathophysiology of colonic ileus and the pharmacology of gut reflex activity. Receptor types involved in this reflex include NK1, BK2, calcitonin gene-related peptide (CGRP), and corticotropin-releasing factor (CRF)-R1. Experimentally, this reflex can be inhibited by CRF-R1 antagonists, kappa opioid agonists, cyclooxygenase (COX)-2 inhibitors, ICAM (intracellular adhesion molecules) antibodies, and mast cell stabilizers. Visceral Hypersensitivity and Hyperalgesia in Functional Gastrointestinal Disease The description of visceral hypersensitivity and hyperalgesia (the phenomenon whereby a previously nonpainful stimulus is now perceived as painful) in several functional gastrointestinal diseases, including noncardiac chest pain, FD, and IBS, has led to a flurry of activity in the areas of gut sensation and perception. While a whole host of receptors, neuropeptides, and neuromodulators is known to be involved at a variety of levels in the mediation of both normal sensation and hyperalgesia, a few have attracted particular interest in view of either their ubiquity and/or apparent key roles. For most visceral sensations, the first-order neuron (primary sensory afferent) synapses with the second-order neuron in the dorsal horn of the spinal cord, which in turn project, thereafter, to the various centers in the brain. Serotonin appears to play a key role. Both 5HT3 and 5HT1A receptor subtypes are involved at different sites in the mediation of gut nociception and several antagonists are currently undergoing study -- some may soon reach the clinical arena. Opioids acting as mu, gamma, and kappa receptors appear to be involved at the peripheral receptor in primary afferents and in dorsal root ganglia, as well as in the spinal cord and the central nervous system. Substance P and NKA also appear to be involved at a number of levels, whereas CGRP has been localized to primary sensory afferents. Professor Bueno placed considerable emphasis on gut hyperalgesia and, in particular, on the role of inflammatory mediators in sensitizing primary afferent neurons. A variety of experimental models have demonstrated that inflammatory mediators will lead to the development of pain in response to a level of gut distention that previously did not elicit this sensation. Several peptides, including BK, CGRP, tachykinins, VIP, 5HT, adenosine, noradrenaline, eicosanoids (including prostaglandin (PG)E2, cytokines [interleukin {IL}-1, IL-8], tumor necrosis factor-alpha [TNF-alpha], and growth factors [nerve growth factor or NGF]), have all been shown to be involved in the sensitization process. A fascinating development has been the realization that such peripheral events can lead to both short- and long-term changes in neural activity in the spinal cord and central nervous system. For example, peripheral sensitization of sensory neurons may alter the membrane properties of the second-order neurons originating in the dorsal horn of the spinal cord through N-methyl-d-aspartate (NMDA) receptors, leading to long-lasting adaptation. SP, dynorphins, and glutamate may also be involved. Thyrotropin-releasing factor (TRF), vasopressin, CCK8, SP, IL-1, TNF-alpha, norepinephrine, dopamine, 5HT1A, and PGE2 have all been shown to modulate the central mediation of events initiated at peripheral sensitization. Motility-Immune Reactions The potential role of gut-immune interactions in the pathogenesis of functional gastrointestinal disorders is, perhaps, best illustrated by the phenomenon of the postinfective IBS. It is now evident that prior exposure to bacterial gastroenteritis may lead to the development of full-blown IBS in a proportion of exposed subjects. Such dysfunction may persist for months or even years after the infectious agent has completely cleared. This observation has stimulated intense interest in the potential interactions between inflammation, intestinal muscle, and the enteric, autonomic, and central nervous systems. Professor Bueno reviewed three animal-based models of disease that have provided considerable insight into these interactions: hypermastocytosis (related to experimental helminthic infestation), lipopolysaccharide-induced allodynia (a model of systemic sepsis), and peripheral inflammation. NK2 receptor antagonists appear to be active in each model, and the NK2 antagonists, SR 48968 and MEN 11420, have been shown to reduce the pain induced by visceral distention in hypermastocytosis models, such as the rat infected with Nippostrongylus brasiliensis, or in experimentally induced inflammation. BK1 and BK2 antagonists, as well as 5HT1A antagonists, such as WAY 100425, also have efficacy in the lipopolysaccharide-induced allodynia model. Serotonin, NK, and BK antagonists appear to hold particular promise for efficacy in the latter setting. Central Input It has been stressed repeatedly that many proposed mechanisms of abnormal nerve-gut responses may include alterations in neurotransmission at the level of the spinal cord and brain. There are other circumstances where gut-motor dysfunction appears to originate centrally. The clinician will immediately recognize the profound effects of stress, be it short- or long-term, on such motor functions as gastric emptying and small bowel transit. Indeed, animal studies and experiments in humans have demonstrated the ability of stimuli of central origin to modulate and disrupt a host of motor and sensory activities in the gastrointestinal tract. Similarly, central nervous system activity may modulate incoming signals from the periphery initiated by physiologic or pathologic events, including inflammation. Many of the receptors identified as active in the peripheral regulation of gut motor activity appear to be at least as important in central regulation. These receptors include 5HT, CRF, NK, CCK, and SP. Cytokines, such as IL-1 and TNF-alpha, also appear to be centrally active. It should come as no surprise, therefore, that the efficacy of some of the newer motility agents that are currently undergoing clinical evaluation may be exerted, at least in part, through effects on the central nervous system. For example, the 5HT4 agonist, HTF 919 (or tegaserod), has been shown to reverse stress-induced delay in gastric emptying. Summary: Implications for Clinical Practice An understanding of the pathophysiology of functional bowel disease should be based on modern concepts of nerve-gut interactions. Experimental animal models have provided tremendous insights into the regulation of a variety of gut motor functions, and have led to the identification of many of the receptors involved. Gut reflexes, visceral hypersensitivity, and hyperalgesia, as well as stimuli of central origin, may all have a role in generating symptoms in functional bowel disease and are likely to interact. Sensitization of visceral afferents by local inflammation, leading to hyperalgesia, may explain some functional bowel disorders. Interventions targeted at serotonin, NK, CCK, and opioid receptors appear to provide the most immediate promise for clinical application in functional bowel disorders. Reference 1.Bueno L. New and future drugs in nerve-gut dysfunctions. State-of-the-Art Lecture. Program and abstracts of the 7th United European Gastroenterology Week; November 13-17, 1999; Rome, Italy. I just want to add thisHe theorizes that the treatment makes the body less reactive to stress and causes it to produce less of a hormone called vasoactive intestinal peptide, or VIP. VIP inhibits smooth muscle contractions in the colon and produces abnormal levels of the hormone that are associated with severe constipation and diarrhea. Palsson previously noticed that IBS patients had elevated levels of the hormone.Here is the whole abstract and some others. Researcher uses hypnosis to alleviate irritable bowel syndrome Last modified at 8:49 a.m. on Saturday, April 4, 1998 NORFOLK, Va. (AP) -- A clinical psychologist is experimenting with hypnosis to alleviate a painful gastrointestinal disorder that affects nearly one out of 10 Americans but is rarely discussed because of its embarrassing nature. The disorder is irritable bowel syndrome, which is characterized by abdominal pain and diarrhea and/or constipation. IBS commonly is managed by a high-fiber diet or anti-spasmodic medication, but neither treatment works for about 25 percent of patients who have frequent, often severe symptoms. Hypnosis may provide relief for those patients by helping them relax, said Dr. Olafur Palsson, director of the behavioral medicine clinic at Eastern Virginia Medical School and assistant professor of psychiatry and behavioral sciences. No one knows what causes IBS, but symptoms often first flare up during a period of stress and may last for years, Palsson said. He has seen patients with such severe, uncontrollable symptoms that they couldn't hold a job. "This is not a trivial problem," he said. "Half of all visits to gastrointestinal specialists are because of this." Previous studies by Palsson and by researchers in England found that hypnosis improved IBS symptoms in 85 percent to 95 percent of patients. Palsson now is leading a study at EVMS to find out how the treatment works. He theorizes that the treatment makes the body less reactive to stress and causes it to produce less of a hormone called vasoactive intestinal peptide, or VIP. VIP inhibits smooth muscle contractions in the colon and produces abnormal levels of the hormone that are associated with severe constipation and diarrhea. Palsson previously noticed that IBS patients had elevated levels of the hormone. Hypnosis first was reported as an effective tool for IBS in a study in England in 1984 and has been used there since, Palsson said. Hypnosis is widely used as a medicinal tool in Europe but has not caught on to the same degree in the United States. Dr. John Lucas, clinical assistant professor of psychiatry at Cornell University Medical College, said the merits of hypnosis have been proven in other studies. It makes sense that it would work in the case of irritable bowel syndrome, he said. Hypnosis can relieve the stress that exacerbates IBS by helping people focus their attention on something else, said Lucas, who often uses hypnosis to help patients manage pain and break habits such as cigarette smoking. Palsson, a native of Iceland, used hypnosis to treat IBS while doing a post-doctoral fellowship in behavioral medicine from 1994 to 1996 at the University of North Carolina-Chapel Hill. Palsson's new study began in September and will conclude this fall. It involves 32 patients who each undergo seven 40-minute hypnosis sessions over 14 weeks. They also listen to a 15-minute hypnosis audiotape once a day, give blood samples and rate their physical symptoms daily on a standard form. Mary, a 34-year-old woman who asked not to be identified by her full name, finished her treatment this month. She was diagnosed with IBS at 18; since then, she has endured abdominal pain almost daily. "There were times when you'd get hit with it with no warning," she said. "You'd be halfway through grocery shopping and all of a sudden you'd be looking for a bathroom and wondering where to stash your grocery cart." Since the treatment, Mary has had regular bowel movements and only occasional, mild abdominal pain. As an added bonus, the migraine headaches she also once suffered have disappeared. "It sounds kind of hokey when you try to explain it to people but it works," she said. "I went into it not knowing anything about hypnosis. It's nothing like on TV. I don't quack like a duck when the phone rings."
 
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Discussion Starter · #18 ·
Thanks everyone for the great information. Flux a couple of questions though. In the research studies that you have quoted, has the hypnotherapy been done one on one, with a doctor and patient or did the patients only use tapes with no individual customization? What credentials did the professionals hold? Was this self hynotherapy or was the individual actually put out in their sessions? I am interested in hypnotherapy for my wife, but I would like to know exactly what type of hypnotherapy was used to get these fantastic results. Another question, how many individuals were in the group? ------------------ http://www.digestioninfo.com[This message has been edited by kwilim (edited 02-26-2000).]
 

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Interesting topic kwilim and info flux, and eric. A good discussion by all.
I new there was a reason I came to this BB!
 
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