# Overly Anxious and Driven People Prone to Irritable Bowel Syndrome



## 19864

Overly Anxious and Driven People Prone to Irritable Bowel SyndromeOverly anxious and driven people are susceptible to irritable bowel syndrome, usually known as IBS, indicates research published ahead of print in the journal Gut. [The cognitive behavioural model of irritable bowel syndrome: a prospective investigation of patients with gastroenteritis Gut 2007; doi: 10.1136/gut.2006.108811] Newswise â€" Overly anxious and driven people are susceptible to irritable bowel syndrome, usually known as IBS, indicates research published ahead of print in the journal Gut. The researchers studied 620 people who had confirmed gastroenteritis caused by a bacterial infection. None had had IBS before, or indeed any serious bowel disorder. Each participant completed a detailed questionnaire when their infection was confirmed. This included questions about mood, perceived stress levels, perfectionism and illness beliefs and behaviours. They were then monitored three and six months later to see whether they had developed the typical symptoms of IBS, which include diarrhoea and/or constipation, abdominal pain and bloating. In all, 49 people had IBS at both time points. Women were more than twice as likely to have IBS as the men. Those with IBS were significantly more likely to have reported high levels of stress and anxiety and psychosomatic symptoms than those who did not develop the condition They were also significantly more likely to be â€œdriven,â€ carrying on regardless until they were forced to rest - a pattern of behaviour which only worsens and prolongs the condition, say the authors. Although not likely to be depressed, those with IBS were more likely to take a pessimistic view of illness. IBS affects between 10 and 15% of adults in industrialised countries, but its exact cause is unknown. â€œGastroenteritis may trigger the symptoms, but cognitions, behaviour and emotions may help to prolong and maintain them over time,â€ conclude the authors, who suggest that cognitive behavioural therapy may be an effective treatment. Click here to view the paper in full: http://press.psprings.co.uk/gut/february/gt108811.pdf --------------------------------------------------------------------------------Â© 2007 Newswise. All Rights Reserved.


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## Kathleen M.

While I do understand how much psychosocial aspects play into who gets IBS and who doesn't, everytime one of these studies come out I always end up wondering what is up with me.Anxiety and perfectionism are two things that just don't play much of a role in my psyche. Guess there is always an exception to prove the rule.







Although I do sometimes have the won't rest thing but only in some ways. I have always been the person that goes to bed when I should and not try to stay up all night to finish things, so I'm not sure how driven I am compared to some people. I'm more of a "they need me at work" I won't take a sick day type than they stay up all night until every little bit of something is perfect. I can sleep just fine if the dishes aren't done, etc. unlike a lot of other people I know.I did participate in the Genetics and IBS study they are doing here. I keep hoping we will find something other than "character flaws" that play a role in who gets IBS. Sometimes I think papers like this can play into the IBS is just in the mind, or no big deal. That isn't likely how the researchers played it out (I'd have to read the paper, and I hope I am right) but I can see how some people will use this as an arguement to say see, we told you we don't need any IBS drugs, if these people would just chill out and calm down and take their fiber they'd be fine.


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## evulienka

Actually for me stress is one of the biggest ( if not the biggest) trigger. I donÂ´t like the way it is presented in media and very often even by the doctors like " it is just a stress you must go through it by yourself and donÂ´t take the space in my surgery any more " . Stress can also cause a lot of suffering and I often feel that the attitude of the society (and the doctors)is like " you are stressed and you are guilty when you are not able to struggle with it" I just think that stress can be a big deal and noone should be forced to feel guilty if they donÂ´t manage stress as well as the others do.


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## 22144

Before my IBS really hit hard, all my friends said I was taking on too much and didn't relax enough.


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## 17902

couldn't they put an IBS patient in a controlled hypnotic state with some fancy narcotic or other, in order to determine if visceral symptoms are at all related to "stress"? If not, surely there must be some way of proving conclusively that the complete lack of intestinal motility I'm experiencing at the moment, for example, is independent of anything within the realm of my will, or even anything susceptible to the most skilled "unconscious" intervention. Then these morons and their research could get on with producing something that might help towards finding for all us sufferers a ticket out of hell. Or else they'd be out of work simply because they're intellectually incapable of approaching the problem this illness poses at its most complex level. For another trial, maybe the subject could be repeatedly stabbed in the stomach, and then taught how to use CBT to deal with it.


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## eric

I think this study again shows that stressors can contribute to the development of IBS at the time of infection. The bodies stress system also helps fight infections.Martin H, they have known for quite a while now years, that stress can contribute to viceral hypersensivity. Via the bodies stress system, HPA Axis and specific cells in the gut called mast cells. Another cell in IBS is the EC cells that release serotonin in the gut. Both these cells are important in PI IBS. IN PI IBS they have found an increase in these cells after infection."Stress and Irritable Bowel Syndrome: Unraveling the CodeBy: Yvette TachÃ©, Ph.D., Center for Neurovisceral Sciences and Women Health, Digestive Diseases Center, Department of Medicine, Digestive Diseases Division, University of California at Los Angeles and VA Greater Los Angeles Health Care System, CaliforniaDr. TachÃ© was the recipient of the IFFGD 2005 Research Award to Senior Investigator, Basic Science. Her early publications put the "brain-gut axis" on the map. Since then, she has been one of the pioneers in this field. In many ways, it has been her energy and enthusiasm that has ensured the continued vibrancy of the field. Her identification of the role of corticotrophin-releasing factor (CRF) signaling pathways in stress-related alterations of gut motor function and visceral pain are of major and lasting importance. "http://www.giresearch.org/Tache.html


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## eric

Hopefully this link worksIBS -- Review and What's New"The Science of IBSGiven the lack of definitive organic markers for IBS, the absence of a unifying hypothesis regarding its underlying pathophysiology is not surprising. Nevertheless, important advances in research made during the past 50 years have brought us closer than ever to understanding the numerous putative etiologic factors involved in this multifaceted disorder, including environmental factors, genetic links, previous infection, food intolerance, and abnormal serotonergic signaling in the GI tract."Serotonin SignalingOf the putative mechanisms underlying the pathophysiology of IBS, the strongest evidence points to the role of serotonin in the GI tract."http://www.medscape.com/viewarticle/532089


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## eric

you migth also want to read thisdealing with stresshttp://ibsgroup.org/groupee/forums/a/tpc/f...261/m/162105482


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## 17902

Eric, I don't have time to read these over right now, but I will later today. Also, I know debates about this type of thing can go on forever, and that's not what I want. I just know I've had IBS-C steady for three and a half years and not even the slightest correlation between my moods and IBS symptoms has emerged. For instance, over Christmas I was an emotional mess for two weeks over family issues, but they were two of the best weeks I've ever had with constipation. If it is emotional, then the effect must be delayed? that seems crazy. anyway, I'll get to your postings soon...thanks


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## 16636

The point of this study was really to determine if cognitive behavioral therapy can be of benefit to people diagnosed with post-infectious IBS. The study was limited to people who had post-infectious IBS. This is a subset of patients, obviously. For example, people with psychological trauma preciptating their symptoms were not part of the study. The study isn't saying it's our "fault" but it is saying that doctors may be well advised to guide recovery from infection in specific ways to avoid the development of "cycles" into and out of illness. From the reading I've done, there are definitely medications being researched which will act on the brain gut axis, hopefully more effectively than Zelnorm. So this is just a behavioral approach to help prevent life-long IBD syptoms. Worth a try, I guess, if intervention is early enough.There's also an emphasis in this study on the concept somatisation. Such as: we manifest enotional/mental illness in our bodies in this vague way called IBS. The use of this concept in this paper is very bothersome to me. It's underexplained, in my opionion,That said, I have no problem with the concept that my emotional condition contributes or even caused my IBS. My emotional condition is intimately connected to my body in every way. The point is that if it's causative for me than it might be causative for a lot of other people, and we all need targeted medications to treat this problem. That's just me.Dana


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## eric

This is also something else to now that is new."Report from the 6th International Symposium on Functional Gastrointestinal DisordersBy: Douglas A. Drossman, MD and William F. Norton, IFFGDThe 6th International Symposium on Functional Gastrointestinal Disorders was hosted by IFFGD on April 7-10, 2005. The biennial meeting was jointly sponsored by the Office of Continuing Medical Education, University of Wisconsin Medical School and the International Foundation for Functional Gastrointestinal Disorders (IFFGD) in cooperation with the Functional Brain-Gut Research Group (FBG). The program, a culmination of two years planning was both stimulating and informative. In fact, our knowledge of the functional gastrointestinal (GI) disorders continues to evolve, and these symposia are in many ways a barometer of the many changes occurring in the field. Nearly 400 persons from around the world attended representing a variety of health care disciplines. Over 80 experts in the field of functional GI disorders presented their work in general sessions, multiple symposia directed toward specialties, and mini-workshops. The attendees included gastroenterologists, other medical physicians, nurses, physician assistants, lab technicians, and related allied health personnel, as well as representatives from the U.S. National Institutes of Health (NIH), the U.S. Food and Drug Administration (FDA), and the pharmaceutical and medical device industry. The summary that follows highlights several of the important aspects presented in the general sessions, including:"Some of the major research advances that support the integrated or biopsychosocial approach include: Genetic and early environmental influences on the functional GI disorders The role of neurotransmitter and neurohormonal signaling in intestinal/enteric functionThe use of animal modelsNewer research relating to altered neuroimmune function, cytokine (cell molecules involved in the immune system response) activation, and brain-gut interactions*Demonstration of post-infectious IBS as a brain-gut disorder*The role of brain imaging in understanding the modulation of visceral pain "http://www.iffgd.org/symposium2005report.html


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## 17902

is wanting to keep a job perfectionism? I'll gladly produce when I feel like lying in bed; but the cognitive behavorial therapist certainly won't be remunerating me for it...Also, I think if people with IBS have "unrealistic personal expectations", it's because the illness keeps them from becoming what they otherwise would have been. It seems to me the leap this study makes from its data to confirming the usefullness of CBT concepts such as "all or nothing behavior" is very suspect. And if what I'm perceiving now is an "illness belief", then I'm more psychotic than someone who sees and talks to people who aren't there.


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## evulienka

I agree that the whole perfectionism thing is quite stupid . I guess I am not exactly perfectionalist







I have mess everywhere and I donÂ´t care about many things which seem to be important for others.


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## eric

This is another article on the same study. It looks like perfectionism didn't play a role.There is important information in the article missing, it part how the psychophysiological interplay between the constant communication with the "gut brain" and the "brain."The study looked to see if the "psychophysiological interplay" contributed to Post Infectious IBS at the time of infection. They have actually known this now for many years.Stress raises risk of irritable bowel syndrome NEW YORK (Reuters Health) - After a bout with a stomach bug, the likelihood that a person will go on to develop irritable bowel syndrome seems to go up if he or she is susceptible to stress and anxiety, according to a new study. ADVERTISEMENT People with irritable bowel syndrome (known as IBS) suffer chronic discomfort with cramping, diarrhea or constipation. The causes of IBS are unclear and there has been debate whether it is mostly due to psychological factors or biological triggers, or perhaps a combination.Dr. Rona Moss-Morris, from the University of Southampton in the UK, and colleagues looked at the impact of psychological factors on the risk of IBS following an episode of gastroenteritis.They studied 620 patients who had no history of IBS or any serious bowel condition but came down with gastroenteritis caused by a bug called Campylobacter.The subjects completed a questionnaire at the time of the infection to assess mood and personality factors, and follow-up questionnaires were administered at 3 and 6 months after the infection.Forty-nine subjects were classified as having IBS at both follow-up visits, the researchers report in the medical journal Gut. Higher levels of perceived stress, anxiety, and negative illness beliefs at the time of infection were all identified as risk factors for IBS.By contrast, depression and perfectionism did not seem to increase the risk of IBS.The study is the first to investigate a combination of emotional and cognitive risk factors "relevant for the development of IBS after Campylobacter gastroenteritis," the researchers state.They conclude, "Gastroenteritis may trigger the symptoms, but cognitions, behavior and emotions may help to prolong and maintain them over time."SOURCE: Gut, online February 26, 2007. http://news.yahoo.com:80/s/nm/20070226/hl_...ress_bowel_dc_1Martin, they have pretty good evidence on why there is d and d/c and c in IBS and it has to do with serotonin and receptors in the gut."IBS -- Review and What's New Previous Page The Science of IBSGiven the lack of definitive organic markers for IBS, the absence of a unifying hypothesis regarding its underlying pathophysiology is not surprising. Nevertheless, important advances in research made during the past 50 years have brought us closer than ever to understanding the numerous putative etiologic factors involved in this multifaceted disorder, including environmental factors, genetic links, previous infection, food intolerance, and abnormal serotonergic signaling in the GI tract.Environmental InfluencesAlthough a patient's psychological state may influence the way in which he or she presents, copes with illness, and responds to treatment, no evidence supports the theory that psychological disturbances are the cause of IBS.[39,40] The biopsychosocial model proposed by Engel takes into account the interplay between biologic, psychological, and social factors.[41] This model proposes that there is an underlying biologic predisposition for IBS that may be acted on by environmental factors and psychological stressors, which contribute to disease development, the patient's perception of illness, and impact on treatment outcomes.[42,43]Studies evaluating the role of acute stress have shown that stress can result in release of stress-related hormones that affect colonic sensorimotor function (eg, corticotropin-releasing factor [CRF] and inflammatory mediators [eg, interleukin (IL)-1]), leading to inflammation and altering GI motility and sensation.[44] For example, CRF-1 receptors located in the central nervous system (CNS) and gut can affect colonic motility, epithelial water transport, and gut permeability.[45] Sagami and colleagues[46] determined that the peripheral administration of a nonselective corticotropin-releasing hormone (CRH) receptor antagonist improved GI motility, visceral perception, and negative mood in response to gut stimulation in patients with IBS. These findings suggest that CRH may play an important role in the pathophysiology of IBS.GeneticsStudies with twins have shown that IBS is twice as prevalent in monozygotic twins as in dizygotic twins.[47-49] Limited research on familial aggregation has found that individuals who have a family member (other than a spouse) with a history of abdominal pain or bowel disorder have more than 2-fold increased odds of having IBS. It is likely that environmental influences may help explain this finding (eg, awareness of the symptom status of family members may make sufferers more open to discussing their symptoms and seeking help for the condition).[50] Preliminary findings also suggest that IBS may be associated with select gene polymorphisms, including those in IL-10, G-protein GNb3, alpha adrenoceptor, and serotonin reuptake transporter (SERT).[47, 51-54] Despite these potential links, however, conclusive evidence for a genetic basis for IBS has not been established.Postinfectious IBSThe presence of postinfectious (PI)-IBS, referring to the development of IBS symptoms -- particularly abdominal pain and diarrhea -- shortly after an enteric infection, is based on research from prospective studies in which IBS symptoms developed in 7% to 32% of patients after they recovered from bacterial gastroenteritis.[52,55,56] Specific risk factors for the development of PI-IBS have been identified, including younger age, female sex, presence of severe infectious gastroenteritis for a prolonged period, use of antibiotics to treat this infection, and presence of concomitant psychological disorders (eg, anxiety).[39,52,55,57] Difficulty in downregulating intestinal inflammation in the colonic mucosa has been suggested as a potential underlying mechanism in this condition.[52] Also suggested as a potential underlying mechanism is the presence of colonic changes shown in patients with PI-IBS compared with controls, including increased gut permeability, increased mucosal enterochromaffin cell production, and increased concentration of mast cells and T lymphocytes in the gut mucosa.[39,52,55,57] Despite considerable evidence linking IBS with an inflammatory etiology (perhaps triggered by enteric infection), in a controlled trial of patients with PI-IBS, anti-inflammatory treatment with prednisolone was not more effective than placebo in improving patient symptoms.[58] The true role of prior infection as a key factor in PI-IBS remains to be established.[59]The use of probiotics (products containing live or attenuated bacteria that have a positive effect on the host) in alleviating symptoms in patients with PI-IBS is an area of recent focus.[60,61] The potential utility of probiotics in this setting stems from their antibacterial, antiviral, and immune-modulating properties; their ability to modify intestinal flora; and their potential to enhance intestinal mucus secretion or influence stool consistency or volume and gas handling.[60] The number of studies evaluating the efficacy of probiotic preparations in patients with IBS is limited but growing.[60-68] Because trials vary in study design, dose, and strain (Lactobacillus and Bifidobacteria alone or in combination; mixture of Lactobacillus, Bifidobacteria, and Streptococcus), direct comparison of results is challenging. Overall, some degree of IBS symptom improvement has been demonstrated in symptoms such as abdominal pain,[65,66] bloating,[63,66] gas,[66] and daily symptom scores.[62,65] O'Mahoney and colleagues[60] have recently demonstrated that results with the Bifidobacterium infantis strain are particularly promising. In a separate analysis, these investigators showed that the baseline characteristics of urgency and hard stool increased the odds ratio of response to this strain, whereas straining and alcohol consumption reduced the likelihood of response.[69,70] The ultimate place in therapy of probiotics in IBS remains to be elucidated.Small Intestinal Bacterial OvergrowthThe presence of a higher than usual population of bacteria in the small intestine (leading to bacterial fermentation of poorly digestible starches and subsequent gas production) has been proposed as a potential etiologic factor in IBS.[71] Pimentel and colleagues have shown that, when measured by the lactose hydrogen breath test (LHBT), small intestinal bacterial overgrowth (SIBO) has been detected in 78% to 84% of patients with IBS.[71,72] However, the accuracy of the LHBT in testing for the presence of SIBO has been questioned.[73] Sensitivity of the LHBT for SIBO has been shown to be as low as 16.7%, and specificity approximately 70%.[74] Additionally, this test may suboptimally assess treatment response.[75] The glucose breath test has been shown to be a more reliable tool,[76] with a 75% sensitivity for SIBO[77] vs 39% with LHBT for the "double-peak" method of SIBO detection.[74] In a recently conducted retrospective study involving review of patient charts for the presence of gastrointestinal-related symptoms (including IBS) in patients who were referred for glucose hydrogen breath tests for SIBO, of 113 patients who met Rome II criteria for IBS, 11% tested positive for SIBO.[78] Thus, results demonstrated that IBS symptoms are often unrelated to the presence of SIBO. Despite the controversy regarding the contribution of SIBO to the underlying pathophysiology of IBS and its symptoms, short-term placebo-controlled clinical studies with select antibiotics, including neomycin and rifaximin, have demonstrated symptom improvement in IBS patients.[61,72,79] Antibiotics may therefore have potential utility in select subgroups of IBS patients in whom SIBO contributes to symptoms. However, the chronic nature of IBS symptoms often leads to the need for long-term treatment. Given the fact that long-term use of antibiotics is generally undesirable, the place of antibiotics in IBS therapy remains to be established.[73]Food IntoleranceFood intolerance has been proposed as a potential cause of GI symptoms in some patients with IBS; however, this link is not well established. Although some patients associate onset of IBS symptoms with ingestion of particular foods, identification of a true food intolerance is challenging, and elimination diets are typically time-consuming and difficult to implement. Recent research involving exclusion of foods to which patients had immunoglobulin (Ig) G antibodies, which are associated with a more delayed response after antigen exposure than IgE antibodies, resulted in significantly better symptom improvement than in patients in the nonexclusion group.[80] Further research into the role of food intolerance in IBS is warranted.Serotonin SignalingOf the putative mechanisms underlying the pathophysiology of IBS, the strongest evidence points to the role of serotonin in the GI tract. The effect of serotonergic mechanisms in the manifestation of IBS symptoms has led to development of a new drug class for the treatment of IBS patients: the GI serotonergic agents.Normal GI function relies on a properly functioning brain-gut axis, which involves the coordinated interplay of the GI musculature, the CNS, the autonomic nervous system, and the enteric nervous system (ENS). The ENS contains millions of neurons embedded in the wall of the digestive tract and functions, at least in part, independently of the CNS. The size, complexity, and independent function of the ENS has resulted in application of the terms "the second brain" and "the mini-brain."[81] Impaired function or coordination of any of these systems, or the communication between these systems and the GI musculature, can lead to symptoms of dysmotility and altered sensory perception, which are characteristic of IBS and select other GI motility disorders.[82]The neurotransmitter serotonin (5-hydroxytryptamine [5-HT]) is a predominant signaling molecule in the ENS. Most (90% to 95%) of the body's serotonin is found in the gut, and smaller amounts are found in the brain (about 3%) and in platelets (about 2%).[83] In the GI tract, serotonin facilitates communication between the ENS and its effector systems (muscles, secretory endothelium, endocrine cells, and vasculature of the GI tract), thus playing a key role in normal GI tract functioning.[84] In addition, serotonin plays a role in the communication between the ENS and the CNS.In the gut, serotonin is synthesized by and stored in the enterochromaffin cells, which are located within the mucosa of the intestinal wall. When material passes through the lumen and the mucosa is stimulated, enterochromaffin cells release serotonin, which then binds to its receptors (primarily 5-HT1P receptors) on intrinsic primary afferent neurons, initiating peristalsis and secretion. Serotonin also binds to 5-HT4 receptors on interneurons, which augments the transmission of signals to motor neurons, resulting in enhanced peristaltic activity. In transgenic mice lacking 5-HT4 receptors, colonic motility is abnormally slow, confirming the role of these receptors in facilitating normal colonic motility.[85] By binding to 5-HT3 receptors on efferent sensory innervations coming from the vagus and the spinal nerves, serotonin mediates signaling between the ENS and the CNS and, thus, modulates pain perception.To regulate the signaling process, excess serotonin must be removed; this is accomplished by the SERT molecule expressed by intestinal epithelial cells.[86] Human studies have shown that defects in serotonin signaling contribute to the pathophysiology of IBS and, potentially, other GI motility disorders. In a recent study by Coates and colleagues,[87] biopsy specimens from patients with IBS showed significantly lower mucosal serotonin concentrations than those from healthy controls, potentially the result of lower mRNA levels for tryptophan hydroxylase (the rate-limiting enzyme in serotonin synthesis), which were also significantly lower in patients with inflammatory bowel disease.[87] There was no significant difference in the number of enterochromaffin cells or in the capacity of these cells to release serotonin under stimulated conditions. In another study, higher serotonin levels were observed in mucosal biopsy samples from patients with IBS with constipation (IBS-C) than in patients with IBS-D or in healthy volunteers.[88]Serotonin levels may also be affected by altering the amount or function of SERT. The study by Coates and colleagues[87] showed a significant decrease in the level of SERT mRNA and SERT protein expressed in the intestinal epithelial cells of IBS patients compared with that of healthy volunteers. In another study,[89] SERT expression and binding capacity in platelets were decreased in women with IBS-D compared with expression and binding capacity in healthy controls. Furthermore, Chen and colleagues[90] showed that mice with a SERT gene deletion had altered colonic motility. It is interesting to note that the mice thrived in laboratory housing conditions, indicating that other transporters could compensate for the lack of SERT. Additional studies have focused on SERT polymorphisms. Yeo and colleagues[91] showed an association between patients with IBS-D and the homozygous short polymorphism of the SERT gene promoter. This mutation results in lower levels of SERT gene transcription and reduced amounts of SERT protein available for reuptake of serotonin. In addition, Camilleri and colleagues[92] showed a possible link between the long promoter polymorphism and patient response to therapy.Thus, a substantially large body of work shows that normal gut physiology is predicated on the interplay between the GI musculature and the ENS, autonomic nervous system, and CNS. One of the central mediators of this complex interplay is the neurotransmitter serotonin. Impairment or imbalance in serotonergic signaling, which can affect GI motility, secretion, and visceral sensitivity, may be affected by defects or deficiencies in serotonin production, specific serotonin receptors, or proteins such as SERT. These changes can manifest in symptoms associated with IBS, including abdominal pain, altered bowel habits (constipation, diarrhea, or alternation between these 2 states), and bloating.http://www.medscape.com/viewarticle/532089_3


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## 17902

Eric, (hadn't seen your last post when I posted this...)Insofar as I can understand them, I don't dispute at all rigorous scientific discoveries about the psychobiology of IBS. I'm firm in my conviction, though, that it is simply impossible for any style of psychological therapy to touch upon whatever layer of the organism it is in which symptoms take root, at least for IBS-C. For years I effectively controlled depression and anxiety with meditation, for example; but these techniques improve neither my emotional perception of pain, nor what actually goes on in my GI tract.


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## 17902

I would equate "driven person" and perfectionist most of the time...I think the "all or nothing thinking" was identified as a factor in the study...how can this be anything but a matter of how things were put on the list of questions they asked?


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## jjohnson

Kathleen,Thanks for that great post. I agree with you completely. Some of the headlines did indeed suggest that these character traits "cause" IBS, even if that was not the intent of the scientists who conducted the study.I think a big part of the problem is that the very term "irritable bowel syndrome" is what invites so much skepticism, trivialization, and even ridicule of this illness we suffer from. Moreover, it conveys absolutely nothing about the great strides that have been made in the past several years in understanding it. Even though the ultimate cause (let alone cure) remains elusive, surely there is enough known about this condition that the name "IBS" has outlived its usefulness (if it ever had any usefulness to outlive, that is.) I wish Dr. Drossman and the rest of the Rome Committee would take that under consideration.


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## eric

"For years I effectively controlled depression and anxiety with meditation, for example; but these techniques improve neither my emotional perception of pain, nor what actually goes on in my GI tract.""these techniques improve neither my emotional perception of pain, nor what actually goes on in my GI tract."That's not the case with most people and IBS and the research. All pain is processed in the brain and these techniques can modulate the signals between the gut and the brain.CBT and HT and meditation are all coping tools.Each has some differences however.It is known now that stress can reinflame previous inflammation in the gut. Part of how this happens in about some of the mechanisms I am pointing out here. If your under stress when you get a gastro infection it increases the risk of developing IBS. Stress effects all peoples guts, especially IBS. In IBS the gut is hypereactive to stimuli. Having IBS is also very stressful. This stress also keep the stress hormones flowing. The vicious cycle in IBS is anxiety=symptoms=anxiety in any order.from the experts."psychophysiological arousal is the core of treating functional gi disorders. There is som much distress, anxiety, antisipatory anxiety, and negative reaction to symptoms, that calming the mind and body often makes a significant difference to symptoms."These aren't "cures" but tools. Its also important that most people with PI IBS who develop IBS have d as their predominate symptom. There are some psycological differences to the symptoms in d and d/c and c IBS. So some of these things might apply more to different subgroups.also treating the brain in IBS is the top down model and the gut down up model. Its known treating both can be very effective.somethings to look overThe Surprising Link Between Mood and Digestion http://www.ahealthyme.com/article/primer/101186767http://www.aboutibs.org/Publications/StressDefined.htmland I emailed some major expert on all this.FYIDr Drossman's comments on foods for IBS Health.Shawn,To say that people with IBS may get symptoms from food intolerances is an acceptable possibility, since the gut will over react to stressors of all types including food (high fat or large volumes of food in particular). Futhermore, there can be specific intolerances. So if you have a lactose intolerance for example, it can exacerbate, or even mimic IBS. Other examples of food substances causing diarrhea would be high consumers of caffeine or alcohol which can stimulate intestinal secretion or with the latter, pull water into the bowel (osmotic diarrhea). The same would be true for overdoing certain poorly absorbed sugars that can cause an osmotic type of diarrhea Sorbitol, found in sugarless gum and sugar substituted foods can also produce such an osmotic diarrhea. Even more naturally, people who consume a large amount of fruits, juices or other processed foods enriched with fructose, can get diarrhea because it is not as easily absorbed by the bowel and goes to the colon where it pulls in water. So if you have IBS, all of these food items would make it worse. However, it is important to separate factors that worsen IBS (e.g., foods as above, stress, hormonal changes, etc.) from the cause or pathophysiology of IBS. Just like stress doesn't cause IBS, (though it can make it worse), foods must be understood as aggravating rather than etiological in nature. The cause of IBS is yet to be determined. However, modern research understands IBS as a disorder of increased reactivity of the bowel, visceral hypersensitivity and dysfunction of the brain-gut axis. There are subgroups being defined as well, including post-infectious IBS which can lead to IBS symptoms. Other work using brain imaging shows that the pain regulation center of the brain (cingulate cortex) can be impaired, as well as good evidence for there being abnormalities in motility which can at least in part explain the diarrhea and constipation. So finding a specific "cause" of IBS has grown out of general interest in place of understanding physiological subgroups that may become amenable to more specific treatments. Hope that helps.Doug http://www.ibshealth.com/ibs_foods_2.htmhttp://www.ibshealth.com/ibsfoodsinfo.htmDr Wood's comments for me"Dr. Jack Wood, a renowned physiologist at The Ohio State University calls the ENS â€œthe little-brain-in-the-gut.â€ "Dear Shawn:Sorry for the delayed reply to your question. I generally agree with Dr. Drosssmanâ€™s response. A subgroup of individuals when they become sensitized to specific molecules in certain foods respond to ingestion of the molecules with symptoms of cramping abdominal pain, fecal urgency and explosive watery diarrhea. These are also the primary symptoms of diarrhea-predominant IBS. Enteric mast cells, by mechanisms we donâ€™t understand, become sensitized to the food molecule and respond to its presence by releasing a signal to the brain-in-the-gut (ENS) which is interpreted as a threat. The ENS responds by â€œrunningâ€ a program which organizes secretion and motility into a behavior pattern of the bowel, which rapidly clears the threat from the lumen. Because to be effective secretion occurs in large volumes and the contractions that accomplish rapid propulsion are strong, running of the program has the side effects of diarrhea and cramping pain. Big brain input to mast cells during stress activates the mast cells to evoke the symptoms resulting from exposure of the mast cells to sensitizing food antigens. Aside from food allergens and mast cells, certain chemicals such as those in hot peppers, stimulate sensory nerves in the ENS and we are beginning to understand how this can also lead to food-related symptoms that might mimic or exacerbate IBS.Hope this helps,Jackie (Jack) D. Wood "FYI"You have two brains: one in your head and another in your gut. Dr. Jackie D. Wood is a renowned physiologist at The Ohio State University. He calls the second brain, "the-little-brain-in-the-gut." This enteric nervous system is part of the autonomic nervous system and contains over one hundred million neurons, which is as many as are in the spinal cord. This complex network of nerves lines the walls of the digestive tract form the esophagus all the way down to the colon. This little brain in the gut is connected to the big brain by the vagus nerves, bundles of nerve fibers running from the GI tract to the head. All neurotransmitters, such as serotonin that are found in the brain are also present in the gut.Dr Wood has discovered that this little-brain-in-the-gut has programs that are designed for our protection and which are very much like computer programs. They respond to perceived threats in the same way that the limbic system or the emotional brain does. So the threat of a gastrointestinal infection can activate the program that increases gut contractions in order to get rid of the infection. The symptoms are abdominal cramping and diarrhea. Dr. Wood has determined that a type of cell found in the body and the gut, called the mast cell, is a key to understanding the connection of the big brain in the head with the little-brain-in-the-gut. Mast cells are involved in defense of the body. In response to certain threats or triggers, such as pollen or infection, mast cells release chemicals, such as histamine, that help to fight off the invader. Histamine is one of the chemicals that causes the symptoms of an allergy or a cold. When an infection of the gut occurs, such as food poisoning or gastroenteritis, the mast cells of the gut release histamine. The little-brain-in-the-gut interprets the mast cell signal of histamine release as a threat and calls up a protective program designed to remove the threat â€" at the expense of symptoms: abdominal pain and diarrhea. The brain to mast cell connection has a direct clinical relevance for irritable bowel syndrome and other functional gastrointestinal syndromes. It implies a mechanism for linking allostasis and the good stress response to irritable states (e.g., abdominal pain and diarrhea) of the gut. Mast cells can be activated to release histamine in response to perceived psychological stress, whether the stressor or trigger is consciously perceived or not. So the end result is the same as if an infection activated the program in the-little-brain-in-the-gut: abdominal pain and diarrhea."http://www.parkviewpub.com/nuggets/n5.html


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## eric

By the way chronic anxiety can contribute to constipation in the activation of the sympathetic nervous system verses the parasympathetic nervous system. Fight or flight or rest and digest. Antisipatory anxiety might be more in d and d/c then C IBSers though for example. C Ibers have more anger they can't go. Although people can have all kinds of emotions to having ibs and to the symptoms.you may not "cure" the underlying disorders, but you can feel better and if you don't have symptoms that s a major plus.


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## eric

> quote:I wish Dr. Drossman and the rest of the Rome Committee would take that under consideration.


I actually think they have been if I remember correctly. I am pretty sure they have discussed it. This is not just an easy thing though to change the name. It would seem that way but I guess its not. One thing though IBS is made up of a bunch of different subgroups. And when they really start to figure those out they may label them each differently perhaps like PI IBS already.


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## 17902

Eric,a question for you, or anyone else, although it's a little off topic. After a colonoscopy two years ago, I went to outpatients a few days after the procedure, concerned that maybe my stomach pain meant something had gone wrong. I was fine, of course. But upon examining the X-ray, the doctor was shocked at how "backed up" I was and insisted on prescribing an enema even though I told him it was actually a good day for me in terms of constipation. Anyway, this suggested to me that I don't merely perceive normal GI processes hyper-sensitively; but rather that there's simply an inordinate amount of fecal matter internally pressuring me. X-rays, it would seem, provide clear physical proof that the pain is psychic only in a very limited sense...like a broken foot. So, for constipation sufferers anyway, do you think X-rays contribute anything to how IBS could or should be interpreted?


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## jjohnson

Eric,Thanks for that interesting piece of info. Please don't think I was trying to criticize these scientists who have, after all, devoted their careers to getting to the bottom of this. You also make a very good point that what we now call IBS may someday be broken down into any number of separate illnesses. Still, it would be hard to argue that the current name IBS has done us many favors in terms of getting it taken more seriously.


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## eric

"Please don't think I was trying to criticize"I didn't think that at all. I basically agree. The name doesn't convey IBS very well at all really. The name just doesn't sound serious enough in comparision with the suffering it can cause.for new people there is a lot of information here on all this.http://www.med.unc.edu/medicine/fgidc/publ...n_materials.htmhttp://www.med.unc.edu/medicine/fgidc/training_articles.htmalso for the info in general, this is on children but it applies."Question--How can you be sure there is no disease? Answer--Worries about the child's health are normal. Repeated explanations may be necessary because the concept of functional symptoms may be new. There are no tests for diagnosis of a functional gastrointestinal disorder, but there are symptom-based diagnostic criteria. Functional gastrointestinal disorders are common; diseases are unusual. If your child's symptoms meet the diagnostic criteria for a functional gastrointestinal disorder, stop worrying that it is something else. Ask your physician to reevaluate the child promptly if the symptoms change. Question--How do you treat the pain in functional disorders? Answer--Conceptually, functional abdominal pain may be treated 1) with education, 2) from the top down, 3) from the bottom up, or 4) with any combination of these. Sometimes getting a diagnosis and learning about a functional disorder is enough to reduce the worries a family has about the health of their child. All parents ask the same four questions when they see a clinician: 1) what is wrong? 2) is it dangerous? 3) will it go away? 4) what can we do about it? In the case of a functional bellyache the answers are: 1) it's a functional bellyache, 2) it is not dangerous, 3) it comes and goes, 4) there are several ways to treat it. If the answers satisfy and the child is not disabled by pain in any way, further treatment may be unnecessary. The goal is to help the child cope with symptoms so that they don't miss daily obligations and activities. Top down treatment--Children can learn to use the thinking parts of their brains to reduce pain. Biofeedback, guided imagery, progressive relaxation, and hypnosis are different ways of training the brain to help control and reduce pain. If these methods are available, the advantage to them is that they teach the child the skills needed to reduce pain without medication. Bottom up treatment--Children may benefit from small doses of chronic pain medicines, or medicine to take away acid or intestinal muscle spasm. These medications are safe and effective in many, but not all, children."http://www.aboutkidsgi.org/Bellyaches.htmlQuestion from a 13-year-old in Oregon -- I have had stomach pains for over one year that make it hard for me to do anything. I have recurring abdominal pain syndrome. My doctor said there is nothing wrong with me and nothing he can do to treat me. Do you have any suggestions?Answer -- We assume that you have been seen by a physician who gave you the diagnosis of "recurring abdominal pain syndrome," (functional recurrent abdominal pain). Tests are done to look for the presence of disease as the cause of symptoms. If the tests find no evidence of disease, the symptoms are termed "functional." Diagnosis of this functional gastrointestinal disorder is based on the symptoms, after ruling out the presence of disease or tissue damage. These symptoms are defined as abdominal pain severe enough to disrupt routine activities three or more times during a three-month period. Studies show that it is pretty common, affecting 10%-15% of school-aged kids. So if it is not a disease that is causing these symptoms (you are not sick and that is good news), what is causing it? The answer is not entirely clear. Ongoing research is looking for the explanation. Recent studies point to an increased sensitivity of the sensory nerves in the intestines. Normal movements of your intestines may be perceived as cramps or other discomfort. The intestines share nerve pathways with the brain. In many situations, when the brain reacts to something -- like the sound of a dentist's drill -- the intestines, or gut, pick up the same signals and react. The majority of people will ultimately have some kind of gastrointestinal (GI) symptom when exposed to stressful situations. If your GI system is a bit too reactive, you will experience symptoms in more types of stressful situations than someone else will whose gut is not quite as reactive. What is stressful for one person may not be stressful to another, and lots of people don't even realize it when they get stressed -- they just feel sick. Finally, there is the "gate theory" of how pain is experienced. When pain originates at some point, nerve messages pass through something like a gate on their way to the brain. The wider open the gate is, the more pain that is experienced. By thinking about and focusing on the pain site, we open the gate. Plus, feelings of anger or worry or sadness can open the gate. However, we can also help close the gate. Turning attention away from the site or feeling of pain, through relaxation or focusing on some other activity, can help close the gate and lessen or even eliminate pain. A well-known phenomenon that demonstrates this is that of the athlete who plays a game while injured, oblivious to the pain. The athlete is completely focused on the game and does not feel pain. Then, after the game is over, the athlete turns attention to the injury and feels pain. Whatever the cause, you can do something about it! It takes some effort but there a number of ways that you can help yourself. First, think about this example. Have you ever experienced a muscle cramp or a side-ache during strenuous running or exercise? You feel real pain in muscles that are not diseased. But they have been stressed beyond some point that in you causes discomfort. What do you do to avoid it in the future? You might think about what you were doing that resulted in the muscle pain. Maybe next time you do more warm-up exercises, or start out slower, or don't run as far. The first time you felt a side-ache, you might have felt concerned and stopped running. After you learned that it was nothing to be concerned about, you may have barely taken notice the next time it happened, perhaps slowed down a bit, but then kept right on going. This is the same type of thing that happens with functional recurrent abdominal pain. Your intestinal muscles may be causing you to feel pain. To get it under control, try this: 1) While the pain you feel is very real, do not worry that you are sick. You are not. Your body is reacting to events in a way that is causing you discomfort but is not cause for alarm. 2) Try to figure out if your symptoms are connected with anything else that may be triggering them. Do symptoms flare at certain times, before certain events, on weekdays, on weekends, etc? If you can identify triggering factors (like certain foods or activities) you can try to avoid them, or if that is not possible, try to deal with them in different ways. 3) Are you missing school because of this? Worry over missing school can make symptoms worse. Try to keep going. 4) Are you doing too much-school plus lots of outside activities? If so, take some time off to relax. Too much of anything can be stressful. 5) The next time you feel the pain, don't let it stop you. Keep on going. Practice focusing your thoughts on what it is you want to do next and then go ahead and do it. Don't let pain take your awareness hostage. http://www.aboutkidsgi.org/questionsandanswers.html#school


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## eric

martin HThe brain is not suppose to get chronic viceral singals all the time. Also when the actual colon distends it sends signals out to the brain via neurotransmitters. Pressure on the gut receptors can activate the signals to the brain where its felt, the brain then responds back to the gut.info on thatVisceral Sensations and Brain-Gut MechanismsBy: Emeran A. Mayer, M.D., Professor of Medicine, Physiology and Psychiatry; Director, Center for Neurovisceral Sciences & Women's Health, David Geffen School of Medicine at UCLAhttp://www.aboutibs.org/Publications/VisceralSensations.htmlIn regards to IBS History of Functional Disorders"MOTILITY In 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 AXIS The 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 issupported by evidence that patients with functional GI disorders have anywhere from a 30 to 80% placebo response rate regardless of treatment. http://216.109.125.130/search/cache?p=hist...&icp=1&.intl=usso just altered motililty alone does not explain IBS. Hope that helps


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## eric

Martin, you might want to get a sitz marker test and and testing for Outlet obstruction type constipation (pelvic floor dyssynergia)The external anal sphincter, which is part of the pelvic floor normally stays tightly closed to prevent leakage. When you try to have a bowel movement, however, this sphincter has to open to allow the fecal material to come out. Some people have trouble relaxing the sphincter muscle when they are straining to have a bowel movement, or they may actually squeeze the sphincter more tightly shut when straining. This produces symptoms of constipation. http://www.iffgd.org/GIDisorders/GIAdults.htmlthis is also a good site on chttp://www.aboutconstipation.org/


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## eric

JJohnsonThere is a good article from the Functional Brain gut research group on Functional GI disorders: what's in a name by dr drossman.you can read it here, its a pdf format.http://www.fbgweb.org/2005-spring-fbg-newsletter.pdf


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## jjohnson

Eric,Thanks for posting this. I think I may have come across this newsletter before since I know you have been posting links to these for some time, in which case, thanks for refreshing my recollection.


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## SteveE

Martinh said: "Also, I think if people with IBS have "unrealistic personal expectations", it's because the illness keeps them from becoming what they otherwise would have been."In response, I'd like to say a loud and clear AMEN! At the same time, I often feel a VERY small debt of gratitude to my IBS for taking me off of the type-A train (uh-oh...I feel another parody coming on...). I may have been a driven perfectionist before it started, but it sure took that out of me in a big way. For awhile I was driven to find answers to the IBS question and I was a perfectionist about in the sense that I wouldn't accept failure. Now I'm accepting that I may never find an answer and that it's a waste of whatever energy/drive I have left to go to great lengths to find one. I do, however, check-in here at the IBS Hotel on the information superhighway to see what the inn keeper and his tenants are learning about periodically, but I'm done pushing myself for answers.On a related note, my wife, who is also chronically ill (not-IBS) is perceived by others as being a driven perfectionist. I know she is about her job, but that goes right out the window at home--and she'd be the first to tell you! The point of me mentioning this is that I doubt any measure of "perfectionism" or "drive" could tell the full story since it is often situation-dependent. I do wish she had the drive to keep a symptom diary like I did since I got the closest thing to an answer I was probably ever going to get about IBS by looking at the resulting patterns, but she expends all of her drive at work and there's really none left.Having two chronically ill people in a household is a rare and unfortunate thing. You'd think it would be a very understanding environment. At times it is--I'm not sure what I'd think of her problems if I had never had IBS. On the other hand, there's a hint of "you don't understand my condition" said once in awhile. I've never thought that hers was all in her head and I still don't, but I do find it amazing that her problems coincided with an incident where she was justifiably REALLY, REALLY mad at someone (not me..thank goodness). Her anger at the time suggested a type of perfectionism based on an expectation that other people should behave in a certain way, and when they didn't, they all but ruined something special (and maybe in her eyes perfect) in her life. Likewise, when my IBS started, I was at a point in my life where I was realizing that something important to me wasn't what I thought it was. Come on...let's take that Type-A TrainAll aboard, cause it's quickest way to perfection.Ugh...Billy Strayhorn will haunt me for that one.Have a perfect day!Steve


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## David LA

Here we go again with "What came first the Egg or the Chicken Theory" For anyone who believes all of this--here's my story..... During my "IBS" Days I still remember so many Drs. saying your just to "anxious" your working to hard or "Driven" and you need to relax, blah, blah, blah.My biggest mis-take looking back is that I actually believed them. I spent so many hours working on all the psychological stuff, (meditation, bio-feedback, etc) that I NEVER bothered to treat my condition. I definitely felt a little better after meditating but as soon as I left my house and entered the real world of LIFE my symptons were still with me.Once I finally started treating my "IBS" by taking supplements and changing my diet. All the Anxious feelings dis-appeared. I still have TONS of work, lots of stuff happening with my relationships--All kinds of " good reasons" for being Anxious but my GI Tract isn't reacting to it.It just doesn't respond the same way it used too. I do believe that their are a small % of people that have so much stress going on in their life that its effecting their GI. But.....this is definitely the MINORITY! 1 or 2 percent seems about right.


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## eric

Dave, how does the bodies stress system help fight infections? What is the mechanism?How often everyday does a persons fight or flight responce go off?If stress is defined as *"In contrast to the common interpretation of the term "stress" as a psychological phenomenon, it should be understood as ANY real or perceived perturbation of an organism's homeostasis, or state of harmony or balance.*So a pain attack is a threat to the organizm or a d attack or not being able to go, all qualify as stressors, as do many other things in life.In this discussion its NOT stress that causes IBS, but a bacterial infection, that happens while a person is under stressors, which contributes to the development of IBS after the infection resolves, that is called PI IBS and a lot is known about it. Including an increase in mast cells embebbed in the colon that can Contribute to pain, because under stessors both physical and mental and both real and perceived they release hitimine unto the smooth muscle of the gut and the gut reacts to that release.Your really only thinking psychological stress it seems here and not the bigger picture of stress systems role in actually fighting infections, because the bacteria is a physical threat to the organism.This is really like catching a cold easier when your under stress.


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## Reta

Stress is one of my biggest triggers for abdominal pain. I don't think it it the actually stress but the results of the stress. I tend neglect my diet, drink too much coffee and do not sleep as well when I am under a great deal of stress. My solution is walking, I can practice my deep breathing and reduce the stress. My little dogs love it.


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## 21782

I have suffered from IBSD since I can remember. I have not posted here before but monitor occasionally. Like many others here, I get frustrated hearing any reports that imply "psycho-somatic" causes of the affliction. I have no doubt that anxiety is a factor in the manifestation of the disorder but I will always maintain the view that the cause is ultimately genetic. The development of the cerebral cortex upon the structure of the reptilian brain stem sets up an evolutionary thread for the genetic progress of DNA information such that basic fight or flight instincts are interpreted through the cerebral cortex in such a way that human "consciousness" cannot interpret these signals correctly. I am not a scientist or scientifically trained, but someone needs to study the relationship between the reptilian brain stem and it's resulting signals to the cerebral cortex and the ability of the cc to interpret that information. I am convinced that the anomaly we seek will be found there. Hey, call me crazy but I just want an answer! I will entertain any postulations that seem rational!


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## eric

NC eddie, they are studying what your talking about.The true meaning really though of psychosomatic.Which I think is used inappropretly really as "Its all in our heads" or "we make it up."EncyclopÃ¦dia Britannica condition in which psychological stresses adversely affect physiological (somatic) functioning to the point of distress. It is a condition of dysfunction or structural damage in bodily organs through inappropriate activation of the involuntary nervous system and the glands of internal secretion. Thus, the psychosomatic symptom emerges as a physiologicalâ€¦when in reality"The American Psychosomatic Society, founded in 1942, is a worldwide community of scholars and clinicians dedicated to the scientific understanding of the interaction of mind, brain, body and social context in promoting health and contributing to the pathogenesis, course and treatment of disease. "http://www.psychosomatic.org/


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## eric

by the way there is Post infectious IBS which serves kind of like a model for developing IBS. In those people enteric infection seems to be a major factor.alsoMechanisms of Disease: Genetics of Functional Gastrointestinal Disorders -- Searching the Genes that Matterhttp://www.medscape.com/viewarticle/553001_1


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