# Do you think it can be just a matter of bad flora?



## SpAsMaN* (May 11, 2002)

I hope someone knows if a bad flora can mimic IBS.Is there any research on the G.i. tract flora?Apparently,many labs works on "effectives" probiotics.Everyone here should include theirs symptoms in their signature.


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## m_m_forth (Oct 21, 2003)

I wish I could direct you to some research but I only have anecdotal evidence. I firmly believe I primarily have a flora problem. Mu recent experience with Digestive Advantage for IBS confirms this for me. It nearly quadrupled my gas problem and made it super smelly!


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## Talissa (Apr 10, 2004)

This is from Medscape Gastroenterology section's article, "What Unifies and Separates Irritable Bowel Syndrome and Inflammatory Bowel Diseases":"Direct and indirect evidence of altered flora of the large and small intestine has been reported in IBS patients. For example, Balsari et al.[36] observed a decrease in coliforms, lactobacilli, and, to some extent, bifidobacteria in a small group of IBS patients. More recently, preliminary evidence of an alteration of bacterial concentration in colonic biopsy specimens from IBS patients has been reported.[37] Indirect evidence for bacterial overgrowth of the small intestine (in the form of altered hydrogen breath test results) has been reported in patients with IBS, and a recent randomized controlled trial found evidence that antibiotic treatment was beneficial for IBS symptoms of bloating and discomfort.[38] Based on the concept of altered interactions between the colonic flora and the gut-associated immune system, probiotics have been proposed as an alternative strategy for the treatment of several gastrointestinal diseases, including IBD[39] and more recently IBS.[40, 41]" Also, regarding the increased permeability of the intestinal wall(leaky gut) which seems to arise due to imbalanced intestinal flora(dysbiosis):"For both syndromes, histologic and functional alterations of the mucosal barrier have been recently reported.[11*, 12, 24, 25] Small intestinal permeability is abnormal in a wide variety of conditions affecting the small intestine, including celiac disease, Crohn disease, and intestinal infections.[18**] Interestingly, gut permeability assessed by the lactulose/mannitol ratio is significantly elevated in PI-IBS(post infectious IBS)patients.[15] This functional alteration of the intestinal barrier function may be a cause or consequence of inflammation, and a direct link between increased intestinal permeability and the exaggerated immune activation in IBD still needs to be confirmed. In addition to a causative role of peripheral factors, gut permeability changes in animal models have also been reported in response to various stressors. " http://www.medscape.com/viewarticle/457728_4 The problem is finding a one-size-fits-all way to reverse the damaged intestinal wall. If you try to solely balance the flora, without healing the intestines, you still have permeability, which causes food reactivity along with altered bowel action. This then causes imbalanced flora, again--a "vicious cycle."It's being studied all over the world, so one day, just maybe....


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## eric (Jul 8, 1999)

"Do you think it can be just a matter of bad flora? "No, there is much more too it then bad flora.Its not just "gut permeability" either.Already they have found molecular changes in the gi tract as well as abnormalities in the gut, and the brain.altered flora, maybe a consequence of abnormal motility, delayed gastric emptiying and post infectious IBS and brain gut dysfunction.Talissa, what damage to the intestinal wall and what inflammation has been found in IBS?Who is Dr Meyer, who wrote the above abstract?


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## eric (Jul 8, 1999)

FYIFrom Current Opinion in GastroenterologyProbiotics and Prebiotics in Gastrointestinal DisordersPosted 04/09/2004Richard N. Fedorak, Karen L. Madsen"Irritable Bowel SyndromeBetween 1996 and 2001, there were five clinical trials that examined various species of Lactobacillus in the treatment of irritable bowel syndrome (IBS).40-44 These studies, along with the role of microflora in IBS, have been reviewed during the past year.45,46In a recent clinical trial, Kim et al.47* examined the effects of a probiotic formulation containing eight different probiotic species, VSL#3 (VSL Pharmaceuticals Inc., Fort Lauderdale, FL), on gastrointestinal transit and symptoms of patients with diarrhea-predominant IBS. After 8 weeks of treatment, there was no significant difference in mean gastrointestinal transit measurements, bowel function scores, or satisfactory global symptom relief between the two treatment groups. However, abdominal bloating was significantly reduced in the VSL#3 treatment group.47*The mechanism of action of probiotics in IBS is poorly understood and has been thought to be attributable to changes in fermentation products. In 10 patients with diarrhea-predominant IBS, administration of VSL#3 probiotics improved the clinical picture without significant alterations in indigenous enterococci, coliforms, Bacteroides, or Clostridium perfringens flora.48 In a similar open-label study, Bazzocchi et al.49 demonstrated that VSL#3 probiotic induced changes in the composition of the colonic microflora together with improvement in colonic dysmotility and visceral perception. In contrast, in a double-masked, placebo-controlled, crossover 4-week trial in 12 patients with IBS, Lactobacillus plantarum 299v did not alter colonic fermentation or improve symptoms compared with placebo.50 Once again, these discordant results support the concept of specific probiotic strains being more effective than others across varied disease states." http://www.medscape.com/viewarticle/470571?src=mp


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## eric (Jul 8, 1999)

FYIPREVALENCE AND EPIDEMIOLOGYIrritable bowel syndrome (IBS) is the most commonfunctional gastrointestinal (GI) disorder with worldwideprevalence rates ranging from 9-23%. Functionaldisorders are conditions where there is an absence ofanatomical or biochemical abnormalities on diagnostictests which could explain symptoms. IBS is a chronicfunctional bowel disorder characterized by abdominal painor discomfort and alterations in bowel habits. It is the mostcommon disorder diagnosed by gastroenterologists andaccounts for up to 12% of total visits to primary careproviders Gender appears to play an important role in IBS.Two-thirds of individuals with IBS are female with anestimated prevalence in women ranging from 14-24%. Ofthose who seek healthcare services including tertiary andambulatory care for IBS and other functional boweldisorders, women lead men by a ratio of 2-2.5:1 whileothers estimate the rate to be higher at 3-4:1. However, thegender distribution appears to be less than 2:1 among IBSnon-patients (individuals with symptoms of IBS but whohave not sought health care) in the community. It is notknown if this increased female prevalence represents areporting bias, i.e. if female patients are more willing thanmen to disclose that they have IBS-related symptoms, or ifit represents a biological difference. Not all individuals with IBS symptoms seek medical carefor their symptoms. Based on different epidemiologicalstudies performed in different countries, 20-75% ofindividuals meeting symptom criteria for IBS will seekmedical care for their symptoms at some point in theirlives. There are between 2.4 and 3.5 million annualphysician visits for IBS in the United States, during which2.2 million prescriptions are written. The cost to society interms of direct medical expenses and indirect costsassociated with loss of productivity and work absenteeismis considerable. It has been estimated that the total cost ofIBS is 30 billion dollars per year which includes 20 billiondollars for indirect costs and 10 billion dollars for directcosts.SYMPTOMS OF IBSGastrointestinal (GI) symptoms.The hallmark symptomsof IBS are chronic abdominal pain and/or discomfort andalterations in bowel habits, such as diarrhea, constipationor alternating diarrhea and constipation. Abdominal painhas been reported as primarily crampy or as a generalizedache with superimposed periods of abdominal cramps,although sharp, dull, gas-like, or nondescript pains are alsocommon. The intensity and location of abdominal pain inIBS are highly variable, even at different times within asingle patient. The abdominal pain and/or discomfortexperienced by IBS patients is often severe enough tointerfere with daily activities. Several factors exacerbate orreduce the pain of IBS. Many IBS patients reportincreased symptoms during periods of stress or emotionalupset such as job or marital difficulties. Defecation mayprovide temporary relief from the abdominal pain of IBS,whereas ingestion of food may exacerbate the discomfortin a subset of patients. Based on bowel habits, patients are commonly sub-classified into those having mainly diarrhea, mainlyconstipation, and those alternating between the twopatterns. IBS patients with constipation may experienceinfrequent bowel movements (3/week), hard stools,straining, and sensation of incomplete evacuation. IBSpatients with primarily diarrhea report frequent bowelmovements (3/day), loose and/or watery stools frequent,and urgency. The prevalence of the difference subgroupsbased on bowel habits is similar. Other common IBSsymptoms include bloating, visible abdominal distension,and mucus in the stool.Upper gastrointestinal symptoms are commonly reportedby IBS patients with 25% to 50% of patients reportingheartburn, early satiety, nausea, abdominal fullness, andbloating. Up to 87% have reported intermittent upperabdominal discomfort or pain (dyspepsia) byapproximately 40% of patients. Extra-intestinal symptoms and overlap with othercommon pain syndromes.Many IBS patients also reportextra-intestinal (non-gastrointestinal) symptoms such asfatigue, muscle pain, sleep disturbances, and sexualdysfunction. Up to two-thirds of IBS patients report extra-intestinal symptoms compared to less than 15% of healthyindividuals. These extra-intestinal symptoms may be dueto IBS co-morbidity with other stress-related syndromessuch as fibromyalgia, chronic fatigue syndrome, andinterstitial cystitis. Epidemiological studies have confirmedthe clinical impression that IBS frequently overlaps withthese other conditions in the same patient, suggestingshared pathophysiologic mechanisms. Psychological symptoms.Some IBS patients also havepsychological distress symptoms such as anxiety anddepression particularly in those with severe symptoms andhealth care seeking behavior. Somatization, anxiety anddepressive disorders are also more commonly seen in IBSpatients than in healthy controls. Psychosocial trauma andearly adverse life events (e.g., parental separation orphysical/verbal/sexual abuse history) may profoundlyaffect symptom severity, daily function, and healthoutcome. Although these adverse events such as abusemay be quite prevalent in IBS patients, a significantnumber have not discussed this with anyone and a smallernumber will actually inform their physicians.DIAGNOSIS OF IBSThe diagnosis of IBS is based on identifying characteristicsymptoms and excluding organic disease. An earlyconfident diagnosis permits tests to be minimized andreassures the patient that there is no lethal disease. Thereare no physical findings or diagnostic tests that confirm thediagnosis of IBS. Therefore, diagnosis of IBS involvesidentifying certain symptoms consistent with the disorderand excluding other medical conditions which may have asimilar clinical presentation. The symptom-based Rome IIdiagnostic criteria for IBS (Table 1) emphasize a ï¿½positivediagnosisï¿½ rather than exhaustive tests to exclude otherdiseases. A validation study of the Rome criteria afterexcluding patients with symptoms suggestive of othermedical conditions other than IBS (ï¿½alarm signsï¿½ e.g.bloody stools, weight loss, family history of colon cancer,refractory and severe diarrhea) showed that 100% ofindividuals who met the diagnosis of IBS based on theRome criteria truly had IBS rather than an alternativediagnosis. At 2 years follow-up, none of the IBS patientsrequired a change in diagnosis.Other medical conditions which may present withsymptoms similar to those seen in IBS includeinflammatory bowel disease, GI infections, lactoseintolerance, thyroid disease, microscopic or collagenouscolitis and malabsorption syndromes such as celiac sprue(Table 2). A medical history and physical examination,laboratory and GI tests can help to exclude these otherdiagnoses. These tests include routine blood tests, stoolstudies for infection, and endoscopic procedures such asupper endoscopy, sigmoidoscopy and colonoscopy. Inpatients 50 years of age who meet diagnostic criteria forIBS and have no ï¿½alarm signsï¿½ suggestive of diseases otherthan IBS, initial screening tests such as a complete bloodcount to check for anemia and a chemistry panel can beobtained. Other screening tests to consider are a thyroidtest (TSH) and a blood test for celiac sprue. However,further tests and procedures such as a colonoscopy are notgenerally recommended. Patients 50 years of age withIBS symptoms should undergo a screening colonexamination with either a colonoscopy or flexiblesigmoidoscopy and barium enema if these tests have notbeen done previously, regardless if they have alarm signs(see Figure 1).In some centers, the presence of bacterial overgrowth isoften determined because this condition may causesymptoms similar to those of IBS. It is most commonlydiagnosed by a lactulose hydrogen breath test. Two studiesfrom the same research group found that 78% to 84% ofpatients with IBS had bacterial overgrowth. In patientswith evidence of bacterial overgrowth, those treated withan antibiotic such as neomycin had a greater reduction intheir GI symptoms compared with placebo. Although thesedata are intriguing, there are some methodologiclimitations in these studies and, therefore, the use ofwidespread hydrogen breath testing for bacterialovergrowth is still not generally advocated. PATHOPHYSIOLOGIC MECHANISMS OF IBSAlthough psychological and physiological abnormalitieshave been described, the overall pathophysiology of IBS isnot well understood. Similar to other chronic medicalconditions, a multi-component conceptual model of IBS,which involves genetic, physiologic, emotional, cognitive,and behavioral factors, has been formulated (Figure 2).Although all factors are closely interconnected, theimportance of individual factors in the generation of IBSsymptoms may vary greatly between individuals.Previously, IBS was considered primarily a disorder ofaltered gut motility. Currently, increased bowel sensitivity(visceral hypersensitivity) and altered brain-gutinteractions are felt to play a principal role in thepathophysiology of IBS. Recently, it has been found thatgenetic and environmental factors are important in IBS butfurther studies are needed to understand the importance ofthese factors in the prevalence, symptoms, physiologicresponses and response to treatment in IBS.Altered intestinal motor function.Altered intestinalmotility has been found in IBS, particularly exaggeratedcontractions (motor response) in the lower (sigmoid) colonto psychological stress and food intake. These alterationsmay explain why many IBS patients experience typicalIBS symptoms following meals and develop exacerbationsduring stressful life events. These changes in bowelmotility are likely due to alterations in the autonomicnervous system outflow to the intestine. Increased gut sensitivity.There has been compellingevidence that IBS patients have enhanced perception ofbowel (visceral) stimuli such as food or distensions of thegut wall. The initial clinical observations that led to thehypothesis that patients with IBS have visceralhypersensitivity included the presence of recurringabdominal pain as a principal symptom, the presence oftenderness during palpation of the sigmoid colon (leftlower abdominal area) during physical examination inmany patients, and excessive pain often reported bypatients during endoscopic examination of the sigmoidcolon. Published studies measuring visceral sensitivitysuggest that a variety of abnormal sensations orperceptions in relation to bowel stimuli may be morefrequent in IBS patients. At least two perceptualalterations can be distinguished, a hypervigilance(increased attention or vigilance) towards expectedaversive events arising from the bowel, and hyperalgesia(lowered threshold to pain) which is inducible by sustainedpainful visceral stimulation. These findings are paralleledby similar findings of target system hypersensitivity inother disorders such as fibromyalgia and myofascial paindisorder. In contrast to their enhanced perception ofvisceral pain, most IBS patients have normal or evendecreased pain sensitivity and tolerance for painful coldand mechanical stimulation of somatic (skin and muscle).However, there is a recent study that has demonstratedincreased somatic sensitivity to thermal heat in IBSpatients. Patients with IBS who also have co-existing fibromyalgia have increased somatic sensitivitycomparable to patients with fibromyalgia alone.Increased stress mediators in IBS.There is increasingevidence to support the prominent role of stress in thepathophysiology and in the clinical presentation of IBSsymptoms. There are few published reports on alterationsin stress mediators, such as catecholamines and cortisol tostress or visceral stimulation in IBS. Several studies havereported increased in catecholamines (norepinephrine andepinephrine) and cortisol levels in IBS patients. However,it remains to be determined whether these neuroendocrinealterations play a direct role in gut function and symptomgeneration. Altered brain-gut communication in IBS.A unifyinghypothesis to explain the functional bowel disorders is thatthey result from a dysregulation of the brain-gut axis. Anevolving theory is that normal gastrointestinal functionresults from an integration of intestinal motor, sensory,autonomic and CNS activity and GI symptoms may relateto dysregulation of these systems. Brain imaging studiessuch as functional magnetic resonance imaging (fMRI) andpositron emission tomography (PET) have been performedin IBS patients to measure brain activation patterns tovisceral stimuli. These studies suggest that brainactivation responses to visceral stimuli are distinctlydifferent in IBS patients compared to healthy individuals.IBS patients may have different emotional and cognitiveprocessing of sensory information from the gut comparedto healthy individuals. Post-infectious IBS.Symptoms suggestive of IBS occurin approximately 7-30% of patients following acute GIinfections, often persisting for years following completeresolution of the infection. A large cohort study identifieda self-reported history of acute gastroenteritis as a majorrisk factor for the development of IBS. Reported riskfactors for the development of post-infectious IBS includefemale sex, the duration of the acute diarrheal illness andthe presence of sustained psychosocial stressors around thetime of infection. Post-infectious IBS is not restricted to aparticular organism and has been documented with avariety of bacterial infections (Salmonella, Campylobacterand E. coli) as well as parasitic infection. However, therole of acute viral gastroenteritis in this condition isunknown.In post-infectious IBS, low grade GI inflammation orimmune activation may be a basis for altered motility,and/or nerve and mucosal (lining of bowel) function of thegut in IBS. Recent studies have also shown that in a subsetof unselected IBS patients (no documented history of apreceding gut infection), there is evidence of increasedinflammatory cells in the colon mucosa. It remains to bedetermined if altered gut immune function is a generalcharacteristic of IBS patients. The implication of stressfullife events in the development of post-infectious IBSsuggests a convergence of central (brain) and peripheral (gut) mechanisms in the clinical presentation of thissyndrome.Gender differences.In addition to IBS, many functionalGI disorders and other chronic visceral pain disorders (e.g.interstitial cystitis and chronic pelvic pain) and somaticpain disorders (e.g. fibromyalgia, myofascial paindisorder) are more common in women than in men.Increasing evidence suggests that gender differences existin the symptoms, pathophysiologic responses and responseto certain treatments in IBS. Female IBS patients are morelikely to be constipated, complain of abdominal distensionand certain extra-intestinal symptoms. Studies have alsosupported an influential role of ovarian hormones (e.g.estrogen and progesterone) on bowel function and painsensitivity which can in part explain the gender differencesin IBS. Several investigators have reported a variation inGI symptoms during different phases of the menstrualcycle, particularly increased abdominal pain and loosestools at the perimenstrual (just prior to and at time ofmenses) phase. TREATMENTTreatment of IBS includes both non-pharmacologic andpharmacologic therapies. An important component of non-pharmacologic treatment for IBS is a successful physician-patient relationship. The physician should strive toestablish effective bi-directional communication with thepatient, gain the patientï¿½s confidence with a concise,appropriate medical evaluation and offer reassurance andeducation that IBS is a real medical condition with apotential impact on health related quality of life butwithout significant long/term health risk. Some IBSpatients, especially those presenting with new onset ofsymptoms, express relief that their symptoms are notcaused by a serious condition such as malignancy. Othercomponents of non-pharmacologic treatment of IBSinclude diet recommendations, lifestyle modifications, andpsychosocial intervention if needed. Patients with mild IBS symptoms comprise the mostprevalent group, and are usually treated by primary carepractitioners, rather than specialists. These patients haveless significant functional impairment or psychologicaldisturbance. These patients do not see a clinician veryoften, and usually maintain normal daily activities.Treatment is directed toward education, reassurance, andachievement of a healthier lifestyle and occasionalmedication. Dietary advice may include avoidingoffending foods which can trigger symptoms (e.g. lactoseor fructose products, fatty foods, caffeine, gas-producingfoods). Fiber supplementation has been shown to beeffective for symptoms of constipation. Pharmacologic therapy is best used in IBS patients withmoderate to severe symptoms refractory to physiciancounseling and dietary manipulations. First line treatmenthas traditionally been aimed at treating the mostbothersome symptom because of the lack of effectivetreatment for the overall improvement of multiplesymptoms in IBS patients. However, new therapies forIBS have been recently introduced and have been shown toeffectively treat multiple symptoms of IBS.Anticholinergic/Antispasmodic agents.After fiberpreparations, antispasmodic agents are the next mostcommonly prescribed group of medications for thetreatment of IBS. However, several studies do not providefirm evidence that anticholinergic agents are efficacious inthe IBS population as a whole. Only a few of theseantispasmodics have been shown to be more effective thanplacebo in relieving abdominal pain in high quality clinicalIBS trials but these are not currently available in the U.S. Antidiarrheal agents.In IBS patients with diarrhea,antidiarrheal agents such as loperamide and diphenoxylatecan be effective in decreasing bowel movement frequency,improving stool form by enhancing intestinal water and ionabsorption, and increasing anal sphincter tone at rest.These physiologic actions seem to explain theimprovement in diarrhea, urgency, and fecal soilingobserved in patients with IBS. These medications do nottypically relieve abdominal pain and may causeconstipation.Psychotropic medications.The rationale of using thisclass of drugs in IBS may relate to several factors, such asthe prominent co-morbidity of IBS with psychologicdistress symptoms and the effects of these agents on gutmotility and pain sensation. Among the classes ofantidepressant medications, the tricyclics have been mostextensively evaluated in IBS. At lower doses than thoseusually used to treat depression (starting at 10 mg and upto 75 mg nightly), amitriptyline and desipramine have beenfound to be significantly more effective than placebo inpatients with IBS. Antidepressants have analgesic (painrelief) properties, which may benefit patientsindependently of the psychotropic effects of the drugs.Treatment with tricyclics should begin with low doses(e.g., 10 mg/day) and increased as needed up to fulltherapeutic doses. Selective serotonin reuptake inhibitors(SSRIs, e.g. paroxetine, citalopram) and selective serotoninand noradrenergic reuptake inhibitors (SNRIs, e.g.venlafaxine) have not been well studied for treatment ofIBS, and are more expensive, but have less side effectsthan tricyclics and empirically may help reduce painfulsymptoms and improve general well-being and quality oflife.Novel serotonin agents.The prominent role of serotoninin GI motility and sensation has led to the development ofnovel serotonin agents such as alosetron and tegaserod inthe treatment of IBS. Most of serotonin (also known as 5-HT) in the body resides in the bowel wall withinenterochromaffin cells lining the gut (mucosa) and nervecell bodies. Serotonin is released from theenterochromaffin cells and acts on receptors on the nerveswithin the bowel wall. These nerves may be part of the nervous system which resides completely within the bowelwall, known as the enteric nervous system, or may benerves that transmit painful and non-painful informationby projecting from the bowel to the spinal cord and brain.Activation of these nerves by serotonin leads to the releaseof other neurotransmitters and through their actions, itplays a major role in gut motility, secretion and sensation.Alosetron (Lotronex&#63194







, which is a 5-HT3 antagonist, hasbeen shown to be effective in relieving pain, normalizingbowel frequency, and reducing urgency in non-constipatedIBS female patients. This medication was approved by theFDA last year but was later withdrawn because of theadverse events of constipation and ischemic colitis, thelatter being observed in 0.1%-1% of patients receiving themedication. Future studies are being planned to determineif there is a causal association of alosetron and ischemiccolitis. However, alosetron has recently been re-approvedand now is available for the treatment of women withsevere diarrhea-predominant IBS under the Restricted UseProgram. Alosetron is indicated only for women withsevere diarrhea-predominant IBS who have: chronic IBSsymptoms (generally lasting ≥ 6 months), no evidence ofanatomic or biochemical abnormalities of the GI tractwhich could explain their symptoms, and failed to respondto conventional therapy. IBS is considered severe if itincludes diarrhea and ≥ 1 of the following: frequent andsevere abdominal pain/discomfort, frequent bowel urgencyor fecal incontinence, or disability or restriction of dailyactivities due to IBS. Physicians must enroll in theRestricted Use Program in order to prescribe alosetron.Patients should discuss with their physicians about therisks and benefits of the medication before beingprescribed it. Both should sign the Patient-PhysicianAgreement form. The starting dose of alosetron is now 1mg orally once daily. If the patient does not experiencecomplete relief of their symptoms after 1 month, the dosecan be increased to 1 mg orally twice daily which was theoriginally approved dose. Any patient who experiencesincreased abdominal pain, blood in their stool and/orconstipation should immediately stop their medication andcontact their physician. Tegaserod (Zelnorm&#63194







is a partial 5-HT4agonist, whichhas been shown to be effective in relieving the globalsymptoms of IBS with constipation. It has been recentlyapproved for the treatment of IBS with constipation inwomen. Tegaserod has been shown to accelerate GI transittime in IBS patients and therefore would increase stoolfrequency, and increase electrolyte secretion in the boweland thus improve stool form. In addition to its motilityenhancing properties, tegaserod has been shown to havepain inhibitory properties in animal studies and thereforemay reduce abdominal pain although human studies areneeded to confirm this effect. Unlike other currentlyavailable medications for IBS with constipation, tegaserodappears to be effective in treating the multiple symptomsof IBS. The subjectï¿½s global assessment of relief of IBSsymptoms, change in number of bowel movements, abdominal pain and bloating are all reportedly improved infemale patients with IBS with constipation takingtegaserod as compared to placebo. The only adverse eventswhich were seen at a small but significantly higher rate inpatients taking tegaserod compared to placebo wereheadache and transient diarrhea. Psychological treatments.Referral for psychologicaltreatment can be recommended as part of a multi-component treatment program to help the patient bettermanage the symptoms, or to address psychosocialdifficulties (e.g., abuse, loss) that may be interfere withdaily function and ability to cope with the illness. Ingeneral, these treatments are reserved for patients withmoderate to severe symptoms, particularly if theyexperience psychological distress. However, the patientmust be motivated and see this type of treatment asrelevant to their personal needs. Psychological treatmentsused to treat IBS include psychotherapy (dynamic andcognitive-behavioral therapy), relaxation therapy,hypnotherapy, and biofeedback therapy. Psychologicaltreatments can also be combined. Review of well-designedtreatment studies of IBS supports the superiority ofpsychological treatment over conventional medicaltherapy. Follow-up studies (duration 9-40 months), havedemonstrated that psychological treatment maintainedsuperiority over placebo, indicating that these methodshave lasting value. The choice of treatment will depend onpatient requirements, available resources and theexperience of the therapist. CONCLUSIONSIBS is a common, chronic disorder characterized byexacerbations and remissions, which presents withsymptoms of abdominal pain and/or discomfort and alteredbowel habits. It has a chronic relapsing course and canoverlap with other functional GI (dyspepsia) and non-GI(fibromyalgia) disorders. The clinical diagnosis of IBS is based on identifyingsymptom criteria with a ï¿½positive diagnosisï¿½ and excludingorganic disease with minimal diagnostic evaluation.Clinicians should feel secure with the diagnosis of IBS, ifmade properly, because it is rarely associated with otherexplanations for symptoms. Although there are manyexpensive and sophisticated tests available for theevaluation of IBS symptoms, these are generally notneeded for patients with typical symptoms and no featuressuggestive of organic diseases.An integrated diagnostic and treatment approach firstrequires an effective physician-patient relationship. Acareful history will also identify the need for diagnosticstudies and treatments as determined by the nature andseverity of the predominant symptoms, and the degree andextent of influencing psychosocial and other factors. The fact that definite structural or biochemicalabnormalities for these disorders cannot be detected withconventional diagnostic techniques does not rule out thepossibility that neurobiological alterations will eventuallybe identified to explain fully the symptoms of mostfunctional disorders. Examples of such a shift inperspective from symptom-based disorders withoutdetectable abnormalities to medically treatable diseasesbased on specific neurobiological alterations includeaffective disorders (depression, anxiety) and migraineheadaches. Similar to other chronic illnesses, amulticomponent model that involves physiologic,affective, cognitive, and behavioral factors can beformulated for IBS. Although all factors are closelyinterconnected, the importance of individual factors in thegeneration of IBS symptoms may greatly vary betweenindividuals. Physiologic factors implicated in thegeneration of IBS symptoms include hypersensitivity ofthe GI tract to normal events, autonomic dysfunctionincluding altered intestinal motility response to stress andfood intake, alterations in fluid and electrolyte handling bythe bowel, and alterations in sleep. Many of the traditional therapies have been used to treatspecific IBS symptoms because they have not been shownto significantly relieve global symptoms, which wouldimprove an overall sense of well-being. However, thediscovery of novel serotonergic agents such as tegaserodand alosetron have been shown to be effective in treatingglobal symptoms in patients with IBS compared withplacebo. More recently published studies evaluating theefficacy of antidepressants, such as tricyclics and SSRIs,suggest that these medications may help improve generalwell-being in addition to treating psychological co-morbidity in affected individuals but further studies areneeded. Psychological and behavioral therapies have alsobeen showed to be effective for IBS however it potentiallycan be limited by the availability of experienced therapists.Instituting a multidisciplinary approach using non-pharmacologic and pharmacologic therapeutic modalitiesmay result in the most effective outcome. Future studieswill further enhance our understanding of this conditionand lead to newer, more effective treatments. http://216.109.117.135/search/cache?p=lin+...&yc=15315&icp=1


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## Talissa (Apr 10, 2004)

Hi Eric,The increased permeability found in IBS patients, as well as imbalanced flora in IBS patients, are outlined in the Medscape Gastroenterology article I posted above.The references are indicated by the numbers following the study information.If you'd like to see the individual references, maybe you should click on the link I provided. I provided the link, so that those who wanted to read further would have The Option of reading the entire article, with references.This was a mainstream source.Take it easy,Talissa


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## anonymoose (Jul 20, 2003)

it couldnt hurt to starve the bad bacteria by cutting out all sugar/grain from your diet. and by taking a quality probiotic. i would think the better ones need to be refrigerated and have more strains of bacteria. best ive come across is jarro-dophillus(probably spelt wrong).


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## Talissa (Apr 10, 2004)

This learning curve linking IBS & bacterial imbalance includes Donald R. Henderson, MD, MPH, Chief of Staff, Daniel Freeman Memorial Hospital & Assistant Clinical Professor of Medicine and Gastroenterology, UCLA School of MedicineHe says:"Physicians also should note that IBS recently has been linked to possible infection or bacterial imbalance. Thus the use of antibiotics and probiotics may prove to be of value. In addition, nutritional supplements like bovine colostrum have been proved to be of great value in treating colitis and, I believe, similarly may be of value in treating IBS. The allopathic model for treating IBS has failed miserably because we do not have much understanding or agreement about how to manage this problem. Therefore, from a therapeutic standpoint, I believe we should look toward the alternative models and further investigate the mindï¿½gut interaction." http://www.medicalcrossfire.com/debate_arc...er_Exchange.htm Dr. Henderson mentions colostrum. If you're wondering why, high quality bovine colostrum has been shown effective in healing the intestinal mucosa barrier of the intestinal wall. Talissa


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## eric (Jul 8, 1999)

I know who the source is quite well and I personally know what inflammation is seen in IBS, macroscopic inflammation of specific cells, but IBS is not an Inflammatory disease like IBD, it is macroscopic inflammation of specific cells, when they peel back some of the muscle layers of the digestive system.Those cells are connected to pain in IBS, stress and IBS, some food reactions and IBS and the bladder and IBS and the HPA axis system to fighting infections and the fight or flight responce and to Fibro and IBS and CFIS and IBS, ect..I am not sure however you understand it well or that Dr Meyer from the above article knows stress can alter the immune barrier. Because your approach and thinking on this is NOT what they believe.Or that "The mechanism of action of probiotics in IBS is poorly understood and has been thought to be attributable to changes in fermentation products." in IBS. Although probiotics have been studied and shown to help heal inflammatory conditions such as IBD.Altered transit/motility can result in altered food fermentation and hence altered flora bacteria. Or that probiotics can help with gas and give relief since small amounts of gas put pressure on the pressure sensitive cells lining the digestive track that are sensitive to ALL stimuli.Or that post infection IBS has a lot to do with gut permeability at the time of enteric infection for one.Or that Mayer is a top neurogastroenterologist in IBS, who has a model of IBS.Who also worte 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.cmecorner.com/macmcm/pcp/pcp2000_01.htm and thisStress and the Gastrointestinal TractV. Stress and irritable bowel syndrome Emeran A. Mayer, Bruce D. Naliboff, Lin Chang, and Santosh V. Coutinho UCLA/CURE Neuroenteric Disease Program, Departments of Medicine, Physiology, and Biobehavioral Sciences, UCLA School of Medicine, Los Angeles, California 90024 http://ajpgi.physiology.org/cgi/content/full/280/4/G519 and this which states inflammation does not completely expalin IBS"Curr Gastroenterol Rep. 2003 Aug;5(4):331-6. Related Articles, Links Current insights into the pathophysiology of irritable bowel syndrome.Schwetz I, Bradesi S, Mayer EA.Center of Neurovisceral Sciences and Women's Health, CURE: Digestive Diseases Research Center, David Geffen School of Medicine at UCLA, VAGLAHS, Bldg. 115, Room 223, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA. emayer###ucla.eduRecent reports have emphasized the possible role of mucosal immune activation and inflammation in neuropathic changes in the pathophysiology of irritable bowel syndrome (IBS). However, novel findings using functional brain imaging techniques have underlined the importance of altered perception of visceral stimuli to symptom generation in IBS. These new developments have rekindled an old debate on peripheral versus central mechanisms in the pathophysiology of IBS. In this review we discuss the latest findings in light of these two concepts. In addition, we provide evidence for the hypothesis that, in the absence of alterations in endogenous pain modulation systems and changes in visceral perception, chronic inflammatory mucosal changes in the gut are not a plausible mechanism to explain the presence of chronic abdominal pain, a cardinal IBS symptom.Publication Types: Review Review, Tutorial PMID: 12864964and this"Dig Dis. 2001;19(3):212-8. Related Articles, Links Basic pathophysiologic mechanisms in irritable bowel syndrome.Mayer EA, Naliboff BD, Chang L.UCLA/CURE Neuroenteric Disease Program, Department of Medicine, Physiology and Biobehavioral Sciences, UCLA School of Medicine, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA. emayer###ucla.eduConverging evidence supports the concept that the irritable bowel syndrome (IBS) symptom complex results from altered regulation of gastrointestinal motility and epithelial function, as well as an altered perception of visceral events. Despite similar symptoms, there is likely heterogeneity of underlying dysfunction and pathogenesis in different subgroups of IBS patients: the syndrome may be produced by primary alterations in the central nervous system (CNS; top down model), or by primary alterations in the periphery (bottom up model), or by a combination of both. One plausible mechanism by which alterations in the CNS result in symptoms, is the enhanced responsiveness of central stress/emotion circuits. The physiological effects of psychological and physical stressors on gut function and brain-gut interactions are mediated by outputs of the emotional motor system in terms of autonomic, neuroendocrine, attentional and pain modulatory responses. IBS patients show an enhanced responsiveness of this system manifesting in altered modulation of gastrointestinal motility, secretion, immune function and in alterations in the perceptual and emotional response to visceral events. Copyright 2001 S. Karger AG, BaselPublication Types: Review Review, Tutorial PMID: 11752839 as well as all these archive articles on there website.Articles Archive Irritable Bowel Syndrome by Lin Chang, MD (You will need Adobe Acrobat Reader to view this article. Click here to get the free Acrobatt Reader.)Gut Feelings: The Surprising Link Between Mood and Digestion (A Healthy Me, 2001)The Neurobiology of Stress and Emotions (Participate, newsletter of IFFGD, 2001) The Inside Trak was a publication written by members of the Neuroenteric Disease Program, now part of the Center for Neurovisceral Sciences & Women's Health. It was aimed at patients suffering from IBS and other chronic disorders of the gastrointestinal tract. The articles dealt with a wide range of issues thought to be of interest to patients and was also a means to update patients on new developments in research, drug development and ongoing clinical studies.Summer 2002 Heartburn and Stress, The Autonomic Nervous System, The New Center for Integrative Medicine Summer 2001 Gender and Stress, Alternative Medicine, Tegaserod: A New Drug for IBS Winter 2000 New IBS Medications, Altered Stress Responses in IBS, Be Your Own Doctor Fall 1999 GERD, Stress and GI Symptoms, Constipation, Sleep Disturbances Spring 1998 Dietary Fiber, Longitudinal Trial, Fibromyalgia and IBS, Abstract Reviews, Why Participate in a Clinical Trial Fall 1997 What is GERD, Nonulcer Dyspepsia, The IBS Class, Pain in the Brain, Becoming a Self Manager, Suggested Readings Spring 1997 Living Healthy with Chronic Illness, How Drugs Become FDA Approved, Sensitization Studies, Breakthroughs in IBS Research, New IBS Drugs, Looking into the Brain for Answers as well as this bookEvolving Pathophysiological Models of Functional GI DisordersEvolving Pathophysiological Models of Functional GI Disorders --From the Chairman's Forward by Emeran A. Mayer, M.D. Despite a recent surge of interest in functional gastrointestinal (GI) disorders by the scientific and clinical community; and by the pharmaceutical industry as well, these disorders remain poorly understood. Few effective treatments exist, and disagreement among experts -- even on such seemingly simple questions as "what is constipation?" or the somewhat more complex issue of the role of psychological "co-morbidity" in symptom generation -- continues to plague rational discussions. Many clinicians still use the term "motility disorders" to refer to functional GI disorders, even though few investigators would agree on even one motility disturbance that might be specific for, or play a pathophysiological role in, functional GI disorders. One of the biggest problems that exists for basic scientists working in this area is that they do not have the opportunity to experience first hand the many characteristic clinical presentations of patients with these disorders. Is there any connection between mechanisms responsible for generating coordinated contractile activity of the gut and symptoms of irritable bowel syndrome (IBS) or functional dyspepsia? Many would agree that progress on this topic thus far is disappointing. The 3-day workshop Pathophysiological Models of Functional Gastrointestinal Disorders that forms the basis of this monograph, sponsored by the International Foundation for Functional Gastrointestinal Disorders (IFFGD) and organized in the Fall of 1999, was designed to explore the feasibility of an emerging consensus process in the area of IBS pathophysiology. The primary goal of the workshop was to provide basic and clinical investigators (with different backgrounds and interests but with a shared interest in functional medical disorders) with an impetus to develop conceptual models that are applicable to functional GI disorders. More than 50 presenters and discussants contributed to five sessions in the workshop. The presenters were charged with developing conceptual pathophysiological models that can explain the key clinical features of the functional GI disorders, particularly IBS. We were fortunate that so many leading international experts in all of the areas addressed in this workshop were able to attend and participate in this endeavor. In the introduction and Session I, presentations included such key areas as minimal diagnostic criteria for functional GI disorders, GI symptoms and temporal variations of symptom presentations, extraintestinal symptoms, comorbid affective disorders and stress, manifestations of functional GI disorders in early life, and alterations in GI motility. These particular topics were chosen to emphasize the following points: Functional GI disorders are not distinct stable entities, but show considerable variations in predominant symptom pattern over time. They are chronic disorders that frequently, perhaps in the majority of patients, start in childhood and run a chronic lifelong course marked by exacerbations and remissions. Functional GI disorders are not isolated problems of the gut, but characteristically include different extraintestinal symptoms as well. They are distinct from the classic GI motility disorders such as chronic intestinal pseudo-obstruction syndrome or gastroparesis. In Session II, basic science investigators addressed different peripheral aspects of afferent and efferent regulation of the gut by the enteric and central nervous systems, including the role of interstitial cells of Cajal and smooth muscle cells, intrinsic and extrinsic afferent neurons, inflammatory cells, and mast cells. They also presented pathophysiological models that were relevant to IBS symptomatology. In the first half of Session III, clinical and basic research investigators with expertise in psychology, psychiatry, and pain physiology presented models relevant to IBS. Topics included central autonomic dysregulation, sleep alteration, and hypervigilance, and were specifically chosen to address several key alterations identified in IBS patients and thought to play a prominent role in IBS symptomatology. During the second half of the session, neuroscientists with a primary research interest in central stress and pain circuits presented models of altered brainstem/forebrain activation, alterations in the stress response, altered neuroendocrine responses, and alteration in pain modulation systems. Alterations in stress responsiveness and pain modulation are currently believed to be key components of evolving models for IBS pathophysiology. In Session IV, several psychiatric investigators presented models that might be relevant to functional GI disorders. Topics included long-term consequences of neonatal maternal separation, abnormal CCK function as a possible pathophysiological model for panic disorder and gastrointestinal disorders, and post-traumatic stress disorder. In Session V investigators presented pathophysiological models of common chronic somatic and visceral syndromes, such as fibromyalgia, asthma, irritable bladder, and migraine. Finally, a summary of all five sessions was presented and identified several converging themes from among seemingly unrelated problems that ranged from asthma to panic attacks and sleep disorders. At the conclusion of the workshop, the majority of participants left with a surprising sense of accomplishment and realization of an evolving interdisciplinary consensus. This monograph captures the essence of this exciting workshop. The Editors hope that this publication will stimulate investigators in academia, clinical medicine, and industry alike to consider the proposed models, put them through rigorous experimental testing, and use them to identify therapeutic targets and develop promising new pharmacological agents. The 117-page volume, Evolving Pathophysiological Models of Functional GI Disorders, is available by contacting IFFGD. or thisGut. 2000 Oct;47(4):497-505. Related Articles, Links Perceptual responses in patients with inflammatory and functional bowel disease.Chang L, Munakata J, Mayer EA, Schmulson MJ, Johnson TD, Bernstein CN, Saba L, Naliboff B, Anton PA, Matin K.UCLA/CURE Neuroenteric Disease Program, Department of Medicine and Physiology, UCLA School of Medicine, Los Angeles, California 90073, USA. linchang###ucla.eduBACKGROUND AND AIMS: Enhanced visceral sensitivity following a transient inflammatory process in the gut has been postulated as an aetiological mechanism of irritable bowel syndrome (IBS). In this study we compared perceptual responses to rectosigmoid distension in patients with mild chronic inflammation of the rectum (ulcerative colitis (UC)) and patients without mucosal inflammation (IBS) to determine if chronic low grade mucosal inflammation may be a plausible explanation for rectosigmoid hypersensitivity reported in both IBS and UC patients. METHODS: UC disease activity was quantified using activity index scores. Perception thresholds for discomfort during rectosigmoid distension were compared between 11 UC patients with quiescent or mild disease activity, 18 IBS patients, and 13 healthy controls. RESULTS: Although UC activity index scores negatively correlated with perceptual thresholds for discomfort (r=-0.76, p=0.016), UC patients had higher discomfort thresholds compared with IBS patients and controls before (p=0.02) and after (p<0.001) a noxious sigmoid conditioning stimulus. CONCLUSIONS: Rectal perception was attenuated in UC but enhanced in IBS. In chronic mild inflammation, activation of antinociceptive mechanisms may prevent the development of visceral hyperalgesia. *Low grade mucosal inflammation alone is unlikely to be responsible for symptoms in functional gastrointestinal disorders.* PMID: 10986209 or thisInflammatory Mediators in Irritable Bowel Syndrome Maria O'Sullivan, PhDDepartment of Gastroenterology, Adelaide & Meath HospitalTrinity College, Dublin, IrelandIrritable bowel syndrome (IBS) is a chronic condition characterized by abdominal pain and altered bowel habit, in the absence of demonstrable structural gastrointestinal abnormality. Essentially the gut functions abnormally - people experience symptoms of pain, diarrhea and/or constipation but no abnormality of the bowel can be identified by standard medical tests. Numerous research studies have now documented physiological changes, including altered motility and hypersensitivity, in the gastrointestinal tract of IBS patients. The mechanisms underlying these events, however, remain unclear. There is growing evidence that inflammation in the gastrointestinal mucosa may play a role in the pathogenesis of at least a sub-set of IBS (1-3). Importantly, overt colonic inflammation precludes a diagnosis of IBS. The challenge for researchers therefore, is to record subtle changes in inflammatory mediators that are not identifiable by usual routine processes. Inflammation and IBS - the EvidenceExperimental (animal) data show that inflammation, even if mild, could lead to persistent changes in gastrointestinal nerve and smooth muscle function, resulting in dysmotility, hypersensitivity and gastrointestinal dysfunction (1, 4-6). In humans, the role of inflammation in the generation of IBS symptoms is less well studied, although there are important findings from people with 'post-infective IBS'. After an acute gastrointestinal infection up to one-third (7-29%) of individuals develop persistent symptoms compatible with IBS (7, 8). In these post-infective IBS subjects, a persistent increase in rectal sensitivity (8) and in inflammatory cells (specifically enteroendocrine cells and lymphocytes) (9) have been documented. To put this in context, however, the majority (over 70%) of people who develop gastroenteritis fully recover and do not develop persistent bowel symptoms. Factors that may predict those who develop post-infective IBS include specific psychological factors, female gender and a longer duration of the initial illness. While there is now reasonable evidence to support a low-grade inflammatory response in those who develop IBS following an acute episode of gastroenteritis, there is still little know about inflammation in IBS patients who have no obvious recent evidence of acute infection. The role of inflammation in non post-infective IBS has been a particular research interest of our group and began with an interest in studying mast cells in IBS. Mast Cells and IBS The mast cell has potential to be a key player in IBS. Although mast cells are most widely known for their role in allergic responses, these cells are normally present throughout the gut and are involved in a range of physiological and pathological activities including mucosal defense mechanisms and inflammation. Mast cells may release an array of inflammatory mediators that act on smooth muscle, nerves and immune cells, which may ultimately result in gastrointestinal dysfunction and symptoms. In addition, mast cells in the gut are located close to nerves providing a structural basis for communication between the gut and the nervous system. In 1993, Weston and colleagues reported increased mast cell numbers in the mucosa of IBS patients(10) - these changes were identified in tissue from the end of the small bowel (terminal ileum). Similarly we identified significant increases in mast cells in IBS patients compared to controls in the colon (specifically at the caecum) (11). There were also trends for increases in other regions of the colon (ascending and descending colon) but no differences could be seen at the rectum. The lack of changes in mast cell infiltration in the rectum has since been confirmed by others (9). Collectively these studies suggest that mast cells were increased in IBS patients - this may be part of a low-grade inflammatory response, although the components and nature of this response remain poorly understood. NITRIC OXIDE AND IBSWe hypothesised that inducible nitric oxide synthase may be a novel and important marker of inflammation in IBS. Enzymes from the nitric oxide synthase family are responsible for the synthesis of nitric oxide (NO) from the oxidation of L-arginine. While at least three enzyme sub-types (isoforms) have been described, our study focussed on one specific isoform, namely inducible nitric oxide synthase (iNOS). This enzyme is thought to be capable of producing large amounts of nitric oxide and to be expressed during inflammation (12). In the human colon, upregulation of iNOS has been implicated in inflammatory processes and increased expression has been documented in inflammatory bowel disease. In colonic mucosa from IBS patients, we found a significant increase in iNOS expression compared to control patients (13). We also measured nitrotyrosine, which is considered a by-product of nitric oxide generation. Overall the nitrotyrosine data in IBS paralleled that of iNOS almost exactly. iNOS could be detected in epithelial cells, lymphocytes (CD3+ T and CD20+ B lymphocytes) and macrophages. Mast cells did not appear to express the iNOS. Overall we demonstrated an increase in iNOS, an enzyme that catalyses the production of nitric oxide, combined with an increase in nitrotyrosine, a by-product of nitric oxide generation. In terms of factors that may affect iNOS expression, there was a trend towards higher iNOS levels in the diarrhea compared to the alternating group although this was not statistically significant. Elevated iNOS may be a marker of general low-grade inflammation in IBS. Induction of iNOS and the generation of NO, could have several other potential roles in IBS - for example NO may have direct effects on intestinal nerve and motor function and intestinal on permeability. OTHER INFLAMMATORY CELLS IN IBSWhile there was some tentative evidence of an associated involvement of other inflammatory markers in our study, these were not striking or clear-cut. On average there were trends for increases in CD3+ lymphocytes and the proportion of lymphoid tissue. Similarly in IBS there was a trend for increased expression of nuclear factor kappa B (NF-?







, a transcription factor for an array of pro inflammatory cytokines and mediators. In our study, none of these changes were statistically significant. In contrast, others have previously reported significant increases in inflammatory cells, for example an increase in CD3+ lymphocytes in post-infective IBS9 and an increase in overall cellularity in the colonic mucosa in IBS (14). CD3 is a 'pan T-lymphocytes marker' and allowed us to estimate the overall number of T-lymphocytes in the lamina propria of the IBS patients. It is possible that specific subclasses of lymphocytes may be altered in IBS (e.g. CD4+ and CD8+ classes). Interestingly, the CD4+ T cell subtype has been implicated in an animal model of inflammation. In this model, stress was shown to reactivate colonic inflammation (15) - susceptibility to reactivation of inflammation by stress appeared to specifically require CD4+ lymphocytes. ANTI-INFLAMMATORY MEDIATORS IN IBS The study of inflammation in IBS has largely focused on the role of pro-inflammatory cells and mediators. From other gastrointestinal inflammatory diseases, we know that inflammatory responses involve a complex balance between pro- and anti- inflammatory mediators. There is emerging data to suggest that people with IBS may have a genetic predisposition to produce low amounts of anti-inflammatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-







(16). Moreover, there is a further preliminary report (17) of dysfunctional mucosal protective mechanisms in IBS characterize by reduced numbers of macrophages. While this data is provisional, it is plausible that people who develop IBS could have poorer defense mechanisms to combat infections or other gut insults.A Link between Inflamation and StressAn increase in inflammatory mediators alone is insufficient to explain the pathogenesis of IBS. From post-infective IBS, we know that the most people who have gastroenteritis and accompanying inflammation do not develop IBS. As discussed earlier, several factors may be important in interacting with the gut insult and in predicting those who develop symptoms - one interesting factor here is the role of stress. Psychological stress is known to affect gut function in normal healthy humans, and in people with IBS stress may trigger or exacerbate symptoms. More recently there is evidence of a link between stress and inflammatory responses. Exposure to stress in both animals and humans has been shown to result in the release of mast cell mediators in the colon (18,19) and in a recent study stress was capable reactivating previous inflammation in rats (15). An important challenge for future work will be to clarify the interaction between inflammation, stress and IBS symptoms.ConclusionWe believe that low-grade inflammation may play a role in the pathogenesis of a sub-set of IBS. There is now evidence from several different studies to suggest that a range of inflammatory mediators may be increased in IBS. It is important to point out, however, that most of this evidence, including our data is preliminary and will need to be confirmed by larger research studies. Important challenges for future work will be to demonstrate the role of specific inflammatory mediators in the generation and resolution of IBS symptoms. Continued research into this area is likely to improve our understanding of the underlying mechanisms in IBS and may lead to the development to better therapeutic approaches for this condition. http://www.med.unc.edu/medicine/fgidc/infl...rymediators.htm with all due respect, please spend more time learning before you convince everyone IBS is leaky gut, or inflammation of the digestive system. Much more is known about IBS at this time in the research. Things like altered flora and gut permeability are a part of a much bigger picture in IBS.There are alreay abnormalities found in IBS patients and molecular cahnges and subgroups of IBSers."Dr. Drossman is Co-director of the Center and Professor of Medicine and Psychiatry at UNC-CH. Dr. Drossman has had a long-standing interest in the research and evaluation of difficult to diagnose and treat gastrointestinal disorders. He established a program of research in functional gastrointestinal disorders at UNC more than 25 years ago and has published more than 350 books, articles, and abstracts relating to epidemiology, psychosocial and quality of life assessment,design of treatment trials, and outcomes of research in gastrointestinal disorders. Dr. Drossman received his MD degree from Albert Einstein College of Medicine in 1970 and completed his medical residency at the University of North Carolina School of Medicine and NYU-Bellevue Medical Center. After his residency, he subspecialized in psychosocial (psychosomatic) medicine at the University of Rochester School of Medicine and in Gastroenterology at the University of North Carolina in 1976-1978. He is currently Professor of Medicine in Psychiatry at UNC.As the medical director of the Center, Dr. Drossman sees patients in the functional GI and motility clinic and precepts GI fellows and visiting gastroenterologists to help develop their clinical skills in treating patients. He also facilitates the learning of medical faculty, psychiatry residents, and medical students, on how to provide biopsychosocial care to patients with functional GI disorders.Dr. Drossman has an active research program, which relates to the clinical, epidemiological, psychosocial, and treatment aspects of irritable bowel syndrome (IBS). He has developed and validated several assessment measures, which are used worldwide for clinical research. Recently he began looking at brain imaging (fMRI) in functional bowel to determine if the reported changes in the brain are responsive to treatment. He also consults with several pharmaceutical and governmental agencies regarding treatment trials. He was responsible for organizing the Functional Brain Gut Research Group as a special interest section within the American Gastroenterological Association, chairs the ROME committee, and is a past president of the American Psychosomatic Society. Dr. Drossman sits on the Board of Directors and is Chair of the Scientific Advisory Board and the Awards Committee 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.In 2001, Dr. Drossman was appointed Associate Editor of Gastroenterology, the official journal of the American Gastroenterological Association and in 2003 became chair of 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. 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 the AGA GI Teaching Project on IBS-II. 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 Senior Editor of the book, Rome III Committees with the book, Rome III, to be published in 2006.Dr. Drossman's educational and clinical interests in the psychosocial/behavioral aspects of patient care was a natural path to his developing 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 considered a world authority in the field of (IBS), functional disorders, and on physician-patient communications. He presents at numerous national and international meetings throughout the year." "However, modern research understands IBS as a disorder of increased reactivity of the bowel, visceral hypersensitivity and dysfunction of the brain-gut axis. There are subgroups being defined as well, including post-infectious IBS which can lead to IBS symptoms. Other work using brain imaging shows that the pain regulation center of the brain (cingulate cortex) can be impaired, as well as good evidence for there being abnormalities in motility which can at least in part explain the diarrhea and constipation. So finding a specific "cause" of IBS has grown out of general interest in place of understanding physiological subgroups that may become amenable to more specific treatments. Hope that helps.Doug Drossman " http://www.ibshealth.com/ibs_foods_2.htm


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## Talissa (Apr 10, 2004)

"The most frequent form of IBS involves abnormal fermentation, producing toxic substances such as hydrogen, generally attributed to the proliferation of certain micro-organisms that are allowed to flourish because of reduced populations of lactobacillus and bifidobacter, usually as a result of gastroenteritis or antibiotic treatment. ..."Overall, the conference revealed that although there is a consensus that gut flora is important, we still know too little about how to manipulate this ecosystem to exploit it to our advantage. Some probiotics may well be beneficial in treating certain conditions, but linking symptoms and probiotic treatments is not easy."<a%20href="http://216.239.39.104/search?q=cache:1yZFp79pP2gJ:www.nursing-standard.co.uk/archives/gin_pdfs/ginvol1-8/ginv1n8p0810.pdf+%22ibs%22+%2B+%22antibiotics%22+%2B+%22probiotics%22&hl=en"%20target="_blank">[url="http://216.239.39.104/search?q=cache:1yZFp...iotics%22&hl=en"]http://216.239.39.104/search?q=cache:1yZFp...iotics%22&hl=en%20</A>%20&start=31" target="_blank">http://216.239.39.104/search?q=cache:1yZFp...2B+%22probiotic s%22&hl=en &start=31://http://216.239.39.104/search?q=cach...hl=en &start=31</a>Here's an easier link in pdf, requiring acrobat reader: http://www.nursing-standard.co.uk/archives...inv1n8p0810.pdf


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## flux (Dec 13, 1998)

> quote:The most frequent form of IBS involves abnormal fermentation,










The source of bogus claim seems to be from a single study which claimed to find excess colonic hydrogen production in a group of IBS patients. But they used a questionable method for measuring the gas, which has never been verified, and their subjects may not have had IBS to begin with. In general, IBSers are believed to have *normal* fermentation.


> quoteroducing toxic substances such as hydrogen,










*False*. Hydrogen is not toxic to human cells. Hydrogen sulfide is, however.(I sent a note to the editor of that journal regarding these errors.)


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## SpAsMaN* (May 11, 2002)

Eric,i agree with the extra-sensitivity in IBS,that's why i suspect that some narcotic will do the trick for me.But again about the extra-sensibility and brain imaging,do you think it would "logical" to reject the bad flora theory when the "spores" of the bacterias can cause sensitivity by themselves as well as big head aches(brain imaging).







Eric,microcopic-colitis have been found in IBS apparently.


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## Talissa (Apr 10, 2004)

Hey Flux,Thanks for the colorful info. I'm sure the editor will love hearing from you!If you're trying to say that imbalanced intestinal flora & the resulting abnormal intestinal permeability have nothing to do with IBS, I'm afraid I'll need more.Here's another tidbit from Medscape":"Inflammatory Bowel Disease and Irritable Bowel Syndrome: Separate or Unified?"Posted 07/15/2003Sylvie Bradesi, PhD, James A. McRoberts, Ph.D, Peter A. Anton, MD, Emeran A. Mayer, MDAbstract and IntroductionAbstractBoth irritable bowel syndrome and inflammatory bowel diseases share symptoms of altered bowel habits associated with abdominal pain or discomfort.... Possible shared pathophysiologic mechanisms include altered mucosal permeability, an altered interaction of luminal flora with the mucosal immune system, persistent mucosal immune activation, alterations in gut motility, and a role of severe, sustained life stressors in symptom modulation. It is proposed that similarities and differences between the two syndromes can best be addressed within the framework of interactions between the central nervous system and the gut immune system. Based on recent reports of low-grade mucosal inflammation in subpopulations of patients meeting current diagnostic criteria for irritable bowel syndrome, therapeutic approaches shown to be effective in inflammatory bowel disease, such as probiotics, antibiotics, and antiinflammatory agents, have been suggested as possible therapies for certain patients with irritable bowel syndrome.Complete article here: http://www.medscape.com/viewarticle/457728_1 ********************************Stick a fork in me, I'm done.


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## scottyswotty (Jun 29, 2000)

Hi TalissaThanks for your interesting posts. Good to see some balance restored to the Force.CheersScott


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## flux (Dec 13, 1998)

> quote:If you're trying to say that imbalanced intestinal flora & the resulting abnormal intestinal permeability have nothing to do with IBS, I'm afraid I'll need more.


Don't you mean to say they do, we need more?


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## Talissa (Apr 10, 2004)

Thanks for the warm welcome Scott!Flux, you are too cool for words. Yes, "they" say that & "we" do need more valid studies to prove otherwise. The studies are happening as we type....Change is in the wind.Talissa


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## flux (Dec 13, 1998)

I suspect it eventually works out that something is specifically amiss with the gut flora in only a small subset of patients, who will then get a different diagnosis (and better treatment). The majority of IBSers will probably turn out to have no problems with the gut flora but will turn out to have intrinsic problems in the brain-gut. Look forward to Rome III


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## SpAsMaN* (May 11, 2002)

Flux or others experts,can you give an exemple who excludeinclude the flora as a culprit?


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## SpAsMaN* (May 11, 2002)

Post-infectious IBS?That may give a signs to the researchers,rigth?Maybe all IBSer are post-stress...Can the flora be mutated this bad?


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## floridian2 (Dec 1, 2003)

Spasman,there is no single known cause of IBS. The disorder occurs in many systems with IBS. There is some evidence that probiotics can help, but there is no clear picture. The first study below claims a beneficial effect from one strain of probiotics; the second found that the same strain had no value. More research is needed.Probiotics are generally considered safe, and are inexpensive. I would suggest that they be tried as one of the first therapies, as probiotics may help some people that present the symptoms of IBS (and who may or may not have IBS). As a diagnosis of IBS may take weeks or months.


> quote: Eur J Gastroenterol Hepatol. 2001 Oct;13(10):1143-7. Related Articles, Links Comment in: * Eur J Gastroenterol Hepatol. 2001 Oct;13(10):1135-6. Click here to read A controlled, double-blind, randomized study on the efficacy of Lactobacillus plantarum 299V in patients with irritable bowel syndrome. Niedzielin K, Kordecki H, Birkenfeld B. Department of Gastroenterology, M. Curie Regional Hospital, Szczecin, Poland. Krzysztof.Niedzielin###mepha.com.pl BACKGROUND: Irritable bowel syndrome (IBS) is a widespread functional disorder of the digestive tract. Its aetiology is unknown and therapeutic options are limited. Recent reports suggest that probiotics may have a role in regulating the motility of the digestive tract. AIM: To assess the efficacy of Lactobacillus plantarum 299V (LP299V) in patients with IBS. PATIENTS AND METHODS: Forty patients were randomized to receive either LP299V in liquid suspension (20 patients) or placebo (20 patients) over a period of 4 weeks. Clinical examination was performed at baseline and at the end of the study. Additionally, patients assessed their symptoms by applying a scoring system. RESULTS: All patients treated with LP299V reported resolution of their abdominal pain as compared to 11 patients from a placebo group (P = 0.0012). There was also a trend towards normalization of stools frequency in constipated patients in six out of 10 patients treated with LP299V compared with two out of 11 treated with placebo (P = 0.17). With regards to all IBS symptoms an improvement was noted in 95% of patients in the LP299V group vs 15% of patients in the placebo group (P < 0.0001). CONCLUSIONS: LP299V seems to have a beneficial effect in patients with IBS. Further studies on larger cohorts of patients and with longer duration of therapy are required in order to establish the place of L. plantarum in the treatment of IBS.





> quote: Dig Dis Sci. 2002 Nov;47(11):2615-20. Related Articles, Links Effect of Lactobacillus plantarum 299v on colonic fermentation and symptoms of irritable bowel syndrome. Sen S, Mullan MM, Parker TJ, Woolner JT, Tarry SA, Hunter JO. Department of Gastroenterology, Addenbrooke's Hospital, Cambridge, UK. A number of recent clinical trials have promoted the use of probiotic bacteria as a treatment for irritable bowel syndrome (IBS). The recent demonstration of abnormal colonic fermentation in some patients with this condition provides an opportunity for the objective assessment of the therapeutic value of these bacteria. This study was designed to investigate the effects of Lactobacillus plantarum 299V on colonic fermentation. We conducted a double-blind, placebo-controlled, cross-over, four-week trial of Lactobacillus plantarum 299V in 12 previously untreated patients with IBS. Symptoms were assessed daily by a validated composite score and fermentation by 24-hr indirect calorimetry in a 1.4-m3 canopy followed by breath hydrogen determination for 3 hr after 20 ml of lactulose. On placebo, the median symptom score was 8.5 [6.25-11.25 interquartile range (IQR)], the median maximum rate of gas production was 0.55 ml/min (0.4-1.1 IQR), and the median hydrogen production was 189.7 ml/24 hr (118.3-291.1 IQR). On Lactobacillus plantarum 299V the median symptom score was 8 (6.75-13.5 IQR), the median maximum rate of gas production 0.92 ml/min (0.45-1.5 IQR), and the median hydrogen production 208.2 ml/24 hr (146-350.9 IQR). There was no significant difference. Breath hydrogen excretion after lactulose was reduced by the probiotic (median at 120 min, 6 ppm; placebo, 17 ppm; P = 0.019). In conclusion, Lactobacillus plantarum 299V in this study did not appear to alter colonic fermentation or improve symptoms in patients with the irritable bowel syndrome.


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## eric (Jul 8, 1999)

Sapsman, microscopic colitus is NOT IBS, so you know, IBD and IBS can coexist however.Talisssa." It is proposed that similarities and differences between the two syndromes can best be addressed within the framework of interactions between the central nervous system and the gut immune system. "another words BRAIN GUT interactions."Based on recent reports of low-grade mucosal inflammation in subpopulations of patients meeting current diagnostic criteria for irritable bowel syndrome,"Your missing a lot of work on post infectious IBS leading to IBS after an enteric infection has subsided. Your missing WHAT KIND OF INFLAMMATION IS SEEN IN IBS!!!Your missing they already see cellular changes in the digestive system, after an enteric enfection has subsided!!!Chronic stressors can reactivate/inflame certain gut immune cells.Mast cells are a big part of this.Advances in Irritable Bowel Syndrome State of the art lectures on IBS from 2000 and more has confirmed a lot of these lectures from leading experts in IBS from many different fields of research including DR Wood and DR Gershon and DR Ester Strenberg a world leader in neuro imune function. http://www.conference-cast.com/ibs/Lecture...dRegLecture.cfm


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## Talissa (Apr 10, 2004)

Flux, thanks for letting us know your thoughts on the flora-IBS connection, or not. I didn't think you would!And you could very well turn out to be correct. It could be just those of us with IBS following an infection & subsequent antibiotic/antibacterial treatment have the flora imbalance problem.Like Spas said, being a PI-IBS person, like myself, could point to effective specific treatment targeting flora & healing the intestinal wall, along with dietary changes due to food reactivity, in conservative circles one day. This is already happening in integrative & functional medicine. It's what I did, & it certainly got my life back on track. But it probably does just apply to a specific subset of IBSr's. For the sake of argument, isn't it possible that digestive disturbance caused by imbalanced flora & increased intestinal permeability could be brought on by high stress, combined w/ say poor diet/NSAIDs/drugs/alcohol? And isn't it possible that because the digestive tract is malfunctioning due to permeability, this could cause a malfunction in the brain/gut axis? Additionally, wouldn't this effect liver function, causing all sorts of hormonal imbalances, making a bad situation worse? (say, more stressful)?But again, I really do feel your assessment could turn out to be the case. And Rome III will hopefully be more useful than the current Rome II diagnostic tool.This is a great exchange..."Those who agree with us give us comfort, those who disagree make us think."Talissa


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## Talissa (Apr 10, 2004)

Hi Eric,Just caught your post. Are you saying there's no hope for us to get back to normal digestion & elimination because of these changes in the mast cells?Other than you always typing in "your", when you mean "you're", this is what I don't like most about your posts--you have alot of facts and the latest medical research from impeccable sources, but you offer no hope to be completely free of the IBS affliction.You do help folks with the hypnosis, & I admire that. But I got back to a normal life(92% normal) after being on the brink, by treating my problem as a bacterial imbalance. This helped me.The medical community is starting to catch on, why fight that? Even if it is just a subset of us who've been diagnosed with IBS who will be helped by this, and if we treat it as a flora imbalance & will be able to work again or go to the mall or go on a picnic again, why discourage it? Why try to stop us from trying to help others?When I was going 14 x's a day, like a faucet, I couldn't go places & do things. I was in pain. Alot of pain. Today, I'm a pilates instructor, I'm able to socialize, I'm not in pain.I want others who are like I used to be to know what it feels like to get back to a mostly normal life. No pain.I will never say a thing against hypnotism, because I haven't tried it.And I have hope I'll get back to 100%--soon.These facts you have don't mean squat if they don't help people.Affectionately,Talissa


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## Talissa (Apr 10, 2004)

P.S. Now I seem to have "D" of the mouth, but in the interest of helping people, I've been taking Digestive Advantage-IBS for 7 days now. While I can't say I'm 100% yet, I have been able to eat things like raw cucumbers & tomatoes without reacting, which is novel for me. My stools are more normal-looking(as opposed to being bloated from the fiber I take), & for the first time in 5 years, I have to strain a bit to go.DA-IBS contains specific strains of lactic acid bacteria, along with the amino acid Lysine. The makers of DA-IBS say to give the product at least a month to get back to normal. It is relatively inexpensive. Some folks here were back to normal after 2 days(lucky blokes).Anyways, here's an interesting study reference re: lactic acid bacteria(LAB):"The enteric flora comprise approximately 95% of the total number of cells in the human body and are capable of eliciting immune responses while also protecting against microbial pathogens. However, the resident bacterial flora of the gastrointestinal tract (GIT) may also be implicated in the pathogenesis of several chronic conditions such as inflammatory bowel disease (IBD). The University College Cork-based Probiotic Research Group has successfully isolated and identified lactic acid bacteria (LAB) which exhibit beneficial probiotic traits. These characteristics include the demonstration of bile tolerance; acid resistance; adherence to host epithelial tissue; and in vitro antagonism of potentially-pathogenic micro-organisms or those which have been implicated in promoting inflammation. The primary objective of this report is to describe the strategy adopted for the selection of potentially effective probiotic bacteria. " http://www.kluweronline.com/article.asp?PIPS=236216&PDF=1 The exciting thing about the new studies happening today is that they are isolating specific strains of probiotics which comply with the necessary traits to have gastrointestinal benefits. (Like adhesion, resistance to acid & bile, etc from the above reference.) I don't know if the LAB strains in this study are the ones in DA-IBS, but it may be the case.The point is people can cite all the inconclusive probiotic trials to treat IBS, and they'll leave out the fact that some folks did indeed get back to normal. Maybe they eat better. Maybe they handle stress better. Maybe they don't smoke & drink. Maybe the folks that were helped are in that subset of IBSr's.There's alot we don't know yet, but it's being studied.For example:"In the treatment of inflammatory bowel diseases (IBD), success has been reported with Escherichia coli Nissle strain in ulcerative colitis, and with a multiple organism product, VSL#3 (VSL Pharmaceuticals, Fort Lauderdale, FL), in Crohn's disease and pouchitis. Initial reports in irritable bowel syndrome (IBS) have resulted in encouraging results with the use of E. coli Nissle strain, and recently with multiple organism probiotic supplements. However, caution must still apply to the use of probiotics in IBD and IBS because the reports and the number of patients treated are limited." http://www.ncbi.nlm.nih.gov/entrez/query.f...itool=iconabstr ...the number of patients treated are limited. That's what needs to change in these studies. They also need to take into account the diets & lifestyles of the participants in the studies.


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## SpAsMaN* (May 11, 2002)

NSaid was my first IBS attack.My altered motilityin my lower tract is exactly at the same place that my first attack.How can i reverse that?I don't think i fit in the PI theory.


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## SpAsMaN* (May 11, 2002)

I have 2 theory for my case.1-The pain receptors are overvigilent and creates spasms then the mast cells are nuts.2-My flora have mutated and and creates gas who irritate the mucosa who affect the pain receptors.


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## SpAsMaN* (May 11, 2002)

Eric,i have read that some tissue(mucosa) are altered in IBS but maybe that is only seen if the bowel is in expension so the colonoscopy would be unable to detect it.


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## eric (Jul 8, 1999)

"Inflammatory Mediators in Irritable Bowel Syndrome Maria O'Sullivan, PhDDepartment of Gastroenterology, Adelaide & Meath HospitalTrinity College, Dublin, IrelandIrritable bowel syndrome (IBS) is a chronic condition characterized by abdominal pain and altered bowel habit, in the absence of demonstrable structural gastrointestinal abnormality. Essentially the gut functions abnormally - people experience symptoms of pain, diarrhea and/or constipation but no abnormality of the bowel can be identified by standard medical tests. *Numerous research studies have now documented physiological changes, including altered motility and hypersensitivity, in the gastrointestinal tract of IBS patients.* The mechanisms underlying these events, however, remain unclear. *There is growing evidence that inflammation in the gastrointestinal mucosa * may play a role in the pathogenesis of at least a sub-set of IBS (1-3). *Importantly, overt colonic inflammation precludes a diagnosis of IBS.* The challenge for researchers therefore, is to record subtle changes in inflammatory mediators that are not identifiable by usual routine processes. Inflammation and IBS - the EvidenceExperimental (animal) data show that inflammation, even if mild, could lead to persistent changes in gastrointestinal nerve and smooth muscle function, resulting in dysmotility, hypersensitivity and gastrointestinal dysfunction (1, 4-6). In humans, the role of inflammation in the generation of IBS symptoms is less well studied, although there are important findings from people with 'post-infective IBS'. After an acute gastrointestinal infection up to one-third (7-29%) of individuals develop persistent symptoms compatible with IBS (7, 8). In these post-infective IBS subjects, a persistent increase in rectal sensitivity (8) and in inflammatory cells (specifically enteroendocrine cells and lymphocytes) (9) have been documented. To put this in context, however, the majority (over 70%) of people who develop gastroenteritis fully recover and do not develop persistent bowel symptoms. Factors that may predict those who develop post-infective IBS include specific psychological factors, female gender and a longer duration of the initial illness. While there is now reasonable evidence to support a low-grade inflammatory response in those who develop IBS following an acute episode of gastroenteritis, there is still little know about inflammation in IBS patients who have no obvious recent evidence of acute infection. The role of inflammation in non post-infective IBS has been a particular research interest of our group and began with an interest in studying mast cells in IBS. Mast Cells and IBS The mast cell has potential to be a key player in IBS. Although mast cells are most widely known for their role in allergic responses, these cells are normally present throughout the gut and are involved in a range of physiological and pathological activities including mucosal defense mechanisms and inflammation. Mast cells may release an array of inflammatory mediators that act on smooth muscle, nerves and immune cells, which may ultimately result in gastrointestinal dysfunction and symptoms. In addition, mast cells in the gut are located close to nerves providing a structural basis for communication between the gut and the nervous system. In 1993, Weston and colleagues reported increased mast cell numbers in the mucosa of IBS patients(10) - these changes were identified in tissue from the end of the small bowel (terminal ileum). Similarly we identified significant increases in mast cells in IBS patients compared to controls in the colon (specifically at the caecum) (11). There were also trends for increases in other regions of the colon (ascending and descending colon) but no differences could be seen at the rectum. The lack of changes in mast cell infiltration in the rectum has since been confirmed by others (9). Collectively these studies suggest that mast cells were increased in IBS patients - this may be part of a low-grade inflammatory response, although the components and nature of this response remain poorly understood. NITRIC OXIDE AND IBSWe hypothesised that inducible nitric oxide synthase may be a novel and important marker of inflammation in IBS. Enzymes from the nitric oxide synthase family are responsible for the synthesis of nitric oxide (NO) from the oxidation of L-arginine. While at least three enzyme sub-types (isoforms) have been described, our study focussed on one specific isoform, namely inducible nitric oxide synthase (iNOS). This enzyme is thought to be capable of producing large amounts of nitric oxide and to be expressed during inflammation (12). In the human colon, upregulation of iNOS has been implicated in inflammatory processes and increased expression has been documented in inflammatory bowel disease. In colonic mucosa from IBS patients, we found a significant increase in iNOS expression compared to control patients (13). We also measured nitrotyrosine, which is considered a by-product of nitric oxide generation. Overall the nitrotyrosine data in IBS paralleled that of iNOS almost exactly. iNOS could be detected in epithelial cells, lymphocytes (CD3+ T and CD20+ B lymphocytes) and macrophages. Mast cells did not appear to express the iNOS. Overall we demonstrated an increase in iNOS, an enzyme that catalyses the production of nitric oxide, combined with an increase in nitrotyrosine, a by-product of nitric oxide generation. In terms of factors that may affect iNOS expression, there was a trend towards higher iNOS levels in the diarrhea compared to the alternating group although this was not statistically significant. Elevated iNOS may be a marker of general low-grade inflammation in IBS. Induction of iNOS and the generation of NO, could have several other potential roles in IBS - for example NO may have direct effects on intestinal nerve and motor function and intestinal on permeability. OTHER INFLAMMATORY CELLS IN IBSWhile there was some tentative evidence of an associated involvement of other inflammatory markers in our study, these were not striking or clear-cut. On average there were trends for increases in CD3+ lymphocytes and the proportion of lymphoid tissue. Similarly in IBS there was a trend for increased expression of nuclear factor kappa B (NF-?







, a transcription factor for an array of pro inflammatory cytokines and mediators. In our study, none of these changes were statistically significant. In contrast, others have previously reported significant increases in inflammatory cells, for example an increase in CD3+ lymphocytes in post-infective IBS9 and an increase in overall cellularity in the colonic mucosa in IBS (14). CD3 is a 'pan T-lymphocytes marker' and allowed us to estimate the overall number of T-lymphocytes in the lamina propria of the IBS patients. It is possible that specific subclasses of lymphocytes may be altered in IBS (e.g. CD4+ and CD8+ classes). Interestingly, the CD4+ T cell subtype has been implicated in an animal model of inflammation. In this model, stress was shown to reactivate colonic inflammation (15) - susceptibility to reactivation of inflammation by stress appeared to specifically require CD4+ lymphocytes. ANTI-INFLAMMATORY MEDIATORS IN IBS The study of inflammation in IBS has largely focused on the role of pro-inflammatory cells and mediators. From other gastrointestinal inflammatory diseases, we know that inflammatory responses involve a complex balance between pro- and anti- inflammatory mediators. There is emerging data to suggest that people with IBS may have a genetic predisposition to produce low amounts of anti-inflammatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-







(16). Moreover, there is a further preliminary report (17) of dysfunctional mucosal protective mechanisms in IBS characterize by reduced numbers of macrophages. While this data is provisional, it is plausible that people who develop IBS could have poorer defense mechanisms to combat infections or other gut insults.A Link between Inflamation and Stress *An increase in inflammatory mediators alone is insufficient to explain the pathogenesis of IBS.* From post-infective IBS, we know that the most people who have gastroenteritis and accompanying inflammation do not develop IBS. As discussed earlier, several factors may be important in interacting with the gut insult and in predicting those who develop symptoms - one interesting factor here is the role of stress. Psychological stress is known to affect gut function in normal healthy humans, and in people with IBS stress may trigger or exacerbate symptoms. More recently there is evidence of a link between stress and inflammatory responses. Exposure to stress in both animals and humans has been shown to result in the release of mast cell mediators in the colon (18,19) and in a recent study stress was capable reactivating previous inflammation in rats (15). An important challenge for future work will be to clarify the interaction between inflammation, stress and IBS symptoms.Conclusion *We believe that low-grade inflammation may play a role in the pathogenesis of a sub-set of IBS. * There is now evidence from several different studies to suggest that a range of inflammatory mediators may be increased in IBS. It is important to point out, however, that most of this evidence, including our data is preliminary and will need to be confirmed by larger research studies. Important challenges for future work will be to demonstrate the role of specific inflammatory mediators in the generation and resolution of IBS symptoms. Continued research into this area is likely to improve our understanding of the underlying mechanisms in IBS and may lead to the development to better therapeutic approaches for this condition. " http://www.med.unc.edu/medicine/fgidc/infl...rymediators.htm "Inflammation, Infection, and Irritable Bowel Syndrome (IBS): An Update04-21-2003 Yehuda Ringel, M.D., Douglas A. Drossman, M.D. IntroductionIrritable bowel syndrome (IBS) is a chronic disorder of gastrointestinal function for which no specific pathophysiologic mechanism is known. However, it is generally accepted that IBS symptoms are multidetermined, and are generated from dysregulation at multiple levels of the brain-gut axis. They are manifest by abnormal motor reactivity to various stimuli, and low sensation and pain thresholds.1 The growing interest of clinicians and researchers in the pathogenesis of functional gastrointestinal disorders led to several research presentations during this year's Digestive Disease Week meeting. Although these presentations addressed various factors implicated in the pathogenesis of these disorders (i.e., behavioral/psychosocial, central and peripheral contributors), this article focuses on some new insights into the possible contribution of gut infection and inflammation in the development of symptoms and other potential clinical consequences. Infection and InflammationStephen M. Collins 2 provided a comprehensive review of the evidence suggesting the need to consider infection and inflammation in the pathogenesis of some patients with IBS. He presented data from clinical studies showing the development of IBS symptoms following acute gastroenteritis (i.e., postinfectious PI IBS) and a higher than expected prevalence of IBS symptoms among patients with inflammatory bowel disease that was in remission. *Additionally, data from animal studies demonstrated that altered gut physiology can persist even after the infection and associated inflammation have resolved.* Furthermore, studies of mucosal biopsies, from both human and animal models, have shown increased inflammatory cells and inflammatory mediators in patients with IBS and in previously sensitized/stressed animals. Finally, some recent studies have shown proximity between nerve trunks and the inflammatory cells, suggesting a local neuroimmune interaction that may contribute to the pathogenesis of IBS. With respect to the latter, several key studies presented during these meeting proceedings provided some supportive evidence relating the role of infection and inflammation to IBS. Wheatcroft and colleagues 3 have shown a significant increase in serotonin-containing entero-endocrine cells (EC) following Trichinella spiralis infection in mice. This finding suggests that the increased EC numbers that have previously been reported in humans after Campylobacter enteritis are likely not specific to bacterial infections. These events may also occur after protozoan and other parasitic infections, and thus may contribute to postinfectious bowel dysfunction. Dunlop and colleagues4 compared the numbers of rectal mucosal lymphocytes, EC, and mast cells from IBS patients (n = 76) and healthy controls (n = 40). Although all biopsies were normal using conventional histology, immunohistochemical studies showed differences in patterns of mucosal pathology between several distinct subgroups of IBS. Patients with PI-IBS showed increased EC and CD3+ lamina propria lymphocytes (LPL),confirming previous findings. However, patients with constipation-predominant IBS were not significantly different from controls, and nonconstipated, non-PI-IBS patients showed increased CD3+, LPLs, and mast cells. These findings suggest that within the broad clinical grouping of IBS, there may be several distinct groups with different patterns of mucosal pathology. The clinical relevance of these findings needs further investigation. The growing interest and the emerging evidence supporting the role of infection and inflammation in the pathogenesis of at least a subset of IBS patients was also manifest in some key studies presented in the American Gastroenterological Association Research Forum on the "Medical Treatment of Functional GI Disorders." As discussed below, these studies explored possible new approaches in the treatment of IBS, while focusing on modulating and reversing infections and/or inflammation. A Role for Anti-inflammatory Agents?Dunlop and coworkers 5 also presented the results of an intriguing multicenter study aimed at assessing the effect of a short course of steroids on intestinal inflammatory cell counts and clinical symptoms in patients with PI-IBS. Thirty-one patients with IBS symptoms 3 or more months after initial acute gastroenteritis were randomized in a double-blind fashion to receive oral prednisolone 30 mg per day or placebo for 3 weeks. Rectal biopsies were taken and symptom questionnaires (modified Talley, Gastrointestinal Symptom Rating Scale [GSRS]-IBS, QOL-IBS & Global Health) were completed prior to and after treatment. Rectal biopsies were immunostained for ECs, lymphocytes (CD3+ lamina propria cells, crypt and surface intraepithelial lymphocytes [IELs]), and mast cells. In addition, a symptom diary was kept throughout the study and a modified GSRS score incorporating pain, diarrhea, looseness, and urgency was used as the primary end point. Prior to treatment, the CD3 count in the lamina propria correlated with the EC counts (Spearman's coefficient 0.429, P = .036) and with the modified GSRS score (Spearman's coefficient 0.482, P = .015). Following treatment, there was a significant fall in CD3 counts. However, this fall was in both the placebo and the prednisolone groups (27, P =.05; and 20, P = .006 vs initial values, respectively) and there was no change in the EC, IEL, and mast cell counts in either group. The modified GSRS score did not change after prednisolone treatment. However, there was a surprising, and unexplained, decrease in GSRS score at the end of the treatment in the placebo group (P = .02 vs initial value). The results of this study show that treatment with 30 mg of prednisolone started 3 or more months after the initial gastrointestinal infection is ineffective in PI-IBS. It is not yet clear if anti-inflammatory treatment started in earlier stages, and/or with higher doses, and/or for longer duration would have other outcomes. *Therefore, despite preliminary evidence for an inflammatory/immune component in some patients with IBS, additional studies are needed before the use of anti-inflammatory agents can be considered in treatment. * A Role for Probiotics?Probiotics are live microbial food supplements or components of bacteria that alter the enteric microflora and have a beneficial effect on health. The most frequently used genera are Lactobacilli and Bifidobacteria. The potential mechanisms of their action include competitive bacterial interactions, production of antimicrobial metabolites, mucosal conditioning, and immune modulation. The emerging use of probiotics in several gastrointestinal disorders (eg, inflammatory bowel disease) has led to increased interest in their use in patients with IBS. Quigley and colleagues 6 presented the results of a double-blind, placebo-controlled treatment study with probiotic bacteria in 77 patients (64% female) with IBS. Following a 2-week run-in period off all medication, patients were randomized to receive, once daily, either Lactobacillus spp, Bifidobacterium spp, each added to a milk drink, or the milk drink alone for 8 weeks. IBS symptoms were recorded daily throughout the entire study. In comparison to placebo, subjects randomized to Bifidobacterium experienced a significant reduction in pain, bloating, and bowel movement difficulty. Benefit with Lactobacillus was limited to an effect on pain in weeks 2 and 7 only, and neither probiotic strain had any effect on the frequency of bowel movements. A composite score, incorporating all symptoms, showed significant improvement in response to Bifidobacterium for all weeks. The improvement in the composite score response was greater with Bifidobacterium compared with placebo and Lactobacillus (Bifidobacterium vs Lactobacillus vs placebo = 3.70 +/- 0.59 vs 5.25 +/- 0.55 vs 5.68 +/- 0.56, P .05 for week 4). The symptomatic response with Bifidobacterium was associated with parallel improvement in quality of life as assessed by using an IBS-specific instrument.7,8 A follow-up 4 weeks after discontinuation of the treatment (washout period) showed that both symptoms and quality of life returned to baseline. The results showed a beneficial effect of probiotic bacteria in IBS. However, it must be kept in mind that data on the use of these agents in IBS are still very limited and not always consistent. (For example, a previous double-blind, placebo-controlled, randomized study showed beneficial effect of Lactobacillus plantarium in IBS.9) In addition, as emphasized by the investigators, it seems that the beneficial effect was short-term and strain-specific. Additional information regarding the variability of strain-specific response was provided by the results of a study presented by another group from Ireland, as discussed below. Sheil and colleagues 10 examined cytokine production by human mononuclear cells that were incubated in vitro in various strains of Lactobacilli and Bifidobacteria. They found strain-specific alterations in cytokine gene expression and strain-specific cytokine responses for both Lactobacilli and Bifidobacteria strains. As proposed by the investigators, these results suggest that experiments on the immunomodulatory effects of one bacterium cannot be extrapolated to other bacteria. Thus, each bacterial strain that is considered for use as a probiotic may need to be validated individually. The results of studies that have thus far been conducted with probiotics are encouraging. However, additional investigations that will better define the potential subgroup of patients, the specific strain, and the duration of treatment are required in order to establish the role of probiotics in the treatment of IBS. Until the latter is accomplished, their use will remain investigational. A Role for Antibiotics?Pimentel and associates 11 tested the utility of antibiotic treatment in IBS. This study follows a recently published provocative report from the same group in which they identified an association between IBS and abnormal findings on lactulose breath test (LBT).12 However, this previous report had limitations due to its study design, primarily related to possible ascertainment bias, the lack of a control arm, and the unblended nature of the treatment. Thus, the results of this study and their clinical significance were uncertain. The current study was designed to test the effect of antibiotic treatment in patients with IBS in a randomized, double-blind, placebo-controlled fashion. One hundred-one consecutive IBS subjects recruited through advertising were randomized to receive neomycin 500 mg (n = 49) or placebo (n = 52) twice daily for 10 days. All subjects underwent LBT before and 7 days after completion of treatment. The LBT was read by a blinded reviewer, and the results remained blinded throughout the study. An IBS symptom questionnaire was administered before and after treatment and a true clinical response was defined as 50% improvement in symptoms. Abnormal LBT was found in 83% of IBS subjects who entered the study compared with 20% in sex-matched controls (P .01). In an intention-to-treat analysis, neomycin resulted in a 39.3% improvement in an IBS composite symptom score compared with 12.3% for placebo (P .05), and 40.1% bowel normalization compared with only 15.1% for placebo (P .001). Of the subjects receiving neomycin, 50% had a true clinical response compared with 17% given placebo (P .01). These results were even greater (up to 75%) in the group in which neomycin was successful in normalizing the breath test. The investigators concluded that abnormal LBT is very common in subjects with IBS and that IBS symptoms can be significantly improved with antibiotic treatment. Important concerns raised during the discussion of this paper related to the following: (1) the unusually high positive LBT rate in this population, possibly due to false-positives likely resulting from rapid transit of lactulose in the small bowel in IBS; (2) the use of a nonstandard measure of primary efficacy (ie, composite symptom score); (3) the significant effect being driven by an unusually low treatment and placebo response rate. The results of this study are provocative and interesting, and therefore deserve replication. They emphasize the need to consider performing LBT, when clinically indicated, as part of the evaluation of patients with IBS. In addition, the definition of IBS is a complex of symptoms that cannot be explained by other conditions. Thus, the finding of positive LBT and positive response to antibiotic treatment suggests the presence of bacterial overgrowth that may be incorrectly diagnosed as IBS. Concluding RemarksThe above discussion seeks to bring to the fore the current state of knowledge regarding the potential role of various factors in the pathogenesis of IBS. Within this context, new insight may be gleaned with respect to the clinical and therapeutic implications for patients with this functional gastrointestinal disorder. http://www.fibromyalgiasupport.com/library...cle.cfm/id/4518 Brain-Gut Interaction in Irritable Bowel Syndrome: New Findings of a Multicomponent Disease Model http://216.109.117.135/search/cache?p=brai...&yc=44382&icp=1


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## Talissa (Apr 10, 2004)

Eric,This was interesting from the article you posted above:"The results of studies that have thus far been conducted with probiotics are encouraging. However, additional investigations that will better define the potential subgroup of patients, the specific strain, and the duration of treatment are required in order to establish the role of probiotics in the treatment of IBS. "Seems to back up my point, thanks.With regards to this, from another article:"Additionally, data from animal studies demonstrated that altered gut physiology can persist even after the infection and associated inflammation have resolved."It appears to me they "resolved" the issue of inflammation by use of steroids, rather than natural treatment allowing the gut to heal, naturally. It seems logical that there would still be altered gut physiology when they only superficially treated the inflammation and didn't address the damaged(with increased permeability) intestinal wall. And they may have cleared up the particular infection, but did it leave the gut with a different kind of imbalance--like maybe they wiped out much of the beneficial bacteria when they treated the infection?(Regarding steroids, some folks may consider them natural. I do too, but the only good ones are the ones produced in our bodies. The others have nasty side effects, like most Rx drugs.)Anyways, this is also encouraging. In my muddled mind, I will always try to treat the problem naturally, never with steroids, & never again with antibiotics not counter-balanced with probiotics, so I may have a decent shot at overcoming this muddlesome IBS. There's no reason to think it's not possible, some day.I really need to stop skimming over all of your enormously long posts!Mine are about as bad, so I really can't throw that one at you







Thanks again,T-


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## SpAsMaN* (May 11, 2002)

Flux,do you have more?I suspect it eventually works out that something is specifically amiss with the gut flora in only a small subset of patients, who will then get a different diagnosis (and better treatment). The majority of IBSers will probably turn out to have no problems with the gut flora but will turn out to have intrinsic problems in the brain-gut. Look forward to Rome III ......I consider going to Australia to have a new flora.I don't think i'm PI but more abnormal sensitivitycause by NSaid.


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## kel1059 (Feb 28, 2003)

Talissa,I enjoy reading your posts. This is really unbelievable. It is almost like i no longer have IBS.I am convinced that the biggest part of my problem was intestinal dysbiosis.Keep up the good work.


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## calid (Aug 4, 2003)

KEL!!!!! Do you believe what Dr. Dahlman gave to you made the difference? It seems as though his treatment put the finishing touch on your recovery. I've been just fine since he found the bad bacterias and treated them, isn't it wonderful? I am SO glad I didn't listen to anyone here who tried to discredit Dr. Dahlman's treatment.


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## Talissa (Apr 10, 2004)

Kel,I've missed your posts!!!, which likewise, I enjoy very much. Calid's too.I'm so, so glad that you're feeling so fine. (Calid too.) Is she correct? Is this new change due to Dr. Dahlman's treatment?I'd personally really like to send in a "sample" to the lab he uses to test for hidden pathogens, like Calid did. Did you have that done? This should probably be on the "Dr Dahlman" thread.....


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## Kathleen M. (Nov 16, 1999)

Personally for me, I do not believe that my symptoms had anything to do with flora.Same very high normal fart frequency (what some people with bad flora say they have...and gas volume can make IBS worse for some). Before IBSDuring mild IBSDuring very severe IBS which responded to non flora changing treatmentsAfter Severe IBS.After that I did find some probiotics that for me reduced the fart frequency (which they should do based on the definition of "good bacteria") but didn't in anyway alter the very infrequent remaining IBS symptoms.If I don't take the probiotics or eat yogurt for awhile the fart frequency will go back up (most probiotics are not normally permanent residents of the gut but they are considered "good" when some of the normal permanent residents are considered "bad" dependin on who is defining it) but no increase in IBS symptoms.That being said.SOME people find that reducing gas volume (whether by altering bacteria or changing what they feed them AKA diet) reduces IBS symptoms.Some people can have lots of gas...based on # times fart a day. (lots of non probiotic bacteria in the gut...probiotic bacteria produce essentially no gas) but do not have IBS symptoms of pain and altered stool consistancy/frequency. So it isn't a strongly coorelated thing from what I can see.Does it help SOME people SOME/MUCH of the time...yep, just like all other IBS treatments known to man."BAD FLORA" is such a hard thing to really decide what it is.Probiotic bactera tend to live in the gut of humans, but do not tend to set up full time permanant residence...more like tourists than anything else.Some of the normal bacteria you find in lots of people can cause large volumes of gas, but are they "bad", really. Not abnormal, just may be a problem for some people some of the time.Generally truely pathogenic bacteria tend to cause things that are "worse" than IBS in some way, but are often acute (but if they damage the nervous system of the gut they can cause problems after they are gone).FWIW, antibiotic use for me was very infrequent, and not at all during my childhood. My diet is generally quite healthy, so many of the "red flags" of "bad flora" do not tend to be that big a factor for me. But some might call my flora "bad" because without the right tourists eating up all the food for them my fart frequency tends to be on the high side.K.


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## eric (Jul 8, 1999)

Talissa The physiological mechanisms responsible for abdominal pain and altered bowel habits occur in healthy control subjects and in persons with IBS. Symptoms can occur in response to a disruption of functioning of the GI tract from an infection, dietary indiscretions (e.g., increased fat or alcohol intake), lifestyle changes (e.g., traveling or vigorous physical activity), or psychologic stress. Among college students and hospital employees, 71% reported that stresses affected their bowel pattern, and 54% reported that stress led to abdominal pain or discomfort.10 Abnormal motility in patients with IBSTable 3 details the studies of altered GI motility in IBS and is summarized below. "The differences between IBS patients and healthy controls are quantitative rather than qualitative. Motility observations in the stomach, small intestine, colon, and rectum are qualitatively similar to those in healthy controls. Moreover, only 25%ï¿½75% of IBS patients exhibit the motility ï¿½abnormalitiesï¿½ listed in Table 3, which are considered to differentiate IBS from healthy controls. These motility parameters cannot be used as diagnostic markers. In the ileum, colon, and rectum, IBS patients show an exaggerated response to a variety of provocative stimuli including meals, distention, stress, cholecystokinin, neostigmine, and corticotropin-releasing hormone injection. No corresponding pattern of hyper-reactivity has been shown in the proximal small intestine and stomach, where the response to stress (inhibition of contractions) differs from the response to meals (increase in contractions). There is no consensus on the patterns of motility responsible for diarrhea and constipation, although accelerated transit is seen in diarrhea and slowed transit is seen in constipation. Among IBS patients exhibiting diarrhea and abdominal pain, there are significantly more high-amplitude propagating contractions, which are of higher amplitude than those observed in healthy controls, and these high-amplitude propagating contractions are more likely to be associated with a sensation of pain. Motility abnormalities may interact with low sensory thresholds to produce symptoms: delayed transit of gas causes greater abdominal perception in IBS,29 and IBS patients are more likely than healthy controls to perceive the occurrence of normal migrating motor complexes""Visceral hypersensitivity in IBSIn 1973, Ritchie first reported that IBS patients have pain at lower volumes and pressures when a balloon is inflated in the bowel.31 This seminal observation has been replicated by a number of research laboratories,31ï¿½36 and the threshold to report pain is below the normal range in 50%ï¿½70% of IBS patients. Consistent with the concept of enhanced perception of visceral events are observations that IBS patients are more likely than controls to notice intestinal contractions37 and gas,29 and their pain thresholds are correlated, albeit weakly, with the amount of clinical pain they experience.32,38,39 Enhanced perception of visceral events is documented throughout the GI tract, including the esophagus,40 stomach,41 duodenum,42ï¿½44 and ileum.45 However, IBS patients do not show somatic hypersensitivity to pain42,46,47 and may have elevated48,49 somatic pain thresholds. One study32 noted that when combining other measures of pain sensitivity, such as the intensity with which the pain sensation is described and the location and size of the somatic referral area, up to 95% of patients show evidence of visceral hypersensitivity. The investigators concluded that visceral hypersensitivity might be a biological marker for IBS, although this interpretation has been challenged.38 InflammationPreliminary evidence for a possible alteration in gut immune function in IBS comes from both unselected and so-called postinfectious IBS (PI-IBS) patients. In unselected patients, increased numbers of mast cells in the muscularis externa of the colon50 and the ileal and colonic mucosa51,52 have been reported. Increased cellularity of the colonic mucosa and lamina propria has also been described in unselected IBS patients using semiquantitative microscopy.53 In patients with intractable IBS, lymphocytic infiltrates of the myenteric plexus were reported,54 and most recently, preliminary evidence for increased iNOS (nitric oxide synthetase) expression was described.55 For subgroups of IBS, these findings suggest there is an up-regulation of gut immune function. However, methodological deficiencies exist, including the influence of the bowel preparation, the classification of the patients, and the nonquantitative analysis of gut cells. Further studies are needed to explore these intriguing findings. Further support for a possible role of altered gut immune function in IBS comes from recent studies in PI-IBS patients.56ï¿½59 A subset of IBS patients associate the development of IBS symptoms with the onset of gastroenteritis.60ï¿½62 In recent prospective studies, IBS-like symptoms were found in 7%ï¿½30% of patients who recovered from a proven bacterial gastroenteritis.59 Reported risk factors included: female gender, duration of the acute diarrheal illness, and the presence of significant life stressor occurring around the time of the infection. Patients with PI-IBS were found to have a variety of functional alterations, including changes in gut motility,63,64 epithelial function,65,66 and an increase in colonic enterochromaffin cells.66 In addition, evidence for increased expression of interleukin 1 messenger RNA, increased cellularity of lamina propria, and an increase in CD3+ lymphocytes were reported from mucosal biopsy specimens.66 The correlation of IBS symptoms with these observed changes has not been established. Furthermore, because the majority of patients do not develop postinfectious diarrhea and the prevalence of IBS is not higher in countries with high rates of enteric infections, further studies are required to determine if vulnerability factors (such as altered neuroimmune system responsiveness) play a role in the development of PI-IBS in a subset of patients. In addition, psychological distress seems to be an important cofactor in determining who retains symptoms after an enteric infection.67 Autonomic activityAbnormalities in extrinsic autonomic innervation of the viscera occur in approximately one fourth of patients with functional bowel disorders.68,69 Aggarwal et al. showed that cardiovagal dysfunction is specifically associated with a constipation-predominant subgroup of patients with IBS, whereas patients with diarrhea-predominant symptoms had evidence of sympathetic adrenergic dysfunction.70 The role of autonomic dysfunction in IBS requires further evaluation. Central nervous system modulationIn general, brain-gut interactions play a prominent role in the modulation of gut function in health and disease.71ï¿½74 Signals from the brain to the gut assure that digestive function is optimized for the overall state of the organism (e.g., sleep vs. wake, stress vs. relaxation).75 Conversely, signals from the gut to the brain play a role primarily in reflex regulation76 as well as in modulation of mood states.77 In addition, certain vagal afferent pathways can influence pain perception.78 The CNS modulates motility, secretion, immune function, and blood flow.79 The emotional motor system in the brain80 is a revised name for the limbic system and some paralimbic structures (including the medial prefrontal cortex, amygdala, and hypothalamus) communicate emotional changes via the autonomic nervous system to the gut. The CNS is also essential in the perception of events occurring within the gut. This brain-gut bidirectional communication is largely not perceived consciously. In effect, the CNS functions as a ï¿½filterï¿½ with regard to the perception of peripheral afferent signals, and the threshold for perception can vary depending on the individual's emotional and cognitive state. Most visceral afferent signals reach the brainstem and thalamus, and only a very few are consciously perceived in the cortex.81 However, one recent study82 suggests that low intensity signals are subliminally registered. Modulation of visceral afferent information occurs at multiple levels from the periphery to cortical regions, as shown in Table 4.""The activation of these modulatory systems is dependent on peripheral as well as central events, even though the latter seem to be dominant. For example, although acute gut inflammation results in sensitization of peripheral, spinal, and central transmission,83 it is hypothesized that chronic inflammation may adaptively down-regulate perceptual sensitivity.49,84,85 Stress, anxiety, or recall of aversive memories all can enhance perception of painful events,86 whereas distraction, hypnosis, and relaxation can decrease perceptual sensitivity.87,88 Stress-induced visceral hyperalgesia89 may be an important mediator of visceral hypersensitivity in IBS patients. Therapeutic approaches aimed at attenuating stress responsiveness may effectively prevent the development of stress-induced visceral hypersensitivity, as well as attenuate autonomic gut responses to stress.90,91 Evidence for the alterations in the way the brain responds to visceral stimuli, and how this response may be altered in IBS patients, comes from recent studies using functional brain imaging techniques.92ï¿½96 Two of the studies, using distal colonic stimulation, have shown a greater activation in IBS patients of the midcingulate cortex, a brain region concerned with attentional processes and response selection.97,98 Modulation of this region by hypnotic suggestion was associated with changes in the subjective unpleasantness of a somatic pain stimulus in another study.88 The extent of abnormal visceral afferent processing by the brain in IBS patients needs to be established because they may be plausible mediators of various therapeutic approaches: cognitive therapies are likely mediated via networks involving the lateral prefrontal cortex, which in turn enhance the restraining effect of the medial prefrontal cortex on the emotional motor system.77 Hypnosis is likely to modulate attentional mechanisms (including the midcingulate cortex),88,99 and relaxation exercises involving deep breathing techniques may alter vagal afferent input to the brain. Centrally targeted medications such as anxiolytics, low dose tricyclic antidepressants (TCAs), NK-1R antagonists, and CRF1R (corticotropin releasing factor 1R) antagonists all involve inhibitory effects on the responsiveness of the emotional motor system and provide options for future therapeutic investigations.""With one exception,101 these studies suggest IBS patients report more lifetime and daily stressful events,10,14,102ï¿½107 including severe abuse history,108,109 than medical comparison groups or healthy controls. Furthermore, in IBS patients, stress is strongly associated with symptom onset105,107,110 and symptom severity.109 Even though the effects of stress on gut function are universal, patients with IBS seem to have greater reactivity to stress.72,111 The identification of specific psychological stressors associated with exacerbation of symptoms may help in planning treatment through psychological or psychopharmacological interventions. 2. Psychological and psychiatric comorbidity is common among patients with IBS. A large proportion of patients with IBS and other functional bowel disorders have concurrent psychological disturbances. As shown in Table 6, when using standardized research interviews, the prevalence of a psychiatric disorder ranges from 40% to over 90% among patients with IBS/functional bowel disorders in tertiary care centers. " http://www.gastrojournal.org/scripts/om.dl...id=agast1232108


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## Talissa (Apr 10, 2004)

EricWhat is your point?


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## SpAsMaN* (May 11, 2002)

What is Nitric oxyde?Is it good or bad?


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## flux (Dec 13, 1998)

> quote:I'm sure the editor will love hearing from you!


Apparently, they were. They say they are going to publish my note in their next issue. This isn't the first time I have encountered an error in a publication, but it is the first time, it isn't being ignored!


> quote:What is Nitric oxyde?Is it good or bad?


Nitric oxide is just a body chemical. It is involved in regulating arterial blood flow and in oxygenating tissues. It also has a role in gut motility.


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## Talissa (Apr 10, 2004)

Flux--that's down right impressive. T-


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## SpAsMaN* (May 11, 2002)

Floridian,lactobacille 299v is what VSL#3 contains and that makes me worst.So the research you have dosen't works apparently. Eric,many researchs claims that the hypersensitivity cause IBS,but Zelnorm FAILED!Why the bad flora can't be the cause for an irritated plumbing?I'm a plumber so that is even more frustrated to cope with a disfunctional plumbing.


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## eric (Jul 8, 1999)

Hypersensitivity is a result not the cause spasman.Bacteria can be irritating and the bowel reacts to ALL stimuli.IBS is very complex and the cause its not known yet, but many things are known about IBS.


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## eric (Jul 8, 1999)

From - Report on the 5th International Symposium onFunctional Gastrointestinal DisordersApril 4, 2003 to April 7, 2003 Milwaukee, Wisconsin By: Douglas A. Drossman, M.D., UNC Center for Functional GI and Motility Disorders at Chapel Hill, and William F. Norton, IFFGDSaturday April 5 Epidemiology/Genetic/Behavioral Factors Moderator: Douglas Drossman MD; Panel: G. Richard Locke III MD, Lin Chang MD, Rona Levy PhD, Shin Fukudo MD. "Shin Fukudo, Tohoku University School of Medicine, Japan discussed Possible Genetic Markers in Functional GI Disorders and Treatment Response, an emerging area of research. For some time it has been believed that brain-gut interactions -- autonomous activity in the GI tract and central nervous activity that influences bowel function in response to stressors -- play a major role in the origin and development (pathogenesis) of irritable bowel syndrome (IBS).Studies suggest that IBS patients have hyper-reactive bowels and unusually stress-sensitive brains. Studies by Dr. Fukudo's group include recent use of models to study serotonin (5-HT) reuptake transporter (SERT) genes, cross-cultural studies of 5-HT agents, and the effects of variations in the regions of the DNA strand that are the beginning of a gene (gene promoter regions) on one's responses to stress. Sensitization of the nerves (neurons) in the brain and the gut (intestines) may be due to a genetic effect as well as an acquired effect (resulting from a stimulus). More investigation on exploring genetic markers and therapeutic responses is warranted. "Full article here. http://www.iffgd.org/symposium2003factors.html


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## SpAsMaN* (May 11, 2002)

"Hypersensitivity is a result not the cause spasman."







My G.I.specialist told me that the hypersensitivity create spasms.Something like that.He told me that when i was in the pipeline of Talnetant(sensitivity stopper).Still searching news about Talnetant(Glaxo).


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## eric (Jul 8, 1999)

The bowel spasming is a motility problem.A lot of work has been done here and serotonin plays a very important role on the d and c and d/c motility problems, which in part explain those symptoms.The bowel hypersensitivity is a nerve problem."Visceral hypersensitivity: Enhanced perception, or over-responsiveness within the gut -- even to normal events." http://www.iffgd.org/GIDisorders/glossary.html The lining of the bowel has cells that are pressure sensitive, so when the bowel is stretched it releases chemicals that can cause pain. "The cardinal symptoms of IBS are abdominal pain and altered intestinal activity - diarrhea or constipation. These are probably related to what is called visceral hypersensitivity; this means the nerve receptors in the intestines are super-sensitive, and fire off signals more readily than those in unaffected people.Visceral hypersensitivity can be demonstrated by inflating a balloon that's inserted in the rectum, and measuring the pressure that produces pain. The pain threshold is lowered in 60% of IBS patients. Interestingly, if the patient is led to anticipate pain, by a stepwise increase in balloon pressure, the pain threshold decreases; on the other hand, if the balloon pressure is randomly altered, there is no lowering of the pain threshold. This indicates that the brain can, indeed, play a part in the symptoms of IBS. And during the anticipation of, as well as actual, distension of the rectum in IBS patients, brain radiographs show increased blood flow in some parts of the brain.Patients with IBS may complain of diarrhea, constipation, or neither of these symptoms. The motility of the colon is clearly an important feature of the condition. Visceral hypersensitivity means the colon will react to a greater extent to stimuli that would produce no obvious effect in unaffected people. A worsening of symptoms after eating, for instance, might be an exaggerated response to the 'gastro-colic reflex', in which a full stomach releases a substance called cholecystokinin-1 that causes contractions of colon musculature.IBS sufferers are sometimes intolerant of certain foods, such as wheat products or milk. An irritant effect can lead, because of visceral hypersensitivity, to poor digestion, excessive gas, bloating, and intestinal 'hurry'.Visceral hypersensitivity implies increased nerve cell signals traveling from the intestines up to the brain (afferent signals), and increased signals going in the opposite direction (efferent signals). These signals are transmitted with the aid of a chemical called serotonin, or 5HT (short for 5-hydroxytryptamine).There are several reasons for believing that 5HT plays a central role in the way IBS symptoms are caused. First, in inflammatory intestinal conditions, such as food poisoning, enteritis, and colitis, the number of special cells that produce 5HT in the intestine wall are greatly increased, and there is increased intestinal motility and hurry. Second, a drug that antagonizes one type of 5HT receptors on the cells (alosetron) is effective in diarrhea-predominant ISB. And third, another drug that antagonizes another type of 5HT receptors (tegaserod) is effective in constipation-predominant IBS.Two other factors are important in how IBS occurs. Stress can make it worse. Acute stress situations are not likely to be a problem; chronic, unrelieved stress, such as separation or bereavement, are more likely triggers."http://216.109.117.135/search/cache?p=pres...A3D53EB061&c=48 2&yc=28196&icp=1[/URL]Also zelnorm and lotronex may not work in some people due to genetic factors they are researching.


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## Talissa (Apr 10, 2004)

Hi Spas,That's pretty funny--you're a plumber with bad plumbing! (not ha,ha funny--ironically funny!)Actually VSL3 contains 8 strains of probiotics. The study Floridian cites is this particular isolated strand l. plantarum.L. Plantarum is the subject of several studies to help IBS. Here's another: At the 12-month follow-up, patients in the test group maintained a better overall GI function than control patients. There was no difference between the groups regarding bloating. Fifty-nine percent of the test group patients had a continuous intake of fermented products, whereas the corresponding figure for the control patients was 73%. CONCLUSIONS: The results of the study indicate that the administration of Lb. plantarum with known probiotic properties decreased pain and flatulence in patients with IBS. The fiber content of the test solution was minimal and it is unlikely that the fiber content could have had any effect. This type of probiotic therapy warrants further studies in IBS patients. http://www.ncbi.nlm.nih.gov/entrez/query.f...3&dopt=Abstract VSL3 didn't help another poster here, but she was helped by a different probiotic mix. Don't give up on probiotics! Here's some more to get you thinking; this was re: results of trials using lactobacillus acidophilus and bifidobacteria infantis:" A retrospective look at IBS patients treated with probiotics indicates that there is a deficiency of Lactobacillus in the gut flora in patients with IBS, Dr. Faber noted, "but we're not ready to call IBS an infectious disease." http://www.medscape.com/viewarticle/455964


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## eric (Jul 8, 1999)

abnormal transit can result in abnormal bacteria flora due to fermentations issues in the digestive tract and altered motility in IBS.The VSL3 study, if I remember correctly was done by them.Probiotics have shown some help and then not in IBS.They are believed to be more preventitive then cure.That they decrease pain and gas, is more that they are reducing gas pressure on the pressure sensitive cells in the gi tract and the hypersensitvity issues in IBS.


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## SpAsMaN* (May 11, 2002)

Thanks Eric.Maybe i will have a rectal manometry to figure out if surgery can be an option.Of course,i will need extremely evidents facts and confidence for a recovery to pass under the knife.







Do you think rectal manometry is needed if i already feel that i have sensitivity?This test is rarely use and a pelvic floor clinic are using it.A colo-rectal surgeon is at the head of the clinic.Sound good,maybe i can learn more to control the spasms who knows.


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## Talissa (Apr 10, 2004)

--Medscape--Probiotics and Prebiotics in Gastrointestinal Disorders *Posted 04/09/2004 * Summary: *The use of probiotics and prebiotics as therapeutic agents for gastrointestinal disorders is rapidly moving into the mainstream. * Mechanisms of action explain the therapeutic effects and randomized; controlled trials provide the necessary evidence for their incorporation into the therapeutic armamentarium...... *Probiotics, prebiotics, and synbiotics are moving from snake oil into the mainstream of medical therapy.* This evolution has been facilitated by our ever-increasing understanding of the mechanism of action of these agents and by the development of molecular methods for analyzing and identifying complex bacterial communities within the mammalian intestine. .... Indeed, the concept of a microbiologic balance existing in the intestine, involving competition between probiotic and pathogenic bacteria for specific binding sites on intestinal epithelial cells, has been well established in the literature. However, recent research has turned toward understanding the role of probiotic bacteria and their secreted products in enhancing and modulating innate and adaptive immune responses in the host by other mechanisms. With the demonstration that immune and epithelial cells can discriminate between different microbial species through activation of Toll-like receptors,[15*] the idea that probiotics may exert some of their protective functions through modulation of immune activity and epithelial function in both the large and small intestine has arisen.The mechanism of action of probiotics in IBS is poorly understood and has been thought to be attributable to changes in fermentation products. In 10 patients with diarrhea-predominant IBS, administration of VSL#3 probiotics improved the clinical picture without significant alterations in indigenous enterococci, coliforms, Bacteroides, or Clostridium perfringens flora.[48] In a similar open-label study, Bazzocchi et al.[49] demonstrated that VSL#3 probiotic induced changes in the composition of the colonic microflora together with improvement in colonic dysmotility and visceral perception. In contrast, in a double-masked, placebo-controlled, crossover 4-week trial in 12 patients with IBS, Lactobacillus plantarum 299v did not alter colonic fermentation or improve symptoms compared with placebo.[50] *Once again, these discordant results support the concept of specific probiotic strains being more effective than others across varied disease states.* ....Two studies examined the mechanism of the probiotic effect and antibiotic-associated diarrhea. Sullivan et al. demonstrated that the probiotics (administered as yogurt) prevented antibiotic-induced changes in Bacteroides fragilis microflora cultured from human feces.[82] Using an anaerobic culture system, Payne et al.[83] demonstrated that L. plantarum 299v diminished antibiotic-induced overgrowth of Candida albicans..... *Level II evidence is emerging in support of the use of probiotics in other gastrointestinal infections, in the prevention of postoperative bacterial translocation, in IBS,* and in both ulcerative colitis and Crohn disease. Nevertheless, one consistent feature has emerged over the past year: Not all probiotic bacteria have similar therapeutic effects. Future clinical trials will need to incorporate this fact into trial planning and design. *The use of probiotics and prebiotics as therapeutic agents for gastrointestinal disorders is rapidly moving into the mainstream. * http://www.medscape.com/viewarticle/470571_4 ****************************ba-da-dum


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## eric (Jul 8, 1999)

FYIHarvard HealthProbiotics: Using Bacteria to Improve HealthWeï¿½re used to taking antibiotics to defeat an infection. Now evidence from clinical trials suggests that consuming, rather than killing, certain kinds of bacteria might offer a way to treatï¿½and perhaps preventï¿½some illness. Probiotic therapy or probiotics, as itï¿½s come to be called, is especially popular in Scandinavia (particularly in Finland), partly because of the tradition there of eating fermented foods like yogurt. But as often happens with products marketed as being more natural, probiotics have been oversold. The claims are seductive: pills, powders, and solutions containing ï¿½friendlyï¿½ bacteria will boost the immune system, prevent cancer, and perform assorted other health miracles. This sort of over-the-top hype is easy to spot. But that doesnï¿½t mean itï¿½s based upon total fiction. All the usual qualifications apply: the studies are small, the results inconsistent, the findings often limited to animal experiments. Nonetheless, the evidence suggests that probiotic therapy could be useful someday as a form of preventive medicineï¿½and not just for diseases affecting the gut. Why it Might WorkMost of us think of the digestive system as a circuitous food processor. But itï¿½s also one of the bodyï¿½s fire walls, keeping out disease-causing microorganisms, as well as proteins that might spur a debilitating immune response, while at the same time letting in vital nutrients. The gut has considerable help in striking this balance between barrier and conduit: some 500 different kinds of bacteria inhabit a healthy intestine. Collectively theyï¿½re known as the gut microflora. These ï¿½good bacteriaï¿½ compete with and tend to crowd out disease-causing bacteria by keeping them from attaching to the intestinal wall and secreting agents that the invaders find toxic. The native bacteria also provide protection by stimulating the patches of lymphoid tissue embedded in the wall of the intestine, causing them to churn out antibodies against pathogens. In young children, the microflora are believed to stimulate the growth of the lymphoid tissue itself. Just as a pollutant can ruin a lake or river, invading viruses or bacteria can lay ruin to this finely balanced intestinal ecosystem. When the invaders win the battle, the gut wall becomes too permeable. Undesirable proteins flood in. The intestine becomes inflamed. Antibiotics can have a similar disruptive effect as they wipe out some of the healthful microflora along with the bacteria that are causing illness. Prodding the Immune SystemDoses of the right kinds of bacteria may also be good for us because they gently stimulate immune systems that have been, in a sense, overprotected. According to the hygiene hypothesis, we may develop allergies and some intestinal problems because we live in relatively germ- and dirt-free environments compared with our ancestors. As a result, our immune systems become overly sensitive and prone to inflammatory responses. The basic notion behind probiotics is pretty straightforward: restore the depleted ecology of the intestine with new, healthful bacteria. Besides having a good local effect in the gut, this might benefit the immune system as a whole. Probiotic therapy is also an old idea. Almost a century ago Elie Metchnikoff, director of the Pasteur Institute, argued that Bulgarian peasants lived long lives because they ate yogurt containing Lactobacillus bacteria. In the 1930s, Minoru Shirota, a Japanese physician, maintained that the right mix of gut bacteria could prevent disease. But working out the practical details of these theories hasnï¿½t been easy. The lingering questions include which bacteria should be used and who will benefit and under what circumstances? Effective in Treating DiarrheaThe best results for probiotic therapy have been in children with bad diarrhea.Infection with rotavirus is the most common cause of severe diarrhea in children. A healthy immune system usually limits a bout of the illness to a few uncomfortable days, but it can last over a week and leave some children so dehydrated that they need to be hospitalized. Finnish researchers, in a series of studies that goes back 10 years, have shown that probiotic therapy cuts the duration of rotavirus-associated diarrhea by 1.4ï¿½2.4 days. Stefano Guandalini, a University of Chicago pediatric gastroenterologist, has published results from a multicenter study in Europe that found value in probiotic therapy for children with diarrhea, regardless of cause. He reported in the January 2000 Journal of Pediatric Gastroenterology and Nutrition that when children hospitalized with severe diarrhea were treated with an oral hydration solution containing Lactobacillus GG, they had a shorter course and a shorter hospital stay than children given the oral solution alone. When people take antibiotics that alter the gutï¿½s microflora, a bacterium called Clostridium difficile often seizes the opportunity, propagates, and produces a toxin. In severe cases, this leads to colitis, an acute inflammation of the lining of the intestine. Two years ago, two large and credible studies, one American and the other Finnish, showed that probiotic therapy reduced the diarrhea experienced by children taking antibiotics for respiratory tract infections. But in other studies of antibiotics, the results have been negative. So the value of probiotic therapy for gut problems caused by antibiotics remains controversial. The evidence for travelerï¿½s diarrhea also ping-pongs. British soldiers traveling to Belize and Finnish tourists visiting Turkey werenï¿½t protected by the probiotics they took, according to studies published several years ago. When a different probiotic was tested on tourists from Long Island the diarrhea rate was cut in half. Useful for Lactose IntolerancePeople are lactose intolerant because they donï¿½t have enough active lactase enzyme in their intestine to break down lactose, a sugar molecule found in milk. Because they feed on lactose, Lactobacillus bulgaricus, Streptococcus thermophilus, and other kinds of bacteria, either in tablets or in foods like yogurt, have been shown to alleviate the problem. Still, some experts warn that dairy products billed as containing active culturesï¿½such as acidophilus milkï¿½may not be depleted of enough lactose to make a difference for people sensitive to the milk sugar. Pills containing the lactase enzyme itself are available and may, for many, be more effective. Potential for Bowel DiseasesThe results are mixed in research on the effectiveness of probiotic therapies against Crohnï¿½s disease, irritable bowel syndrome (IBS), and other bowel disorders. Much of the published research consists of reports on one or several patients, which is the kind of information that yields interesting hypotheses but not good, solid proof of efficacy. But two years ago, Irish investigators reported results from a small, randomized trial that showed Lactobacillus GG reduced the number of unformed bowel movements in IBS patients with diarrhea. But for pain, urgency, and bloating, the probiotics werenï¿½t any more helpful than the placebo used in the trial. Probiotics in Food Yogurt has been cast as a health food ever since Elie Metchnikoff drew a connection nearly a century ago between the good health of Bulgarian peasants and their consumption of yogurt containing various species of Lactobacillus bacteria. But, in the early 1980s, Tufts University researcher Sherwood Gorbach and his group conducted a series of experiments showing that the Lactobacillus species commonly found in yogurt (L. acidophilus and L. bulgaricus) didnï¿½t colonize the intestine and, therefore, couldnï¿½t have much beneficial effect. Not everyone agrees with this point of viewï¿½a really steady diet of L. acidophilus might still have some benefitsï¿½but it certainly took some of the steam out of the idea that bacterial cultures make yogurt a super health food. Itï¿½s not common in the United States, but food makers elsewhere are adding probiotic bacteria to their products. In Australia, for example, a product called Bio-Cheese has added Lactobacillus rhamnosus HN001. Adding bacteria to foods, particularly to dairy products, is feasible. Many of the successful clinical trials of probiotics have used milk laced with bacteria. You can find reports in the published medical literature suggesting that probiotic therapy might help people with Crohnï¿½s disease, but theyï¿½re preliminary. Bowel disorders are often difficult to treat, so people are going ahead and giving probiotics a try before the definitive studies are done. Some say theyï¿½re getting good results. Might Prevent AllergiesA study published in the April 7, 2001, Lancet hinted that probiotics might be used to prevent allergies. Expectant mothers in the treatment part of the study took two capsules of Lactobacillus GG daily for two to four weeks before delivery, which was followed by a six-month course for the infant. Infants who received the bacteria had a rate of chronic allergic eczema half that of infants who didnï¿½t. Infants with chronic allergic eczema are at increased risk for having allergies later in life. Might Boost the Immune SystemVarious studies have hinted that probiotics might boost the effectiveness of vaccines. Other researchers have shown that they might promote overall health by revving up the immune system. For example, a study published in the June 2, 2001, British Medical Journal found that children attending daycare centers in Helsinki who drank milk spiked with Lactobacillus GG were absent 11% less often and had 17% fewer respiratory infections during the seven-month study than children drinking regular milk. With age, our immune systems flag. Probiotics might be used to perk them up, according to a study in the December 2001 American Journal of Clinical Nutrition . New Zealand researchers gave 30 healthy volunteers, ages 63ï¿½84, milk containing a bacterium called Bifidobacterium lactis HN019 for three weeks. At the end of the study, numbers of several kinds of white blood cells had risen. Itï¿½s worth noting that this study was sponsored by the New Zealand Dairy Board and that there was no evidence that the higher white blood cell counts improved health. Which Bugs Work?The bacteria most commonly used as probiotics fall under the general heading of lactic acid bacteria. These bacteria feed on sugars and produce lactic acid, which is part of the reason they are so useful in the food industry: by generating acid and lowering the amount of sugar, they make foods like yogurt, cheese, and sauerkraut inhospitable environments for disease-causing organisms. Some yeasts, principally Saccharomyces boulardii, have also been used as probiotics. The bacterial strains tested most often belong to the Lactobacillus and Bifidobacterium genera. So far, researchers have had more success with a strain called Lactobacillus GG than with any other. ï¿½GGï¿½ is for the initials of the Tufts University researchers who isolated it, Sherwood Gorbach and Barry Goldin. Itï¿½s also known as Lactobacillus rhamnosus or Lactobacillus rhamnosus GG. But if you want to buy Lactobacillus GG, it can be hard to find. Gorbach and Goldin have a patent on it, and so far, itï¿½s available commercially only in a product called Culturelle, which is sold through a Web site and a toll-free phone number. The strains that are used in commonly available probiotics include L. acidophilus and L. reuteri. Whether L. acidophilus, even in large doses, can populate the gut is doubtful. L. reuteri has shown some promise as a treatment for childhood diarrhea. Researchers and companies are competing to show that their particular bacterial strain works best. Some are placing their bets on combinations. For example, VSL Pharmaceuticals, a Gaithersburg, Md. company, is selling a product called VSL #3 that contains eight different kinds of bacteria.


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## Nath (Jan 5, 1999)

Theres a good article in New Scientist (24th april edition) about the role of intestinal flora in gasto diseases, including IBS. Theres no web link that I can find, unless you are an online subscriber. I think new scientist sells in the US, so it might be worth picking up a copy.


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## SpAsMaN* (May 11, 2002)

In the mouth,a bacteria call Mutant is responsible for the tooth decay by creating acid lactic with the contact of the sugars.Maybe there is a similar reaction in the bowel causing irritation and spasms.I have noted that my mouth bacterias are worst with IBS and very irritating too.


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## not well (Mar 18, 2004)

when is the Rome 3 report going to published anyone know?


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## eric (Jul 8, 1999)

not well, Rome 3 will come out the end of the year or beginning of the next.Nath, is that in the new issues I did not see it?But I did see this.Brain-watching helps suppress pain http://www.newscientist.com/news/news.jsp?id=ns99994931


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## flux (Dec 13, 1998)

> quote:Rome 3 will come out the end of the year or beginning of the next


Eric, the website http://www.romecriteria.org/romeIII.html says 2006.


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## eric (Jul 8, 1999)

I asked Dr Drossman and he said the dates I mentioned, although maybe they postponed it. I will check again with them to make sure.


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## not well (Mar 18, 2004)

thanks eric you also mentioned that abnormal transit time can result in abnormal bactiera flora if you could maybe explain a bit more cause still a bit confused on this whole issue of why after every meal does it go through me and sit at the end, and why if i don't get the right urge bms are incomplete? ten years ago in the summer i remember having a salad and after that i've has non stop symtomns which are desribed belowi swear to **** something invaded my GI tract that day


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## Talissa (Apr 10, 2004)

Hi not well,I hope you don't mind me butting in--just wanted to add that it can also work the other way: abnormal/imbalanced intestinal flora can bring about abnormal transit time--esp. when intestinal hyperpermeability, which leads to food reactivity, is added to the mix. "i swear to **** something invaded my GI tract that day"We have a wisdom within us if we listen--you know your body. You're probably right.T-


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## eric (Jul 8, 1999)

" intestinal hyperpermeability, which leads to food reactivity, is added to the mix. "This is BAD Information and has nothing to do with IBS. IBS is not caused by foods and is not dybosis or "leaky gut" its just a popular theory at the moment with a very few people on the bb right now, who cannot explain it, post IBS studies about it or understand the inflammation they see in a subgroup of IBS patients and post infectious IBS. "From the new IFFGD."There is no evidence that digestion is different in those with IBS compared to those without IBS. Although the exact cause is not known, there are factors that appear to aggravate symtoms or make people feel worse."While dietary factors do not cause IBS, they may aggrvate symptoms in some persons. Increased intestinal muscle reactivity and/or heightened sensitvity in IBS can cause the bowel to over respond to stimuli. Even the act of eating itself, and not a particular food, ay aggravate symptoms."Nonetheless certain foods are known to simulate gut reactions in general."There is more from there news letter."Irritable Bowel Syndrome: An Overview By: Lin Chang, M.D., CNS: Center for Neurovisceral Sciences & Womenï¿½s Health; CURE: Digestive Diseases Research Center, Division of Digestive Diseases, UCLA School of Medicine Irritable bowel syndrome (IBS) is a chronic functional bowel disorder characterized by abdominal pain or discomfort and alterations in bowel habits. The clinical diagnosis of IBS is based on identifying symptom criteria with a ï¿½positive diagnosisï¿½ and excluding organic disease with minimal diagnostic evaluation. Although there are many expensive and sophisticated tests available for the evaluation of IBS symptoms, these are generally not needed for patients with typical symptoms and no features suggestive of organic diseases. This article provides a comprehensive overview of the prevalence, symptoms, diagnosis, and treatment options for IBS." http://www.aboutibs.org/Publications/currentParticipate.html IT is possible on the other hand you may have gotten a bug from the salad, an enteric infection or shock to the digestive system can be the start of molecular changes in the digestive system, especially cells that release serotonin and mast cells in the gi track leading to full blown IBS. That's what happened to me.They already know in IBS there is an altered gastro colonic responce to food, and hence the act of eating can trigger symptoms.The stomach sends signals to the lower colon food is on the way and you have to go.They also know in IBD d patinets there is an increase in serotonin released from the cells in the gut and that causes the bowel to over react and the result is d.The food is still in the the throat and sigmoid colon over reacts.These are a little blurry. Sorry







"Schuster and his colleagues conducted a series of studies in which volunteers wore tiny pressure transducers that recorded the pressure of the muscles lining their colon and rectum. Recordings were made over a 24-hour period, while volunteers went about their normal daily routines.The researchers found that many IBS patients have disorganized and significantly more vigorous contractions. The muscles tend to spasm. "There's a more prolonged contraction, over a larger area," says Schuster. "It's like having a Charlie horse in the gut."The Hopkins team found that while healthy volunteers had between six to eight peristaltic contractions in their colon within a 24-hour period, IBS volunteers who tended to be constipated had almost none, and volunteers who frequently had diarrhea had as many as 25 peristaltic contractions per day. "This is not caused by foods, dybosis or "leaky gut" or gut permeability, however there is a lot of evidence for neurotransmitter dysregulation being involved in moltility in IBS. There are three important factors in IBS research right now.Altered motilityviceral hypersensitivityand brain gut axis dysfunction between the enteric nervous system and the central nervous system and the bidirectional communication between the two.


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## eric (Jul 8, 1999)

1"Michael Camilleri, MDHead, Motility Interest GroupDivision of Gastroenterology and HepatologyMayo Clinic The last decade has seen a dramatic increase in our understanding of the mechanisms and management (diagnosis and therapy) of irritable bowel syndrome. Dr. Camilleri is a physician investigator with specialist expertise in motility, sensory and functional disorders of the gastrointestinal tract. He summarizes the clinical and scientific advances and provides the evidence basis for future therapies in irritable bowel syndrome. Dr. Camilleri's presentation reviews the mechanisms of motor and sensory functions of the colon, and outlines the diagnosis, current approaches to therapy and potential future therapies for this common disorder. "2Douglas Drossman, MDProfessor of Medicine and PsychiatryCo-Director, UNC Center for Functional GI and Motility DisordersUniversity of North Carolina at Chapel Hill Recently, the irritable bowel syndrome (IBS) has gained a great deal of prominence within the field of Gastroenterology. An explosion of basic and clinical research has advanced our understanding of the pathophysiology of this condition. We now understand the IBS not only as a disorder of motility, but also as one associated with visceral hypersensitivity with brain-gut modulation. This new knowledge has been associated with the development of symptom-based criteria for diagnosis, and has led to new forms of treatment. Dr. Drossman, is a nationally recognized investigator and clinician in the field of functional gastrointestinal disorders. He presents an update using an integrated Biopsychosocial approach that applies our new knowledge of the pathophysiology of IBS in order to develop a practical approach to diagnosis and treatment. 3Jack Wood, PhDProfessor of Physiology and Internal MedicineChairman Emeritus, Department of PhysiologyThe Ohio State University College of Medicine Dr. Wood was the first to use microelectrodes to record the electrical and synaptic behavior of neurons in the enteric nervous system. He coined the term "brain-in-the-gut" in view of emerging evidence that the enteric nervous system had neurophysiological properties like the brain and spinal cord. In recent years he has focused on signaling interactions between the enteric immune system and the brain-in-the-gut during infectious enteritis and food allergy. In this lecture he shows how the central nervous system, enteric nervous system and intestinal immune system are integrated during physical and emotional stress to produce irritable bowel symptoms of diarrhea and abdominal pain and discomfort. 4Barbara Yawn, MDDirector of ResearchOlmsted Medical Center Dr. Yawn combines her experience as a primary care physician with a research agenda designed to elucidate the physician's and the patient's contribution to the diagnostic process. The ability to study patients from primary care and specialty clinics as well as community populations affords her work a view of the entire scope of the IBS. By including qualitative research techniques, Dr. Yawn gives voice to the patients' concerns and their recommendations to improve their medical care. 5Michael Gershon, MDChair, Department of Anatomy and Cell BiologyColumbia University College of Physicians And Surgeons Dr. Gershon's earliest work involved investigations of the function of serotonin in the bowel, but it soon also came to involve studies of the cellular and molecular basis of intrinsic reflex control and ontogeny of the ENS. Dr. Gershon's work has been vital in the rediscovery of the unique ability of the enteric nervous system (ENS) to function independently of CNS input, and he has become the acknowledged world leader in research in enteric neuronal development. In this lecture he shows how and why blocking signals from the brain to the gut with alosetron, a potent, long-lasting and specific 5-HT3 antagonist, relieves many of the symptoms of IBS. This lecture also includes a discussion of the 5-HT1P, 5-HT4 and 5-HT3 receptors. 6Nigel 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. 7Margaret Heitkemper, RN, PhD, FAANUniversity of WashingtonDepartment of Biobehavioral Nursing & Health SystemsMargaret McLean Heitkemper, RN, PhD, FAAN is Professor and Chairperson, Department of Biobehavioral Nursing and Health Systems, Adjunct Professor, Division of Gastroenterology, School of Medicine, University of Washington. She is also Director of the NIH-NINR funded Center for Womenï¿½s Health Research at the University of Washington. Dr. Heitkemper received her BSN in 1973 from Seattle University, her MN in gerontological nursing from the University of Washington in 1975, and her PhD in Physiology and Biophysics from the University of Illinois at the Medical Center, Chicago in 1981. She has been on faculty at the University of Washington since 1981. Her research related to women, stress, and gastrointestinal function has been continuously funded by NIH since 1983. She is the author of two nursing textbooks and over 60 data based papers. At this time, Dr. Heitkemper serves as Chairperson of the Nursing Science Review Group at the NIH. 8William Orr, PhDPresident/Chief Executive OfficerLynn Health Science InstituteDr. Orr, one of the pioneers in the field of sleep medicine, will focus on a description of sleep physiology and how sleep alters gastrointestinal functioning in normal volunteers as well as in patients with irritable bowel syndrome. In addition, the presentation will cover disruptions in autonomic functioning in patients with IBS, and how this may be involved in the pathogenesis of irritable bowel syndrome. William Whitehead, PhDUniversity of North Carolina at Chapel HillUNC Functional GI Disorders CenterAbdominal pain is the defining symptom of irritable bowel syndrome, and patients rate pain as more bothersome than diarrhea or constipation. Consequently, pain reduction is the primary goal of treatment. The relative contributions of biological and psychological influences on pain experience remain controversial. New drugs about to be released decrease pain by regulating serotonin (5HT3 antagonists and 5HT4 antagonists). However, antidepressants and psychotherapy also reduce abdominal pain and may do so through psychological mechanisms. 9Esther 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. 10Howard Mertz, MDAssociate Professor of MedicineDivision of GastroenterologyVanderbilt UniversityDr. Mertz has done extensive research on the role of intestinal hypersensitivity in a variety of functional bowel disorders including IBS, constipation, and functional dyspepsia. Currently his work has identified cerebral centers which are activated by visceral pain and how they are different in IBS. Dr. Mertz has reported the largest series of constipated patients studied, and classified their physiology and symptoms into a coherent picture. These findings and implications will be discussed in the presentation that follows. 11Bruce Naliboff, PhDCURE Digestive Disease Research CenterDepartment of Medicine, Physiology and PsychiatryIt is increasingly recognized that Irritable Bowel Syndrome is a common and diagnosable disorder that has a significant impact on Quality of Life. Dr. Naliboff is a leading authority on the interplay between psychological, behavioral, and biological factors in IBS. His research includes perceptual, autonomic, and brain imaging studies of visceral sensitivity, as well as studies of psychosocial variables that impact Quality of Life and symptoms in IBS. His lecture will review the most recent data on the broad range of intestinal and extra-intestinal symptoms in IBS, the overlap of IBS with psychiatric disorders, and the role of both symptoms and psychosocial factors in determining Quality of Life for IBS sufferers. 12Stephen Collins, MBBS, FRCP, FRCPC - McMaster University, Faculty of Health Sciences Title: The Effect of Mucosal Inflammation on Enteric Neuromotor Function: Implications for the Development of IBS post-infectious gastroenteritis 13 Arnold Wald, MD - University of Pittsburgh Medical Center Title: Irritable Bowel Syndrome: Psychotropic and Medical Aspects Benny Kerzner, MD - National Children's Medical Center Title: Functional Abdominal Pain: A Pediatric Perspective http://www.conference-cast.com/ibs/Lecture...dRegLecture.cfm GutReactions http://www-fhs.mcmaster.ca/idrp/leading.htm Inflammation, Infection, and Irritable Bowel Syndrome (IBS): An Update http://www.fibromyalgiasupport.com/library...cle.cfm/id/4518


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## SpAsMaN* (May 11, 2002)

I like these photos Eric.I hope one day,all these researchs will come to a breakthrough.


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## SpAsMaN* (May 11, 2002)

This graphic not necessary rule out bad flora.But the researchs dosen't seems to go toward the flora theory .It would be surprising to discover that the spasmscontractions are rules by bowel bacterias in a near future.What do you think?It would be like returning to your highschool girlfriend.


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## Talissa (Apr 10, 2004)

Eric,You are seriously brainwashed.One day (& god-willing I'll be here to "see" it) you're going to have to eat your words Big Time.I'm guessing you used to say probiotics were useless? Now they're moving from snakeoil to mainstream. So will the connection btn LGS & IBS. Here's a little something from a medical MD, who knows just a bit more than you on the subject of intestinal hyperpermeability & its devastating consequences:"Altered Immunity & Leaky Gut Syndrome"by Zoltan P. Rona MD, MSc.....Due to the enlarged spaces between the cells of the gut wall, larger than usual protein molecules are absorbed before they have a chance to be completely broken down as occurs when the intestinal lining is intact. The immune system starts making antibodies against these larger molecules because it recognizes them as foreign, invading substances. The immune system starts treating them as if they had to be destroyed. *Antibodies are made against these proteins derived from previously harmless foods.*...The Leaky Gut and IBSThe mainstream thinking on IBS is that it is caused by stress. Irritable bowel syndrome is the number one reason for general practitioner referrals to specialists. In well over 80% of the cases, tests like the intestinal permeability test (a special urine test involving the determination of absorption rates of two sugars called lactulose and mannitol), CDSA or livecell darkfield microscopy reveal the presence of an overgrowth of fungi, parasites or pathogenic bacteria. The one-celled parasite, blastocystis hominis and different species of candida are the most common microbes seen in IBS. The only stress associated with IBS is that which is generated by infection and the leaky gut syndrome. If allowed to persist without the correct treatment, IBS can progress into more serious disorders like the candidiasis syndrome, multiple chemical sensitivities, chronic fatigue syndrome, many autoimmune diseases and even cancer. If treated medically, IBS is rarely cured. To treat it correctly, natural treatments work best and must include the removal of the cause, improvement of gastrointestinal function and healing the lining of the gut....In addition to the creation of food allergies by the leaky gut, the bloodstream is invaded by bacteria, fungi and parasites that, in the healthy state, would not penetrate the protective barrier of the gut. These microbes and their toxins, if present in large enough amounts, can overwhelm the liver's ability to detoxify. This results in symptoms such as confusion, memory loss, brain fog or facial swelling when the individual is exposed to a perfume or to cigarette smoke that he or she had no adverse reactions to prior to the development of the leaky gut syndrome.************** http://www.crossroadsinstitute.org/newsletter/mar04.html (The entire article is extremely interesting! This is an online magazine, so you just need to scroll down about half way--its the 15th short article or so.)


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## Talissa (Apr 10, 2004)

Eric,You can also read the following article(in pdf) called:"Persistent epithelial dysfunction and bacterial translocation after resolution of intestinal inflammation" http://upload.mcgill.ca/parasitology/Chadee1.pdf The article is addressing the difficulty in treating IBS & IBD. It is obviously ALL about increased permeability along the intestinal wall.


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## Talissa (Apr 10, 2004)

And yet there's more..."...Food allergies and food intolerances may be caused by several factors including heredity, gut permeability, an overly sensitive immune system, poor digestion, or an excessive exposure to a limited number of foods.....The food is inadequately digested in the stomach and small intestine causing intact proteins come into contact with the cells lining the intestine. Antibodies in and on the intestinal lining combine with the food protein, initiating an inflammatory reaction. The inflammatory reaction causes damage to the nearby intestinal cells. Continued exposure results in progressive damage to the intestinal cell lining. The damaged lining decreases the surface area of the intestine, resulting in fewer nutrients being absorbed, and allows antigens to "leak" into the body. In this way, food causes Leaky Gut Syndrome. Leaky Gut Syndrome, in turn, causes food allergies. An undigested protein "leaks" across the intestinal lining and is tagged as an antigen, antibodies are made, and a food allergy is born. The person is now sensitized to this food and whenever it is eaten, the body will launch an immune response damaging nearby cells which again leads to Leaky Gut Syndrome if the "nearby" cells are in the intestinal lining. " http://www.ibdanswers.com/AppA-ClinicalDef...eakyGutSyndrome This article is also very good. Definitely worth the time to check out.


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## Talissa (Apr 10, 2004)

Spas,The researchers ARE turning now toward gut flora as a big key to IBS--hence the point of the above Medscape article.For ex, what I find most encouraging is they've found certain strains of LAB(lactic acid bacteria) are capable of healing the intestinal wall. (There are many others which battle pathogens.)Speaking of specific strains of LAB, the Digestive Advantage-IBS really is making the most marked improvement in me--much faster than any other probiotic I've tried.I need to post this on the other thread too, but I can certainly can eat many, many things which previously made me set aside an hour before bed to repeatedly go to the loo.T-


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## Nath (Jan 5, 1999)

Eric, it was in last weeks print edition(24th april no.2444 p42). Its not available online unless you subscribe to new scientist. I could scan it if you would like a copy, too much typing for me


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## SpAsMaN* (May 11, 2002)

Anyway,we all walk in darness.I feel that i may have permeability,even through the skin.The 5 of May,i have a phone consultation with the "flora expert" from the Australian clinic.If you have few goods questions,i can ask her.They treat IBS-C and D by changing the sick flora by an healthy one.Visit my recent Australian clinic thread... I don't need trapped gas anymore and i never had the need.


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## SpAsMaN* (May 11, 2002)

I don't know any others flora experts,which is odd.


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## SpAsMaN* (May 11, 2002)

But be quick for your "questions to ask" because in Australia they already are the 3 of May because they are one day ahead of the America.


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## not well (Mar 18, 2004)

eric i understand what your saying about transit time but even after having a small bite of a meal, 25 peristalis movements WILL make you D in a very short time and so forth. mine is completly different every i eat something i feel it's not being digested properly(read the symtomns below) i've been taking prebio 7 and i've noticed a small change(less bloating and slight improvement in bms) like talissa said abnormal intestine flora can probably cause havoc with the functioning of motility and sphincter movements. but I DO NOT SUFFER FROM D ONE MINUTE AFTER A MEAL. i seriously believe that when i had the salad ten years back either some unknown bacteria or anything else for that matter came in to my gi tract. i know this sounds gross but even the stools stench differently from ten years back before i had this, and i remember well.but as for nerve dysfunction yes ten years back i could have a complete bm without straining and be free for the whole day. but i think if it is abnormal intestine flora it could have had an effect on the anal sphincter muscules, but certain nerve receptors could be responsible as well.i'm still confused on this whole issueregards


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## Talissa (Apr 10, 2004)

Eric,It was early this am when I posted, I forgot about the Medcape article I posted earlier that does prove :LGS linked to IBS is already moving into mainstream.******************************Remember this article? : " _What Unifies and Separates Irritable Bowel Syndrome and Inflammatory Bowel Diseases_ ""Both irritable bowel syndrome and inflammatory bowel diseases share symptoms of altered bowel habits associated with abdominal pain or discomfort...Possible shared pathophysiologic mechanisms include altered mucosal permeability..." "A comparison of published data on the activation of the gut-associated mucosal immune system in IBS and IBD reflects both the similarities and the differences in the altered immune response observed in these disorders...""Increased PermeabilityFor both syndromes, histologic and functional alterations of the mucosal barrier have been recently reported.[11*, 12, 24, 25]...."(increased permeability & alterations of the mucosa barrier ARE leaky gut)" *Despite the common assumption that chronic gut mucosal inflammation is associated with sensory-motor dysfunction of the gastrointestinal tract in inflammatory as well as functional intestinal disorders, the relationship between chronic inflammation and the generation of gastrointestinal symptoms remains unclear.* The development of IBS-like symptoms in some patients with quiescent ulcerative colitis was suggested as an indication of the role of inflammation on altered sensory and motor function.[8] The concept of long-lasting postinflammatory changes in gut motility is supported by the observation of altered anorectal and colonic motility in patients in remission from ulcerative colitis and Crohn disease.[52] " " *The recent observation of an activated immune system in some IBS patients associated with persistent low-grade mucosal inflammation provides evidence for the reconsideration of the symptom-criteria-based diagnosis of functional bowel disorders.* "


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## Talissa (Apr 10, 2004)

> quote:"increased permeability & alterations of the mucosa barrier ARE leaky gut"


TRUEI realize the term "LGS" is distasteful, and was formerly only used by alternative medicine practitioners, but times have changed:The following are just a few PubMed references to leaky gut:"Intestinal permeability, leaky gut, and intestinal disorders." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=10980980 "Zinc supplementation tightens "leaky gut" in Crohn's disease." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=11383597 "A porous defense: the leaky epithelial barrier in intestinal disease." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=14767487 "Crohn's disease, TNF-alpha, and the leaky gut. The chicken or the egg?" study reviewed by the American Journal of Gastroenterology:"Anti-tumor necrosis factor treatment restores the gut barrier in Crohn's disease." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12190145 ****************Bottom line: stick to hypnotherapy to help people, but leave this alone.You don't have a clue.


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## eric (Jul 8, 1999)

Nath if you could an email me it that would be great.Notwell, I have to come back to your questions.Talissa,False and this has to do with post infectios IBS, but its something you have to completely learned about in regards to gut permeability and IBS. There are also MOLECULAR CELL CHANGES YOUR TOTALLY IGNORING!!! You do not have the whole picture on the complexities of this, I gurantee you that and because of that, before you promote leaky gut, please understand what you are saying to people, because you are dealing with other people's health and your information and it needs to be accurate.Your in medscape all the time, read the WHOLE IBS Resource center, not cherry pick for "leaky gut and permeability."There are macroscpopic inflammed cells, they believed inflammed by chronic stressors and a biderectional communication between the gut and the brain in a subset of IBS patients.This has to do with the HPA axis and the limbic system.I have said this to you before in regards to the above abstract your using, read all of Dr mayers works and you will soon find out what he is really talking about in regards to IBS, and it might totally surprize you for sure. You are talking about something completely different then what Dr Mayer believes as a top expert neurogastroenterologist in IBS research.I am waiting for the experts to write a paper for me on this to set the record straight.Its maddening when people continouly post totally inaccurate information on IBS.Since Talissa, you are using Dr Mayers work to promote leaky gut, I would suggest you read all his work, to understand exactly what his work has lead to in IBS."Substantial data (Mayer et al review) now support the concept of an enhanced responsiveness of central stress circuits and associated alterations in neuroimmune interactions to external (eg, anxiety, fear, psychosocial factors) or internal (eg, nutrient, inflammation, infection) stressors as part of the underlying pathogenesis of IBS. Such stress hyperresponsiveness results in altered autonomic, neuroendocrine outputs as well as alterations in endogenous pain modulation. This process in turn leads to dysregulation of gut motility, altered gut epithelial function, and enhanced perception of visceral events, ultimately altering brain-gut interactions and producing the characteristic IBS symptoms."He also argues without the abnormalities of brain processing of gut information, "chronic inflammatory mucosal changes in the gut are not a plausible mechanism to explain the presence of chronic abdominal pain, a cardinal IBS symptom."Inflammation does not explain totally pain in IBS."Curr Gastroenterol Rep. 2003 Aug;5(4):331-6. Related Articles, Links Current insights into the pathophysiology of irritable bowel syndrome.Schwetz I, Bradesi S, Mayer EA.Center of Neurovisceral Sciences and Women's Health, CURE: Digestive Diseases Research Center, David Geffen School of Medicine at UCLA, VAGLAHS, Bldg. 115, Room 223, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA. emayer###ucla.eduRecent reports have emphasized the possible role of mucosal immune activation and inflammation in neuropathic changes in the pathophysiology of irritable bowel syndrome (IBS). However, novel findings using functional brain imaging techniques have underlined the importance of altered perception of visceral stimuli to symptom generation in IBS. These new developments have rekindled an old debate on peripheral versus central mechanisms in the pathophysiology of IBS. In this review we discuss the latest findings in light of these two concepts. In addition, we provide evidence for the hypothesis that, in the absence of alterations in endogenous pain modulation systems and changes in visceral perception, chronic inflammatory mucosal changes in the gut are not a plausible mechanism to explain the presence of chronic abdominal pain, a cardinal IBS symptom. Publication Types: Review Review, Tutorial PMID: 12864964"Frome RomeIrritable Bowel Syndrome: How far do you go in the Workup?"Is it possible that some simple and inexpensive tests will emerge to accurately diagnose IBS? I do not think that IBS can by diagnosed by ordering tests, either to make a unitary diagnosis, or by default by excluding other disorders. There is evidence that IBS is a heterogeneous disorder where different physiological subgroups contribute to the clinical expression of the syndrome. For example, there is a subgroup of patients, called "post-infectious IBS" who appear to respond to an enteric infection such as campylobactor jejuni with an increased inflammatory cell response (22). This is associated with activating enterochromaffin cells to produce 5HT, and CD3 cells to produce cytokines, which in turn leads to enhanced motility and lowered visceral sensation thresholds (22;23). But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it. All patients with active celiac disease have microscopic inflammation, but a large proportion do not have abdominal pain, and patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds (24). In individuals with these disorders, there may be central nervous system counter-regulatory measures responding to the peripheral pain/inflammatory processes that increase pain thresholds. With regard to IBS, the gut-related effects of microscopic inflammation may be only one component of a dysfunctional brain-gut system. In addition, and often in response to stress, there may be a failure to activate descending pain inhibitory systems that enable the clinical experience of pain and other symptoms that typify this disorder (25). In one prospective study of post-infectious IBS, it was found that those who retained their symptoms 3-months after an enteric infection had not only increased mucosal cellularity, but also had increased psychosocial distress at the time of the infection. Furthermore, lowered visceral sensation thresholds and increased motility were present after the infection regardless of whether or not the patients retained their symptoms (26). Therefore, the microscopic inflammation and its physiological effects on motility and sensation contribute to, but are not always sufficient for the clinical expression of IBS pain. At least for post-infectious IBS this provides some evidence that psychological distress alters brain pain regulatory pathways to amplify incoming visceral signals leading to the full clinical expression of this syndrome http://www.romecriteria.org/reading1.html You can also read his paper on The Neurobiology of Stress and EmotionsBy: Emeran A. Mayer, M.D.UCLA Collaborative Centers for Integrative Medicine, UCLA School of Medicine, California how altered stress circuits and throwing the balance of homeostasis out of whack leads to the symptroms of IBS. http://www.ibs.med.ucla.edu/Articles/PatientArticle003.htm "Readers' ExchangeDefining Stress in IBSFall 2003From Arizona -- Thank you so much for your efforts and support for those of us with GI disorders. Your first issue (Spring 2003) of Digestive Health Matters is both professional and informative. I would like to comment on one of the articles - "The CNS: Center for Neurovisceral Sciences and Women's Health at UCLA." I am encouraged to know that steps are being taken for funding research of IBS and interstitial cystitis. However, it is discouraging that researchers are still expending time and money to research "neurobiological mechanisms by which stress modulates brain-visceral interaction." I realize that stress is a popular theory in the discussion of IBS triggers, however, I believe this is completely backward and it is the chronic pain and totally unreliable bowel function of an IBS sufferer which causes the greatest stress. If research would focus on "fixing" the bowel, no doubt the panic and fear of IBS would be greatly alleviated. Comment from Emeran Mayer, M.D. -- 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. For example, in this viewpoint a severe hemorrhage, starvation, extreme temperature, or worry about the unpredictable onset of abdominal pain all qualify as stressors -- some as "physical" stressors, others as "psychological" stressors. The fear to leave the house in the morning without knowing if one can make it to work without having to stop on the freeway because of an uncontrollable bowel movement, or the fear of experiencing uncontrollable abdominal discomfort during an important business meeting are sufficient stressors to activate the central stress system. The central stress system involves the release of chemical stress mediators in the brain (such as corticotropin releasing factor), which in turn orchestrate an integrated autonomic, behavioral, neuroendocrine, and pain modulatory response. This biological response in turn will alter the way the brain and the viscera interact, and this altered brain-gut interaction can result in worsening of IBS symptoms. Thus, pain and discomfort, fear of these symptoms, activation of the stress response, and modulation of the brain-gut interactions by stress mediators are part of a vicious cycle which need to be interrupted to produce symptom relief. The neurobiology of stress is not a theory, but a topic that can be studied in animal models, and one of the hottest topics in drug development for treatment of IBS (e.g., substance P antagonists, corticotropin releasing factor antagonists)." http://www.aboutibs.org/Publications/StressDefined.html This is the real research and Talissa , does not even understand the Dr's work she is posting about. Talissa What other problems do they see in IBS? How about the last five years from the expert symposiums on IBS and functional disorders that overlap and their connections? "IFFGD Professional Symposium (April 2003) The IFFGD 5th International Symposium on Functional Gastrointestinal Disorders was held April 4-7, 2003. Click here for details. --------------------------------------------------------------------------------From past issues of ParticipateClick to view reports from the previous Symposiums: 4th International Symposium on Functional GI Disorders, 20013rd International Symposium on Functional GI Disorders, 19992nd International Symposium on Functional GI Disorders, 19971st International Symposium on Functional GI Disorders, 1995" http://www.aboutibs.org/Publications/symposium.html


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## eric (Jul 8, 1999)

This is a problem when Kel and Talissa, promote issues, which if you look on every accurate IBS resource souch as medscape, mayo, ucla and UNC and the cleveland clinic all top IBS research centers do not promote "leaky gut" or IBS as an infection with a known pathogen! Why is that, why is it just kel, Talissa and a few others along with DR D a chriropracter promoting this? The experts look at IBD conditions along with IBS, right now IBS is under the microscope for sure, yet, the cause is unknown and points to, motility issues, neruotransmitter dysregulation and , abnormal gut cells, altered stress ciruits and abnormalties in brain processing of gut information and rectal sensitivity and nerve sensitivity and sleep abnormalities and the prevalance between men and women and it for most people going away when you sleep, and releif after defication which points more to IBS and less to organic disease. There is a bigger picture then "leaky gut" applied to post infectious IBS and gut permeability. Why does the new drugs for IBS help people, why is HT so effective in IBS, as well as CBT and other phycophysiological treatments, why do relaxation techniques work so well in IBS, why does simple diet changes help people, why does education itself help people symptoms. These people are making "gut permeability into a mountain", instead of the real role it may possibly play in all IBS research. Then disregard the Mountain of eveidence on other factors because there focus is extremely narrow to the research.


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## eric (Jul 8, 1999)

With permissionIBS - Beyond the Bowel: The Meaning of Co-existing Medical ProblemsOlafur S. Palsson, Psy.D., Research Associate William E Whitehead, PhDUNC Center for Functional GI & Motility Disorders Irritable bowel syndrome (IBS) is a disorder that is defined by a specific pattern of gastrointestinal symptoms in the absence of abnormal physical findings. The latest diagnostic criteria for IBS, the Rome II criteria created by an international team of experts, require that the patient has abdominal pain for at least 12 weeks in the past 12 months, and that the pain satisfies two of three criteria: It is relieved after bowel movement, associated with change in change in stool frequency or associated with stool form. It is becoming clear, however that these bowel symptoms do not tell the whole story of symptoms experienced by IBS patients. People with this disorder often have many uncomfortable non-gastrointestinal (non-GI) symptoms and health problems in addition to their intestinal troubles.Symptoms All Over the Body in IBSSeveral research reports have established that IBS patients report non-bowel symptoms more frequently than other GI patients and general medical patients. For example, four studies that have asked IBS patients about a wide variety of body symptoms(1-4) all found headaches (reported by 23-45% of IBS patients), back pain (28-81%) and frequent urination (20-56%) to be unusually common in individuals with IBS compared to other people. Fatigue (36-63%) and bad breath or unpleasant taste in the mouth (16-63%) were found by three of these four studies to be more common among IBS patients. Additionally, a large number of other symptoms have been reported to occur with unusually high frequency in single studies. In our recent systematic review of the medical literature(5), we found a total 26 different symptoms, listed in Table 1, that are reported to be more common in IBS patients than comparison groups in at least one study. Table 1. Non-gastrointestinal symptoms more common in irritable bowel syndrome patients than in comparison groups(5). 1. Headache2. Dizziness3. Heart Palpitations or racing heart4. Back pain5. Shortness of breath6. Muscle ache7. Frequent urinating8. Difficulty urinating9. Sensitivity to heat or cold10. Constant tiredness11. Pain during intercourse (sex)12. Trembling hands13. Sleeping difficulties14. Bad breath/unpleasant taste in mouth15. Grinding your teeth16. Jaw pain17. Flushing of your face and neck18. Dry mouth19. Weak or wobbly legs20. Scratchy throat21. Tightness or pressure in chest22. Low sex drive23. Poor appetite24. Eye pain25. Stiff muscles26. Eye twitchingOverlap with Other Medical ConditionsResults from numerous studies (reviewed by Whitehead, Palsson & Jones, 2002(5)) also indicate that IBS overlaps or co-exists more often than would be expected with other medical conditions that appear to have little logical connection with the gut. The most researched example of such an overlap is the co-existence of IBS with fibromyalgia, a disorder characterized by widespread muscle pain. Fibromyalgia affects an estimated 2% of the general population, but in contrast, 28-65% of IBS patients have the disorder. Similar results are obtained when this overlap is examined the opposite way, by studying fibromyalgia patients and looking for IBS: 32-77% of fibromyalgia patients have IBS.Chronic fatigue syndrome (CFS) is another medical condition that has been found to have many times the expected co-occurrence with IBS. CFS is thought to affect only 0.4% of people in general, but it has been reported to be present in 14% of IBS patients(2), and conversely, 35-92% of chronic fatigue syndrome patients have IBS. Other conditions documented in multiple studies to have excess overlap with IBS are temporomandibular joint disorder (TMJ), found in 16-25% of IBS patients(2,6), and chronic pelvic pain (35% of IBS patients(7). In addition to these well established relationships, many other medical conditions appear (judging from single study reports) to have an excess overlap with IBS, although the frequencies of most of them in IBS are much lower than for the disorders already discussed. In fact, we recently(8) compared the frequencies of a broad range of diagnoses in the medical records of 3153 IBS patients in a large Health Maintenance Organization in the U.S. Northwest to an equal number of non-GI patients in the same HMO, and found that the IBS patients had a higher frequency of almost half of all non-gastrointestinal diagnoses, or 64 of the 136 sampled diagnoses.In summary, non-GI symptoms and co-existing medical problems seen in many IBS patients far exceed what is typical for medical patients or GI patients in general. This raises important questions about what causes this phenomenon, and what the implications of it are for IBS patients.What Explains Non-GI Symptoms and Co-existence of Other Disorders in IBS?There are several possible explanations for the preponderance of general symptoms and disorders in IBS. Our research group is currently conducting several research studies that may help shed some light on this mystery, but it is far too early to come to definite conclusions. We will list here some of the possible explanations, and discuss relevant data coming from work by our team and other investigators.A common physical cause? One rather obvious explanation for the high rates of co-existing symptoms and conditions in IBS patients would be that there is something biologically wrong in IBS that also causes the other symptoms or conditions. There are a number of distinct physiological characteristics or "abnormalities" that are seen in many IBS patients, although none of them are found in all patients. These include heightened pain sensitivity in the gut, increased intestinal contractions (motility) or hyper-reactivity to meals or stress (too much movement of the intestines - this is the reason why IBS was called spastic colon in the past), patterns of dysfunction in the autonomic nervous system (the part of the nervous system that helps regulate our inner body functions) and vague signs of immune activation seen in some IBS patients. Although one can suggest ways in which these physiological abnormalities would play a role in some other disorders that co-exist with IBS, there is little evidence so far of a common pattern of physical abnormality that could link IBS and its most common coexisting conditions and symptoms. Patterns of autonomic dysfunction in IBS are not like the ones seen in fibromyalgia and chronic fatigue syndrome, for example; and fibromyalgia patients do not show the same gut pain sensitivity as IBS patients, and conversely, IBS patients do not show the pain-sensitive tender points that are characteristic of fibromyalgia(9-10). Furthermore, as can be seen from reviewing the symptom list in Table 1, the non-GI symptoms that plague IBS patients are so varied, and cover so many different organ systems, that it would be hard to identify any biological connection between them. On the contrary, it seems like the only overall commonality between these symptoms may be that they are non-specific - they are, in other words, not clear symptoms of any identifiable disease processes or diagnosable disorders. Indeed, the symptoms that are most common among IBS patients are generally those that are also common in the general healthy population - they just tend to occur at an even higher rate in people with IBS.Physical expression of emotional discomfort? Another possible explanation for the high number of non-GI symptoms and disorders in IBS is the tendency to translate strong emotions into physical "symptoms". This is sometimes called somatization ("soma" is the Greek word for "body" and somatization therefore literally means "to express in the body"). All people "somatize" to some degree: It is normal to feel butterflies in your stomach, to blush or go pale, get a lump in your throat, or feel the heart beating in your chest if you get very emotional. Shaky hands, stiff neck or excess sweating are likewise quite ordinary when people are under a great deal of stress. However, some people are more vulnerable than others to letting negative emotions express themselves physically. This is often thought to be an alternative and less healthy way of exhibiting or feeling emotional discomfort. Some people may develop a strong tendency to do this because they have a basic personality style that shies away from interpersonal expressiveness. For others, it could be the result of growing up in the care of strict, repressive or abusive parents or caretakers, where normal expression of negative emotions was not allowed or would have been dangerous: Getting a headache or a stomach ache may be an alternative way to "give voice" to negative emotions under such circumstances. It seems that excessive habitual suppression of ordinary verbal and emotional expression of negative emotions, regardless of the reason for it, may lead to the tendency to somatize. There is evidence that this tendency may be at work in IBS, at least among some women with the disorder. Dr. Brenda Toner has found in two studies(11-12) that women with IBS score higher than depressed women and healthy women on questionnaires measuring of the tendency to avoid expression of negative emotions or views.Learned over-attention to body symptoms and excess disease attribution? All people ignore most of the sensations from their bodies most of the time. This is necessary so that we are not overwhelmed by the vast amount of information our senses supply to our brains every moment of our lives. For example, if you are reading this sitting down, you have probably not been at all aware of the sensations of the seat under your body until right now - nor the feeling in your scalp, etc. Our brains constantly sift through the mass of incoming body information and decide what is important for us to become consciously aware of, based on such things as our past experiences and how likely the information is to indicate threat to our health or well-being. Most minor symptoms (those that might be uncomfortable and bothersome if they would get our attention), are simply dismissed in our busy everyday lives, because other things win out in the moment-to-moment competition for our limited attention resources.More frequent attention to mild physical symptoms can be learned, however, and can become a habit. As with most things, such habitual over-attention is probably most easily learned in childhood. It would seem reasonable, for example that a child would get into the habit of noticing physical symptoms more if his or her parents are always talking about their own symptoms. We have recently found(13) that the more medical problems the parents in the childhood home had, the more general physical symptoms adult IBS patients report.A possible consequence of a childhood where the child grew up with parents or others who were seriously ill, is a tendency to interpret common normal physical sensations as symptoms of serious illness. Such serious view of symptoms can also be modeled after the parents' approach to common illness. Dr. Whitehead and colleagues found in a telephone survey of 832 adults 20 years ago(14) that people whose parents paid more attention to cold or flu symptoms in childhood were more likely to view such symptoms as serious in adulthood and to visit doctors for them. They were also more likely to have IBS diagnosis.Evidence that IBS patients interpret physical sensations differently than others is emerging from brain imaging studies. This type of research takes a "snapshot" of the amount of activity in different parts of the brain in response, using techniques such as PET scans (positron emission tomography) and functional MRI (functional Magnetic Resonance Imaging). By examining which parts of the brain react most to painful sensations, it is possible to deduce to some degree how the brain processes the information. In one such study, by Silverman and colleagues(15) , IBS patients but not control subjects reacted to physical sensations from a painful balloon inflation in the rectum with increased blood flow in the left prefrontal cortex, a part of the brain known to process personally threatening information. In contrast, that study and others(16-17) found that IBS patients do not show activity in the anterior cingulate cortex that is indicative of general discomfort in healthy subjects. IBS patients are also more likely to respond to physical stimuli in the GI tract by activating brain centers that handle emotional events. Collectively, this suggests that IBS patients may process body information associated with bowel sensations (and perhaps other physical sensations as well) differently than other people, interpreting them as personally threatening and more emotionally relevant events rather than ordinary discomfort. Such different interpretations of physical sensations would also explain hyper-attention to such sensations.Faulty neurological filtering? After entering the spine (the information highway from the body to the brain), information destined for the brain about body pain is sent along nerves through gates that control how much of this information passes through. Our brains continually send signals down to these spinal gates to cause them to block signals that are of too low intensity to provide valuable information (you do not want to constantly know about all your minor aches and discomforts from regular body activity). This is one of the ways that the brain uses to limit the vast amounts of information constantly streaming in from millions of nerve sensors throughout our bodies. A current popular hypothesis in the field of IBS research is that an inadequate amount of this "descending inhibition" of incoming pain information is at least partly to blame for the hypersensitivity to intestinal discomfort and pain seen in IBS, and causes signals from pain sensors that would normally be blocked to pass on through to the brain. Some researchers have further suggested that the same kind of slack traffic control could be more widespread in IBS and may explain the observed proneness to headaches, back pain or muscle aches. People who have more open pain gates because of faulty inhibition would theoretically be like the princess in H.C. Andersen's classic story "The Princess and the Pea" who could feel a pea through 20 mattresses. The problem with this as an explanation for symptom overabundance in IBS is, first, that it would explain only excess in pain-type symptoms, which are but one of many types of overabundant symptoms in IBS, and secondly, that there are no direct data on IBS patients yet to show us how valid this view is.Result of greater psychological distress?As was explained above, it is normal for people who are emotionally distressed to experience more physical symptoms. At least half of IBS patients who have consulted doctors have been diagnosed with an affective ("emotional") disorder - typically either depression or an anxiety disorder. Additionally, many people with IBS who have no affective disorder diagnosis have significant symptoms of anxiety and depression. One might therefore ask whether the physical symptoms reported could simply be a side effect of psychological distress. We have addressed this question in two studies presented at this year's Annual Meeting of the American Gastroenterological Association(18-19). In the HMO data18 mentioned above, we found that having a psychological diagnosis was associated with increased numbers of physical diagnoses these IBS patients had received (from an average of 7.1 to 9.7). However, we also found that even patients with no psychiatric diagnosis had more physical diagnoses per person than the other HMO patients (7.5 vs. 5.5), so the presence of psychological problems is not the whole answer. In the other study(19), we examined the relationship between depression and anxiety scores of 795 people with IBS and the number of physical symptoms they had experienced over the past month. Statistical methods that estimate how much of the variability in one measured characteristic can be explained by other measured factors tell us that the psychological symptoms roughly accounted for 25-30% of physical symptoms of these people. In short, psychological distress is almost certainly a part of the explanation for greater body symptoms in IBS, but not nearly the whole story. Future research will have to determine which of the above explanations are applicable in IBS, but it is likely that more than one of them, and maybe some other factors unrecognized so far, work together to account for the high frequency of symptoms and disorders that co-exist with IBS.The Impact of Extra Physical Symptoms and Disorders on IBS PatientsWhat do these extra (or "non-IBS") symptoms and co-existing medical conditions mean in practical terms for patients with IBS? The first thing to note is that not all IBS patients experience additional health problems and symptoms, so it is not a concern for all people with IBS. For those who do, however, symptoms and disorders beyond the bowel can add measurably to the overall burden of illness for the individual, and also lead to greater health care needs and health care costs for IBS patients.It is by now well established that IBS patients visit doctors more than is typical for other people. Only recently has it been recognized, though, that most of the extra health care visits people with IBS make are not for their bowel problems. Levy et al.(20) reported that IBS patients had about twice as many doctor visits compared to other patients in the same HMO, but they found that 78% of the additional visits were due to other problems than IBS. It seems quite likely that these extra non-gastrointestinal doctor visits of IBS patients are due to the tendency to experience more general body symptoms over time, based on study results we presented at the Annual Meeting of the American Gastroenterological Association last year(21). Using a scale asking patients about the 26 physical symptoms in Table 1, we found that those IBS patients who report an unusually high number of these symptoms over the past month missed six times as many days from school or work due to illness (see Figure 1 below) compared to those with low or moderate (normal) symptoms. The "high-symptom" IBS patients also had twice as many doctor visits and more hospital days (see Figure 2 below), and their quality of life was furthermore measurably poorer on the average. A general tendency to have a large number of body symptoms is therefore very costly in terms of the IBS patient's overall well-being and ability to function normally in life, and increases substantially the health care costs for these individuals. These findings clearly underline the need to find a way to help the many IBS patients who score unusually high on body symptom questionnaires to reduce that tendency.Is It Possible to Reduce Non-gastrointestinal Symptoms in IBS?It is unknown to what degree standard medical treatment for IBS, when successful, also results in improvement in non-GI symptoms. The problem is that most IBS treatment research has not examined how non-IBS symptoms change. Non-IBS symptoms have also not been a focus of standard IBS treatment. An exception to this is psychological treatment trials for IBS, which sometimes have included general physical symptom questionnaires among the measures of treatment effects. We therefore know from our two studies of hypnosis treatment for IBS(22) as well as from research in England(23) that hypnosis treatment for IBS regularly improves non-GI symptoms substantially in addition to beneficial effects on bowel symptoms. Less is known about improvement in non-GI symptoms from cognitive-behavioral therapy, which is the other widely researched psychological treatment for IBS. However, there is every reason to believe that cognitive-behavioral treatment can reduce the tendency to experience a lot of general physical symptoms, based on a review of over 30 such treatment studies(24). These benefits of psychological treatment for IBS point to extra value of such treatments for the subgroup of IBS patients who have many non-GI symptoms.Research in coming years will hopefully identify other ways to improve the well-being and life functioning of IBS patients by reducing non-GI symptoms, and this is likely to become an integral part of managing IBS effectively in the subset of patients who suffer many symptoms and conditions beyond the bowel.References: http://www.med.unc.edu/wrkunits/2depts/med...d_the_bowel.htm


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## Talissa (Apr 10, 2004)

Do you even read the posts here Eric? Many, many people that have IBS are using probiotics & are concerned with healing the intestinal wall. Somebody forgot their smart pill today....


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## calid (Aug 4, 2003)

> quote: Why is that, why is it just kel, Talissa and a few others along with DR D a chriropracter promoting this?


The answer is simple:WE'RE GETTING WELL.


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## Talissa (Apr 10, 2004)

Well said, Calid.It was also brief. I promise to work on that!But I've got just a quick, simple question Erico you even know what this means?


> quote:" The recent observation of an activated immune system in some IBS patients associated with persistent low-grade mucosal inflammation provides evidence for the reconsideration of the symptom-criteria-based diagnosis of functional bowel disorders."


In case you skimmed over this in _your_ Medscape forays, and in the above post, let me clarify.It means you're wrong. It means the medical community has recognized that reconsideration of the symptom-criteria-based diagnosis in IBS is called for, due to new findings regarding increased intestinal permeability(leaky gut).Connect the dots, please, I'm getting soooo tired of this. (I know, I know, others of you are as well.)I really will try to be better in the future. Talissa


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## SpAsMaN* (May 11, 2002)

From Eric post...neurobiological mechanisms by which stress modulates brain-visceral interaction." I realize that stress is a popular theory in the discussion of IBS triggers, however, I believe this is completely backward and it is the chronic pain and totally unreliable bowel function of an IBS sufferer which causes the greatest stress. If research would focus on "fixing" the bowel, no doubt the panic and fear of IBS would be greatly alleviated. I could not say it better.


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## SpAsMaN* (May 11, 2002)

Neurogastroenterologist,maybe that's enough years in the school specialty to be beleive.There is probably only few in America.Sadly.


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## Talissa (Apr 10, 2004)

> quote: I believe this is completely backward and it is the chronic pain and totally unreliable bowel function of an IBS sufferer which causes the greatest stress.


You're so right, you couldn't say it better!!


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## eric (Jul 8, 1999)

Talissa, first I have many friends of the doctors who's information you posted. "Many, many people that have IBS are using probiotics & are concerned with healing the intestinal wall."Since there is no overt inflammation in IBS, the way you perceive it to be in IBS, that may or may not be how it works, it maybe working on reducing gas from bad bacteria from foods fermenting in the bowel due to altered transit. Which then creates gas bubbles that add pressure to the ALREADY sensitive nerves lining the digestive tract. The cells lining the digestive tract are pressure sensitive and in IBS to ALL stimuli, not just bacteria.I am not against probiotics in the slightest. I recommend them!There is preliniary evidence probioitcs may help some IBSers, although the specific strains are not known, nor the complete mechansims of action.That does not mean we should call IBS leaky gut or an inflammatory bowel disease. Which is what your promoting.They have found some specific markers in IBS, just not in all IBSers.However, in IBS there is no overt inflammation like there is in miscroscopic colitus or inflammatory bowel disease.It is macroscpopic specific cells embedded in the digestive wall."Do you even know what this means?quote:--------------------------------------------------------------------------------" The recent observation of an activated immune system in some IBS patients associated with persistent low-grade mucosal inflammation provides evidence for the reconsideration of the symptom-criteria-based diagnosis of functional bowel disorders." "yes, I understand it quite well, but you certainly don't from the infromation in your posts.Your quoting a doctors research who does not hold your views. I have emailed him and he is away right now. I think he would be very concerned about this for sure.You should also read his work before you presume you know what he is saying!"It means the medical community has recognized that reconsideration of the symptom-criteria-based diagnosis in IBS is called for, due to new findings regarding increased intestinal permeability(leaky gut)."That is not what it means and he works very closely with the IFFGD and the UNC and the rest of the IBS researchers around the world.a quick note on franks comment here."I realize that stress is a popular theory in the discussion of IBS triggers, however, I believe this is completely backward and it is the chronic pain and totally unreliable bowel function of an IBS sufferer which causes the greatest stress."It is not a theory but a very real phycophysiological responce in all humans. It just happens to pertain a whole lot more in IBS.That's what the vicious cycle is all about in IBS.Symptoms=stress and anxiety= symptomsThe brain can trigger the gut and the gut can trigger the brain.This is well known and a fact.Talissa , you might want to read the rest of DR Mayers work in IBS. Especially this, because one of his main focuses is on the neruobiology of stress and emotions on IBS!The Neurobiology of Stress and EmotionsBy: Emeran A. Mayer, M.D., UCLA Mind Body Collaborative Research Center, UCLA School of Medicine, California "What does this have to do with IBS Converging 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. Sovik Why 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 responsiveness Based 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. http://www.ibsgroup.org/ubb/ultimatebb.php...=1;t=037740;p=2 If you want to take it further the chronic stressors activate the bodies fight or flight responce, to a real or perceived threat. The HPA axis launches and sends signals to the gut that triggers mast cells lining the digestive system wall. In post infectious IBS there is an increase in both mast cells and ec cells that sotre serotonin. After resolution of the intitial enteric infection and inflammation WHICH RESOLVES, chronic stressors reactivate infalmmation of those specific cells without a pathogen. These cells are then degradulated and release toxins on to the smooth muscle and contribute to pain in IBS. If you really want to read more about his work, instead of quoting him out of context, then read more of his work, including this.Publication from IFFGD: The Neurobiology Basis of Mind Body Medicine (Click on title to view excerpts)By: Emeran A. Mayer, M.D.How do the mind and body interact with each other and the environment . . . and in this process actively maintain health and prevent disease? This accessable publication describes the basis for a growing awareness of an evolving convergence of many "alternative" concepts of health and disease with cutting edge concepts proposed by science, information that can be helpful to anyone with a chronic disorder such as irritable bowel syndrome. The 22-page publication is available by contacting IFFGD. http://www.aboutibs.org/IBSpublications.html Which by the way I have just finished reading.You might also want to read these articles of his.Or what they just got a grant to build a new facility for?"Center will study role of brain, stress and emotions in IBS, IC and related disordersThe National Institutes of Health awarded UCLA $3.75 million to create a new national research center to be named the Center for Neurovisceral Sciences and Women's Health (C.N.S). The new center -- the first of its kind -- will study how the brain, stress and emotions impact the development of disorders that affect mainly women -- including such common diseases as irritable bowel syndrome (IBS) and interstitial cystitis (IC). The new center will develop research programs as well as a comprehensive clinical center that will see patients.The funding is through two organizations, both part of the National Institutes of Health the National Institute of Diabetes, Digestive and Kidney Diseases and the Office of Research for Women's Health.C.N.S will be the first national center in the country to explore the role of sex and gender factors in women's increased risk to develop a wide range of common, chronic disorders affecting the digestive and urologic systems. The center will bring together multidisciplinary teams from the UCLA departments of Medicine, including Digestive Diseases, Urology, Psychiatry, Psychology and Neurology, as well as the Department of Veterinary Clinical Sciences at Ohio State University."We will explore differences in the way women respond to psychological and physical stress, and how these differences predispose them to develop common clinical disorders, such as chronic abdominal and pelvic pain syndromes" said Dr. Emeran Mayer, principal investigator for the grant who is also UCLA Professor of Medicine, Physiology and Psychiatry and Bio-behavioral Sciences, Chair of the UCLA Center for Integrative Medicine and co- director of the CURE







igestive Diseases Research Center. Dr. Yvette Tache, Professor of Medicine, UCLA Division of Digestive Diseases, is a world-renowned researcher on the neurobiology of stress and gastrointestinal function and is co-principal investigator of the grant."We hope to develop a better understanding of some of the most common digestive and urological disorders like Irritable Bowel Syndrome and Interstitial Cystitis, which will help improve treatment," added Mayer.In addition to building a cutting edge research program on the neurobiology of stress and chronic visceral pain, the vision for the C.N.S. includes establishing a new clinical center specializing in digestive system disorders that occur mostly in women; a health outcomes research arm of the center, which will explore quality of care and evaluate patient-centered outcomes, including health-related quality of life, patient satisfaction with care, and costs in this patient population; a specialty training program for research and patient care and a pilot and feasibility study program to fund research projects.C.N.S. will receive $750,000 annually over five years from a partnership between the National Institute of Diabetes, Digestive and Kidney Diseases and the Office of Research for Women's Health (ORWH). C.N.S. has been designated a Specialized Center of Research (SCOR) -- a prestigious National Institute designation.C.N.S. researchers will study key areas including: how circuits within the brain are activated differentially under stress based on genetic factors, early life experiences and sex-related differences. Investigators will study how specific hormones released in the brain under stress may affect the immune response in the colon and urinary bladder, and what role this neuro-immune interaction plays in the development of IBS and IC. Researchers will address how stress hormones released in the brain may also influence pain perception as well as contractions of urinary bladder and colon.Irritable Bowel Syndrome affects 15 to 20 percent of Americans and causes discomfort in the abdomen, along with diarrhea and/or constipation. Interstitial Cystitis affects more than 700,000 Americans; 90 percent are women. Both disorders occur much more commonly in women than in men, for as-yet unknown reasons." http://www.npi.ucla.edu/news/neurovisceralsciences.html How about this article he wrote?Altered stress responce in IBS!The majority of patients with irritable bowel syndrome (IBS) associate stressful life events with the initiation or exacerbation of their symptoms. Emerging evidence suggests that this association may be due to an alteration in the way the brain communicates with the gut during periods of prolonged or severe life stresses. While stress and stress related symptoms have long been regarded as a domain of psychology, tremendous progress has been made in our understanding of the biological processes that mediate the body's response to stress. The brain network which plays a central role in the stress response is the 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. Activation of the HPA axis in response to stress leads normally to a coordinated series of adaptive physiologic and behavioral changes which attempt to maintain and restore our body's homeostasis (in a state of equilibrium). In the setting of stress, adaptive behaviors such as increased arousal, vigilance, focused attention, and alertness occur. Altered function of the HPA axis in response to stress may play a primary role in behavioral abnormalities such as fatigue, lack of motivation, abnormal sleep and appetite, which are commonly seen in patients with functional bowel disease, such as IBS. In our patient database of functional bowel disease, 71% reported frequent tiredness and fatigue and the two-thirds reported sleep disturbances. These symptoms in turn play an important role in the impact of IBS on quality of life.Stress responses involving the HPA axis are mediated by the release of corticotropin releasing hormone (CRH) from a brain region called the hypothalamus. Stressful events activate the HPA axis which result in the eventual release of CRH which then results in release of adrenocorticotropin hormone (ACTH) from the pituitary gland. ACTH then acts on the adrenal cortex causing it to release cortisol into the bloodstream. Cortisol and ACTH are secreted in a specific rhythm over the course of 24 hours each day, and both reach their highest levels in the early morning and their lowest in the late afternoon and evening. The cortisol peaks correlate with the state of greatest alertness and energy in the majority of healthy people. Cortisol can be measured in the blood and urine. Regulation of the HPA axis has not been studied well in IBS. We have preliminary evidence which suggests that IBS patients have blunted or decreased levels of cortisol in response to a stressor such as balloon distension of the lower colon and rectum. There is also evidence that IBS and fibromyalgia patients have lower baseline levels of 24-hour urine cortisol. In order to learn more about how stress may play a role in chronic pain disorders, the UCLA Neuroenteric Disease Program has several ongoing studies in IBS, fibromyalgia and gastroesophageal reflux disease (GERD). There is a study measuring ACTH and cortisol levels in the blood over a 24-hour period in patients with IBS and/or fibromyalgia, and healthy individuals. In addition, we are studying how stress may affect the perception of signals originating from the intestine. We are completing another study which has examined the relation of stressful life events and increase in heartburn symptoms in patients with GERD.In summary, alterations in the HPA axis in patients with chronic pain syndromes such as IBS or fibromyalgia may play a role both in the inadequate activation of the body's own pain inhibition systems (including the "endorophin system"), resulting in bowel and/or muscle hypersensitivity. A better understanding of the way the body responds to stress via the HPA axis will therefore help in the development of novel therapies for these common conditions.and a graph of how it works http://www.cns.med.ucla.edu/Articles/Patie...teredStress.htm 4th international symposium on IBS"Basic Principles: Brain-Gut Moderators: Emeran Mayer MD and Jackie Wood PhD; Panel: Michael Gershon MD, Brent Vogt PhD, Stuart Derbyshire PhD, Santosh Coutinho PhD During the last decade the concept of unique bi-directional interactions between the gut and the brain as an important factor in coordinated gut function in health has become widely accepted. More recent speculations have considered the possible role of these brain-gut interactions in brain function and the regulation of emotions. A dysregulation of brain-gut interactions is thought to play an underlying role in the functional GI disorders and may account for accompanying disorders related to emotional states (e.g., anxiety). This session focused on basic physiological principles (i.e., the characteristics of vital processes or functions). Michael Gershon from Columbia University, New York began this session discussing the enteric nervous system (ENS). Also called "the little brain," the ENS is a complex and independent division of the autonomic nervous system (ANS). It contains nerves and neurotransmitters (chemical messengers between nerve cells) that are also present in the brain. Certain cells within this system act upon sensory input to the central nervous system and amplify signals that can be associated with increased release of the neurotransmitter 5HT (serotonin, which affects intestinal motility) in response to pressure or injury within gut tissue. This action, and the recent work looking at the role of the serotonin transporter in mediating reuptake function may play a role in explaining why people develop IBS. (Neurotransmitters interact with nerve cell receptors to communicate from one nerve cell to another. They must be removed by a transporter in a process called reuptake before the cell receptor can reactivate.) Stuart Derbyshire from the University of Pittsburgh gave an overview of nerve function going from the gut to the central nervous system (visceral afferent function) and an introduction to brain imaging. Positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) can help us study brain-gut connections, and differentiate brain activity in response to cognitive function, stimuli from the internal organs in contrast to other parts of the body, and input from specific areas in the gut. The receptive areas of the brain in this interaction can be influenced by localized stimuli and by emotion, memory, and cognitive function. Brent Vogt from Wake Forest University, North Carolina discussed the important role of an area of the brain called the anterior cingulate cortex and its subdivisions in influencing the subjective experience of pain by translating emotion and cognitive awareness into pain regulatory actions. For example, one area of the cingulate cortex is rich in internally produced opiates and may be an area of inhibition of pain through pathways descending to the spinal cord. One of the foundations of basic science is the development of animal models to correspond to the study of disease processes in humans. Santosh Coutinho from UCLA discussed possible animal models for IBS. Mechanical or chemical inflammation in the rat colon, as well as maternal separation of rat pups, can lead later to excessive sensitivity to pain within the gut (hyperalgesia). Both factors may play a role in the origin and development of IBS in humans. Inflammation Moderator: Robin Spiller MD; Panel: Jackie Wood PhD, Mary Perdue MD, Robin Spiller MD The last few years have led to a greater understanding of the role of inflammation in influencing intestinal hypersensitivity in the functional GI disorders. For example, a well-defined subgroup (up to 25% of IBS patients) appear to develop their IBS after an infectious illness. Jackie Wood from Ohio State University, discussed how inflammation alters the neurophysiology of the enteric nervous system (ENS) by activating nerves within the ENS. There are a variety of ENS neurons that can direct responses within the body leading to altered motility, sensation and secretion, and ultimately, symptoms of diarrhea, constipation, and pain. Mary Perdue from McMaster University, Ontario discussed the importance of the epithelial intestinal barrier to maintain immune tolerance to potentially harmful matter, such as bacteria, ingested when we eat or drink. (Everything that enters the human body must pass through an epithelial layer. Various types of epithelial tissues line not only the body cavities, blood vessels, and most organs, but also our outer surface-our skin. Within the intestines, epithelial tissue forms an intestinal barrier involved with absorption, secretion, sensation, contractility, and protection.) Studies in animal models show that psychological stress can disrupt this barrier, leading to the penetration of bacteria into the gut, inflammation, an immune system response (inflammatory cytokines), and ultimately sensitization of neural signals from the gut to the brain that can heighten the perception of pain. Robin Spiller from the University of Notingham, UK brought this basic information to the human model of post-infectious IBS. The predictors of post-infectious IBS include increased life events and psychological distress, female sex, and longer duration of diarrhea episode. In response to bacterial infection, there is an increase in certain gut (enterochromaffin) secretory cells (5HT producing) and inflammatory cells (cytokine producing) leading to prolongation of pain and diarrheal symptoms, and this may be aggravated by the presence of psychological stressors. *These findings suggest ways in which infection-induced inflammation might interact with chronic stress to produce long lasting bowel dysfunction. * They also suggest possible treatments that need study. Brain Imaging Moderator: David Thompson MD; Panel: Qasim Aziz PhD, Howard Mertz MD Pain is a subjective experience that is interpreted differently from person to person. This makes precise understanding of individual pain symptoms difficult. Objective measures of gastrointestinal signal processing in the brain, that could differentiate between people with functional GI disorders and those without the disorders, would help to measure symptoms such as intestinal pain. New imaging techniques offer the prospect of measurements independent of symptom reporting and the use of positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) in humans with GI disorders has become an active area of investigation. These tests identify areas of the brain that respond to stimulus by detecting an increase in blood flow. Qasim Aziz from the University of Manchester, UK reviewed the concept of central sensitization. This can occur when an event, such as acid reflux injury to the esophagus or an infection in the gut results in sensitization of nerves in the spinal cord. This central sensitization can sometimes persist long after the original injury or inflammation has healed. When this happens, a sensation that was previously non-painful may now be perceived as painful. Additionally, Dr. Aziz discussed how emotional states can influence symptom severity in some individuals with painful functional disorders, such as IBS. Individuals with functional GI disorders with this type of response would likely benefit from appropriate psychological therapies. Howard Mertz from Vanderbilt University, Tennessee discussed the effects of rectal distension on brain activation as measured with fMRI. Compared to controls, IBS patients had increased activity in areas of the brain (anterior cingulate and prefrontal cortex) associated with emotional arousal, pain memory and interpretation, and physiological response. Disruption of this circuitry may be a factor leading to increased pain in IBS. Altered Bowel Function Moderator: John Kellow MD; Panel: Charlene Prather MD, Juan Malagelada MD, John Kellow MD, Arnold Wald MD Charlene Prather from St. Louis University reviewed the role of motility abnormalities in explaining symptoms of diarrhea and constipation among patients with functional bowel disorders. Clustered contractions, which are brief bursts of intestinal activity that occur in people both with and without IBS, may be associated with abdominal pain and discomfort. High Amplitude Propagated Contractions are propulsive contractions that often are followed by an urge to defecate. These contractions appear to occur less frequently and of shorter duration in people with constipation. Efforts are being made to move toward non-invasive assessment of bowel motility and more standardized testing methods. Juan Malagelada from Autonomous University of Barcelona, Spain discussed the possible role of physiological handling of intestinal gas in IBS. Those who usually do not experience bloating have greater efficiency in expelling gas compared with those with IBS or functional bloating who have altered gut motility that results in greater retention of gas. This effect, coupled with heightened sensitivity (which can be aggravated by large fatty meals) within the gut may doubly contribute to symptoms of pain and bloating. Treatments may be directed toward increasing the speed of movement through the gut (transit rate) of accumulated gas with medication or increasing flexibility (compliance) of the bowel wall, possibly with medication, to better accommodate the distension. John Kellow from University of Sydney, Australia discussed how diarrhea is associated with more rapid transit related to altered motor activity, an exaggerated contractile response to food, CCK (Cholecystokinin, a hormone that stimulates intestinal motility) and other physiological stressors, increased sensitivity of the intestines (compared to patients with constipation), and possibly altered colonic and rectal muscle tone. Dietary restriction of poorly absorbed carbohydrates (e.g., fructose or sorbitol) may reduce diarrheal symptoms. Arnold Wald from the University of Pittsburgh discussed the subgroups of constipation. About half of individuals reporting constipation to their physician have normal transit, or movement through the colon. People with uncomplicated constipation may benefit from dietary fiber and bulk laxatives such as psyllium or methylcellulose. Wheat bran is one of the most effective fiber laxatives, however not everyone responds well or tolerates fiber. Other laxatives may be useful when prescribed by a physician and used appropriately. The remaining group of individuals reporting constipation have either colonic inertia (slow transit) associated with decreased colonic motility and decreased reactivity to meals and other bowel stimulants, or ineffective defecation (e.g., pelvic floor dyssynergia-failure to relax or inappropriate contraction of the muscles in the anal canal) which may respond to anorectal biofeedback treatment. It may be difficult for a physician to distinguish these subgroups based on the clinical presentation and tests may be required (e.g., colonic transit study, anorectal manometry). http://www.iffgd.org/symposium2001.html The 5th symposium"Epidemiology and Behavioral FactorsThe incidence of IBS is 20 times greater than that for inflammatory bowel disease. Risk factors include abuse, post-infectious state, genetic/familial factors, and possibly even analgesics.Gender effects seem to appear after puberty. Also, it is important to consider that gender-related treatments need to be developed and tested. Recent research has shown that children of IBS parents consume greater health care costs and have more clinical visits than children of parents without IBS.Early learning factors are quite important is explaining the development of IBS. PhysiologyThe use of PET and fMRI in humans with GI disorders has become an active area of investigation. Emotional states, like fear and disgust can activate areas of the limbic system [amygdala, Anterior Cingulate Cortex (ACC)]. This area is associated with emotional arousal, while the prefrontal cortex is associated with pain memory and interpretation. Disruption of this circuitry may be a factor leading to increased pain in IBS.Efforts are being made to move toward noninvasive assessment of bowel motility and more standardized testing methods.While normals have greater efficiency in expelling gas, those with IBS/functional bloating have altered gas dynamics with greater retention. This effect, coupled with visceral hypersensitivity may doubly contribute to symptoms of pain and bloating. Treatments may be directed toward increasing transit rate of accumulated gas (e.g., with neostigmine or prokinetic agents) or increasing compliance of the bowel wall to better accommodate the distention.Diarrhea is associated with more rapid transit related to altered MMC (e.g., increased HAPC) activity, an exaggerated contractile response to food, CCK and other physiological stressors, increased visceral hypersensitivity compared to patients with constipation, and possibly altered colonic and rectal tone.About half of patients reporting constipation have normal transit. The remaining group have either colonic inertia associated with decreased HAPC's and decreased reactivity to meals and other bowel stimulants, or outlet dysfunction (e.g., pelvic floor dyssynergia) which may be amenable to anorectal biofeedback treatment. Clinical FeaturesThe clinician needs to be able to elicit and integrate the dietary, lifestyle, gut physiology and psychosocial features unique to the patient, and to use this information through application of a multidisciplinary treatment approach. The importance of good interview skills and an effective physician- patient relationship was emphasized.Dietary restriction of poorly absorbed carbohydrates {fructose or sorbitol} may reduce diarrheal symptoms.Globus and rumination syndrome are distinctly different from functional chest pain, heartburn and dysphasia. What may be different from previous assumptions is that the latter three diagnoses overlap in pathogenesis, and are not as easily distinguished physiologically. In one study these complaints were found to be associated with increased wall thickness at the time of symptom presentation.Rumination is a unique condition, more often affecting males.Functional biliary disorders and emphasized the importance of excluding other conditions (e.g. GERD, ulcer disease, functional bowel disorder), which may mimic the less common biliary disorders. Newer noninvasive tests are used to assess bile duct emptying, thereby reducing the risks related to ERCP and biliary manometry.Functional anorectal disorders including fecal incontinence, pelvic floor dyssynergia and functional anorectal pain (levator ani syndrome and proctalgia fugax). Unlike most functional GI disorders (though similar to the functional biliary disorders) diagnostic testing using physiological methods is important in confirming the diagnosis and directing treatment, which can include anorectal biofeedback.The high health costs and unnecessary procedures (including hysterectomies) may be obviated through physician education about diagnostic criteria. Physicians who address psychosocial factors may further reduce health care costs.Good communication skills were emphasized. Building an effective physician-patient relationship depends on active listening, providing empathy, validating the patient's feelings, educating and reassuring through interactive dialog and mutually negotiating treatments. This is associated with improved patient satisfaction, adherence to treatment and improved clinical outcome. " http://www.med.unc.edu/wrkunits/2depts/med...gdsymposium.htm Maria O'Sullivan, PhDDepartment of Gastroenterology, Adelaide & Meath HospitalTrinity College, Dublin, IrelandIrritable bowel syndrome (IBS) is a chronic condition characterized by abdominal pain and altered bowel habit, in the absence of demonstrable structural gastrointestinal abnormality. Essentially the gut functions abnormally - people experience symptoms of pain, diarrhea and/or constipation but no abnormality of the bowel can be identified by standard medical tests. Numerous research studies have now documented physiological changes, including altered motility and hypersensitivity, in the gastrointestinal tract of IBS patients. The mechanisms underlying these events, however, remain unclear. There is growing evidence that inflammation in the gastrointestinal mucosa may play a role in the pathogenesis of at least a sub-set of IBS (1-3). Importantly, overt colonic inflammation precludes a diagnosis of IBS. The challenge for researchers therefore, is to record subtle changes in inflammatory mediators that are not identifiable by usual routine processes. Inflammation and IBS - the EvidenceExperimental (animal) data show that inflammation, even if mild, could lead to persistent changes in gastrointestinal nerve and smooth muscle function, resulting in dysmotility, hypersensitivity and gastrointestinal dysfunction (1, 4-6). In humans, the role of inflammation in the generation of IBS symptoms is less well studied, although there are important findings from people with 'post-infective IBS'. After an acute gastrointestinal infection up to one-third (7-29%) of individuals develop persistent symptoms compatible with IBS (7, 8). In these post-infective IBS subjects, a persistent increase in rectal sensitivity (8) and in inflammatory cells (specifically enteroendocrine cells and lymphocytes) (9) have been documented. To put this in context, however, the majority (over 70%) of people who develop gastroenteritis fully recover and do not develop persistent bowel symptoms. Factors that may predict those who develop post-infective IBS include specific psychological factors, female gender and a longer duration of the initial illness. While there is now reasonable evidence to support a low-grade inflammatory response in those who develop IBS following an acute episode of gastroenteritis, there is still little know about inflammation in IBS patients who have no obvious recent evidence of acute infection. The role of inflammation in non post-infective IBS has been a particular research interest of our group and began with an interest in studying mast cells in IBS. Mast Cells and IBS The mast cell has potential to be a key player in IBS. Although mast cells are most widely known for their role in allergic responses, these cells are normally present throughout the gut and are involved in a range of physiological and pathological activities including mucosal defense mechanisms and inflammation. Mast cells may release an array of inflammatory mediators that act on smooth muscle, nerves and immune cells, which may ultimately result in gastrointestinal dysfunction and symptoms. In addition, mast cells in the gut are located close to nerves providing a structural basis for communication between the gut and the nervous system. In 1993, Weston and colleagues reported increased mast cell numbers in the mucosa of IBS patients(10) - these changes were identified in tissue from the end of the small bowel (terminal ileum). Similarly we identified significant increases in mast cells in IBS patients compared to controls in the colon (specifically at the caecum) (11). There were also trends for increases in other regions of the colon (ascending and descending colon) but no differences could be seen at the rectum. The lack of changes in mast cell infiltration in the rectum has since been confirmed by others (9). Collectively these studies suggest that mast cells were increased in IBS patients - this may be part of a low-grade inflammatory response, although the components and nature of this response remain poorly understood. NITRIC OXIDE AND IBSWe hypothesised that inducible nitric oxide synthase may be a novel and important marker of inflammation in IBS. Enzymes from the nitric oxide synthase family are responsible for the synthesis of nitric oxide (NO) from the oxidation of L-arginine. While at least three enzyme sub-types (isoforms) have been described, our study focussed on one specific isoform, namely inducible nitric oxide synthase (iNOS). This enzyme is thought to be capable of producing large amounts of nitric oxide and to be expressed during inflammation (12). In the human colon, upregulation of iNOS has been implicated in inflammatory processes and increased expression has been documented in inflammatory bowel disease. In colonic mucosa from IBS patients, we found a significant increase in iNOS expression compared to control patients (13). We also measured nitrotyrosine, which is considered a by-product of nitric oxide generation. Overall the nitrotyrosine data in IBS paralleled that of iNOS almost exactly. iNOS could be detected in epithelial cells, lymphocytes (CD3+ T and CD20+ B lymphocytes) and macrophages. Mast cells did not appear to express the iNOS. Overall we demonstrated an increase in iNOS, an enzyme that catalyses the production of nitric oxide, combined with an increase in nitrotyrosine, a by-product of nitric oxide generation. In terms of factors that may affect iNOS expression, there was a trend towards higher iNOS levels in the diarrhea compared to the alternating group although this was not statistically significant. Elevated iNOS may be a marker of general low-grade inflammation in IBS. Induction of iNOS and the generation of NO, could have several other potential roles in IBS - for example NO may have direct effects on intestinal nerve and motor function and intestinal on permeability. OTHER INFLAMMATORY CELLS IN IBSWhile there was some tentative evidence of an associated involvement of other inflammatory markers in our study, these were not striking or clear-cut. On average there were trends for increases in CD3+ lymphocytes and the proportion of lymphoid tissue. Similarly in IBS there was a trend for increased expression of nuclear factor kappa B (NF-?







, a transcription factor for an array of pro inflammatory cytokines and mediators. In our study, none of these changes were statistically significant. In contrast, others have previously reported significant increases in inflammatory cells, for example an increase in CD3+ lymphocytes in post-infective IBS9 and an increase in overall cellularity in the colonic mucosa in IBS (14). CD3 is a 'pan T-lymphocytes marker' and allowed us to estimate the overall number of T-lymphocytes in the lamina propria of the IBS patients. It is possible that specific subclasses of lymphocytes may be altered in IBS (e.g. CD4+ and CD8+ classes). Interestingly, the CD4+ T cell subtype has been implicated in an animal model of inflammation. In this model, stress was shown to reactivate colonic inflammation (15) - susceptibility to reactivation of inflammation by stress appeared to specifically require CD4+ lymphocytes. ANTI-INFLAMMATORY MEDIATORS IN IBS The study of inflammation in IBS has largely focused on the role of pro-inflammatory cells and mediators. From other gastrointestinal inflammatory diseases, we know that inflammatory responses involve a complex balance between pro- and anti- inflammatory mediators. There is emerging data to suggest that people with IBS may have a genetic predisposition to produce low amounts of anti-inflammatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-







(16). Moreover, there is a further preliminary report (17) of dysfunctional mucosal protective mechanisms in IBS characterize by reduced numbers of macrophages. While this data is provisional, it is plausible that people who develop IBS could have poorer defense mechanisms to combat infections or other gut insults.A Link between Inflamation and StressAn increase in inflammatory mediators alone is insufficient to explain the pathogenesis of IBS. From post-infective IBS, we know that the most people who have gastroenteritis and accompanying inflammation do not develop IBS. As discussed earlier, several factors may be important in interacting with the gut insult and in predicting those who develop symptoms - one interesting factor here is the role of stress. Psychological stress is known to affect gut function in normal healthy humans, and in people with IBS stress may trigger or exacerbate symptoms. More recently there is evidence of a link between stress and inflammatory responses. Exposure to stress in both animals and humans has been shown to result in the release of mast cell mediators in the colon (18,19) and in a recent study stress was capable reactivating previous inflammation in rats (15). An important challenge for future work will be to clarify the interaction between inflammation, stress and IBS symptoms.ConclusionWe believe that low-grade inflammation may play a role in the pathogenesis of a sub-set of IBS. There is now evidence from several different studies to suggest that a range of inflammatory mediators may be increased in IBS. It is important to point out, however, that most of this evidence, including our data is preliminary and will need to be confirmed by larger research studies. Important challenges for future work will be to demonstrate the role of specific inflammatory mediators in the generation and resolution of IBS symptoms. Continued research into this area is likely to improve our understanding of the underlying mechanisms in IBS and may lead to the development to better therapeutic approaches for this condition. http://www.med.unc.edu/wrkunits/2depts/med...rymediators.htm All of the things and people I posted all share there work together including the research you posted.Were also leaving out a ton of work already done on serotonin and IBS and motility and brain gut axis communication and dysfunction."What are neurotransmitters and what role do they play in IBS?Neurotransmitters are substances that transmit nerve impulses. Serotonin is a major neurotransmitter throughout the nervous system in the gut. Serotonin has been shown to be very important in gut peristalsis, which relates to the movement of contents in the intestinal tract from the mouth through the stomach, through the small intestine and colon. Gut peristalsis occurs all the time: it's how we empty our food and digest our meals. It also seems to be important in gut sensation. As a result, we believe that serotonin may play a major role in IBS and may be a unifying link in these patients who have disordered gut motility and disordered sensation. " http://dhn-online.healthology.com/focus_ar...i_misunderstood I am also surprized out of all the IBS information in medscape you left a ton out iincluding this!!!IBS: Improving Diagnosis, Serotonin Signaling, and Implications for Treatment http://www.medscape.com/viewprogram/2750 The person who wrote this is the worlds leading authority on the enteric nervous sytem! MEDLINE Abstracts: Serotonin Signaling and Visceral Hypersensitivity in IBS"Our understanding of the enteric nervous system (ENS) has evolved from the "classical" view, in which the brain controls all enteric behavior, to the current view, which holds that enteric innervation is one of local control within the bowel, modified by a bidirectional "dialogue" with the brain. The ENS independently controls enteric reflexes through intrinsic primary afferent neurons, which monitor intraluminal conditions. This monitoring is accomplished through the use of enteroendocrine cells in the mucosa, the best known of which are the serotonin-containing enterochromaffin cells. This article describes the roles that serotonin, specific serotonin-receptor subtypes, and the serotonin reuptake transporter play in the ENS and in the communication between the ENS and central nervous system. The way in which these findings have implicated serotonin in irritable bowel syndrome is discussed." http://www.medscape.com/viewarticle/462728 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. http://www.medscape.com/viewarticle/462728 and again I will point out all these top doctors are working together on IBS, including DR mayer who you posted."Michael Camilleri, MDHead, Motility Interest GroupDivision of Gastroenterology and HepatologyMayo Clinic The last decade has seen a dramatic increase in our understanding of the mechanisms and management (diagnosis and therapy) of irritable bowel syndrome. Dr. Camilleri is a physician investigator with specialist expertise in motility, sensory and functional disorders of the gastrointestinal tract. He summarizes the clinical and scientific advances and provides the evidence basis for future therapies in irritable bowel syndrome. Dr. Camilleri's presentation reviews the mechanisms of motor and sensory functions of the colon, and outlines the diagnosis, current approaches to therapy and potential future therapies for this common disorder. "2Douglas Drossman, MDProfessor of Medicine and PsychiatryCo-Director, UNC Center for Functional GI and Motility DisordersUniversity of North Carolina at Chapel Hill Recently, the irritable bowel syndrome (IBS) has gained a great deal of prominence within the field of Gastroenterology. An explosion of basic and clinical research has advanced our understanding of the pathophysiology of this condition. We now understand the IBS not only as a disorder of motility, but also as one associated with visceral hypersensitivity with brain-gut modulation. This new knowledge has been associated with the development of symptom-based criteria for diagnosis, and has led to new forms of treatment. Dr. Drossman, is a nationally recognized investigator and clinician in the field of functional gastrointestinal disorders. He presents an update


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## calid (Aug 4, 2003)

28 pages.....GEESH


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## scottyswotty (Jun 29, 2000)

Yeeghad! that is even longer than the posts Mike NL used to post!!


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## Talissa (Apr 10, 2004)

Eric,You've got issues.NO ONE IS SAYING IBS IS LEAKY GUT!Get it through your membrane.It's been confirmed through research to play a role in IBS for an unknown % of IBS patients and to discount it as some alternative medicine hocus-pocus could be detrimental to getting better.And I'm not promoting anything. (I teach pilates and help wayward animals.)I vividly remember what it was like my first year or so with IBS. I read stories here from folks who are there now. I want to help them. You put down Dr. D's program, but it is textbook natural medicine. It's how I got better. It just took longer because I was on my own.Whenever you come on saying these untruths, you're possibly stopping others from getting better. LEAKY GUT IS NOT IBS, FOR SOME IT PLAYS A ROLE.


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## Talissa (Apr 10, 2004)

PS--After today, I promise to never refer to "leaky gut". I will say "increased intestinal permeability" or "altered mucosa barrier" as they do at Medscape._______________________The Canadian GI's aren't so afraid of the term LGS:"CDDW: Intestinal permeability linked to IBS following Walkerton outbreak"..." Intestinal permeability, or "leaky gut syndrome," is a condition whereby the bowel lining allows more particles and chemicals to pass through, which could irritate its deeper tissue layers. In other words, large spaces develop between the cells of the gut wall, and bacteria, toxins and food leak in." http://www.medicalpost.com/mpcontent/artic...321_163831_4140


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## SpAsMaN* (May 11, 2002)

Maybe you should write a book.







I don't like the 5 htp family,they are too many members,too complicated reactions and nothing works to stabilize them.By the facts,Why they call them 5-htp?This is odd to name something like that.


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## Kathleen M. (Nov 16, 1999)

Standard nomenclature for scientific types.5-HTP is an abreviation for the full technical name for serotonin.this way scientists in papers do not have to right out 5-hydroxytryptophan (or whatever the full name is really spelled).Pretty much all of biology does it this way.For receptors for a compound you name them (whatever it is)-1,-2,-3,-4 because the body never has just one receptor for just one chemical.By using 5-HTP-1,2,3,4 etc rather than calling them fred, george, ron, percy, bill and charlie it helps keep track of them better.Basically it is like naming popes or kings George the first George II George III, etc.Same sort of thing. Technical naming conventions do take awhile to get use to but ALL receptor families are all named the same sort of way and they do not let you invent your own nomenclature for each different researcher...that would be much more confusing.K.


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## eric (Jul 8, 1999)

intestinal permeability in IBS is a CONSEQUENCE not a cause, the cause for some was the intial enteric infection, and molecular cell changes. http://www.gastrojournal.org/scripts/om.dl...&id=a0020100493 Leaky gut or intestinal permeablity is NOT a disease by itself!People can have intestinal permeability issues regardless if they have IBS for other reasons!In IBS, the gut reacts to ALL stimuli. The complete cause of IBS is unknown.Current research understands IBS as:"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.Dr 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.htm "What is understood about the cause? Is stress an issue? One way to understand the condition is that there's a dysregulation in the way the brain and the gut are functioning with each other. Stress does not cause IBS. Stress may modify signals between the brain and the intestinal tract. Factors that might normally affect the bowel might then affect it more; there's an increased response of the bowel. This could be psychologic stress - but I also mean stress in a broader concept like dietary, physical, or environmental. Women who have their period are going through a cycle where hormonal changes occur and this can have an effect. A person with IBS might eat a regular meal and experience a bowel problem. For them, it's an overreaction of the bowel to the stressors." http://www.aboutibs.org/Publications/clinicalIssues.html There is altready quite a bit of eveindece on why this happens.Food allergies and food intloernces are not IBS, only triggers to the underlying disorder.There is no evidence that digestion is different in those with IBS compared to those without IBS. Although the exact cause is not known, there are factors that appear to aggravate symtoms or make people feel worse."While dietary factors do not cause IBS, they may aggrvate symptoms in some persons. Increased intestinal muscle reactivity and/or heightened sensitvity in IBS can cause the bowel to over respond to stimuli. Even the act of eating itself, and not a particular food, ay aggravate symptoms."Nonetheless certain foods are known to simulate gut reactions in general."There is more from there news letter."Irritable Bowel Syndrome: An Overview By: Lin Chang, M.D., CNS: Center for Neurovisceral Sciences & Womenï¿½s Health; CURE: Digestive Diseases Research Center, Division of Digestive Diseases, UCLA School of Medicine Irritable bowel syndrome (IBS) is a chronic functional bowel disorder characterized by abdominal pain or discomfort and alterations in bowel habits. The clinical diagnosis of IBS is based on identifying symptom criteria with a ï¿½positive diagnosisï¿½ and excluding organic disease with minimal diagnostic evaluation. Although there are many expensive and sophisticated tests available for the evaluation of IBS symptoms, these are generally not needed for patients with typical symptoms and no features suggestive of organic diseases. This article provides a comprehensive overview of the prevalence, symptoms, diagnosis, and treatment options for IBS." http://www.aboutibs.org/Publications/currentParticipate.html Although some people have oerlapping disorders and some people believe because they eat and it causes pain, it must be foods. And certain foods themselves act as triggers.Other things where intestinal permeabilit is a consequence.Some medschronic stress Overuse of antibiotics Overuse of NSAIDS (aspirin, ibuprofen, Tylenol) Overuse of stomach antacids A diet high in processed foods and refined sugars Frequent consumption of alcohol Exposure to environmental chemicals and toxins Intestinal infections Things that can change gut flora other then IBS:alcoholdietEnvironmentacid / alkaline balance some supplementsantibioticsPromoting healthy bacteria in the digestive system is a plus.Inflammation, Infection, and Irritable Bowel Syndrome: An Update http://www.immunesupport.com/library/showarticle.cfm/ID/3692 "Maria O'Sullivan, Dublin, IrelandNitric oxide, mast cells and inflammations in the pathogenesis of IBS Summarized by Sara Ewert, Ph.D-student, Dep. of Physiology and Pharmacology, Gï¿½teborg univeristyThe group (Dr. Maria O'Sullivan, Prof. Colm O'Moran) has experimental data, patient-based data and data from post-dysentery IBS patients. Their data shows that IBS is correlated to a low-grade inlammatory process involving the mast cell, type I hypersensitivity and potent inflammatory mediators. The reason to believe that the mast cell might be the link between the brain and gut are the close proximity to nerves and the fact that stress induces degranulation. " http://wwwhost.gu.se/cgf/fouschema.html#Maria "InflammationPreliminary evidence for a possible alteration in gut immune function in IBS comes from both unselected and so-called postinfectious IBS (PI-IBS) patients. In unselected patients, increased numbers of mast cells in the muscularis externa of the colon50 and the ileal and colonic mucosa51,52 have been reported. Increased cellularity of the colonic mucosa and lamina propria has also been described in unselected IBS patients using semiquantitative microscopy.53 In patients with intractable IBS, lymphocytic infiltrates of the myenteric plexus were reported,54 and most recently, preliminary evidence for increased iNOS (nitric oxide synthetase) expression was described.55 For subgroups of IBS, these findings suggest there is an up-regulation of gut immune function. However, methodological deficiencies exist, including the influence of the bowel preparation, the classification of the patients, and the nonquantitative analysis of gut cells. Further studies are needed to explore these intriguing findings. Further support for a possible role of altered gut immune function in IBS comes from recent studies in PI-IBS patients.56ï¿½59 A subset of IBS patients associate the development of IBS symptoms with the onset of gastroenteritis.60ï¿½62 In recent prospective studies, IBS-like symptoms were found in 7%ï¿½30% of patients who recovered from a proven bacterial gastroenteritis.59 Reported risk factors included: female gender, duration of the acute diarrheal illness, and the presence of significant life stressor occurring around the time of the infection. Patients with PI-IBS were found to have a variety of functional alterations, including changes in gut motility,63,64 epithelial function,65,66 and an increase in colonic enterochromaffin cells.66 In addition, evidence for increased expression of interleukin 1 messenger RNA, increased cellularity of lamina propria, and an increase in CD3+ lymphocytes were reported from mucosal biopsy specimens.66 The correlation of IBS symptoms with these observed changes has not been established. Furthermore, because the majority of patients do not develop postinfectious diarrhea and the prevalence of IBS is not higher in countries with high rates of enteric infections, further studies are required to determine if vulnerability factors (such as altered neuroimmune system responsiveness) play a role in the development of PI-IBS in a subset of patients. In addition, psychological distress seems to be an important cofactor in determining who retains symptoms after an enteric infection.67 " http://www.gastrojournal.org/scripts/om.dl...id=agast1232108 Their data shows that IBS is correlated to a low-grade inlammatory process involving the mast cell


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## eric (Jul 8, 1999)

Basic Principles -- Brain-Gut Moderators: Emeran Mayer MD; Robin Spiller MD. Panel: Robin Spiller MD; Jackie Wood PhD; George Chrousos MD; Yvette Tachï¿½ PhD; Lisa Goehler PhD; G.F. Gebhart PhD; Emeran Mayer MD. Click on Titles to View Other TopicsIntroductionOutcomes of Pediatric Functional GI Disorders Epidemiology/Genetic/Behavioral Factors Brain Imaging Emerging Techniques to Evaluate and Treat Functional GI and Motility Disorders Clinical Applications of Diagnosis and Treatment Functional GI DisordersGeneral Principles of TreatmentPharmacological Treatment Psychological Treatment IFFGD Research AwardsThe brain-gut axis refers to the continuous back and forth interactions of information and feedback that take place between the gastrointestinal tract, and the brain and spinal cord (which together comprise the central nervous system). These interrelated feedback circuits can influence brain processes and bowel functions -- affecting pain perception, thoughts and one's appraisal of symptoms, gut sensitivity, secretions, inflammatory responses, and motility. The brain-gut circuits can be activated by an external or internal factor or stimulus that makes a demand on the system, such as a stressful event, an injury, an emotional thought or feeling, or even the ingestion of food. Symptoms of functional GI disorders may result from a maladaptive response to stimuli at some point within the complex interactions that take place along the brain-gut axis. Basic science is the fundamental approach to understanding how systems work. Basic research takes place in the laboratory and often involves the study of molecules and cells. From this body of knowledge is drawn the means to investigate practical applications and to formulate clinical practices. Translational science converts basic science discoveries into the practical applications that benefit people. One of the more exciting areas of recent research relates to the basic and translational aspects of the effects of stress on inflammation, cytokine and immune modulation, and pain. (Cytokines are a type of protein released by cells of the immune system, which act through specific cell receptors to regulate immune responses.) This series of presentations address three important research areas in the field of functional GI disorders, which have recently attracted considerable attention: the role of immune activation in the gut and the interactions of the gut immune and nervous systems; the role of the central nervous system in the regulation (modulation) of pain perception (nociception); and the emerging field of animal models with relevance for functional GI disorder research. This section demonstrates the rapid progress seen in the last few years in better understanding of basic mechanisms, in particular the neuroimmune interactions underlying symptom generation in patients with "functional" GI disorders. There are immune responses to infections. To defend itself from a foreign substance or invader, such as a bacterium or virus, the body mounts an immune response controlled by the brain. There needs to be a balance between infection and the body's immune response; the immune system needs to turn on and turn off at the right times to destroy the invader but not to the degree that it may harm healthy tissue. Robin Spiller, University Hospital, Nottingham, England began the session by noting the difficulty in separating disorders of structure ("organic") from disorders of function. He noted, "The difference is based on how high the power of your microscope is." This was elaborated upon in his presentation on Post-infectious Functional GI Disorders. It has been observed that IBS-like symptoms, that persist for 6 months to a year or longer, may appear after a bout with an acute infection in the gastrointestinal tract (e.g., food-poisoning). This is termed, "post-infectious IBS." A study by Gwee et al showed that the presence of unusual or amplified life stress at the time of onset of infection increased the chances of developing IBS symptoms. Inflammation persisted in patients with IBS-like symptoms but did not in patients whose symptoms resolved. This suggests that the brain's management of certain stressful stimuli (i.e., psychologic distress) affects the brain-gut system's ability to inhibit inflammation. It has frequently been observed that some individuals with more severe symptoms of IBS have coexisting psychologic distress. Stress has been thought to influence health-care seeking behavior, either by increasing motility, visceral hypersensitivity or inflammation, or by enhancing one's perception of gut symptoms, all of which lead to a greater need to seek care for them. The concept of post-infectious IBS suggests that in some circumstances stress (the biological process by which the body adapts in response to a stimuli) may influence symptoms. An initial response to an infection in the gastrointestinal tract can involve the neurotransmitter, serotonin, which acts as a messenger (mediator) to cells involved with the immune response. Immune cells -- mostly in the blood, but also in the lymphatic system -- enter the infected area and remove the invader. Additionally, the body adaptively removes the infection (e.g., via vomiting or diarrhea -- normal beneficial responses that help the body expel an infecting organism). Persistence of the underlying inflammatory response may lead to post-infectious disorders of function. A variety of neuroimmune responses can lead to intestinal over-responsiveness (sensitization) and other clinical effects. These responses include direct toxicity to nerves that influence intestinal contractions, alteration in gut immune activation, abnormalities of serotonin metabolism, and persisting low-grade inflammation. IBS developing after infective gastroenteritis is associated with subtle increases in enteroendocrine and chronic inflammatory cells in the gut mucosa. The net effect may be to increase serotonin availability in the gut and enhance secretion and propulsive motility patterns. Serotonin antagonists may be beneficial in such patients Notably, the concept of "post-infectious IBS" has grown to include studies of their application in post-infectious gastroparesis and dyspepsia. 1Major inflammatory responses have not been observed in most IBS patients. However, in some studies subtle changes associated with inflammation have been noticed, such as increased presence of mast cells (a type of immune system cell present in blood and tissue). Jackie Wood, Ohio State University College of Medicine discussed the Effects of Inflammation on the Gut Enteric Nervous System, specifically noting the importance of mast cell degranulation (the release from within the cell of granules, or small sacs, containing chemicals that can digest microorganisms and fight infection). In tissue mast cells accumulate around nerve endings of nerves that contain the neurotransmitter serotonin. The release of substances that can induce activity in excitable tissue (i.e., histamine, Interleukin-1 (IL-1), and bradykinin) by mast cells can affect receptor and neurotransmitter function in the enteric nervous system - the part of the autonomic nervous system that controls function of the gastrointestinal tract. In other words, when mast cells in the intestinal lining empty their contents in response to an infection, they activate nearby nerve endings. In a subgroup of patients, this can have significance in terms of resulting clinical consequences of diarrhea and abdominal discomfort.2Yvette Tachï¿½, University of California Los Angeles discussed Stress and Inflammation. The experience of stress is an adaptive behavior common to all living organisms. The activation of corticotropin releasing factor (CRF) signaling pathway, is the major mediating mechanism involved with the body's stress response system in which gastric emptying is inhibited (with possible loss of appetite) while colonic motor activity is stimulated (producing a loose stool or a sensation of bowel urgency). There is growing evidence that activation of this CRF pathways impacts on inflammation, autonomic nervous system function, immunity, and clinical behavior or illness, all of which may be linked to the pathophysiology of the functional gastrointestinal disorders. While we often talk about how the brain -- influenced for example by arousal and/or psychosocial factors -- can affect immune function, the reverse is also true. Immune activation, following infection for example, can influence brain function. Lisa Goehler, University of Virginia discussed Cytokines and Vagal Afferents: Immune Signaling to the Brain. Cytokines are substances that are produced by white blood cells to regulate certain functions during inflammatory and immune responses. The vagus is a nerve made of both sensory and motor fibers that innervates nearly every internal organ. The gastrointestinal (GI) tract, along with the lungs and liver, is an area of tissue that most commonly comes in contact with microorganisms (pathogens), such as bacteria or viruses, capable of activating an immune response. Cytokine mediators activate neurons that convey messages from tissue to the brain (afferent neurons) through the vagus nerve. The GI tract is richly supplied with vagal afferents that can signal immune activation in the tissue. This process may underlie the mechanism that causes individuals to feel sick. The concept of "sickness symptoms" is not always recognized. The cytokine inflammatory and immune mediators distributed throughout the body (peripheral), which appear to interact through vagal pathways, have systemic effects that manifest as symptoms in the body. (Mediators are substances released from cells to regulate immune responses.) Such symptoms include fever, increased sensitivity to pain, loss of appetite, and decreased desire for social interaction. The process may provide the basis for a role of the vagus as an interface between the site of the immune response and the brain that results in symptoms of altered mood, including anxiety or depression, that are sometimes associated with gastrointestinal disease.4 Jerry Gebhart, The University of Iowa discussed the CNS Modulation of Visceral Nociceptive Responses. The central nervous system (CNS) is composed of the brain and spinal cord. The brain interprets and influences our perceptions of the pain sensation signals transmitted from the gut (visceral nociceptive responses) to the spinal cord and then to higher centers. Several structures in the brain (periaqueductal gray, dorsolateral pons, and rostroventral medulla) can facilitate or inhibit signals sent to the CNS and influence the perceived discomfort, or even whether the signals are experienced as pain. Inflammation of the bowel can produce increased sensitivity to pain or enhanced intensity of pain sensation (hyperalgesia) via increased activity of certain cells (for example, those that contain nNOS) in these higher brain modulatory centers.5 To close the Brain-Gut sessions, Emeran Mayer, University of California Los Angeles discussed Evolving Animal Models of Visceral Hypersensitivity. In contrast to most other disorders of the digestive system, functional disorders of the gut continue to be defined by symptom criteria rather than by biological markers. Realistic animal models of functional gastrointestinal (GI) disorders in which to test hypotheses have not been available until recently. While it is unlikely that there will ever be an animal model to replicate all complexities of the human functional GI disorders, animal research is likely to help us understand some of the key underlying mechanisms responsible for symptom generation. This includes over-responsiveness of central stress circuits to visceral and psychological stimuli, resulting in altered autonomic responses (motility, secretion), increased pain sensitivity (visceral hypersensitivity) and possibly altered immune function of the gut. Future studies with genetically altered (i.e., transgenic) mice that become models for studying specific human diseases and their treatments may further increase our understanding of these mechanisms.6 http://www.iffgd.org/symposium2003brain-gut.html "Bacteria and IBSMany have wondered if IBS is caused by an infection. To date, no virus, bacteria, or parasite has been found to directly cause IBS. It has, however, been hypothesized that these microbes may indirectly cause IBS or at least exacerbate its symptoms. Some researchers question whether IBS begins with a common bacterial gastroenteritis. [Gastroenteritis is an inflammation of the lining of the stomach and intestinal tract often caused by a bacterial infection. Symptoms may include vomiting, abdominal pain, and diarrhea.] Other investigators question whether the number or type of bacteria that normally live in the colon affects symptoms.Some individuals with IBS recall that their symptoms began with a gastroenteritis. The first theory of a "post-infection diarrhea" as a possible link has been explored in greater depth this past year. A post-infection diarrhea is a common, temporary phenomenon resulting from the destruction of intestinal digestive enzymes during an infection. Even after the infection has cleared, certain foods will cause the persistence of loose stools for several weeks until the intestine rebuilds its digestive enzymes.One recent Canadian study looked at the occurrence of IBS in people who travel overseas and acquire a "traveler's diarrhea." These investigators found that 10% of travelers who acquired an infectious gastroenteritis subsequently developed IBS. Those who did develop a traveler's diarrhea, compared to those who did not, had an approximate 6-fold increased risk of developing IBS.Another study from England found that 23% of their patients hospitalized for an infectious gastroenteritis went on to develop IBS. Regardless of whether these individuals developed IBS, they all had increased rectal sensitivity and increased colon movements several weeks after their infection had cleared. However, the researchers also found that the individuals who developed IBS reported more life events suggesting that that there may have been a psychological component to their symptoms in addition to the infectious component.Can bacteria cause IBS without a preceding infection? There are trillions of bacteria that normally reside in the gastrointestinal tract where they help digest nutrients. [Fermentation and intestinal gas are a byproduct of this digestive process.] Some investigators have questioned whether the number or type of bacteria normally present is different in individuals with IBS. A group of German investigators found that the tissue taken from the colons in people with IBS had higher bacterial concentrations than the tissue from individuals without IBS. The researchers believe that this finding suggests that the colons of some people with IBS are colonized by a greater number of bacteria than those without IBS. This may alter how nutrients are fermented in the colons of IBS patients.A group of British investigators also believe that colonic fermentation (gas production) is different in some people with IBS. They confirmed this in one study, which may explain why some individuals respond to dietary restriction and why some do not. The investigators went on to measure gas production in IBS patients before and after antibiotic treatment. The antibiotics appeared to reduce the total volume and rate of hydrogen gas production in the people studied. The investigators felt that this second study provided additional evidence of the role of colonic fermentation in IBS symptoms and supported the use of dietary modification or antibiotics to reduce gas production and improve symptoms in people with IBS.These findings are promising. It is too early however, to say conclusively that bacteria and antibiotics have a role in the development of IBS symptoms and in effective treatment."Where is the Problem in IBS?The definition of IBS suggests that all routine investigations such as blood tests, endoscopy, and radiological imaging should be normal. The condition is diagnosed on the basis of symptoms, elicited through history and physical examination, in the absence of obvious gut abnormality. So what is the problem?Much work has been done to explain the underlying pathology (disease characteristics or cause) in IBS in the hope that treatment could be directly targeted to an abnormality. This approach could be hugely beneficial compared to available treatments that work symptomatically.In IBS, we know the problem is not only in the gut but is also in the brain-gut axis and the autonomic nervous system.Is the problem in the gut? Increased perception of sensations in the gut, or visceral hypersensitivity, has consistently been observed in IBS. Mertz and colleagues from California checked the discomfort threshold in IBS patients and in a control group. In response to balloon distention of the rectum, almost all (94%) of IBS patients showed lowered pain thresholds. The investigators proposed that increased rectal perception could be used as a reliable biological marker for IBS.Is the problem in the brain?Silverman and colleagues from UCLA used a special brain imaging technique, positron emission tomography (PET), to measure the changes in the pattern of blood flow in the brains IBS patients and a control group in response to balloon distention of the rectum. They found that different areas of the brain were activated in IBS patients when rectal stimuli were delivered. This suggests that the brains of people with IBS process signals from the gut differently.Is the problem in the general autonomic nervous system?Monga and colleagues from London checked bladder and esophageal perception and pain thresholds and found that women with IBS have both lower bladder and esophageal sensory thresholds. They suggested that IBS is part of a generalized disorder of smooth muscles. These women also had "irritable bladders." Francis and colleagues from Manchester, UK found that a higher proportion of patients who are seen in the urology clinic have IBS compared to patients seen in other clinics (dermatology; and ear, nose, and throat).There seems to be increasing evidence that the pathology in IBS is not limited to the gut, brain, or autonomic nervous system only. *Rather there may be an involvement of all three systems. Therefore, any potential new therapy should be aiming at this widespread pathology.* http://www.aboutibs.org/Publications/resea...ml#anchor147531


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## Talissa (Apr 10, 2004)

Eric,You say:


> quote:intestinal permeability in IBS is a CONSEQUENCE not a cause


Hugo Rodier, M.D. says:


> quote:"We now know that a shift toward more pathogenic bacteria causes this permeability...Even a less-serious infection like the stomach flu can create this problem for years to come (J. Gut, 2001, 47:804). *Later, Irritable Bowel or Spastic Colitis may develop* , but because the stomach flu episode happened so long before, the two are not correlated. *Irritable Bowel, then, is a disorder of intestinal flora, made worse by stress.* It is characterized by spasms of the guts after meals, bloating, cramping, and alternating diarrhea and constipation.


 http://www.healthypath.com/Classes/GastroIntestinal.htm Joseph Mercola, MD, says the same thing. Different opinions, but their credentials sure beat yours....


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## eric (Jul 8, 1999)

"We now know that a shift toward more pathogenic bacteria causes this permeability...Even a less-serious infection like the stomach flu can create this problem for years to come (J. Gut, 2001, 47:804). Later, Irritable Bowel or Spastic Colitis may develop , but because the stomach flu episode happened so long before, the two are not correlated. Irritable Bowel, then, is a disorder of intestinal flora, made worse by stress. It is characterized by spasms of the guts after meals, bloating, cramping, and alternating diarrhea and constipation."The head of the four winds nutrition club. There is a world expert for you for sure. LOL I don't think so.THE UNC CENTER for FUNCTIONAL GASTROINTESTINAL & MOTILITY DISORDERS http://www.med.unc.edu/medicine/fgidc/sitemap.htm Dr. Drossman is Co-director of the Center and Professor of Medicine and Psychiatry at UNC-CH. Dr. Drossman has had a long-standing interest in the research and evaluation of difficult to diagnose and treat gastrointestinal disorders. He established a program of research in functional gastrointestinal disorders at UNC more than 25 years ago and has published more than 350 books, articles, and abstracts relating to epidemiology, psychosocial and quality of life assessment,design of treatment trials, and outcomes of research in gastrointestinal disorders.Dr. Drossman received his MD degree from Albert Einstein College of Medicine in 1970 and completed his medical residency at the University of North Carolina School of Medicine and NYU-Bellevue Medical Center. After his residency, he subspecialized in psychosocial (psychosomatic) medicine at the University of Rochester School of Medicine and in Gastroenterology at the University of North Carolina in 1976-1978. He is currently Professor of Medicine in Psychiatry at UNC.As the medical director of the Center, Dr. Drossman sees patients in the functional GI and motility clinic and precepts GI fellows and visiting gastroenterologists to help develop their clinical skills in treating patients. He also facilitates the learning of medical faculty, psychiatry residents, and medical students, on how to provide biopsychosocial care to patients with functional GI disorders.Dr. Drossman has an active research program, which relates to the clinical, epidemiological, psychosocial, and treatment aspects of irritable bowel syndrome IBS. He has developed and validated several assessment measures, which are used worldwide for clinical research. Recently he began looking at brain imaging (fMRI) in functional bowel to determine if the reported changes in the brain are responsive to treatment. He also consults with several pharmaceutical and governmental agencies regarding treatment trials. He was responsible for organizing the Functional Brain Gut Research Group as a special interest section within the American Gastroenterological Association, chairs the ROME committee, and is a past president of the American Psychosomatic Society. Dr. Drossman sits on the Board of Directors and is Chair of the Scientific Advisory Board and the Awards Committee 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.In 2001, Dr. Drossman was appointed Associate Editor of Gastroenterology, the official journal of the American Gastroenterological Association and in 2003 became chair of 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. 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 the AGA GI Teaching Project on IBS-II. 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 Senior Editor of the book, Rome III Committees with the book, Rome 3, to be published in 2006.Dr. Drossman's educational and clinical interests in the psychosocial/behavioral aspects of patient care was a natural path to his developing 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 considered a world authority in the field of IBS, functional disorders, and on physician-patient communications. He presents at numerous national and international meetings throughout the year. http://www.med.unc.edu/medicine/fgidc/drossman.htm


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## Talissa (Apr 10, 2004)

Eric,I hate to be the one to break it to you, but you are not Dr. Drossman.


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## SpAsMaN* (May 11, 2002)

I think the particulars inflammatories cells who are found in 90% of the IBSers,can be the CAUSE of my altered motility.Eric in the first page of this thread i found this quotes from your post who does not seems to corellate the others researchs.:chronic inflammatory mucosal changes in the gut are not a plausible mechanism to explain the presence of chronic abdominal pain, a cardinal IBS symptomThe only consequence that i feel is altered motility.


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## eric (Jul 8, 1999)

No Tal, I am not and never said I was, it was the sources.Maybe this will help though.From my IBS website."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.htm Spasman, it maybe one of many possiblities and I would get some particular tests done.Have you ever had a sitz marker test done?Comprehensive Overview of Constipation: http://www.med.unc.edu/wrkunits/2depts/med...ve_overview.htm


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## Talissa (Apr 10, 2004)

Hi Eric,The point of my post was to compare your absolute truths with that of MDs.I'll try & use words with fewer syllables next time.Btw, even Dr. Drossman cannot say that there absolutely is no bacterial connection that leads to getting IBS, or prevents recovery for some because...NO ONE knows that yet, with certainty. It is being studied.Dr. Drossman is an expert in the mechanisms of IBS, not the cause. It's being studying. You find the cause, a way to a cure is more plausible, rather than simply masking symptoms with drugs. Drugs that cause other problems within the body.Talissa_____________He HIMSELF thinketh he have all answers.


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## kel1059 (Feb 28, 2003)

also Dr Drossman was the former editor of a journal called "Psychosomatic Disorders" or something to that effect.It tells me that he just don't give a darn about bacteria.He is going to preach what he knows best.--and that is that IBS is "ALL IN THE HEAD".okay maybe that is an exageration but i get sick of eric referring to this Dr drossman as some type of all knowing God -- which he ain't!


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## kel1059 (Feb 28, 2003)

talissa,it is like talking to a wall.a couple of years ago eric was complaining because not enough people were donating money to him for constructing a website on IBS.







If you combine that fact with his business dealings then the picture starts to get a little more clear.eric if you take the time to read the works of Dr H Rodier you would see that he makes excellent sense. of course since that flies in the face with your business strategy you will not pay attention to it.


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## eric (Jul 8, 1999)

Kel, having another episode?Kel, What is the defintion of Psychosomatic?I don't think you actually know what it means and just fear the word itself?"Merriam-Webster Online DictionaryMain Entry: psyï¿½choï¿½soï¿½matï¿½ic Pronunciation: -s&-'ma-tikFunction: adjectiveEtymology: International Scientific Vocabulary1 : *of, relating to, concerned with, or involving both mind and body * the psychosomatic nature of man -- Herbert Ratner2 : of, relating to, involving, or concerned with bodily symptoms caused by mental or emotional disturbance psychosomatic illness psychosomatic medicine So Kel, your saying that emotions, stress, anxiety has nothing to do with the body or with health and disease and there is no such thing as Mind body medicince?Are there other things that can go wrong OTHER then bacteria in IBS? IN IBS research they sure have found quite a few that are all connected.I know you really want IBS to be a chronic bacterial infection, your are completely focused on that and nothing else, that's a big problem.Funny it does not show up in IBS in blood work or colonoscopies or get worse over timeTal, I posted and lost it and will post it again later.Hoiwever you must not be reading what I am posting to begin with, because most of the posts are trying to explain."bacterial connection that leads to getting IBS"They alreay know a lot about this which is what I am trying to point out to you and what I posted above, if you read it.So here it is again.The brain-gut axis refers to the continuous back and forth interactions of information and feedback that take place between the gastrointestinal tract, and the brain and spinal cord (which together comprise the central nervous system). These interrelated feedback circuits can influence brain processes and bowel functions -- affecting pain perception, thoughts and one's appraisal of symptoms, gut sensitivity, secretions, inflammatory responses, and motility. The brain-gut circuits can be activated by an external or internal factor or stimulus that makes a demand on the system, such as a stressful event, an injury, an emotional thought or feeling, or even the ingestion of food. Symptoms of functional GI disorders may result from a maladaptive response to stimuli at some point within the complex interactions that take place along the brain-gut axis. Basic science is the fundamental approach to understanding how systems work. Basic research takes place in the laboratory and often involves the study of molecules and cells. From this body of knowledge is drawn the means to investigate practical applications and to formulate clinical practices. Translational science converts basic science discoveries into the practical applications that benefit people. One of the more exciting areas of recent research relates to the basic and translational aspects of the effects of stress on inflammation, cytokine and immune modulation, and pain. (Cytokines are a type of protein released by cells of the immune system, which act through specific cell receptors to regulate immune responses.) This series of presentations address three important research areas in the field of functional GI disorders, which have recently attracted considerable attention: the role of immune activation in the gut and the interactions of the gut immune and nervous systems; the role of the central nervous system in the regulation (modulation) of pain perception (nociception); and the emerging field of animal models with relevance for functional GI disorder research. This section demonstrates the rapid progress seen in the last few years in better understanding of basic mechanisms, in particular the neuroimmune interactions underlying symptom generation in patients with "functional" GI disorders. There are immune responses to infections. To defend itself from a foreign substance or invader, such as a bacterium or virus, the body mounts an immune response controlled by the brain. There needs to be a balance between infection and the body's immune response; the immune system needs to turn on and turn off at the right times to destroy the invader but not to the degree that it may harm healthy tissue. Robin Spiller, University Hospital, Nottingham, England began the session by noting the difficulty in separating disorders of structure ("organic") from disorders of function. He noted, "The difference is based on how high the power of your microscope is." This was elaborated upon in his presentation on Post-infectious Functional GI Disorders. It has been observed that IBS-like symptoms, that persist for 6 months to a year or longer, may appear after a bout with an acute infection in the gastrointestinal tract (e.g., food-poisoning). This is termed, "post-infectious IBS." A study by Gwee et al showed that the presence of unusual or amplified life stress at the time of onset of infection increased the chances of developing IBS symptoms. Inflammation persisted in patients with IBS-like symptoms but did not in patients whose symptoms resolved. This suggests that the brain's management of certain stressful stimuli (i.e., psychologic distress) affects the brain-gut system's ability to inhibit inflammation. It has frequently been observed that some individuals with more severe symptoms of IBS have coexisting psychologic distress. Stress has been thought to influence health-care seeking behavior, either by increasing motility, visceral hypersensitivity or inflammation, or by enhancing one's perception of gut symptoms, all of which lead to a greater need to seek care for them. The concept of post-infectious IBS suggests that in some circumstances stress (the biological process by which the body adapts in response to a stimuli) may influence symptoms. An initial response to an infection in the gastrointestinal tract can involve the neurotransmitter, serotonin, which acts as a messenger (mediator) to cells involved with the immune response. Immune cells -- mostly in the blood, but also in the lymphatic system -- enter the infected area and remove the invader. Additionally, the body adaptively removes the infection (e.g., via vomiting or diarrhea -- normal beneficial responses that help the body expel an infecting organism). Persistence of the underlying inflammatory response may lead to post-infectious disorders of function. A variety of neuroimmune responses can lead to intestinal over-responsiveness (sensitization) and other clinical effects. These responses include direct toxicity to nerves that influence intestinal contractions, alteration in gut immune activation, abnormalities of serotonin metabolism, and persisting low-grade inflammation. IBS developing after infective gastroenteritis is associated with subtle increases in enteroendocrine and chronic inflammatory cells in the gut mucosa. The net effect may be to increase serotonin availability in the gut and enhance secretion and propulsive motility patterns. Serotonin antagonists may be beneficial in such patients Notably, the concept of "post-infectious IBS" has grown to include studies of their application in post-infectious gastroparesis and dyspepsia. 1 *Major inflammatory responses have not been observed in most IBS patients. However, in some studies subtle changes associated with inflammation have been noticed, such as increased presence of mast cells * (a type of immune system cell present in blood and tissue). Jackie Wood, Ohio State University College of Medicine discussed the Effects of Inflammation on the Gut Enteric Nervous System, specifically noting the importance of mast cell degranulation (the release from within the cell of granules, or small sacs, containing chemicals that can digest microorganisms and fight infection). In tissue mast cells accumulate around nerve endings of nerves that contain the neurotransmitter serotonin. The release of substances that can induce activity in excitable tissue (i.e., histamine, Interleukin-1 (IL-1), and bradykinin) by mast cells can affect receptor and neurotransmitter function in the enteric nervous system - the part of the autonomic nervous system that controls function of the gastrointestinal tract. In other words, when mast cells in the intestinal lining empty their contents in response to an infection, they activate nearby nerve endings. In a subgroup of patients, this can have significance in terms of resulting clinical consequences of diarrhea and abdominal discomfort.2Yvette Tachï¿½, University of California Los Angeles discussed Stress and Inflammation. The experience of stress is an adaptive behavior common to all living organisms. The activation of corticotropin releasing factor (CRF) signaling pathway, is the major mediating mechanism involved with the body's stress response system in which gastric emptying is inhibited (with possible loss of appetite) while colonic motor activity is stimulated (producing a loose stool or a sensation of bowel urgency). There is growing evidence that activation of this CRF pathways impacts on inflammation, autonomic nervous system function, immunity, and clinical behavior or illness, all of which may be linked to the pathophysiology of the functional gastrointestinal disorders. While we often talk about how the brain -- influenced for example by arousal and/or psychosocial factors -- can affect immune function, the reverse is also true. Immune activation, following infection for example, can influence brain function. Lisa Goehler, University of Virginia discussed Cytokines and Vagal Afferents: Immune Signaling to the Brain. Cytokines are substances that are produced by white blood cells to regulate certain functions during inflammatory and immune responses. The vagus is a nerve made of both sensory and motor fibers that innervates nearly every internal organ. The gastrointestinal (GI) tract, along with the lungs and liver, is an area of tissue that most commonly comes in contact with microorganisms (pathogens), such as bacteria or viruses, capable of activating an immune response. Cytokine mediators activate neurons that convey messages from tissue to the brain (afferent neurons) through the vagus nerve. The GI tract is richly supplied with vagal afferents that can signal immune activation in the tissue. This process may underlie the mechanism that causes individuals to feel sick. The concept of "sickness symptoms" is not always recognized. The cytokine inflammatory and immune mediators distributed throughout the body (peripheral), which appear to interact through vagal pathways, have systemic effects that manifest as symptoms in the body. (Mediators are substances released from cells to regulate immune responses.) Such symptoms include fever, increased sensitivity to pain, loss of appetite, and decreased desire for social interaction. The process may provide the basis for a role of the vagus as an interface between the site of the immune response and the brain that results in symptoms of altered mood, including anxiety or depression, that are sometimes associated with gastrointestinal disease.4 Jerry Gebhart, The University of Iowa discussed the CNS Modulation of Visceral Nociceptive Responses. The central nervous system (CNS) is composed of the brain and spinal cord. The brain interprets and influences our perceptions of the pain sensation signals transmitted from the gut (visceral nociceptive responses) to the spinal cord and then to higher centers. Several structures in the brain (periaqueductal gray, dorsolateral pons, and rostroventral medulla) can facilitate or inhibit signals sent to the CNS and influence the perceived discomfort, or even whether the signals are experienced as pain. Inflammation of the bowel can produce increased sensitivity to pain or enhanced intensity of pain sensation (hyperalgesia) via increased activity of certain cells (for example, those that contain nNOS) in these higher brain modulatory centers.5 To close the Brain-Gut sessions, Emeran Mayer, University of California Los Angeles discussed Evolving Animal Models of Visceral Hypersensitivity. In contrast to most other disorders of the digestive system, functional disorders of the gut continue to be defined by symptom criteria rather than by biological markers. Realistic animal models of functional gastrointestinal (GI) disorders in which to test hypotheses have not been available until recently. While it is unlikely that there will ever be an animal model to replicate all complexities of the human functional GI disorders, animal research is likely to help us understand some of the key underlying mechanisms responsible for symptom generation. This includes over-responsiveness of central stress circuits to visceral and psychological stimuli, resulting in altered autonomic responses (motility, secretion), increased pain sensitivity (visceral hypersensitivity) and possibly altered immune function of the gut. Future studies with genetically altered (i.e., transgenic) mice that become models for studying specific human diseases and their treatments may further increase our understanding of these mechanisms.6 http://www.iffgd.org/symposium2003brain-gut.html


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## eric (Jul 8, 1999)

Kel, emotions and stress have nothing to do with IBS or even intestinal permeability?"Mary Perdue from McMaster University, Ontario discussed the importance of the epithelial intestinal barrier to maintain immune tolerance to potentially harmful matter, such as bacteria, ingested when we eat or drink. (Everything that enters the human body must pass through an epithelial layer. Various types of epithelial tissues line not only the body cavities, blood vessels, and most organs, but also our outer surface-our skin. Within the intestines, epithelial tissue forms an intestinal barrier involved with absorption, secretion, sensation, contractility, and protection.) Studies in animal models show that *psychological stress can disrupt this barrier, leading to the penetration of bacteria into the gut* , inflammation, an immune system response (inflammatory cytokines), and ultimately sensitization of neural signals from the gut to the brain that can heighten the perception of pain." http://www.iffgd.org/symposium2001.html Maybe your so stressed and worried about bacteria in IBS that it's the reason it is entering your "epithelial intestinal barrier."Wow there is a concept huh.


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## norwood (Jan 28, 2004)

JEEEEEESSSSSSHHHHH! Of course money is necessary...after this thread, there is no more space on the server!


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## missC (Oct 16, 2002)

" kel,emotions and stress have nothing to do with IBS or even intestinal permeability?"uhh....kel.... did you EVER say that?putting words into people's mouths makes it pretty easy to knock down their (alleged) arguments. if we all observed basic rules of debate and logic then maybe things wouldn't get so heated here.i haven't forgotten that i promised to actually read one article from you unarguably proving the existence of a brain-gut axis, Eric. i have a day free coming up and plan to spend a couple of hours doing that. one, not the fifteen or so you posted in full rather than as links in response. your attitude doesn't cause me to look forward to it. it's true you're getting plenty of attitude back, but as an observer and non-participant in Dr D's trials, that's the way it seems to operate - you go on the offensive and get your own mud thrown back at you. it's not tremendously surprising.


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## eric (Jul 8, 1999)

Miss c its in reference to "Dr Drossman was the former editor of a journal called "Psychosomatic Disorders" or something to that effect.""--and that is that IBS is "ALL IN THE HEAD".Also"also Dr Drossman was the former editor of a journal called "Psychosomatic Disorders" or something to that effect.It tells me that he just don't give a darn about bacteria."he's also the chair of the rome committe!!!Well that's funny he wrote these then"IBS PublicationsAnother look at bacteria and IBSBy Douglas A. Drossman, M.D. http://www.aboutibs.org/Publications/bacteria.html "Bacterial infection as a possible factor in irritable bowel syndrome (IBS) has long been a subject for research."Bacterial Overgrowth in IBS http://www.med.unc.edu/wrkunits/2depts/med...rowthandibs.htm I remeber kel, arguing in the chat with the experts and Kel telling them they knew nothing about the immune system and IBS? They then had to figure out a way to ban people after that, because she just went off and would not stop or listen and bascially implied she knew more then they did. How many times can we count her information just plain upsurd and the majority of times down right inaccurate.What is the brain gut axis?"Modern IBS research has focused on the importance of the relationship between events that affect the function of the central nervous system (brain) and the influence these factors ultimately have on the function of the intestines via the specialised enteric nervous system of the intestine (The Brain Gut Axis).Its a fact, not a theory. http://www.ibs-research-update.org.uk/ibs/brain1ie4.html It is my hope people learn about the brain in the gut, the "enteric nervous system" and that it is majorally connected to and communicates with the brain and that they effect each other which is very very important in IBS and in IBS research.There are more nerve fibers in the gut brain then the spinal cord.It is a serious mistake, not to take the brain gut axis into account in IBS.If you do not believe in the brain gut axis, you don't believe your gut and your brain are connected to each other and communicate back and forth to each other. Its a bidirectional system not a theory. They effect each other, again that is not a theory.Gut Thoughts http://www.kiwiterapi.dk/whiplash/frames/gutthoughts.htm


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## eric (Jul 8, 1999)

IFFGD glossary of terms:"Brain-gut axis: The continuous back and forth interactions of information and feedback that take place between the gastrointestinal tract, and the brain and spinal cord (which together comprise the central nervous system). "


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## Talissa (Apr 10, 2004)

Eric,Kel isn't stressed about bacteria, she's almost 100%. And for myself, I'd sure rather IBS have a bacterial connection than simply believe I'm a headcase that will need drugs the rest of my life. Oh, & of course hypnotherapy to correctly direct my brain.Have you ever heard of the term "psychologization" of disease. This is what happened to "IBS" when it first came on the radar screen.Things are changing.It is GOOD._______________________Maxx--you crack me up!


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## not well (Mar 18, 2004)

here's a little testtake some glycerin suppositories in the morning and empyty yourself.straight afterwards take either some anti D drug from the pharmacy eg : kaolin/morphine mixutre or immodium whatever.if there's no feeling of fullness/bloating later on, then the anti D has proberly slowed down the peristalsis movements( which i feel is happening to me)if there still is then it could be a digestive flora bacteria imbalance thats causing this whole thing .i'mm gonna try this over the weekend,cause i've done more then half the prebio 7(probiotic formular) packet already and feel bloated evenmore after a complete bm.but why is my anal sphincter muscle not working properly?


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## not well (Mar 18, 2004)

talissa,eric,kel any comments?


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## Talissa (Apr 10, 2004)

not well,Probiotics don't work overnight for most of us. And sometimes there's an adjustment period. And sometimes what you're eating can affect their effectiveness. Any medications you're taking may affect this. We're all different. It may even be those probiotics--I don't know about that brand. Therein lies the one problem with natural medicine. It's not exact. It's also why it's good to see someone trained in naturopathy who's had success treating IBS.Regarding your experiment for the wkd, you got me. Off the top of my head, it sounds a bit wacky. And I've never taken immodium or Pepto & I've no idea the ramificatins of taking glycerin.Maybe someone else can better advise.T-


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## SpAsMaN* (May 11, 2002)

Not well have you even been on Morphine?


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## skinny (Jul 27, 2002)

Eric just demonstrated what propagandistic tool he knows how to use best: *stacking the deck*. His amateurish cut and paste jobs look like it too.


> quote:Stacking the Deck: One stacks the deck when *he/she leaves out relevant information, tells half-truths*, exaggerates, or otherwise tampers with the facts. We often see this technique used in the presenting of statistics and polling results.Reference: http://rhetorica.net/propaganda.htm Card Stacking. "Stack the cards" or "arrange the deck" of facts against the truth. *Use under-emphasis and over-emphasis. Suppress facts that don't support your side.*Reference: http://brainstorm-services.com/wcu/propaganda.html


Eric wrote:


> quote:Well that's funny he wrote these then"IBS PublicationsAnother look at bacteria and IBSBy Douglas A. Drossman, M.D. http://www.aboutibs.org/Publications/bacteria.html "Bacterial infection as a possible factor in irritable bowel syndrome (IBS) has long been a subject for research."Bacterial Overgrowth in IBS http://www.med.unc.edu/wrkunits/2depts/med...rowthandibs.htm


Eric why are you quoting outdated information? Dr. Drossman's critiques on the SIBO study is outdated and moot. With the gobs of time you spend compiling your database of articles and links, I'd expect you to be up to snuff on this.Normalization of lactulose breath testing correlates with symptom improvement in irritable bowel syndrome: a double-blind, randomized, placebo-controlled study http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12591062 Pimentel, Chow, Lin, et. al are on to something. The study was well done. They did follow-ups and used a single antibiotic with a placebo in a double blinded fashion. The antibiotic had resulted in ~35% bowel normalization compared to the placebo ~14%. Pimentel reported he got better results on the liquid elemental diet study (Vivonex Plus), but I haven't seen the data on that.skinny


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## SpAsMaN* (May 11, 2002)

Maybe the stress they seems to miss is the stress of IBS itself rather than the phantom stress they never clearly identify.


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## eric (Jul 8, 1999)

Glossory of terms http://www.iffgd.org/GIDisorders/glossary.html "believe I'm a headcase that will need drugs the rest of my life"This is a belief not the research and people probaly won't feel that way when they learn more about IBS! That it is a physcial condition. Because then it will be clear its not all in the head perhaps or all in the gut perhaps, but in the way the brain and the gut communicate and things that can go wrong all along these systems. The research is certainly getting somewhere for sure and it is working on the connections of the brain gut axis and ALL abnormalities in both the gut and the brain in IBS. And where things can go wrong both in the gut and in the brain and in between the two. This involves bacteria studies, central nervous sytem studies, enteric nervous sytem studies, the interation of the two studies, surgery and IBS and genetics and IBS and many many other factors. But a lot has been done already as well. *Neuroimaging has provided evidence of physiological differences between normal individuals and those suffering from IBS in the way a visceral stimulus (ie, rectal distention) is processed in the brain.* 14,15 Initial data from positron emission tomography (PET) scans demonstratedincreased activation of the anterior cingulate cortex (ACC) among normal individuals, comparedto IBS patients. The ACC is a cerebral cortical area that is rich in opiate receptors and is thought to be a major component of cognitive circuits relating to perception as well as descending spinal pathways involving pain. More recently, fMRI was used to demonstrate increased activity in the ACC, prefrontal (PF), and insular cortex areas, and in the thalamus of IBS patients compared to normal individuals."





















They have also learned to maniplulate those signals however and make people feel better, in a way that has nothing to do with bacteria, but through neurotransmission. They then can see brain changes that correlate with them feeling better."The cardinal symptoms of IBS are abdominal pain and altered intestinal activity - diarrhea or constipation. These are probably related to what is called visceral hypersensitivity; this means the nerve receptors in the intestines are super-sensitive, and fire off signals more readily than those in unaffected people.Visceral hypersensitivity can be demonstrated by inflating a balloon that's inserted in the rectum, and measuring the pressure that produces pain. The pain threshold is lowered in 60% of IBS patients. Interestingly, if the patient is led to anticipate pain, by a stepwise increase in balloon pressure, the pain threshold decreases; on the other hand, if the balloon pressure is randomly altered, there is no lowering of the pain threshold. This indicates that the brain can, indeed, play a part in the symptoms of IBS. And during the anticipation of, as well as actual, distension of the rectum in IBS patients, brain radiographs show increased blood flow in some parts of the brain.Patients with IBS may complain of diarrhea, constipation, or neither of these symptoms. The motility of the colon is clearly an important feature of the condition. Visceral hypersensitivity means the colon will react to a greater extent to stimuli that would produce no obvious effect in unaffected people. A worsening of symptoms after eating, for instance, might be an exaggerated response to the 'gastro-colic reflex', in which a full stomach releases a substance called cholecystokinin-1 that causes contractions of colon musculature.IBS sufferers are sometimes intolerant of certain foods, such as wheat products or milk. An irritant effect can lead, because of visceral hypersensitivity, to poor digestion, excessive gas, bloating, and intestinal 'hurry'.Visceral hypersensitivity implies increased nerve cell signals traveling from the intestines up to the brain (afferent signals), and increased signals going in the opposite direction (efferent signals). These signals are transmitted with the aid of a chemical called serotonin, or 5HT (short for 5-hydroxytryptamine).There are several reasons for believing that 5HT plays a central role in the way IBS symptoms are caused. First, in inflammatory intestinal conditions, such as food poisoning, enteritis, and colitis, the number of special cells that produce 5HT in the intestine wall are greatly increased, and there is increased intestinal motility and hurry. Second, a drug that antagonizes one type of 5HT receptors on the cells (alosetron) is effective in diarrhea-predominant ISB. And third, another drug that antagonizes another type of 5HT receptors (tegaserod) is effective in constipation-predominant IBS.Two other factors are important in how IBS occurs. Stress can make it worse. Acute stress situations are not likely to be a problem; chronic, unrelieved stress, such as separation or bereavement, are more likely triggers.Finally, genetic factors can play a role. Twin studies suggest that environmental factors are probably more important than genetic factors. However, there are some rare congenital conditions with abnormalities in intestinal motility, and others where the inflammatory reaction to infection is exaggerated.Psychological factors have been frequently blamed for IBS, and it's true that psychiatric diagnoses are increased in IBS patients referred to specialist clinics; however, there doesn't seem to be any association between psychiatric disorders and IBS in the general population." http://www.healthandage.com/Home/gid2=2071 IN PI IBS there is an increase of mast cells and serotonin storing EC cells.Tal, I will give you another analogy.A person can be standing on railroad tracks. Your only looking one way down the tracks for the bacteria train and you get nailed from a train going the other direction. Or you can stand off the tracks and look both ways for all incoming trains.Also, how many bacterial infections have you had and what were the symptoms, Usally a fever and perhaps vomiting and such, people with c-dif for example could tell basically between there IBS and the effects of C-dif. Everyday we are exposed to different ones, they protect us from our environment and mine in Oregon are not the same as someone in florida. They protect us from all kinds of things and that protection has evolved for millions of years. They are not all bad, the majority are not bad. If a bad one is found by your doctor, then that is not IBS.Diet and other factors we have discussed are important to gut flora, if people effect them for all or any of those reasons when they send a stool sample in for testing, how do you seperate its from IBS or any of the other reasons. I also don't think I have ever seen exactly what bacteria all humans should have in their guts and the counts. Bacteria for sure plays a role in digestion, a very important role for sure. They are researching this and have been for a while. Symptoms are important here also.IBSers will also react to bacteria in the colon just like they would to stress, hormones, foods and any other items that put pressure on the nerve cells or effect the nerve cells in the gut or mess with the digestive system. Everytime you eat left overs this can happen.There are also tests in regards to these issues. Some more accurate then others, and technology has gotten way better in testing in and of itself.I have not however seen any pet scans or fmri between people with only intestinal permeability and those with IBS? Its also not like all these doctors don't now anything about infection and inflammation or disease. A lot of work has also been done in inflammatory bowel disease and many other conditions. The first thing if there is inflammation in the gut is to rule out microscopic colitus or celiac sprue or inflammatory conditions. IN IBS, major inflammation is not seen and its not the kind of inflammation most people think about when they think inflammation. Its important not to scare people into things they may already be scared about. Its important I believe to let there doctors figure out why they have inflammtion and be tested.I have shown you a ton of research on bacteria and IBS and hesitate to post more since the first has not been understood yet.You can be reactive or proactive, and I know sometimes I am reactive, by certain peoples comments, that is not the way I would like it at all, but certain people just want to push buttons and they have for longer then you have been here, they dont want to be proactive and say, hey what does that mean? They are reactive and might read something and automatically be reactive to a particlur item instead of proactive, and say, well there is a lot of reserch on this and what does it really mean.I have been extremely proactive in looking at research in IBS and have had a ton of expert help. I certainly in know way what so ever, know everything, but I am past the basics for sure, something I believe your still struggling with, but at least your trying. It is a huge learning curve for sure and IBS is super complex. IBS is not just about bacteria or bacteria research, there are many many more things that can go wrong and that is what IBS research is sifting through right now. However, they already have some specific clues and reasons for certain treatments in IBS from what they have seen in IBS research, not all of them have to do with bateria or probiotics either.There are conditions and problems in which bacteria does not play a role and in the things they do know it plays a role, then they need to make sure if its the cause or the result. That's what basic science is about.Knowledge is power over a persons condition. I am going to try to be less reactive in the future. Personally. of course that may depend on how many times someone contionuosly works on pushing my buttons, because I also won't lie down dead for that either.One focus in IBS is on the neurotransmitter serotonin, do you know why?Glossory of terms http://www.iffgd.org/GIDisorders/glossary.html "believe I'm a headcase that will need drugs the rest of my life"This is a belief not the research and people probaly won't feel that way when they learn more about IBS! That it is a physcial condition. Because then it will be clear its not all in the head perhaps or all in the gut perhaps, but in the way the brain and the gut communicate and things that can go wrong all along these systems. The research is certainly getting somewhere for sure and it is working on the connections of the brain gut axis and ALL abnormalities in both the gut and the brain in IBS. And where things can go wrong both in the gut and in the brain and in between the two. This involves bacteria studies, central nervous sytem studies, enteric nervous sytem studies, the interation of the two studies, surgery and IBS and genetics and IBS and many many other factors. But a lot has been done already as well. *Neuroimaging has provided evidence of physiological differences between normal individuals and those suffering from IBS in the way a visceral stimulus (ie, rectal distention) is processed in the brain.* 14,15 Initial data from positron emission tomography (PET) scans demonstratedincreased activation of the anterior cingulate cortex (ACC) among normal individuals, comparedto IBS patients. The ACC is a cerebral cortical area that is rich in opiate receptors and is thought to be a major component of cognitive circuits relating to perception as well as descending spinal pathways involving pain. More recently, fMRI was used to demonstrate increased activity in the ACC, prefrontal (PF), and insular cortex areas, and in the thalamus of IBS patients compared to normal individuals."





















They have also learned to maniplulate those signals however and make people feel better, in a way that has nothing to do with bacteria, but through neurotransmission. They then can see brain changes that correlate with them feeling better."The cardinal symptoms of IBS are abdominal pain and altered intestinal activity - diarrhea or constipation. These are probably related to what is called visceral hypersensitivity; this means the nerve receptors in the intestines are super-sensitive, and fire off signals more readily than those in unaffected people.Visceral hypersensitivity can be demonstrated by inflating a balloon that's inserted in the rectum, and measuring the pressure that produces pain. The pain threshold is lowered in 60% of IBS patients. Interestingly, if the patient is led to anticipate pain, by a stepwise increase in balloon pressure, the pain threshold decreases; on the other hand, if the balloon pressure is randomly altered, there is no lowering of the pain threshold. This indicates that the brain can, indeed, play a part in the symptoms of IBS. And during the anticipation of, as well as actual, distension of the rectum in IBS patients, brain radiographs show increased blood flow in some parts of the brain.Patients with IBS may complain of diarrhea, constipation, or neither of these symptoms. The motility of the colon is clearly an important feature of the condition. Visceral hypersensitivity means the colon will react to a greater extent to stimuli that would produce no obvious effect in unaffected people. A worsening of symptoms after eating, for instance, might be an exaggerated response to the 'gastro-colic reflex', in which a full stomach releases a substance called cholecystokinin-1 that causes contractions of colon musculature.IBS sufferers are sometimes intolerant of certain foods, such as wheat products or milk. An irritant effect can lead, because of visceral hypersensitivity, to poor digestion, excessive gas, bloating, and intestinal 'hurry'.Visceral hypersensitivity implies increased nerve cell signals traveling from the intestines up to the brain (afferent signals), and increased signals going in the opposite direction (efferent signals). These signals are transmitted with the aid of a chemical called serotonin, or 5HT (short for 5-hydroxytryptamine).There are several reasons for believing that 5HT plays a central role in the way IBS symptoms are caused. First, in inflammatory intestinal conditions, such as food poisoning, enteritis, and colitis, the number of special cells that produce 5HT in the intestine wall are greatly increased, and there is increased intestinal motility and hurry. Second, a drug that antagonizes one type of 5HT receptors on the cells (alosetron) is effective in diarrhea-predominant ISB. And third, another drug that antagonizes another type of 5HT receptors (tegaserod) is effective in constipation-predominant IBS.Two other factors are important in how IBS occurs. Stress can make it worse. Acute stress situations are not likely to be a problem; chronic, unrelieved stress, such as separation or bereavement, are more likely triggers.Finally, genetic factors can play a role. Twin studies suggest that environmental factors are probably more important than genetic factors. However, there are some rare congenital conditions with abnormalities in intestinal motility, and others where the inflammatory reaction to infection is exaggerated.Psychological factors have been frequently blamed for IBS, and it's true that psychiatric diagnoses are increased in IBS patients referred to specialist clinics; however, there doesn't seem to be any association between psychiatric disorders and IBS in the general population." http://www.healthandage.com/Home/gid2=2071 IN PI IBS there is an increase of mast cells and serotonin storing EC cells.Tal, I will give you another analogy.A person can be standing on railroad tracks. Your only looking one way down the tracks for the bacteria train and you get nailed from a train going the other direction. Or you can stand off the tracks and look both ways for all incoming trains.Also, how many bacterial infections have you had and what were the symptoms, Usally a fever and perhaps vomiting and such, people with c-dif for example could tell basically between there IBS and the effects of C-dif. Everyday we are exposed to different ones, they protect us from our environment and mine in Oregon are not the same as someone in florida. They protect us from all kinds of things and that protection has evolved for millions of years. They are not all bad, the majority are not bad. If a bad one is found by your doctor, then that is not IBS.Diet and other factors we have discussed are important to gut flora, if people effect them for all or any of those reasons when they send a stool sample in for testing, how do you seperate its from IBS or any of the other reasons. I also don't think I have ever seen exactly what bacteria all humans should have in their guts and the counts. Bacteria for sure plays a role in digestion, a very important role for sure. They are researching this and have been for a while. Symptoms are important here also.IBSers will also react to bacteria in the colon just like they would to stress, hormones, foods and any other items that put pressure on the nerve cells or effect the nerve cells in the gut or mess with the digestive system. Everytime you eat left overs this can happen.There are also tests in regards to these issues. Some more accurate then others, and technology has gotten way better in testing in and of itself.I have not however seen any pet scans or fmri between people with only intestinal permeability and those with IBS? Its also not like all these doctors don't now anything about infection and inflammation or disease. A lot of work has also been done in inflammatory bowel disease and many other conditions. The first thing if there is inflammation in the gut is to rule out microscopic colitus or celiac sprue or inflammatory conditions. IN IBS, major inflammation is not seen and its not the kind of inflammation most people think about when they think inflammation. Its important not to scare people into things they may already be scared about. Its important I believe to let there doctors figure out why they have inflammtion and be tested.I have shown you a ton of research on bacteria and IBS and hesitate to post more since the first has not been understood yet.You can be reactive or proactive, and I know sometimes I am reactive, by certain peoples comments, that is not the way I would like it at all, but certain people just want to push buttons and they have for longer then you have been here, they dont want to be proactive and say, hey what does that mean? They are reactive and might read something and automatically be reactive to a particlur item instead of proactive, and say, well there is a lot of reserch on this and what does it really mean.I have been extremely proactive in looking at research in IBS and have had a ton of expert help. I certainly in know way what so ever, know everything, but I am past the basics for sure, something I believe your still struggling with, but at least your trying. It is a huge learning curve for sure and IBS is super complex. IBS is not just about bacteria or bacteria research, there are many many more things that can go wrong and that is what IBS research is sifting through right now. However, they already have some specific clues and reasons for certain treatments in IBS from what they have seen in IBS research, not all of them have to do with bateria or probiotics either.There are conditions and problems in which bacteria does not play a role and in the things they do know it plays a role, then they need to make sure if its the cause or the result. That's what basic science is about.Knowledge is power over a persons condition. I am going to try to be less reactive in the future. Personally. of course that may depend on how many times someone contionuosly works on pushing my buttons, because I also won't lie down dead for that either.One focus in IBS is on the neurotransmitter serotonin, do you know why?


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## SpAsMaN* (May 11, 2002)

Eric,i don't know why you sent me a constipation link because i go 1 to 4 tims a day.Sitz marker?Maybe i should talk about that to my G.I.specialist.Trapped gas is my predominant symptoms.


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## Talissa (Apr 10, 2004)

Skinny,You are one of many people here who astound me in their intelligence and great ability to get their point across clearly, with some humor mixed in!Thanks for the study link.T-


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## Jhouston (Nov 9, 2003)

Eric, Question: If there is a bacteria problem, will HT work? Joann


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## kel1059 (Feb 28, 2003)

terrorist eric,i had to hit the page down button 39 times on my computer for your post at the top of this page. you're insane, insane i tell you ---insane!go skinny go!







--and eric, quit putting words in my mouth. i agree that negative emotions play a role in our downward spiral.Talissa,your post about bifidobacteria was very good. my GSDL (stool analysis) showed no bifido bacteria growth and no good e coli growth. --and my peristalsis was terrible. now my peristalsis is actually pretty good. simply amazing!poor peristalsis was one of my worst symptoms. i still don't trust what is going on with me and live in fear that it will come back.


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## Talissa (Apr 10, 2004)

Eric,Thanks for actually presenting your views in a reasonable manner. I hear what you're saying. It seems contradictory though, to your blanket statements while seemingly trying to stop folks from approaching the problem as a bacterial imbalance &/or permeability problem. Whether you believe there's more to it than that, I know first hand, you get your life back when approaching it this way. And you don't need a prescription.For ex, "IBS is not a bacteria problem," well yeh, it could be if that's what got you to having IBS.For ex, "intestinal permeability is a consequence of IBS, not the other way around," when that exact question has not been answered and is being studied by unsung heroes.Talk about pushing buttons!And you mistakingly believe that because I'm new to this board, that I've no real knowledge of IBS. I assure you that since that Dr looked into my eyes and told me I had it & there's not much to do about it, I've studied IBS.And I spent two years becoming a CN. Studied digestion, body systems, nutrients, diseases, everything. I did it solely because that MD broke me with Flagyl, then told me there was nothing he could do but write another bloody prescription.Then I realized during my studies that the MD who had me taking Tetracycline for over a year back in HS probably started the whole dysbiosis cycle. And why did he have me taking the drug for 365+ days, when today it's not to be taken more than 10 consecutive days? Because I had a few zits. Seriously, not many. Well, wow, I feel better. This bb has got to be better than therapy. But I gotta quit spending so much time here...Talissa


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## flux (Dec 13, 1998)

> quote: Eric why are you quoting outdated information? Dr. Drossman's critiques on the SIBO study is outdated and moot. With the gobs of time you spend compiling your database of articles and links, I'd expect you to be up to snuff on this.


It isnï¿½t outdated.


> quote: Pimentel, Chow, Lin, et. al are on to something. The study was well done


Perhaps, but at the moment, there is no corroboration. It would seem something fishy is going on, no?


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## kel1059 (Feb 28, 2003)

talissa,the time you spend here is going to a good cause.your story about the antibiotics is a credible testimony. many people here can share the same story. antibiotics took me from bad to terrible about 7 or 8 years ago.hopefully people will see this information and pass it on to their loved ones. at the very least our idiot doctors should be clued in to the benefit of probiotics during antibiotic use but sadly they are not.


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## not well (Mar 18, 2004)

spasman i've never tried morphine but there some antidioraeals that combine the mixture with calcium.talissa what i am trying to say is why the food goes down quicker in us then in ppl without ibs,i've noticed thisevery morning i have to have a bm it HAS to be complete. (cause if it aint my colon gets more c*** later on and the feeling is horrible) the struggle to get the urge is unbelivable(before i had this i could have a complete bm and ever thing would be empty regardless of what i ate later on during the day)if a get the right urge i'm free until i eat something no matter how small it is.then gradualy throught the day the fullness/ bloated feeling comes along like there's something stuck up my a**.then i have to have another urge to get it out and so forth after the next meal thats why i hardly eat anything, only something afternoon and evening.now why does it feel like my anal sphincters not working correctly? maybe cause there is not enough stool in the rectum?maybe the nerves are damaged or dysfunctioned?(eric could tell me something about this cause he knows about the brain-gut thing) why can't it all come out at once?every time i clean there's still c*** on the paper. that means i can't do normal things or be around ppl everyone else cause i HAVE to be around toilets every day.this has ruined me i'm telling you. why do i feel like s*** every day?it seems the more comfortable i am the better the urge i get to have a bm. but i can't stay indoors for the rest of my life so there is two things here that is wrong with me1)anal sphicter does not evacuate like it used to, only on right sensation/urge and if i try and hold a D burst the sphicter sometimes has no effect thats why i have to wear dark coloured underwear. and IT STILL dont make no difference2)anything i eat goes through me and sits there at the end with an uncomfortable fullness feeling.3)if i don't have a bm to get rid of it, the next meal makes it even worse.so two things :bacteria imbalance? digestion not working properly? maybe i dont know much about it yet to tell you the truthenteric nervous infection dysfuntion? oversensitive nerves throughout the whole system?i dont know thats eric's knowledgetoo long for me to read your posts eric cause i've only got about an hour before the cafe shuts but eric if what your saying is correct about brain gut axis are there any solutions to getting my system back to the way it was?you know instead of giving out the mass of information you do(which is helpfull) maybe you should give some advice on whats the effective treatment for different the symtomns that we all have.almost ten years now NO career NO social life NO relasionships NO nothing just lonleynessthis is a nightmare i am upset and i should bei just can't believe after i ate that bit of salad that i got this and its never stoppedsame cycle over and over againonly had pain a few times when i've been constipated but nothing major for the GI who found nothing by sticking a tube camera up my a**all i am trying to say is there any way of getting my gi tract back ot normal like all those years back?spasman,eric,flux,talissa,kel what you think about this? i don't care what it is, brain gut flora nerve hypersensation or whatever thats hard to understand i just WANT to get rid of this to lead a normal life again.have any of you got simular symtomns to me?thanks for reading


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## SpAsMaN* (May 11, 2002)

High amplitude contraction?







Is it what we call spasms?







Visit this link for a photo of the PAIN IN ACTION: http://www.med.unc.edu/wrkunits/2depts/med...ve_overview.htm Eric,having spasms dosen't necessary means chronic constipation!


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## scottyswotty (Jun 29, 2000)

not well - that sounds like some kind of ordeal. what alternative health systems/modalities have you tried?where do you live in the UK?PM me if you want to.Scott


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## SpAsMaN* (May 11, 2002)

Not Well ,visit my Methadone topic,there is hope.Comment on this photo of a spasms.I crave a comment. http://www.med.unc.edu/wrkunits/2depts/med...ve_overview.htm


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## eric (Jul 8, 1999)

First Kel, garlic kills e coli , look it up."no good e coli growth"Flux, is simon2004 another of the many Kel is signing on to the bb with? Just curious?Second Tal if your doing all the studying on IBS what do you know about serotonin? Because anybody actually studying it, would have to know about it in regards to IBS?also"For ex, "IBS is not a bacteria problem," well yeh, it could be if that's what got you to having IBS."This caused my IBS also and why I am trying to really explain it to you. There is a ton of information on this out there and a lot I have already posted.Dr Robin Spiller in the UK is a leading expert on PI IBS.Here you go, one of the percipating factor in PI IBS is stress and the other is in part the severity of tissue damage and ulceration from the infection itself.I also keep mentioning mast cells and enteroendocrine cells, of which the main content is serotonin and why I ask the question to you, do you know about serotonin and IBS?And"It is important that patients should understand the important roles of anxiety, stress, and diet and persisting low-grade inflammation in this condition." http://www.med.unc.edu/wrkunits/2depts/med..._infectious.htm also I am not responsible for the bad doctors you have had! However, even if a person has a bad experience with a doctor, doesn't mean there are not still good ones out there that help people. There are and they can help people, answer questions, do any needed testing ect.. Does one or more bad apples mean all apples are bad? On the other hand also, I have seen patients give up on what doctors try to say to them.Jhoston, HT is a proven effective treatment for IBS, which at this time is not a bacterial infection and they have reasons for it working in IBS. One recently on why it works for foods and IBS and others on the brain and pain and many others reasons. Have you read all the studies and information on it and IBS. It is one of the most effective treatments to date in IBS statistically.On the other hand it helps boost the immune system, so no matter what it can help in that regard. It also depends on what were talking about here in regards to bacteria. It is however to much of a blanket statement to give you a clearer answer.skinny First as flux mentioned it is not outdated, second it was that Kel said they don't study it which is totally inaccurate and they have studies on it going on right now as we speak.You might also notice from those articles the UNC see's only ten percent of the people they test with sibo. Also what are the symptoms of SIBO?Also SIBO is not IBS. And I have seen that artcile already. You might also want to look at the wording."symptom improvement"That is very important.also their is a test for this to rule it out!!! So that in a way is a moot point.Gastrointestinal Motility Disorders The UNC Breath Testing Center http://www.med.unc.edu/wrkunits/2depts/med...gidc/breath.htm Not well, your post concerns me very much.What you are posting is consistent with an IBS diagnoses, although I am not diagnosing you or even know what tests you have had done.Are you seeing a doctor now or have you seen one lately, how long has it been?"what i am trying to say is why the food goes down quicker in us then in ppl without ibs"This is pretty well known why now for the most part in IBS.although there can be other reasons for it or other coexisting conditions.But in IBS they have a pretty good idea of why this happens.This is important not well, even though it makes you upset and it sucks its important not to stress out as much as possible, because that is well known to make it all worse, which I fully understand in thirty years of severe IBS myself, but try not to, its very important, it makes pain and discomfort worse, causes more bowel spasms, and takes more of a toll on your whole body.That is not the only answer for you and like I said I think I could find real help for you in the UK.also, have you only seen one doctor?I can find help for you I believe in the UK.


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## flux (Dec 13, 1998)

> quote:is simon2004 another of the many Kel is signing on to the bb with? Just curious?


I believe kel has appeared as other people as well presumably to help spread misinformation, but I don't think so in this case. simon2004's misinformation seems to focused on pH.


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## I'll B Snookered (Apr 9, 2004)

flux, do you think eric is Dr. Drossman? I don't think I've seen an eric post without a reference to this omnipotent being, Dr. Drossman. No offense, eric.


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## Arnie W (Oct 22, 2003)

not wellI know where you're coming from. For years I have never been complete, and yeah I can relate to the toilet paper saga. There's something which is preventing complete evacuation, no matter how many toilet trips you make a day. And sometimes I wonder where it's all coming from.As suggested earlier, antibiotics, esp for acne, seem to be a major culprit for some people. It doesn't seem to matter how relaxed or stressed I am. No rhyme or reason to this monster. I've been following Dr D's protocol and am finally begining to see some improvement. It's still early days, so there's no point in saying that this is the way to go just yet, but I feel something is happening. I'll keep you posted.


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## Talissa (Apr 10, 2004)

Eric,Do you get off on fighting?I'm really not in a contest with you to see who knows more. The reason I don't mention the serotonin is because there's not much we can do right now about that.But I've gotten back to a normal life by going to the source--the flora in my digestive tract.What kind of a person tries to stop others from doing the same just because they get some ego trip from being friends with MDs & have alot of studies etc & want desperately to appear to be smarter than everyone else?


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## Talissa (Apr 10, 2004)

I should add, that there's not much we can do naturally about the serotonin uptake problem --except maybe try 5-htp.And it seems to me that if you normalize your digestive tract, you'll be absorbing nutrients more efficiently & thus you will naturally correct these other IBS symptoms.I know once I starting improving--the insecurity, anxiousness, depression by way of feeling powerless & helpless ag the IBS, they just slowly left.I fixed myself. It was actually pretty cool.Further, the long-term risks and consequences of taking low-dose antidepressants for IBS are unknown. But here's an example of some of the ways Paxil can totally screw your body up:Less commonAgitation; chest congestion; chest pain; chills; cold sweats; confusion; difficulty breathing; dizziness, faintness, or lightheadedness when getting up from a lying or sitting position; fast, pounding, or irregular heartbeat or pulse; muscle pain or weakness; skin rash. RareAbsence of or decrease in body movements; bigger, dilated, or enlarged pupils [black part of eye]; difficulty in speaking; inability to move eyes; incomplete, sudden, or unusual body or facial movements; increased sensitivity of eyes to light; low blood sodium (confusion, convulsions [seizures], drowsiness, dryness of mouth, increased thirst, lack of energy); red or purple patches on skin; serotonin syndrome (confusion, diarrhea, fever, poor coordination, restlessness, shivering, sweating, talking and acting with excitement you cannot control, trembling or shaking, twitching); talking, feeling, and acting with excitement and activity you cannot control. Incidence not determinedBack, leg, or stomach pains; bleeding gums; blindness; blistering, peeling, loosening of skin; bloated, full feeling; bloody or black, tarry stools; bloody urine; blue-yellow color blindness; blurred vision; coma; constipation; cough or hoarseness; dark urine; decreased frequency or amount of urine; decreased vision; depression; difficulty opening the mouth; difficulty swallowing; electric shock sensations; epileptic seizure that will not stop; excessive muscle tone; eye pain; fainting; fixed position of eye; fluid-filled skin blisters; general body swelling; general feeling of tiredness or weakness; headache; high fever; hives; inability to move arms and legs; inability to sit still; increased blood pressure; increased sweating; increased thirst; incremental or ratchet-like movement of muscle; indigestion; itching skin; joint pain; lab results that show problems with liver; light-colored stools; lockjaw; loss of appetite; loss of bladder control; low blood pressure; lower back or side pain; muscle spasm, especially of neck and back; muscle tension or tightness; nausea; need to keep moving; nosebleeds; painful knees and ankles; painful or difficult urination; painful or prolonged erection of the *****; pale skin; puffiness or swelling of the eyelids or around the eyes, face, lips, or tongue; raised red swellings on the skin, the buttocks, legs, or ankles; red irritated eyes; rigid muscles; seizure or coma late in pregnancy; sensitivity to the sun; skin redness or soreness; skin sores, welts or blisters; skin thinness; sore throat; sores, ulcers, or white spots on lips or in mouth; swelling of breasts; swollen or painful glands; shortness of breath; slow heart rate; slow movement; slow reflexes; spasms of throat; stiff muscles; stomach pain; sudden numbness and weakness in the arms and legs; swelling of face, fingers, lower legs; tightness in chest; unexpected or excess milk flow from breasts; unusual bleeding or bruising; unusual or decreased blood cell production; unusual tiredness or weakness; vomiting; weight gain; wheezing; yellowing of the eyes or skin. Symptoms of overdoseDizziness; drowsiness; dryness of mouth; flushing of face; irritability; large pupils; nausea; racing heartbeat; trembling or shaking; vomiting. Other side effects may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine. However, check with your doctor if any of the following side effects continue or are bothersome:More commonAcid or sour stomach; belching; decreased appetite; decreased sexual ability or desire; excess air or gas in stomach or intestines; heartburn; nervousness; pain or tenderness around eyes and cheekbones; passing gas; problems in urinating; runny or stuffy nose; sexual problems, especially ejaculatory disturbances; sleepiness or unusual drowsiness; stomach discomfort, upset, or pain; sweating; trauma; trembling or shaking; trouble in sleeping. Less commonAbnormal dreams; anxiety; bladder pain; body aches or pain; change in sense of taste; changes in vision; cloudy urine; confusion; congestion; difficulty in focusing eyes; difficulty in moving; discouragement, feeling sad or empty; drugged feeling; dryness of throat; excessive muscle tone; fainting or loss of consciousness; fast or irregular breathing; feeling of unreality; feeling of warmth or heat; flushing or redness of skin, especially on face and neck; frequent urge to urinate; headache, severe and throbbing; heavy bleeding; increase in body movements; increased appetite; irritability; itching, pain, redness, or swelling of eye or eyelid; itching of the vagina or genital area; lack of emotion; loss of interest or pleasure; loss of memory; lump in throat; menstrual changes; menstrual pain or cramps; muscle twitching or jerking; pain during sexual intercourse; problems with memory; problems with tooth; rhythmic movement of muscles; sense of detachment from self or body; severe sunburn; slow heartbeat; sneezing; thick, white vaginal discharge with no odor or with a mild odor; tightness in throat; tingling, burning, or prickling sensations; trouble concentrating; voice changes; watering of eyes; weight loss; yawn. After you stop using this medicine, your body may need time to adjust. The length of time this takes depends on the amount of medicine you were using and how long you used it. During this period of time check with your doctor if you notice any of the following side effects:Abnormal dreams; agitation, confusion, or restlessness; burning, crawling, itching, numbness, prickling, "pins and needles" , or tingling feelings; diarrhea; dizziness or light-headedness; electric shock sensations; fear; headache; increased sweating; muscle pain; nausea or vomiting; nervousness; runny nose; trembling or shaking; trouble in sleeping; unusual tiredness or weakness; vision changes. Other side effects not listed above may also occur in some patients. If you notice any other effects, check with your doctor. http://www.mayoclinic.com/invoke.cfm?objec...9A5A2A3115076DA **********************Is it Paxil or is it Poison?


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## kel1059 (Feb 28, 2003)

(edited to add that i wrote this before reading T's post on anti-depressants)T,one other important thing to remember is that eric went off his medication (prozac) a while ago.i think that might be an important clue as to what is going on here.eric, i know the side effects can be troubling but can't you try others to see if those might be a little more gentle on your system? have you tried lexapro? i hear it may be a little easier.something tells me that marijuana should NOT be substituted for psychiatric drugs.eric, i care about you. i really do! --and i want you to get the help you need. if not for yourself then do it for your family. i am going to put your name in the church basket next sunday so people pray for you.have you ever tried meditation or prayer to calm yourself down? maybe the HT has lost its effectiveness. maybe you need other modalities.(flux --- are you loulou? are you jr katz? when jeff banned you for your obnoxious behavior a few years ago how many aliases did you create?)


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## kel1059 (Feb 28, 2003)

t.,i just read your post on antidepressants. i agree with you about the risks, but in the case of eric --- i think it's a chance that i am willing to take.


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## eric (Jul 8, 1999)

First, I quite anti depressant over 15, maybe twenty years ago.Tal, why are you talking to be about anti depressant here and their side effects. I know about them. But that is also not what this thread is about. However, since you did mention it, why are they effective in IBS?Anti depressants for IBS are given at low doses to control pain.For some they are effective and usally perscribe short term, or long term depending on the person.This is something for the doctor and the person to decide and make the call.The Use of Antidepressant in Irritable Bowel Syndromeand Other Functional GI Disorders http://www.med.unc.edu/wrkunits/2depts/med...essants_ibs.htm Second, there are a ton of things a person can do for the serotonin issue, and taking 5ht may help, but that's not the problem either, its not the amount its the dysregulation of it. Taking 5ht supplement are likely to effect the brain but not the gut problem. see info below.How do you not mention the problem and leave it out? If its a problem in IBS, then it should be understood and dealth with as much as possible.Since it is very much connected in IBS to motility issues and the communication back and forth to the brain and back. Its a very important issues even to gut preability.If alter reactions to serotonin are causing the d and c and d/c, which they have a lot of evidence on, you don't think its worth talking about?and this is one of the way'"I know once I starting improving--the insecurity, anxiousness, depression by way of feeling powerless & helpless ag the IBS, they just slowly left."That is an example of dealing with serotonin and the altered stress responce seen in IBS and other issues in IBS, the anxiety/emotional link which is connected to that inflammatory issues you were talking about.Also, for Arnie and others, stress in IBS is define as a unconcious or concious perceived or real threat to the organism. So this is a kind of stress a person maynot be conciously aware of.Arnie, this may be a possiblity for you."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.html or *sensation* of incomplete evacuation -- the patient never feels like they evacuate their stool completely -- urgency, particularly in patients with diarrhea, and sometimes mucus in the stool. http://www.healthology.com/printer_friendl...&c=gi_ibswhatis "FYIPathophysiologyAltered 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.Ask The Expert.Image of a cadeusus. .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 "Thanks Flux, simon is not kel, Kel has sneakily sign on with quite a few other names its hard to tell sometimes who a person is talking to her or her as sommeone else she has sign on for a new identity.


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## Talissa (Apr 10, 2004)

Eric,What's up with this?CONCLUSIONS: The mucosal 5-HT concentrations in the colon showed an ascending cephalocaudal gradient in all study groups. Although the mucosal 5-HT concentrations were elevated in patients with constipation-predominant IBS as compared with those with diarrhea-predominant IBS and the control subjects, *further studies are necessary to determine whether the elevated mucosal 5-HT is a cause or a result of abnormal colonic motility. * http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=11351146 I'm confused. I could've read you wrong, but aren't you saying with CERTAINTY that abnormal motility IS DEFINITELY due to elevated serotonin levels????This is from 2001, has new info come out saying one way or the other?From my own experience, I'm pretty ctn that once the motility was normalized through diet & balancing the flora, my serotinin levels in the colon lowered, making me sunny again.But maybe a newer study has come out since then?"Tal"


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## Talissa (Apr 10, 2004)

This is kind of fun.I'm glad you steered me in this direction, himself.READ THIS:"Antidepressants in IBS: Are We Deluding Ourselves?Am J Gastroenterol. 2004 MayTalley NJ.The benefit of selective serotonin reuptake inhibitors (SSRIs) in the irritable bowel syndrome (IBS) has not been clear. In the latest randomized trial published this month in the Journal, paroxetine was superior to placebo in terms of improving well-being, but not abdominal pain or bloating. Based on the results of the most recent studies, both tricyclic antidepressants and SSRIs may improve patient satisfaction or quality-of-life without relieving most of the primary gastrointestinal symptoms. *This suggests that antidepressant therapy represents at best only a "band-aid" approach to management.* Optimizing the use of antidepressants in IBS is a challenge, and these issues are explored in this Editorial." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15128361


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## kel1059 (Feb 28, 2003)

once again, it is a chance that I am willing to take.


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## Talissa (Apr 10, 2004)

Adding On--So the quality of life improves because SSRI's have people floating through their life, but it doesn't seem to help the primary gastrointestinal problems....Do you ever advise people to take SSRI's Eric?I'm off now--back to the real world. But look forward to researching this further!!!


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## kel1059 (Feb 28, 2003)

he often hangs himself with his own posts. the Dr esther sternberg post of his is my personal favorite.i will be rolling that one out again shortly.


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## Talissa (Apr 10, 2004)

Kel,You're my humor therapy this am!!! Thanx!


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## kel1059 (Feb 28, 2003)

off the top of my head, the sternberg post is about how the HPA axis is assaulted by various factors -- toxins (which eric denies), bacterial endo and exo toxins, fungal toxins, viruses, (also stress).


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## eric (Jul 8, 1999)

First off, Kel, you have never been able to understand Dr Strenberg's work. She also left out the various factors, one of which is how the chronic stress responce triggers the HPA axis which then degranulates mast cells in the gut, which then release toxins onto the smooth muscle. This is part of the inflammatory issues in IBS. This is also consistent with Tal's orginal posts from DR Mayer and the inflammatory bowel disease and IBS, as well as many other IBS researchers around the world!Tal, that is an older 2001 post, more is known now.Why I have also said read this three times now.IBS: Improving Diagnosis, Serotonin Signaling, and Implications for Treatment CMEAuthors: Lucinda Harris, MD; Lin Chang, MD http://www.medscape.com/viewprogram/2750 You also have to look at the entire serotonin and IBS research.Serotonin is important in the big picture. SSRI have not been studied well in IBS.Tricyclic antidepressants have had more success.I do not tell people to take them or not, just post info, it is up to a doctor to prescribe them to an indivdual on an indivdual basis, with a patients consent. Some people have a bad time with them, while others do not. Its not up to me to judge any of it. ITs up to the doctor patient relationship.There was a preliminary study on a person with severe IBS for 16 years, where they pet scanned them, before treatment and noticed brain abnormalities.Then they adminstered anti d's and CBT and then pet scan the peson I think six months later. They got better and on the second pet scan the abnormalities of the brain were improved. Preliminary, but extremely interesting. I also do recommend learning about these systems, then you learn how to deal with anxiety and emotions and the effects they have on the symptoms and pain and that anti' d's should be used if needed, but that serotonin regulation can be dealth with for most people through stress and anxiety reductions that very much help IBS. This is very consistent with IBS research. Negative emotions, antisipatory anxiety, worry, threats, real or perceived, conciously and unconciously all trigger symptoms.Anti depressants relief anxiety and work on serotonin transmission and pain. Exactly what stress reduction techniques do. And emotions are very much connected to pain and even how bad pain can be to a person.You have said yourself, getting rid of the "I know once I starting improving--the insecurity, anxiousness, depression by way of feeling powerless & helpless ag the IBS, they just slowly left."That is in part why that happened and consistent as well with IBS research.Two important systems in IBS, the serotonin system and the HPA axis system, which are very much connected. The HPA axis system is also very much connected to fibro and CFIS, which overlaps frequently in IBS and vise versa.


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## eric (Jul 8, 1999)

PS, Kel, can you say anything construtive to this post and the information, or are you just here to critize and ###### and attack?


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## kel1059 (Feb 28, 2003)

> quote:First off, Kel, you have never been able to understand Dr Strenberg's work.


if you say so.


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## Talissa (Apr 10, 2004)

Eric,Couldn't resist popping back on real quick.********************Do you have any studies which PROVE that altered motility causes the low serotonin levels?You know, one that outdates the study from 2001?Because if you don't, I'll stand by my word that once you normalize motility through diet & balancing gut flora, the depression so often is absolved.(Exercise & a whole foods diet thereafter will help keep severe depression away.)To put it simply,Please answer this,Do you really believe that if the serotonin levels are lowered in the colon by drugs, that the motility will normalize???Don't need 28 pages.Just a simple yes or no & a study to back it up.**********************Another point--THIS was the article's conclusion from your post above: "The antidepressants, SSRIs, SNRIs, and TCAs *may* be effective in treating IBS, particularly in those patients with severe disease, * but further studies are needed* . Other neuropeptides and receptors are also being actively investigated, and certainly a number of pharmacologic agents are on the horizon."***********I would say that altered motility is a CONSEQUENCE of low serotonin.I'll further add that low serotonin in the colon is due to imbalnced gut flora is seriously derailing nutrient absorption & proper assimilation.THINK before you answer this time. I'm sure you are intelligent.You're just too quick to react w/o thinking things through.Talissa****************I also think all of this research to find a drug for fixing the problem artificially, while making a huge profit for the Rx companies & the MDs who will be able to just write a prescription out, getting to the next patient in under 10 minutes, is criminal.These drugs are poison & you can get better naturally.


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## Talissa (Apr 10, 2004)

Also pls read this again,Am J Gastroenterol. 2004 May; *Antidepressants in IBS: Are We Deluding Ourselves?* Talley NJ.The benefit of selective serotonin reuptake inhibitors (SSRIs) in the irritable bowel syndrome (IBS) has not been clear. In the latest randomized trial published this month in the Journal, paroxetine was superior to placebo in terms of improving well-being, but not abdominal pain or bloating. Based on the results of the most recent studies, *both tricyclic antidepressants and SSRIs may improve patient satisfaction or quality-of-life without relieving most of the primary gastrointestinal symptoms.* This suggests that antidepressant therapy represents at best only a "band-aid" approach to management. Optimizing the use of antidepressants in IBS is a challenge, and these issues are explored in this Editorial.PMID: 15128361 [PubMed] I think this review from THIS month may be most up-to-date and reliable.It was written for MAY. This is MAY.Please start thinking.Please start realizing you don't know everything.Neither do I.But when I post my OPINION, I let folks know it's an OPINION & not try to make it fact by posting long studies failing to prove what you say is anything, but your OPINION.Talissa**************This time I'm really done for today. I can hear the collective sigh


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## flux (Dec 13, 1998)

> quote: imbalnced gut flora is seriously derailing nutrient absorption & proper assimilation


But digestion and absorption is *normal* in IBS!


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## eric (Jul 8, 1999)

Tal, first do you know what 5ht 3 and 5ht 4 cell receptors do in the gut and how they work?"Do you have any studies which PROVE that altered motility causes the low serotonin levels?"This is backwards.Its the release of serotonin from specific cells that causes altered motility. It is also in part a signaler to the brain and pain. Serotonin is a very important brain gut mediator.They have also manipluted it and made people better. IS it the entire answer, that has not been totally established. It may also be that this problem leads to abnormalities of other systems.First, the above receptors control important parts of digestion. Serotonin is a very important neurotransmitter that intiates the peristaltic reflex (gut contractions).Ninety-five percent of all serotonin is localized in the GI tract where it plays a key role in the motor, sensory and secretory functions of the gut. There are increased cells that store it in IBS, one major thing I have been trying to point out to you in PI IBS.It is also not low serotonin levels, its the release of serotonin from those cells that intiate the peristaltic reflex, when to much is released from the cells, then you get d, when to little is released then you get c and alternating is just that.There are enough studies to implicate it in IBS. People with d have been found to release more after eating for one. I could post tons of them.MEDLINE Abstracts: Serotonin Signaling and Visceral Hypersensitivity in IBS http://www.medscape.com/viewarticle/462728 "Other neuropeptides and receptors are also being actively investigated"This is a fact, but needs to be put into perspective of the whole disorder, IBS is not completely figured out yet and why they call it research."Do you really believe that if the serotonin levels are lowered in the colon by drugs, that the motility will normalize???"They have already normalized motility in IBSers, by manpiluation of serotonin receptors. There is also evidence of it lowering pain in the brain in IBS via pet scans. However, this gets even more complex and I will not go there at the moment.Altered transit of food in the gut maybe WHY there is altered flora for one. Leaky gut also can cause malabsorbtion, in IBS there is no eveidence that digestion itself is different from normals. IBSers still absorb nutrients like normals. The exception to this would be coexising problems. Like fructose for one or lactose.Two lack of fiber can increase gut permeabiltiy and diet and stress and foods, meds (nasids) and many other factors can upset gut flora. Since a lot of IBSers have bad diets,, some women take nasids for PMS or other reasons and IBSers are under stressors, that needs to be seperated and figured out, what roles everything plays, some of which has been.again"I would say that altered motility is a CONSEQUENCE of low serotonin." Wrong, because its the other way around, serotonin helps starts digestion. I will also say go into pubmed and type in "leaky gut and IBS" or "intestinal permeability and IBS", then type in serotonin in IBS. See how much info there is on these things in the national library of medicine database."This is why I said read the above. This is a CME for doctors.IBS: Improving Diagnosis, Serotonin Signaling, and Implications for Treatment CMEAuthors: Lucinda Harris, MD; Lin Chang, MD http://www.medscape.com/viewprogram/2750 "IntroductionMany patients with irritable bowel syndrome (IBS) have walked into their physician's office and said, "The last doctor told me my symptoms were all in my head." Those physicians may have been right, but not in a way they anticipated.Over the past 50 years, evolving conceptual mechanisms have been proposed to explain the pathophysiology of IBS. These mechanisms have ranged from a purely psychological disorder to such physiologic conditions as a primary abnormality in gastrointestinal (GI) motility or visceral hypersensitivity. *However, recent scientific data have increasingly supported that a dysregulation in brain-gut interactions resulting in alterations in GI motility, secretion, and sensation is the principal pathophysiologic mechanism underlying IBS* .1 Brain-gut interactions are mediated largely by the autonomic nervous system, which is comprised of the parasympathetic (vagal and sacral parasympathetic), sympathetic, and enteric nervous systems (ENS). Many factors (both central and peripheral) may contribute to an altered brain-gut axis, including genetic predisposition, chronic stress, inflammation/infection, and environmental parameters.1 *These alterations may subsequently lead to disturbances in intestinal motility, visceral sensitivity, and mucosal immune response and permeability.* In IBS, these disturbances result in symptoms of abdominal pain or discomfort and altered bowel function, the defining characteristics of this disorder.2There are many neurotransmitters and hormones that mediate bidirectional brain-gut communication. *Serotonin (5-hydroxytryptamine [5-HT]) is one of the key mediators of gut motility, secretion, and sensation.* Most of the serotonin is localized in the GI tract and is found in enterochromaffin (EC) cells and enteric neurons.3 EC cells sense luminal factors such as food or mechanical distension in the gut, and release serotonin; 5-HT receptors on intrinsic primary afferent neurons (IPANs) as well as extrinsic spinal or vagal afferent neurons are activated. The ENS regulates secretion and peristalsis, whereas vagal and spinal afferents modulate nonpainful and painful sensations, respectively.4 There are at least 7 main classes of 5-HT receptors. Particularly important for lower gut function and regulation are the 5-HT1P, 5-HT3, and 5-HT4 receptors. These receptors have been the focus of research evaluating the pathophysiologic mechanisms of IBS as well as targets for the development of novel agents in the treatment of functional gastrointestinal disorders. There is also evidence to suggest that other older serotonergic agents -- that is, tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs) -- may modulate intestinal function as well.3 The roles of other neuropeptides and their receptors are also currently being explored as potential molecular targets for drug development.The development of more effective treatment for IBS is crucial because it is one of the most common disorders seen by gastroenterologists and primary-care physicians, but patients are often not satisfied with traditional therapies. In addition, proper diagnosis and treatment are particularly critical for a number of reasons. Studies have demonstrated the dramatic impact of this disorder on the quality of life of patients with IBS compared with the general population and with individuals with other chronic health conditions.5,6 In addition, patients with IBS utilize the healthcare system for both GI and non-GI complaints more than patients without IBS.7 The latter in turn impacts the productivity of patients with IBS such that their absenteeism from work or school has been found to be 3 times higher than that of patients without IBS.8 Not surprisingly, economic studies have demonstrated that this disorder is costly to the healthcare system and to the economic system as a whole, resulting in an annual associated cost of up to $30 billion.9,10The challenge for clinicians is to identify individuals with IBS despite the fact that no diagnostic biologic marker currently exists for this disorder, and to manage their symptoms despite the lack of effective treatment. Studies evaluating the utility of symptom-based criteria and medical tests in the diagnosis of IBS vs organic GI disorders have resulted in recent recommendations for a more cost-effective diagnostic approach.11 Although many patients may respond to reassurance, life-style changes, and traditional therapies, it is important for healthcare providers to familiarize themselves with advances in the pathophysiologic mechanisms of IBS that have subsequently led to the development of novel therapeutic agents, such as the serotonergic medications. In addition, these advances have inspired a new look at older medications that affect the serotonin receptors." http://www.medscape.com/viewarticle/463521 By the way, women have higher serotonin evels then men.and"The majority of patients with irritable bowel syndrome presenting to a gastroenterologist demonstrate affective dysregulation."""The ENS (gut brain) independently controls enteric reflexes through intrinsic primary afferent neurons, which monitor intraluminal conditions. This monitoring is accomplished through the use of enteroendocrine cells in the mucosa, the best known of which are the serotonin-containing enterochromaffin cells. This article describes the roles that serotonin, specific serotonin-receptor subtypes, and the serotonin reuptake transporter play in the ENS and in the communication between the ENS (gut brain) and central nervous system (brain)."MEDLINE Abstracts: Serotonin Signaling and Visceral Hypersensitivity in IBSPosted 10/23/2003 http://www.medscape.com/viewarticle/462728 Serotonin is majorally implicated in IBS.


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## kel1059 (Feb 28, 2003)

serotonin is an intermediate player in the whole mess, but it is the source of billions of $$$ for the drug companies.supressing symptoms is a good business strategy.


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## eric (Jul 8, 1999)

Kel, wow thats contructive for sure? You know this for a fact do you?The whole world of doctors and drug companies are all in a huge conspiracy out to get kel.So they post tons of medical information to the national library of medicine and include it in continuing medical education information to doctors and pass it all on to UCLA, Harvard, UNC, mayo, cleveland clinic, Johns Hospkins and everyone else.Go back to figuring out quantum mechanics and homeopathy, what you do best.But again its wrong. This is the combined research from around the world and from many sources other then drug company money. A lot of this research has also been funded by the National Institute of health and other organizations, not connected to drug companies.It is also basic science research over a broad spectrum of sciences from almost every country and peer reviewed for many many years now.You have no idea what your taking about.I am glad you understand this all so well and consider yourself such an expert to make those statements. It was not drug company money that lead to the discovery of serotonin and its role in gut function, it was a Doctor, the worlds leading expert on the enteric nervous sytem and a NIH grant.The Enteric Nervous System:A Second BrainMICHAEL D. GERSHONColumbia University Once dismissed as a simple collection of relay ganglia, the enteric nervous system is now recognized as a complex, integrative brain in its own right. Although we still are unable to relate complex behaviors such as gut motility and secretion to the activity of individual neurons, work in that area is proceeding briskly--and will lead to rapid advances in the management of functional bowel disease. http://www.hosppract.com/issues/1999/07/gershon.htm Kel, what kind of Dysbiosis do you have?Putrefaction Dysbiosis?Lack of fiber Dysbiosis?Fermentation Dysbiosis ?Diet Dysbiosis?


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## Talissa (Apr 10, 2004)

Now that my IBS is under control, I need to seriously work on my self control...Flux,As far as I know this is old school thinking:


> quote:But digestion and absorption is normal in IBS


This is what


> quote: Some symptoms of IBS are now understood to result from abnormal colonic fermentation subsequent to damaged gut flora by antibiotics or gastroenteritis. The excess production of hydrogen, along with a range of other compounds, is thought to impact colonic functioning.


I na ddition, you will notice that most every site for IBS encourages using digestive enzymes.Case in point: "Digestive enzymes taken 20 minutes before meals can help enhance digestion and normalize bowel function." http://www.healthandage.com/html/res/com/C...Syndromecc.html Maldigestion is defined as the incomplete breakdown (digestion)of foods and can lead to malabsorption, a term that refers to the disordered or incomplete uptake of nutrients from the intestinal tract.And to further muddy up the issue:" Gut associated lymphoid tissue (GALT) represents nearly 60% of the immune system, and can promote and induce gut inflammation. This is especially true in cases of maldigestion and duodenitis when undigested food constituents trigger inflammatory responses. [17]" http://www.findarticles.com/cf_dls/m0ISW/2...cle.jhtml?term= I can tell you from my own muscle wasting back in the old horrific days, I sure wasn't properly assimilating protein. And using digestive enzymes definitely allowed me to eat a wider variety of foods w/o reacting in painful "D".Anyways, if you have something, Flux, that's recent to support this view, I'd be very interested!


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## Talissa (Apr 10, 2004)

Er,


> quote:This is backwards.Its the release of serotonin from specific cells that causes altered motility.


This is the same as saying increased serotonin in the colon. This I can agree with, I did misread what you were saying. HOWEVER, it's my opinion that normalizing this, allowing the cells to transport the serotonin where it needs to go, can ONLY be accomplished by balancing gut flora & any submucosa inflammation, which is made worse if int'l permeability is altered. Thus, say I, you normalize gut flora, lowering inflammation, which normalizes serotonin levels in the colon, & you've just help normalize motility.Thus, motility can be normalized naturally. (In my experience & in my opinion.)_________________Back to this side effect, depression, of many IBS patients. Nothing to do w/ motility.I'll restate my belief that flora imbalances in the gut can trigger corresponding imbalances in the brain.In addition, regarding stress-- I'm also a believer of this statement:"If you're like most people with IBS, you probably find that your signs and symptoms are worse or more frequent during stressful events, such as a change in your daily routine or family arguments. *But while stress may aggravate symptoms, it doesn't cause them.*"Stress doesn't cause IBS symptoms, it aggravates them.That's from the Mayo Clinic, reprinted at CNN: http://www.cnn.com/HEALTH/library/DS/00106.html Doesn't mean I like the rest of the article, but I agree with that & much of the rest.Tal


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## Talissa (Apr 10, 2004)

Flux--Don't know why this didn't show up:John Hopkin's Gastroenterology & Hepatology site says:


> quote:Some symptoms of IBS are now understood to result from abnormal colonic fermentation subsequent to damaged gut flora by antibiotics or gastroenteritis. The excess production of hydrogen, along with a range of other compounds, is thought to impact colonic functioning.


 http://www.hopkins-gi.org/pages/latin/temp...12&pagenum=1872 I think I'm in too much of a rush!


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## eric (Jul 8, 1999)

well first I am not flux if your were addressing me?Second this has been known for a while.This is brand new in the IFFGD newletter on IBS"From the new IFFGD. 2004 *"There is no evidence that digestion is different in those with IBS compared to those without IBS. Although the exact cause is not known, there are factors that appear to aggravate symtoms or make people feel worse."* While dietary factors do not cause IBS, they may aggrvate symptoms in some persons. Increased intestinal muscle reactivity and/or heightened sensitvity in IBS can cause the bowel to over respond to stimuli. Even the act of eating itself, and not a particular food, ay aggravate symptoms." *Nonetheless certain foods are known to simulate gut reactions in general."* There is more from there news letter."Irritable Bowel Syndrome: An Overview By: Lin Chang, M.D., CNS: Center for Neurovisceral Sciences & Womenï¿½s Health; CURE: Digestive Diseases Research Center, Division of Digestive Diseases, UCLA School of Medicine Irritable bowel syndrome (IBS) is a chronic functional bowel disorder characterized by abdominal pain or discomfort and alterations in bowel habits. The clinical diagnosis of IBS is based on identifying symptom criteria with a ï¿½positive diagnosisï¿½ and excluding organic disease with minimal diagnostic evaluation. Although there are many expensive and sophisticated tests available for the evaluation of IBS symptoms, these are generally not needed for patients with typical symptoms and no features suggestive of organic diseases. This article provides a comprehensive overview of the prevalence, symptoms, diagnosis, and treatment options for IBS." http://www.aboutibs.org/Publications/currentParticipate.html They also know there is an altered gastro colonic responce in IBS, do you know what that means?The Dr Who worte that is also an expert on Fibro and IBSThe Association of Irritable Bowel Syndromeand Fibromyalgia http://www.med.unc.edu/medicine/fgidc/fibromyalgiaandibs.htm She is also the co director of a new center in CA.Co-Director of the UCLA/CURE Neuroenteric Disease Program,Director of the UCLA Motility UnitWhere did this come from there is no link to it. but"Some symptoms of IBS are now understood to result from abnormal colonic fermentation subsequent to damaged gut flora by antibiotics or gastroenteritis. The excess production of hydrogen, along with a range of other compounds, is thought to impact colonic functioning. "Some symptoms can happen from the weather so what?These things can trigger IBS.also"subsequent to damaged gut flora by antibiotics or gastroenteritis."Can antibiotics actually damage cells in the gut or make changes in other ways, besides altering gut flora?Enteric infection, why are people taking the anitbiotics in the first place? for a gut infection, already we have gone over Post infectious IBS." na ddition, you will notice that most every site for IBS encourages using digestive enzymes."They do? They maybe somewhat benefical, but depends on what were taking about? What kind of digestive enzymes? That does not say, perhaps lactase?alsoEnzyme Supplements Claims, Benefits: Digestive aids and/or substitutes for the enzymes you need but lack. Many are advertised from a "more is better" angle. Bottom Line: No clinical evidence supports the idea that swallowing, injecting, or otherwise consuming enzymes can benefit healthy people or prevent disease, let alone keep you young. http://wellnessletter.com/html/ds/dsEnzymeSupps.php One exception however is lactase enzyme."And to further muddy up the issue:" Gut associated lymphoid tissue (GALT) represents nearly 60% of the immune system, and can promote and induce gut inflammation. This is especially true in cases of maldigestion and duodenitis when undigested food constituents trigger inflammatory responses. [17]" http://www.findarticles.com/cf_dls/m0ISW/2...cle.jhtml?term=" You still have not gotten inflammation in IBS. This is MAJORALLY IMPORTANTThis is from a non conventional doctor not a researcher and he already believes IBS is leaky gut right from the start, so this information is completely biased.he also sells products http://www.quantumenergycenter.com/Add_HealthCarePros.aspx Show me a actual real study where IBSers are not absorbing nutrients and are different then controls?


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## Talissa (Apr 10, 2004)

Er, I was addressing Flux.Let me address the Wellness Letter first. That's published by UC Berkley. I have on pretty da** good authority one of that school's lgt contributors is a biggy in the pharmaceutical industry. I subscribe to it also, just to see what the other side is saying...._________________________Regarding the John Hopkin's site info, from their fair assessment's of IBS, I think it's fair to say they aren't tied to Rx companies.Your question:"Can antibiotics actually damage cells in the gut or make changes in other ways, besides altering gut flora?" in reference to John Hopkins info, I think with the new information about the immune response along the intestinal wall & how altered flora can cause permeability, which causes a histamine reaction, causing more problems in a vicious cycle--yes, I do feel this can change cells.Imbalanced gut flora is the catalyst.Luckily the cells of the intestinal wall renew every 3 days or so.____________________It is quite hysterical to me that IBS, a digestive disorder, a digestive problem, can be presented as a condition with normal digestion.I'm pretty sure that little tidbit will change in the future!Tal


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## not well (Mar 18, 2004)

tallisa you mentioned :some symptoms of ibs(or maybe chronic intestine pseudo obstruction in my case) are now understood to result from abnormal colonic fermation subsequent to damaged gut flora by antibiotics or gastroenterisis. the excess production of hydrogen along with a range of other compounds, is thought to impact colon fuctioning.could this be the cause of my sypmtoms like i mentioned above or could it be a case of faster peristalsis movements that explain why every time my meal goes through me?i'm thinking of trying digestive enyzmes after my morning bm(if complete) to see if i feel less bloated and full by late afternoon evening time.spasman, we seem to have the same sypmtoms in common along with meribaibs.talking bout the methadone i never tried it but you said you had two days relief on it meaning your bms were normal just like before you had ibs, aslo you tried the enyzmes?eric how do i contact you?i've looked up all the info on testing,and i do need to see someone, i have come to a conclusion that a camera pill endoscopy would help(i think this sees the digestion clearer with a picture every two seconds summit like that)aslo i want to rule out bacteria so an sibo would be usefullaslo a motility transit time test and,something to see if my anal sphincter nerves are damaged.there is a GI clinic in a place in north west london called stmark's hospital.i hope they can refer me straight away without the usual"you have to see your gp first because your not important enough and besides he'll only prescribe you the antispasmodics like he did before"so to the gastroenterologists, read my post above becuase i think, and i know my symptoms are serious to the extent of the grief they have casued me for the last ten years i'm only spending two to three hours on the net now and most of it is on the bbi usualy post in the early evening GMTif someone wants to PM me feel freeregards


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## Talissa (Apr 10, 2004)

not well,From what I've read of your incredibly disabling symptoms, my instinct is to say parasites. Was this ruled out by 3 stool analyses?Also, you may find this interesting:"This is called 'post-infective IBS'. The resulting IBS may be either diarrhoea-predominant or constipation-predominant IBS, which suggests that both chronic diarrhoea and chronic constipation may be bacterially derived. Because metronidazole and vancomycin markedly reduce diarrhoea and constipation-predominant IBS respectively during treatment and so it appears that these forms of IBS may be mediated by an ongoing, bowel flora infection rather than a persisting damage of gut nerves. After all, such antibiotics would scarcely have affect dead or dying nerves. Hence, currently, the most likely cause of IBS would appear to be a chronic infection of the luminal bacteria which live within the bowel. Nonetheless, progressively nerve damage can develop with such an infection, and this can be seen in some patients with severe constipation." http://www.cdd.com.au/html/expertise/diseaseinfo/ibs.html Again, currently, the most likely cause of IBS would appear to be a chronic infection of the luminal bacteria which live within the bowel.I think you've got severe dysbiosis, & just taking probiotics & digestive enzymes may not be enough.I'd try my "ParaGone", readily available in health stores, & is mainly for folks with constipation, or better but more expensive--try to get a thorough stool analysis done. You may need some stronger antibacterials---but pleeeease, if you do, counter them with probiotics, so the cycle doesn't continue.Other tips I've heard for "C"--drink buckets of water(Maxx) & grind up some flax seeds, a tbsp, & mix it w/ 8 oz water, drink each morning(..).Controversial opinion obviously, but I've gone this far, why stop now???







I REALLY want you to be able to change your screen name!Talissa


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## Talissa (Apr 10, 2004)

not well,Read this sad tale with a happy ending. Some of it -may- sound familiar. She was diagnosed IBS-C, and many, many stool samples failed to reveal D.fragilis and Blasto. hominis (including samples from great smokies diagnostic lab). http://www.ibstales.com/happy_tales Click on happy tales 2 under constipation.Damn bugs.


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## flux (Dec 13, 1998)

> quote:Some symptoms of IBS are now understood to result from abnormal colonic fermentation subsequent to damaged gut flora by antibiotics or gastroenteritis. The excess production of hydrogen, along with a range of other compounds, is thought to impact colonic functioning


I'm not sure where this "information" is coming from, but I will inquire about it. It's odd to see this kind of misinformation published at such a web site.


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## missC (Oct 16, 2002)

"One focus in IBS is on the neurotransmitter serotonin, do you know why?"Oh my GOD, Eric, is it hard work trying to be that patronizing? i say 'trying' - headsup, man, everybody knows you're not a doctor! do you just work p/t, cheffing away in yr cute lil hat, while yr girlfriend pays the bills and buys your weed, to have time to pretend to read and struggle to comprehend every medical journal going?normally i like a bit of aggro, but i'm gaining in sympathy with the folks who say, 'for god's sake, just IGNORE them!' 'cause any of us could read exactly what you do, if we didn't have anything better to do with our lives. And as far as comprehension goes, don't try that trick with me sonny - i can read too and i have the mediocre biochemistry bsc to prove it. personally i have plenty better things to do than hang around medline for kicks. just how empty must your life BE?


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## bonniei (Jan 25, 2001)

Flux, Talissa, I woinder if John Hopkins site posted by Talissa is referring to the King et al studyT.S. King, M. Elia and J.O. Hunter , Abnormal colonic fermentation in irritable bowel syndrome. Lancet 352 (1998), pp. 1187ï¿½1189. and this studyA. Koide, T. Yamaguchi, T. Odaka et al., Quantitative analysis of bowel gas using plain abdominal radiograph in patients with irritable bowel syndrome. Am J Gastroenterol 95 (2000) 1735ï¿½1411 .where gaseous distension of the colon has been observed


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## bonniei (Jan 25, 2001)

Also this "As has been previously reported, we found that bran significantly increased pain and bloating in IBS patients compared to placebo. It is tempting to speculate that the pain and bloating experienced by our IBS group is a result of rapid filling of the ascending colon, with a failure of the latter to respond with accelerated clearance"The American Journal of Gastroenterology Volume 97, Issue 9 , September 2002, Pages 2315-2320 doi:10.1016/S0002-9270(02)04342-3 Cite or link using doi Copyright ï¿½ 2002 Am. Coll. of Gastroenterology. Published by Elsevier Science Inc. Original contribution Abnormalities of GI transit in bloated irritable bowel syndrome: effect of bran on transit and symptoms John M. Hebden M.D., Elaine Blackshaw, Massimo D'Amato M.D., Alan C. Perkins Ph.D. and Robin C. Spiller M.D.,


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## bonniei (Jan 25, 2001)

And also I want to say Talissa, If it hasn't been mentioned already on the thread, that the serotonin solution is not antidepressants but Lotronex and Zelnorm as they work directly on the receptors in the gut while the antidepressanrs work on those in the brain


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## not well (Mar 18, 2004)

talissa my incredibly disabling are real and you would be shocked at how my life has been over the last ten years.if having to revovle your life every day around toilets like i do means NO SOCIAL LIFE, NO GOING OUT, NO RELASIONSHIPS NOT EVEN TELLING YOUR FRIENDS WHAT YOU HAVE.WHAT FRIENDS? so imagine the isolation that can lead to mental illnessthis place where i live is hostile and aggresive and theres no way i'm walking around telling everyone i have irritible foul syndrome(whatever you want to call it)how can you call it that? just a name made up by doctors years ago for mystery functional disorder of your gi tract that gives everyone an excuse to say it's all in the mindwhen the GI stuck a camera tube up my a** five years ago and found nothing wrong, the feeling i had was beyond despair but since coming to this board i hope to find information that might lead to a solution.i'm not an expert in what theother members know of but i do read the links frequentlyi don't own a computer so i have only a limtied amount of time in cybers cafesand then when i have to go i have to find a public toilet somewhere and it's not nice having a c*** away from home so being fair i'm only asking ppl for their advice becuase i don't yet know what i have. yes it could be bacteria overgorwth,flora imbalance or maybe somtehing elsebut why when the weather changes, so do my bms?there's something wrong with my gut and i intend to find out the link http://www.ibstales.com/happy_tales and the other storys on there i've read i can't relate to my symtoms, but thats good if they have been cured cause i thought no ones been 100% yetregards


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## not well (Mar 18, 2004)

and no you can't get 3 stool anaysis in the uk on the NHS


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## bonniei (Jan 25, 2001)

not well


> quote:now why does it feel like my anal sphincters not working correctly? maybe cause there is not enough stool in the rectum?maybe the nerves are damaged or dysfunctioned?(eric could tell me something about this cause he knows about the brain-gut thing) why can't it all come out at once?every time i clean there's still c*** on the paper. that means i can't do normal things or be around ppl everyone else cause i HAVE to be around toilets every day.this has ruined me i'm telling you.


It is because you are suffering from incomplete evacuation which is not a sign of IBS but pelvic floor dysfunction. Biofeedback and Kegels and Beyond Kegels can help. Your pelvic muscles have become weak by not using them. However IBS-C have a higher thresholld for defecation which means you will need a lot more stool before you sense it and feel the urge to defecate.


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## Talissa (Apr 10, 2004)

not well,I'm so incredibly touched & saddened by your "tale." And it is hard to stay mentally sound when everything is so wrong in your life.I really wish I could look into a crystal ball & know EXACTLY what you should do to get better.But I've no doubt, one day your life will be better, because you are so determined to find a way. Just try & focus on the good things, and keep the faith you'll find a way to even 90% better.


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## SpAsMaN* (May 11, 2002)

Talissa said:Case in point: "Digestive enzymes taken 20 minutes before meals can help enhance digestion and normalize bowel function." FALSE as a chiro!!! I have tried few times Creon25(enzyms tested in lab) before meals.It give me more gas and i was unable to continued.


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## Talissa (Apr 10, 2004)

Er & Flux, Is it so much of leap to think that the intestinal wall cells have trouble with nutrient uptake, when they have trouble with serotonin uptake?It just hasn't been studied, funded by lg Rx companies.Bonniei,Thanks for the info. But aren't Lotronex & Zelnorm catalysts for some people ending up dead or in the hospital?


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## bonniei (Jan 25, 2001)

Talissa,Only when wrongly prescribed by careless doctors. If Lotronex is prescribed to people who have C for example.


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## SpAsMaN* (May 11, 2002)

Eric,if your tiny friends 5 htp is a solution, why don't we just put some in our coffee and adjust the dose as needed???







Running down a dream(Tom Petty,best of)




























In fact,what mean running down a dream?


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## eric (Jul 8, 1999)

Not well, my email is on my websitewww.ibshealth.comI would be happy to help out.Be extremely careful of what information you gleam from this thread on infection and inflammation and bacteria.This is accurate however on it. And are some of the leading expert on IBS from around the world. http://www.iffgd.org/symposium2003brain-gut.html here is more.Post infectious IBS from one of the world authoirties on it, if not the top.Post Infectious Irritable Bowel Syndrome Robin C. Spiller, MDReader in Gastroenterology at the University Hospital, Nottingham, UKAn important subgroup of patients with Irritable Bowel Syndrome describe a previously entirely normal bowel habit with all their symptoms developing immediately after an acute bout of diarrhea and vomiting. This phenomenon has been recognized by clinicians for many years and was well described by Truelove and Chaudary who studied 130 patients with Irritable Bowel Syndrome, 34 of whom were described as having post-infective IBS. Most of the infections were bacillary dysentery but some were amoebic. Interestingly, they found there was an important interaction between psychological problems and infection. They found that a post-infectious origin and absence of anxiety, depression or neurotic features both predicted a good outcome. The commonest causes of gastroenteritis are viral, followed by Campylobacter, Salmonella and Shigella. Viral gastroenteritis typically heals rapidly with little residual injury, while the bacterial infections often produce ulceration and bleeding. They are generally associated with more prolonged illness and it is these infections which have been associated with post-infective Irritable Bowel Syndrome. The first prospective study was reported by McKendrick 1 who studied 38 individuals following a salmonella outbreak. He found that 11 out of the 38 met the Rome I criteria for IBS 6 months after the initial illness. Two further prospective studies of hospitalized patients from an infectious disease unit in Sheffield also confirmed this high incidence of post-infective IBS 2 3. Our own study of 386 cases of bacterial gastroenteritis obtained from a community survey showed a lower incidence of post infective IBS (7%) possibly reflecting a less severe illness, since only 1 in 10 of these patients were hospitalized However these were not trivial illnesses since the average duration of illness was 7 days with a third reporting bloody diarrhea and a median weight loss of 6kg. Interpreting this data requires knowledge of the normal incidence of new IBS, as was obtained in a large survey based on the British general practice database. This study of 584,308 patients found the incidence of new IBS per annum in non-infected patients to be 0.35%. However, in 300 patients who had a culture positive infectious gastroenteritis, the annual incidence was 4% giving a relative risk of 11.9% 95% CI (6.9-21) 4. Traveller's diarrhea is of course extremely common in Canadian citizens travelling to Mexico and Ilnyckyj prospectively surveyed this group. Nearly 50% developed travellers diarrhea and in this group the incidence of new IBS three months later was 17.5% compared with just 2.7% for those who did not get travellers diarrhea, a relative risk of 6.6(0.8-53) 5. Risk FactorsMost patients with bacterial gastroenteritis recover fully and only a small minority develop post-infective Irritable Bowel Syndrome. Female sex, hypochondriasis and adverse life events in the previous year all give an increased risk 6 7 with a relative risk of 3.4, 2.0 and 2.0 respectively. A much stronger risk factor is the duration of the initial illness, with a steadily increasing relative risk for each week of illness, reaching 11.4 for those with diarrhea lasting more than 21 days. Bacterial factors are likely to be important since we found around 1 in 10 of Campylobacter infected individuals developed post-infective IBS compared with just 1 out of 100 with Salmonella. It is likely therefore that the severity of tissue damage and ulceration is a major predictor.PathophysiologyDiarrheal illnesses are characterized by accelerated GI transit and increased gut sensitivity. This gradually returns to normal but at a variable rate. By three months most of those who are going to recover will have done so and thereafter the rate of recovery is much slower. As Gwee found colonic transit is accelerated in all infected individuals at 3 months, but those who meet the Rome I criteria for IBS have a faster transit than those who do not. Similarly rectal sensitivity is increased in those meeting Rome criteria, though again all those infected show a similar trend.Although conventional histological examination of mucosal biopsies in IBS shows no abnormality, when detailed quantification is undertaken changes are noted. We performed serial rectal biopsies in individuals recovering from Campylobacter gastroenteritis at 2, 6, 12 and 52 weeks. We note initial increases in both inflammatory cells and enteroendocrine cells, which mostly returned towards normal, but remained abnormal in a few markedly symptomatic individuals 8. Similar abnormalities were noted in patients attending the outpatients with a history of post-infectious Irritable Bowel Syndrome. There is a good correlation between the inflammatory cells and the enteroendocrine cells suggesting that cytokines might drive the enteroendocrine cell hyperplasia. The main content of the enteroendocrine cells is 5HT, an agent that stimulates peristalsis and intestinal secretion causing diarrhea in normal subjects. Drugs, which inhibit the action of 5HT such as Alosetron, are likely to show benefit in this group thought they have not been specifically studied.Other authors have noted increased enteroendocrine cells in unselected irritable bowel patients 9 but this needs confirmation. More important than increase in numbers may be the increase in release of 5HT. Several pilot studies 10 including some reported at DDW this year suggested that there was an exaggerated release of 5HT following a meal particularly in those who got meal related symptoms 11.ManagementIt is important that patients should understand the important roles of anxiety, stress, and diet and persisting low-grade inflammation in this condition. Providing the Rome criteria are met and general physical examination is normal then the probability of another diagnosis is low. However, infections can unmask other disease particularly coeliac disease, inflammatory bowel disease such as Crohn's and tropical sprue together with hypolactasia. Such patients should therefore undergo a minimum set of screening tests including endomysial antibodies, hemoglobin, CRP, ESR, albumin and stool culture. In the absence of alarm features such as weight loss, fever, rectal bleeding and nocturnal diarrhea, only 5% of all these tests will be abnormal. Since microscopic colitis has also been reported to develop acutely after an infectious illness it is important to do a colonic biopsy and, if suspicions are high, also a duodenal biopsy to exclude coeliac disease. Lactose intolerance developing after a viral gastroenteritis is well recognized by pediatrician. This occurs because lactase, the enzyme responsible for digesting lactose, is expressed fully only in the mature enterocyte at the tip of the villus. Since viral gastroenteritis generally specifically damages the villi, lactose levels remain low for some months. A low lactose diet is therefore worth trying, particularly in those racial groups with an a priori greater risk of lactose intolerance such as Asians, Africans and Chinese. A low lactose diet is only relevant if the subjects take more than 240 mls of milk. Even those with documented lactose intolerance can tolerate amounts smaller than this when spread throughout the day. Since psychological factors are so important, it is necessary to make some formal assessment of this. Where anxiety and depression levels are high they should be treated on their own merits since it is unlikely the patient will recover without addressing these issues. There are no specific diets recommended for post infective IBS but reduction of poorly absorbed carbohydrates, particularly wheat, potatoes together with other items such as citrus fruits have been reported to be beneficial in patients with diarrhoea-predominant IBS and should be tried 12. Loperamide and codeine are well tried treatments for diarrhea predominant IBS regardless of origin and are likely to be effective though at the risk of some side-effects, including sedation and nausea in the case of codeine and abdominal pain in the case of Loperamide. Alosetron has also been reported to be effective in diarrhea predominate IBS but again has not been specially tried in post infective patients. PrognosisWhatever treatments are offered, the clinician can afford to be reassuring since the prognosis is relatively good. Chaudary's original study found 77% had recovered within 2 years 13 while Harvey also found 82% of those with acute illness at onset had recovered by 5 years 14. In our own follow-up 5 to 6 years following the initial survey we found that 11 out of 17 post infective Irritable Bowel Syndrome patients had actually recovered though we also noted that a past history of psychiatric disorder predicted a poor outcome.Key PointsPost infective Irritable Bowel Syndrome accounts for around 1 in 10 of all cases of IBS. Females with prolonged illnesses and previous adverse life events are more likely to develop post-infective IBS. Low-grade inflammatory changes may persist in some of these patients. Overall prognosis is good with 2 out of 3 recovering over a period of 3-5 years. http://www.med.unc.edu/wrkunits/2depts/med..._infectious.htm This is not all IBS patients either.MissC, perhaps if you took the time to read the thread, you would have seen why I said that. " i have the mediocre biochemistry bsc to prove it."Well then, where is serotonin stored and what function does it have in gut functioniong and communication with the brain, why don't you help?Perhaps if you read the articles and looked at the sources, your anger would subside?I have studied IBS for three years, almost ten hours everyday, because I have it, not to prove anything to you my dear. You have no idea who I am or what I do in my life, thank you. *This is a fact, no bacteria or virus has been found to cause IBS to date!!!!!!!* This was an old discussion on Pimentals work from 2000.Bacteria May Be Root Of Bowel Disorder California researchers say they may have found the cause -- and possibly the cure -- for irritable bowel syndrome, the most common gastroenterological complaint in the United States. Physician Martin Pimentel, writing in Wednesday's edition of the American Journal of Gastroenterology, says that excess bacteria in the small intestine are found in nearly four of every five IBS sufferers. Treatment with antibiotics improves the condition in most patients, he said. "This is the first time there's an identifiable target in IBS," Pimentel said. "All treatments to date have been controlling the symptoms or covering up the symptoms." But if there's a link between bacteria and IBS, commented physician Michael Levitt of the Veterans Administration Medical Centre in Minneapolis, it's odd that no one has noticed it before. "Enormous numbers of people with irritable bowel syndrome have been treated with antibiotics, for one reason or another," he said. But he said there have been no reports of large numbers of such patients saying the IBS had gotten better. Levitt added that test used by Pimentel was only applied to people with IBS. "They never tried it on healthy people," he said. If healthy people also had excess bacteria, but no IBS, it would tell against the theory, he said. The study, he said, is "interesting" but not conclusive. Pimentel, a gastroenterologist at Cedars-Sinai Medical Center in Los Angeles, said about 20 per cent of Americans complain of irritable bowel syndrome, whose symptoms include bloating, nausea, diarrhea and constipation. Many of the symptoms, he said, are like those that would be caused by a bacterial "overgrowth" in the small intestine, where food is digested. To examine the idea, Pimentel said he and colleagues studied 202 IBS patients, using a test that shows the presence of bacteria. Nearly four in five of the IBS patients -- 78 percent -- showed signs of bacterial overgrowth, Pimentel said. Patients with the overgrowth were treated with antibiotics. Of the 48 who returned for follow-up testing, more than half showed no sign of excess bacteria, he said. The complete or partial elimination of the bacterial overgrowth, he said, also resulted in a complete or partial reduction of IBS symptoms. "We found that 50 per cent of subjects got rid of it altogether," Pimentel said, and the others had reduced symptoms. In fact, he said, the numbers could be even better, because more than two-thirds of the treated patients didn't return for a follow-up test -- possibly a sign that their disease had been cleared up. The study, he admitted, is not conclusive, because it doesn't meet the "gold standard" for scientific research -- it's not a randomized, double-blind trial. Instead randomly assigning patients to receive treatment or placebo -- without patients or researchers knowing which is which -- Pimentel and his colleagues studied patients who were referred from local clinics and doctors; and all of the patients who showed signs of excess bacteria were treated. Levitt said he'd be reluctant to place too much reliance on the current study, just because it doesn't meet those standards. "Anything that's uncontrolled in this field is highly speculative," he said. Pimentel said a randomized, double-blind study is now under way, and more than 60 of the planned 100 patients have been recruited. Results of that study should be available within months, he said. -- http://www.applesforhealth.com/bactbowel2.html More from Dr Spiller. Post infectious IBS refers to cases of IBS, which can be shown to have arisen after a distinct case of gastroenteritis caused by an infection. This lecture gave a comprehensive review of the literature on the subject, including a large amount of data from R. Spiller and his group.Studies have looked at patients with IBS, and shown a large proportion with an acute stage of onset, suggesting an infectious cause:Many IBS studies have been performed on patients seeking medical treatment and within Gastrointestinal units. More recent studies have used databases of patients within the community as a whole, and have suggested that an acute episode of gastritis can lead to IBS. Several studies have focused on communities and the incidence of post-infectious IBS seen within patients visiting their doctors. A study published in the British Medical Journal by Rodriguez and Ruigï¿½mez showed that in the year following an episode of gastritis, patients were 10 times more likely to have IBS then patients in the general population. This study used patients identified using the British General Practice Research Database, containing data on patients recorded by general practitioners (Rodriguez and Ruigï¿½mez 1999, BMJ 318: pp. 565-566), allowing this study to contain 584 308 subjects in the general cohort and 318 in the gastroenteritis cohort.Other studies with smaller patient groups have shown similar results:28 (7%) of the patients went on to develop functional IBS. However, a further 78 of the cases developed altered bowel habits, with similar symptoms to that of the new IBS cases, lacking the pain. As a result they did not meet the Rome criteria for IBS (Neal et al, BMJ 1997, 314(7083): pp. 779-782).Other studies have looked at specific infections; McKendrik (McKendrik and Read, J Infect. 1994; 29(1)







p. 1-3) presented a study of patients with salmonella infections, 31% of the patients acquired IBS post infection. Gwee et al (Gwee et al, Lancet. 1996; 347(8995): pp. 150-3) looked at cases of gastroenteritis, and found that 29% of patients suffered from new IBS after resolution of the infection. One of the major problems with this type of study results from the fact that people often have a bout of vomiting or stomach distress due to food. Consequently few people specifically remember having a bacterial infection that rapidly resolves. This would suggest that the number of cases of IBS resulting from a bacterial infection is actually higher than that shown in studies.Several groups have compared differing factors with an increased risk of IBS. One new method involves using specific cells (e.g. Hep2 cells) and reacting them with bacteria. If you get an increased elongation of the cell, then the bacterial strain used can be considered to be capable of inducing IBS. This induced elongation gives a much higher risk of IBS than other factors, such as gender or life stress.Prospective studies have shown that there are elevated CD8+ lymphocytes in patients with post-infectious IBS after 1 year. This coincides with an increased permeability during a bacterial infection, and an increase in inflammatory cells in IBS patients, suggesting that PI-IBS patients suffer from a lack of down regulation of the inflammatory response. Indeed, some studies have shown that some IBS patients are deficient in TGFb and IL-10.Following infections with campylobacter enteritidis there is an increase in entero-endocrine cells. In the case of IBS patients this increase does not return to normal, remaining up to 10 fold higher then that seen in normal controls.Long-term prognosis for PI-IBS patients:This study, and others like it, suggests that 2/3 of PI-IBS patients recover within 6 years. The majority of recovering patients showed no anxiety, while the persistent sufferers did, suggesting that anxiety impairs recovery from PI-IBS.The take home message from this lecture what that there appears to be significant evidence leading to the role of post-infectious IBS, although host factors play a large role in susceptibility. However, PI-IBS has a reasonably high chance of recovery over the long term, if there are no other contributing factors (such as anxiety). http://wwwhost.gu.se/cgf/fouschema.html#Robin graphs are included *"An initial response to an infection in the gastrointestinal tract can involve the neurotransmitter, serotonin, which acts as a messenger (mediator) to cells involved with the immune response. Immune cells -- mostly in the blood, but also in the lymphatic system -- enter the infected area and remove the invader. Additionally, the body adaptively removes the infection (e.g., via vomiting or diarrhea -- normal beneficial responses that help the body expel an infecting organism). Persistence of the underlying inflammatory response may lead to post-infectious disorders of function. A variety of neuroimmune responses can lead to intestinal over-responsiveness (sensitization) and other clinical effects. * *"The predictors of post-infectious IBS include increased life events and psychological distress, female sex, and longer duration of diarrhea episode. In response to bacterial infection, there is an increase in certain gut (enterochromaffin) secretory cells (5HT producing) and inflammatory cells (cytokine producing) leading to prolongation of pain and diarrheal symptoms, and this may be aggravated by the presence of psychological stressors. "* http://www.iffgd.org/symposium2001.html Mnay people get gut infections, but not all get IBS, the perdictors are gut damage and people under stress at the time of infection then get IBS. a reason for this is the same sytem used too fight infection, fights stress, after the infection resolves chronic stress reactivates the cells.


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## bonniei (Jan 25, 2001)

> quote:Is it so much of leap to think that the intestinal wall cells have trouble with nutrient uptake, when they have trouble with serotonin uptake?


Talissa it is not as simple as seotonin uptake in IBS with Lotronex and Zelmorm. This is how they workZelnorm is a 5HT4 agonist. That means it binds to 5HT4 receptors and initiates events like peristalsisLotronex is a 5HT3 anatagonist which essentially means it blocks the effect of 5HT3 agonists or blocks the 5HT3 receptors from releasing serotonin and slows down motility"Mucosal stimulation (eg, after a meal) stimulates the enterochromaffin cells to release serotonin, which then activates 5HT3 receptors in the submucosal plexus as well as in the myenteric plexus and longitudinal muscle (figure 2).[23] Blocking 5HT3 receptors is of clinical relevance in chronic diarrhoea as this leads to reduced contractility, slows colonic transit, and increases fluid absorption.[31] "I don't know if you are referring to SSRI's.


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## SpAsMaN* (May 11, 2002)

Not well,i never been on Methadone sadly.







For sure it make good works on IBS-D.Methadone is very tough to get,even a week trial.Often,you have to try(if you can)others pain medecine before Methadone can be prescribe to you.


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## bonniei (Jan 25, 2001)

Also I found this about flora and colonic function.The American Journal of Gastroenterology Volume 95, Issue 9 , September 2000, Page 2533 doi:10.1016/S0002-9270(00)01573-2 Cite or link using doi Copyright ï¿½ 2000 Am. Coll. of Gastroenterology. Published by Elsevier Science Inc. Abstract *Treatment of abnormal gut flora improves symptoms in patients with irritable bowel syndrome *Steven M. Faber Elizabeth City, N.C., USA Available online 14 September 2000. Purpose: IBS is a common GI disorder without effective medical therapy. Studies suggest that IBS pts. have an imbalance of their Gut Flora and show improvement in symptoms of abdominal pain, gas and bloating after supplementation with exogenous flora. In addition to flora we used pancreatic enzymes, antibiotics and antifungals when indicated based on stool analysis results.Methods: We performed a retrospective analysis of 26 pts. with IBS by ROME criteria who completed a stool analysis and health questionnaire before and 4ï¿½6 weeks after treatment. 20F, 6M mean age 57 y/o were treated with a combination of lactobacillus acidophilus NCFM, bifidobacterium infantis, pancreatic enzymes, antibiotics and/or antifungals. Stool Analysis: Below normal levels of stool lactobacillus 21/26 (80%) and bifidobacterium 13/26 (50%) were noted. Major pathogenic organisms identified included Klebsiella Pneumonia 16/26 (62%) Citrobacter Freundi 15/26 (19%)Pseudominas Aeuroginosa 3/26 (12%)Klebsiella Oxytoca 3/26 (12%). Significant yeast organisms abnormally present in stool includedCandida Albicans 10/26 (38%) and Candida Glabrata 4/26 (15%). Abnormal yeast growth was found in 18/26 (69%) of pts.. Undigested meat fibers were found in 9/26 (35%) pts.Results: Patients noted improvement in bloating 19/26 (73%), reduction in passage of excess gas 14/26 (54%), decreased abdominal pain/cramps 16/26 (62%), decrease in diarrhea 16/26 (62%), improvement in constipation 14/26 (54%), decrease in alternating diarrhea and constipation 15/26 (58%), decrease in the sensation of incomplete evacuation 7/26 (27%).Conclusions: Some IBS pts. have an imbalanced gut flora including a deficiency of beneficial organisms such as Lactobacillus and Bifidobacterium. This imbalance may also predispose to an overgrowth of pathogenic bacteria and yeast Inadequate protein digestion may also produce classical IBS symptomatology. Supplementation with beneficial indigenous microflora, treating culture positive growth of pathogenic bacteria/yeast and using pancreatic enzymes in our study showed a significant improvement in the most common IBS symptoms.------*I find this interesting. "Significant yeast organisms abnormally present in stool includedCandida Albicans 10/26 (38%) and Candida Glabrata 4/26 (15%). Abnormal yeast growth was found in 18/26 (69%) of pts.." Oh no! I am going to be attacked for this!







Edit in bold*


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## SpAsMaN* (May 11, 2002)

Good Bonnei.Very rare research.Not stunning but interesting.I just hope that eventually somethingpositive for us will be available from this kind of results.


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## Talissa (Apr 10, 2004)

Spas,If you've got inflammation along the intestinal wall, taking the enzymes before a meal is the wrong way to take them.I always take them during the meal, of for dinner,enzymes with HC1, after the meal. This is because I seem to have the inflammation.If you read what I said, it was a "case in point", an ex to show that most sites on IBS say using digestive enzymes is helpful fo the condition. ________________Bonniei,You're funny too! You tend to see things from both sides, don't you? The first time I posted about "fermentation & altered colonic function in IBS" & met Flux(BAM! like an aberration he appeared), someone mentioned he "proved" there is no candida in the GI tract....you may indeed seen an attack with pictures even.Anyways, regarding this statement of mine--"Is it so much of leap to think that the intestinal wall cells have trouble with nutrient uptake, when they have trouble with serotonin uptake?",I wasn't referring to any drugs.I was referring to IBSr's not properly breaking down & absorbing nutrients. If the intestinal cells have trouble with serotonin uptake in IBS, doesn't it follow that the cells for nutrient uptake could be malfunctioning as well?I know I just got back from dinner out. I had a nice eggplant parmesan, with salad, followed by a beer.Even 3 years ago, this would've done me in. With the eggplant, even last month(eggplant's high in fructose).But between the mixed strain probiotics, digestive enzymes & the DA-IBS probiotics which mfr enzymes in the body--no rumbling, no pain, & no need to go to the loo.I don't want to prove I'm smart(sometimes I'm astounded at what an airhead I can be







. I want to prove others can be better too. Since I'm PI-IBS D, maybe my way to recovery could just apply to them.Maybe PI IBS D isn't really IBS at all.Thanks for the study on gut flora. I was starting to drown there! Good night, T-____________Edited for typos which were probably due to consumption of beer & not wanting to type ANYMORE


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## meribaibs (Jan 18, 2004)

Notwell needs a referral to a top-notch GI in the UK. If anyone knows one, please help her out. As for the bad flora theory, I'm in, but nobody wants me. I sent two e-mail inquiries to the GSDL in Canada, and I got zip. What gives? How do I go about contacting them? Is Dr. Dalhman's office the only route?


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## bonniei (Jan 25, 2001)

> quote:If the intestinal cells have trouble with serotonin uptake in IBS, doesn't it follow that the cells for nutrient uptake could be malfunctioning as well


I haven't read that there is a problem of serotonin uptake in IBS. But I am sure eric or flux will comment on it if I am wrong. Serotonin reuptake is usually spoken about when talking about SSRI's.


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## Talissa (Apr 10, 2004)

not well,Here's more to think on regarding IBS:For both syndromes, histologic and functional alterations of the mucosal barrier have been recently reported.[11*, 12, 24, 25] Small intestinal permeability is abnormal in a wide variety of conditions affecting the small intestine, including celiac disease, Crohn disease, and intestinal infections.[18**] Interestingly, gut permeability assessed by the lactulose/mannitol ratio is significantly elevated in PI-IBS patients.[15] This functional alteration of the intestinal barrier function may be a cause or consequence of inflammation...Despite the common assumption that chronic gut mucosal inflammation is associated with sensory-motor dysfunction of the gastrointestinal tract in inflammatory as well as functional intestinal disorders, the relationship between chronic inflammation and the generation of gastrointestinal symptoms remains unclear. The development of IBS-like symptoms in some patients with quiescent ulcerative colitis was suggested as an indication of the role of inflammation on altered sensory and motor function.[8] http://www.medscape.com/viewarticle/457728_4 And here's more info:"On a more chronic basis, it has been suggested that some probiotics can help maintain remission in the inflammatory conditions, ulcerative colitis and pouchitis. They have also been suggested to repress enzymes responsible for genotoxin formation. Moreover, studies have suggested that probiotics are as effective as anti-spasmodic drugs in the alleviation of irritable bowel syndrome. The approach of modulating the gut flora for improved health has much relevance for the management of those with acute and chronic gut disorders. "On probiotics:Br J Nutr. 2002 "Mechanisms of effect are likely to include the excretion of acids (lactate, acetate), competition for nutrients and gut receptor sites, immunomodulation and the formation of specific antimicrobial agents. As such, persons susceptible to diarrhoeal infections may benefit greatly from probiotic intake. On a more chronic basis, it has been suggested that some probiotics can help maintain remission in the inflammatory conditions, ulcerative colitis and pouchitis. They have also been suggested to repress enzymes responsible for genotoxin formation. Moreover, studies have suggested that probiotics are as effective as anti-spasmodic drugs in the alleviation of irritable bowel syndrome. The approach of modulating the gut flora for improved health has much relevance for the management of those with acute and chronic gut disorders. " http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12215180 Just more to think about in this very mysterious & complex condition...


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## Talissa (Apr 10, 2004)

Er


> quote:This is a fact, no bacteria or virus has been found to cause IBS to date!!!!!!!


Really?Medline:


> quote:A history of acute gastroenteritis caused by a variety of bacterial infections as well as parasitic infections was found to increase the risk of the development of persistent IBS symptoms.


 http://www.medscape.com/viewarticle/457728_2 ________________It sure did for me! But if I'd had balanced gut flora to begin with , the bacterial infection (Giardia) would have gone away in three days on it own, like it does in healthy people.And if the unknowledgeable about gut flora MD had had me taking probiotics to counteract the Flagyl, maybe I'd never had gone into having persistent IBS symptoms(IBS?). That's what my doc told me I had.I've got company for the weekend, so see you guys on Monday! Have a good weekend.


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## SpAsMaN* (May 11, 2002)

Eric,is it what you're trying to say? There are also those who believe that chronic physical pain is really the end result of accumulated, unaddressed, unhealed emotional pain that has found its expression via the wounding of the body as vehicle for this transport. Amongst the pain variables, sometimes there's direct damage to, and compression of the nerves themselves, and sometimes disturbances within the body cause nerve signals to remain active although they aren't directly damaged themselves. Injury, trauma, disease, degenerative processes, inflammatory processes, biochemical imbalances, neurological injury and dysfunction, mechanical imbalances are all broad-based categories of conditions that can keep pain signals firing. Sometimes nerve cells that were once involved in a pain-producing situation but no longer so, remain ultra-sensitive and continue to send pain signals when normally, none would be sent. A growing body of research suggests that chronic pain is not just a symptom of an abnormality, but is the abnormality itself. And so, when one portion of the nervous system breaks down and causes ongoing pain, other parts of the nervous system are affected as well.


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## SpAsMaN* (May 11, 2002)

IBS and flora link: http://www.dollingers.com/colon.html


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## kel1059 (Feb 28, 2003)

> quote: Not well, my email is on my websitewww.ibshealth.comI would be happy to help out.Be extremely careful of what information you 'gleam' from this thread on infection and inflammation and bacteria.This is 'accurate however on it'. And are some of the 'leading expert' on IBS from around the world.


If I didn't know better i'd swear i'd be talking to a street junkie.


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## flux (Dec 13, 1998)

> quote: Is it so much of leap to think that the intestinal wall cells have trouble with nutrient uptake


But they do *not* have this problem.


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## missC (Oct 16, 2002)

"Well then, where is serotonin stored and what function does it have in gut functioniong and communication with the brain, why don't you help?"but why would i need to when you already have all the answers luvvie? you ain't telling me that that's not a rhetorical question, the answer to which you are eagerly waiting to spring upon us?i thought you were cured, E? so you read ten hrs a day to help us out? awwwwwwwww. i take it you really don't have a job then. does yr girlf do all the housework as well? or maybe the tapes you sell us guys cover the bills?you know, it's not yr reading that's irritating - i'm glad somebody does it, cause i'm sure as hell not going to, having a job and a life - although links instead of C & P would still be lovely. it is, in fact, the anxious patronage and showing off. if yr erudition was for erudition's sake you wouldn't need to go on (and on and ON) about it like you do, giving people attitude from a great height of learning (!) instead of producing concise and helpful suggestions in yr own words.ah, Eric. STILL gonna do that reading. it's looming up like a cloud on the horizon.


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## eric (Jul 8, 1999)

Miss C, I have a computer business and three Jobs and am getting married in two months. We have over three hundred websites, so I am online quite a bit. Not that I really need to tell you any of this, I don't even know you or you me.My life is not only my business, but my girlfriend and I are very happy and I have a super tight relationship with my family and friends,if you really want to know. My girlfriend also has IBS and knows I am helping people here and very much likes that about me that I care, regardless of the frustration certin members give me. My nephew also has IBS and my stepdad. And a couple of my other friends.What I have ever done to you? "so you read ten hrs a day to help us out?"I still very much believe in good will personally, especially towards fellow IBSers.I am online quite a bit with my computer business and I read a lot to help out and yes that very much is the reason. I really do care and don't consider this some kind of game like a few do, I understand all to well people suffering with IBS and how much this disorder sucks and how badly people need help and accurate information.You don't know how many things I have turned down for money, because people have contacted me to sell bogus treatments or MLM level marketing to IBSers. I will not do that to any IBSer. I am not here to scam one soul, period.And no I don't work with the Tapes anymore, because people were so nasty about it here over the years and attacked HT and my work with Mike as his webmaster, like yours and Kels comments here, to get at me personally, he did not deserve that nor did I, we have helped hundreds and hundreds of people. Hypnotherapy is the most effective treatment statistically to date. IT is a researched treatment for over 15 years now.That is a fact at this time. His product is exceptional for IBS, that is why I worked on his sites. Not only have I helped hundreds of people with HT of which its hard enough to explain why someone would use HT for IBS, I have helped thousands and thousands of people with IBS through education, both here on other bb's and through local support groups I have started. People have contacted me to use those support groups as models around the country. If you would have read what I posted on this thread, this was never about money. This is about people who need help with IBS, like I did when I first started here. Its to bad you don't help out. Just complain and say you don't have time, well I have made time.I Have also told you why I post the info and not in my own words, but right from the experts articles. So there is no confusion about the info. I have permission from the AGA and many other sources to post the info, so I do. Read it or don't your choice. Above we can see what happens when people put it in their own words or cut only certain parts of a site out for discussion or thier arguement, or post any old site off the net, on a lot of posts here. I will also tell you, you build a IBS website and answer hundreds of emails and make lots of phone calls and spend lots of time staying up on the most current IBS research and spend time helping here and see if you can afford it, without being rich. I have spent a lot of money helping IBSers, you have absolutely no idea what so ever over the last four years. But this is not about money. People who really know me and there are a lot on this bb, know that about me.And even through all this, while I help, I have people get extremely rude and nasty to me. Call me names, say I am only in this for money, say the experts information is bogus ect. ect..Not well, please email me and I will help you out with doctors and sources in the UK. I am very concerned about you. I know of excellent resources in the UK, where you can get real help.


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## Talissa (Apr 10, 2004)

not well-Parasites are imp to rule out:"In diagnosing IBS, a physician should first rule out other diseases that share similar symptoms, such as ulcerative colitis, colon cancer, diverticulosis, *parasites* , and dysentery and other infectious illnesses, says Schuster. Once those conditions have been excluded, a brief checklist called the Rome Criteria for IBS is used to diagnose the condition." http://www.jhu.edu/~jhumag/0497web/gastro1.html


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## Talissa (Apr 10, 2004)

Best Pract Res Clin Gastroenterol. 2004 AprPubMed(This is what I've been saying, as I've learned from studying nutritional science & natural medicine, now finally I've got it MAINSTREAM!!)







"Irritable bowel syndrome."Verdu EF, Collins SM.Intestinal Research Programme, McMaster University, Hamilton, Ont., Canada.The intestinal microbiota interacts with several aspects of gastrointestinal function that may affect the expression or progression of disease....Normal gut physiology is molded by the interaction between the intestinal microbiota and the host's gastrointestinal tissues, including motility, absorption and secretion, and intestinal permeability. ... *Early studies in axenic mice demonstrated gross morphological abnormalities and gut motor dysfunction related to the absence of a normal microflora, raising the possibility that shifts in commensal bacterial populations could play a role in the development of altered motility states including functional disorders of the gut. * ...This chapter concentrates on the experimental evidence for a role of intestinal microbiota and the potential therapeutic value of probiotics in functional diseases such as irritable bowel syndrome. http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15123072 This is big.I think it deserves it's own new thread, but I've not time right now!!!!


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## Talissa (Apr 10, 2004)

Flux,I can pretty much prove that the problem IBS folks have with serotonin transport out of the gut is AN EXAMPLE of nutrient uptake problems in IBS.Will be my "thesis", no time now, but it's coming!Bet ya can't wait...


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## missC (Oct 16, 2002)

you do three jobs and run a business in the four hours or so you have left over from reading? blooming heck. how? what time is there left over for things like personal hygiene and shopping?Eric, have a nice LIFE! and wedding, the lot. we're never going to agree about most things, so (I hope) i'll leave it at that.


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## SpAsMaN* (May 11, 2002)

Don't be more irritated Eric but "...say the experts information is bogus ect..."














It just that i don't really understand the researchs in your post.And have no solution to it.


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## eric (Jul 8, 1999)

"I can pretty much prove that the problem IBS folks have with serotonin transport out of the gut is AN EXAMPLE of nutrient uptake problems in IBS."Now that is going to be interesting.also"A history of acute gastroenteritis caused by a variety of bacterial infections as well as parasitic infections was found to increase the risk of the development of persistent IBS symptoms. "This is well known and its PI IBS, but you have not made the speration between PI IBS and IBS and also that not just bacteria cause it, there has to be other things going on, stress for one at the time of infection. Not everyone with an infection comes down with IBS!! If that were the case almost everyone on the planet would have IBS. What have I been saying here, Mast cells infection the hpa axis and stress!!Mast cells are inflammed in some IBSers, chronic stressors can reactivate the inflammation after the inflammation has resolved!You have not fully grasped this in regards to infection and IBS. Your not fully reading what their saying. Also, there is no way on earth you will understand IBS just from the persceptive of gut functioning or leaky gut. The communication between the ENS (gut brain) and the Central nervous system (brain) is not only crucial in understanding IBS, its a fact they both work together, even in fighting infection. The brain and the immune system continuously signal each other!! *The hypothalamo-pituitary-adrenal (HPA) axis maintains a homeostatic response to stress and infection!* Tal, this information you posted above left out the rest of the VERY important information."For both syndromes, histologic and functional alterations of the mucosal barrier have been recently reported.11*, 12, 24, 25 Small intestinal permeability is abnormal in a wide variety of conditions affecting the small intestine, including celiac disease, Crohn disease, and intestinal infections.18** Interestingly, gut permeability assessed by the lactulose/mannitol ratio is significantly elevated in PI-IBS patients.15 This functional alteration of the intestinal barrier function may be a cause or consequence of inflammation...Despite the common assumption that chronic gut mucosal inflammation is associated with sensory-motor dysfunction of the gastrointestinal tract in inflammatory as well as functional intestinal disorders, the relationship between chronic inflammation and the generation of gastrointestinal symptoms remains unclear. The development of IBS-like symptoms in some patients with quiescent ulcerative colitis was suggested as an indication of the role of inflammation on altered sensory and motor function.8"from the rest of the article."For both syndromes, histologic and functional alterations of the mucosal barrier have been recently reported.11*, 12, 24, 25 Small intestinal permeability is abnormal in a wide variety of conditions affecting the small intestine, including celiac disease, Crohn disease, and intestinal infections.18** Interestingly, gut permeability assessed by the lactulose/mannitol ratio is significantly elevated in PI-IBS patients.15 This functional alteration of the intestinal barrier function may be a cause or consequence of inflammation, and a direct link between increased intestinal permeability and the exaggerated immune activation in IBD still needs to be confirmed. In addition to a causative role of peripheral factors, gut permeability changes in animal models have also been reported in response to various stressors. For example, in a rat model of chronic stress, an increase in intestinal epithelial permeability, associated with an increase in mucosal neutrophils and mast cells, has been demonstrated.34** In this model, the combination of stress-induced increases in intestinal permeability, allowing easier access of antigens to gut-associated macrophages and dendritic cells, together with stress-induced changes in HPA axis responsiveness and cytokine profiles, resulted in the development of colitis, without any additional chemical or immunologic manipulations. Rats with a history of aversive early life events were more susceptible to these stress-induced changes in gut permeability,35* possibly related to early programming of the HPA axis.31*"and the next paragraphChanges in Luminal FloraA change in intestinal microflora has been implicated, in association with genetic factors, as a putative mechanism responsible for the initiation and persistence of inflammation in IBD. Indeed, it has been suggested that the failure to maintain immunologic tolerance toward the indigenous microflora leads to a disease-associated dysregulation of the gut-associated immune system. Direct and indirect evidence of altered flora of the large and small intestine has been reported in IBS patients. For example, Balsari et al.36 observed a decrease in coliforms, lactobacilli, and, to some extent, bifidobacteria in a small group of IBS patients. More recently, preliminary evidence of an alteration of bacterial concentration in colonic biopsy specimens from IBS patients has been reported.37 Indirect evidence for bacterial overgrowth of the small intestine (in the form of altered hydrogen breath test results) has been reported in patients with IBS, and a recent randomized controlled trial found evidence that antibiotic treatment was beneficial for IBS symptoms of bloating and discomfort.38 Based on the concept of altered interactions between the colonic flora and the gut-associated immune system, probiotics have been proposed as an alternative strategy for the treatment of several gastrointestinal diseases, including IBD39 and more recently IBS.40, 41 However, the reported results are conflicting, and only a small number of double-blind controlled clinical trials support a beneficial health effect in IBD or IBS.42 The epithelium has recently been recognized as playing an important role in innate immune responses in response to intestinal microorganisms.43, 44 It expresses a variety of receptors (Toll-like receptor) involved in the recognition of a spectrum of microbial products. This recognition capability may enable an appropriate cytokine and chemokine secretion in response to changes in luminal flora.and the next paragraphs"Influence of Sustained Psychosocial Stressors on Mucosal Immune System ActivationEven though stress has been less recognized as a factor in the natural history of IBD, considerable evidence supports a prominent role for it in the pathophysiology and clinical presentation of both IBD and IBS symptoms.45 Patients with IBS seem to have a greater reactivity to stress than do control subjects or IBD patients. Yet, sustained psychologic stressors have been associated with the onset and exacerbation of symptoms in both IBS and IBD.46-48 The development of persistent IBS symptoms after acute gastroenteritis has been associated with major life events around the time of infection.14 Similarly, for IBD, a wide range of clinical studies indicates a strong link between sustained psychosocial stressors and IBD activity.49 Levels of long-term perceived stress have been shown to correlate with changes in mucosal appearance and relapse in ulcerative colitis.50* Further evidence of an influence of stress on inflammatory processes comes from animal studies showing a modulation of the immune function at different levels, including immune cell distribution, cytokine profiles, or susceptibility to infection in naï¿½ve or colitic animals.51 In view of the established concept of an altered immune response in IBD patients, and the suspected low-grade inflammation in some patients meeting the symptom criteria for IBS, it is reasonable to consider a bidirectional model of brain-gut interactions as an important determinant of gut-associated immune activation in both disorders.Chronic Inflammation and Alteration of Sensory-Motor Functions of the Gastrointestinal TractDespite the common assumption that chronic gut mucosal inflammation is associated with sensory-motor dysfunction of the gastrointestinal tract in inflammatory as well as functional intestinal disorders, the relationship between chronic inflammation and the generation of gastrointestinal symptoms remains unclear. The development of IBS-like symptoms in some patients with quiescent ulcerative colitis was suggested as an indication of the role of inflammation on altered sensory and motor function.8 The concept of long-lasting postinflammatory changes in gut motility is supported by the observation of altered anorectal and colonic motility in patients in remission from ulcerative colitis and Crohn disease.52 However, chronic abdominal pain and visceral hypersensitivity-classic features in patients with IBS-do not appear to be a hallmark of ulcerative colitis or Crohn disease.53 One may speculate that various patient populations with different degrees of intestinal inflammation (patients with IBD and PI-IBS, and possibly small subsets of those with IBS) do not necessarily experience pain and discomfort from these mucosal changes. Whereas the effects of the immune activation are likely to affect enteric nervous system circuits and smooth muscle function, altering intestinal compliance and reflex activity and producing such symptoms as diarrhea and urgency, the effects on visceral perception are less predictable. An important variable in symptom generation is the differences in the ability of the brain and its endogenous pain inhibitory pathways to counteract the changes in peripheral viscerosensory pathways. http://www.medscape.com/viewarticle/457728_2 alsoResearchers identify molecular alterations in patients with irritable bowel syndromeNew research demonstrates abnormal serotonin signaling in IBSBALTIMORE, Md. ï¿½ Novel research shows that alterations in serotonin signaling in the gastrointestinal (GI) tract are present in patients with Irritable Bowel Syndrome (IBS). These data shed light on the alterations in gut motility, secretion, sensation, as well as the clinical manifestations of IBS, which include abdominal discomfort, pain, bloating, constipation and/or diarrhea. The study findings were presented today by two lead investigators from the University of Vermont, Peter Moses, M.D., Associate Professor of Medicine and Director of Clinical Research in the Digestive Diseases, and Gary Mawe, Ph.D., Professor of Anatomy and Neurobiology, in an oral presentation during the plenary session at the 68th Annual Scientific Meeting of the American College of Gastroenterology in Baltimore. "Serotonin is a critical signaling molecule necessary for normal gut function ï¿½ when released, it causes gut motility and secretion, and triggers signals to the brain and spinal cord," said Moses. "Our finding that key elements of serotonin signaling are changed in IBS lends credibility to the notion that IBS is not simply a psychological or social disorder as was once thought, but instead due to altered gut biochemistry and interactions between the gut and the brain." Serotonin (5-HT) is a naturally occurring neurotransmitter and signaling molecule. Ninety-five percent of all serotonin is localized in the GI tract where it plays a key role in the motor, sensory and secretory functions of the gut. For some time, scientists have suspected that alterations in serotonin may contribute to abnormal conditions in the GI tract. "Now we have a perspective on molecular changes in the intestines of individuals with IBS that we did not have before," said Mawe. "We identified a significant decrease in the serotonin transporter in cells that form the inner lining of the bowel ï¿½ the same serotonin transporter that is located in cells in the brain. In the gut, this transporter acts as a sponge to remove serotonin once it is released, and therefore stops its actions. Because the transporter is diminished in IBS, serotonin stays around longer, and this can lead to changes in motility, secretion and sensitivity." The study examined tissue obtained from 43 healthy controls and 32 patients with IBS and 22 patients with inflammatory bowel disease (IBD). IBS patients were defined strictly using ROME II criteria. Each biopsy was evaluated by five parameters: immunohistochemical staining, histological assessment, serotonin content, serotonin release and the measurement of mRNA encoding. The study also examined the molecular components of serotonin signaling, including the serotonin re-uptake system. Specifically, the investigators measured serotonin content, the endocrine cell number, serotonin release and presence of serotonin transporters (SERT). Serotonin transporters are regulatory molecules that control the activity of serotonin within nerve endings in the GI tract to coordinate motility, visceral sensitivity and intestinal secretion. In patients with IBS, the study found a significant decrease in serotonin content and significantly higher endocrine cell (EC) populations in patients with IBS compared to controls, while the release of serotonin from EC cells was not significantly different. In terms of the way the body inactivates serotonin signaling, or the serotonin re-uptake system, SERT mRNA and SERT immunoreactivity were markedly reduced. This reduction led to a decrease in the capacity to remove serotonin from intracellular space once it was released, thus increasing serotonin availability. http://www.eurekalert.org/pub_releases/200...v-rim100803.php last but not least.From the Rome sitediscomfort and pain are a must for an IBS diangoses!!!!Irritable Bowel Syndrome: How far do you go in the Workup? *"But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it.* " *With regard to IBS, the gut-related effects of microscopic inflammation may be only one component of a dysfunctional brain-gut system.* In addition, and often in response to stress, there may be a failure to activate descending pain inhibitory systems that enable the clinical experience of pain and other symptoms that typify this disorder (25). In one prospective study of post-infectious IBS, *it was found that those who retained their symptoms 3-months after an enteric infection had not only increased mucosal cellularity, but also had increased psychosocial distress at the time of the infection.* *Furthermore, lowered visceral sensation thresholds and increased motility were present after the infection regardless of whether or not the patients retained their symptoms * (26). *Therefore, the microscopic inflammation and its physiological effects on motility and sensation contribute to, but are not always sufficient for the clinical expression of IBS pain.* At least for post-infectious IBS this provides some evidence that psychological distress alters brain pain regulatory pathways to amplify incoming visceral signals leading to the full clinical expression of this syndrome. http://www.romecriteria.org/reading1.html


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## bonniei (Jan 25, 2001)

Hi Talissa, Your study http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15123072 shows that colnic functiuon is affected by flora only in mice and not in humans.


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## flux (Dec 13, 1998)

> quote:Will be my "thesis", no time now, but it's coming!Bet ya can't wait...


No, because it is just not so.


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## Talissa (Apr 10, 2004)

Bonniei,Why do you think they do these tests on mice?Think about it.IBS is ALL about imbalanced gut flora, the cause & the direction of how to fix. This study proves it.There will be more to come.______________Flux,Forget the thesis, y'all don't seem to be bright enough to get it anyways. But think about the 6 amino acids that are synthesized into serotonin within the EC cells(mast cells) along the brush border of the intestinal wall . Where do you think nutrients go, if they aren't digested by pathogens first? Epithelial cells within the brush border. The nutrients have trouble getting transported when there is mucosa inflammation in that border(along the wall). That's the over-simplified, short answer that I don't have time to care whether you buy or not.But that is another truth that will be revealed in mainstream. It's a fact. And here is a non-mainstream source that spells out poor nutrient uptake in IBS: http://articles.findarticles.com/p/article...une/ai_75178726 It's 5 pages w/ references.Mainstream will soon catch up to the researchers at the Townsend letter.The GI's in Canada already know this, but their research isn't funded solely by Rx companies:" * Normal gut physiology is molded by the interaction between the intestinal microbiota and the host's gastrointestinal tissues, including motility, absorption and secretion, and intestinal permeability. * "_____________________I'm am so amazed that you guys would dig your heels in, not wanting to admit you may be wrong, when this information will one day help millions of IBSr's get well.It's mind-blowing. And kind of sad.


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## bonniei (Jan 25, 2001)

Talissa, in your opinion, what would serotonin uptake accomplish?


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## not well (Mar 18, 2004)

ok i'll give my reply,firstly bonnie you said, "incomplete evacuation is a pelvic floor dysfunction and not in ibs"could be but a good number of ibs sufferers have similar problems with bowel movements"however ibs c sufferers have a higher threshold for defecation which means you will need a lot more stool before you sense it and feel the urge to defecate"true cause i sometimes feel like when there isint enough in there i cant get it outbut the only time i get the urge is when my mind gives the signal. i feel like my sphincter muscle cant work on its own.if the sphincter nerves are partly controled by the enteric nervous system then there could be a link with other symptoms of ibs toonow just to clear this up talis NCREDIBLY" SARCASTIC WITH ME like you think imm an idiot or something else.you don't know me and you don't know the state of mind i am inyou wanna think i'm an idiot then PM me and tell me what you think im only telling ppl how i feel about this whole mess im in and believe me your in no position to think i'm a fool but telissa i want to ask you something,what were your INCREDIBLY horrible sypmtoms before you improved on the probiotics?and talissa do tell us please of your harrowing "TALE" now wont you#don't get me wrong i still think gut flora imbabalnce could be a cause for thisand i'll make sure the first test i want to have done is the SIBO before all the othershere's a link for you talilssa :www.bowelcontrol.org.uk/causes/htmlread about anal sphincter damage please and tell me what you think if it could be the bacteria that keeps stressing it regards eric i will e-mail you in a couple of dayshang in there meribaibs we're gonna get rid of this once and for all


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## not well (Mar 18, 2004)

ok i'll give my reply,firstly bonnie you said, "incomplete evacuation is a pelvic floor dysfunction and not in ibs"could be but a good number of ibs sufferers have similar problems with bowel movements"however ibs c sufferers have a higher threshold for defecation which means you will need a lot more stool before you sense it and feel the urge to defecate"true cause i sometimes feel like when there isint enough in there i cant get it outbut the only time i get the urge is when my mind gives the signal. i feel like my sphincter muscle cant work on its own.if the sphincter nerves are partly controled by the enteric nervous system then there could be a link with other symptoms of ibs toonow just to clear this up talissa do not get INCREDIBLY SARCASTIC WITH MElike you think imm an idiot or something else.you don't know me and you don't know the state of mind i am inyou wanna think i'm an idiot then PM me and tell me what you think im only telling ppl how i feel about this whole mess im in and believe me your in no position to think i'm a fool but telissa i want to ask you something,what were your INCREDIBLY horrible sypmtoms before you improved on the probiotics?and talissa do tell us please of your harrowing "TALE" now wont youdon't get me wrong i still think gut flora imbabalnce could be a cause for thisand i'll make sure the first test i want to have done is the SIBO before all the othershere's a link for you talilssa :www.bowelcontrol.org.uk/causes/htmlread about anal sphincter damage please and tell me what you think if it could be the bacteria that keeps stressing it regards


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## SpAsMaN* (May 11, 2002)

Talissa:What is the solution for IBS in your last link?There is the first paragraphefining Caustive FactorsThis article will attempt to examine the causes, consequences, and clinically proven remedies that help to reestablish gut health and enhance gut repair routines. With the help of new Quantum Medicine[TM] test protocols and computerized regulation thermography, we have discovered that a high percentage of IBS sufferers have duodenitis, dysbiosis, stagnant lymph flow and drainage in the deep lymph channels of the gut, silent/hidden dental foci, and dysregulation of the extracellular matrix caused by xenobiotic toxicity.







What is the "new Quantum Medecine"?I have bad mouth flora too but i will eventually get rid of it.


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## SpAsMaN* (May 11, 2002)

Good wedding Eric.I hope everybody will


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## bonniei (Jan 25, 2001)

not well, You are right that many ibs'ers could be having pelvic floor problems.Secondly my mind gives the signal to go only every 3 gays when enough stool has accumulated in thr rectum to be able to sense it. if there is no urge i just don't try to go as it could lead to straining which needs to be avoided. How often do you get the urge? If your nerves were damaged you would never get the urge i think


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## flux (Dec 13, 1998)

> quote: The nutrients have trouble getting transported when there is mucosa inflammation in that border(along the wall


This does *not* happen in IBS. Nutrient absorption is normal. Period.


> quote: http://articles.findarticles.com/p/article...une/ai_75178726


A joke?


> quote: Mainstream will soon catch up to the researchers at the Townsend letter


Researchers?


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## Arnie W (Oct 22, 2003)

not wellIt is not up to me to be a spokesperson for other members of the board, but you have completely over-reacted and misinterpreted what was said to you. Maybe I'm one of those people without a life, but I took a good half hour out of my day to go over the preceding posts to check what was said that offended you. All I could see was the said person offering you advice and empathising , yes, repeat, empathising, with you.I think you have misconstrued what was said, esp, I imagine, the "tale" in inverted commas. I don't think for one moment that she was implying that you were telling a tale or a tall story.That's the problem with the internet. It is so easy to read too much into what is written and to take from it something that was not intended. I've been caught out myself that way. Take what I say with a grain of salt, but most of us have some idea of what it's like to be in your shoes because we ourselves have various afflictions which make life uncomfortable. I myself have bared my soul on this board with the most personal things I would NEVER share with anyone else. No one is discounting what you are going through.Hoping that this board will help you, and all of us, in finding a solution.


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## Talissa (Apr 10, 2004)

not well,I am really really sorry you took what I said as talking down to you. I'm genuinely wanting to see you get better, I genuinely want your life to change.Maybe when I put the JH post about needing to rule out parasites before an IBS diagnosis is made, maybe I should explained it better.While I had over a year of IBS hell, long story & I've got company, it was incredibly difficult, but I had different symptoms overall than you.From what I've learned about parasitic infections, that's what I think you have, & you asked for an opinion. They are tricky to detect & mimic IBS symptoms.It's just my opinion, or another good possibility is pelvic floor dysfuntion, like Bonniei said.Again, I'm sorry if I caused you more stress & if I could take it back I would.Talissa


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## Talissa (Apr 10, 2004)

Bonniei,Serotonin, mfr'd primarily from Tryptophan, has many functions when its mfr & transport to the brain are homeostatic--including regulation of food intake(via motility), good sleep, and mood stability.Aside--Did you know that Questran is one of hundreds of drugs that was first tested on mice before humans? Apparently their internal systems are remarkably similar to ours. So are canines. I'm glad they do this to mice & not dogs though!!!


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## Talissa (Apr 10, 2004)

Flux,It's hard for nurtients to be absorbed from cells that are literally flattened(microscopically speaking) by the changes in the brush border with inflammation. They can't, for ex, split dissacharides into mono's for transport/absorption when they are damaged. This is well documented in IBD inflammation & now we know IBS also involves inflammation & in severe cases, inc'd permeability, which makes it even harder due to histamine response.Along with this final stage of digestion b4 absorption getting derailed by inflammation, we also have fewer enzymes being produced in the pancreas, & with rapid peristalsis, nutrients go too quickly thru the tract to be properly ushered into intestinal celll walls. Because of dysbiosis, we also have more pathogens competing for nutrients than do "healthy people".Obviously, not all nutrients fail to be assimilated, but IBS is classic poor nutrient uptake:___________________________________From an interview with Dale Guyer, M.D"Another area of challenge for the patient revolves around the irritable bowel symptoms, poor digestion, gas and bloating particularly after eating, and general overall poor nutrient absorption. What are some of the things you have noted seem to be primary contributors to such problems, and what are the things in your experience that seem to be most helpful? Dr. Guyer: Indeed I think the digestive - and for that matter the detoxification system, are often the crux or limiting pieces that get in the way of significant healing, and of course when someone does not digest and absorb effectively their cellular nutrient profiles are going to be inherently deficient....Also, most patients have alterations of the intestinal ecology and will need supplementation of probiotic bacteria, and sometimes initially at least many patients will need a broad array of different types of probiotics, and so often times initially for the first several weeks I will have patients take 3 or 4 different brands which different spectrums of biologically active probiotic bacteria. Also of course, there will often tend to be yeast overgrowth especially in those who have ever been on any kind of antibiotic therapy, and to help in that sense it is often beneficial to do a comprehensive digestive stool analysis (Great Smokey Diagnostic Laboratory performs such analyses). http://www.immunesupport.com/library/showa...e/1/T/CFIDS_FM/ This was an MD, who's done her research!P.S. What's a major cause of abdominal region pain, gas & bloating? incompletely digested food moving into the colon...


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## bonniei (Jan 25, 2001)

Talissa, Well there is a difference between serotonin in the brain and serotonin in the gut.i have come across serotonin in the gut inducing peristalsis and thus you would think that excess serotonin in the gut would cause diarrhea.Which is why lotronex blocks the release of serotonin in the gut and helps diarrhea. And you would think that people with D have a problem with serotonin reuptake leading to excess serotonin and D. However here is something counterintuitive which suggests reuptake is a problem withh IBS-C only so serotonin reuptake would help only IBS-C."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" So I am trying to make sense of this and I was hoping that you would havve more info. Also, are you saying serotonin in the brain could affect motility? Because if there is reuptake it goes to the brain.As for the mice, better that they be guinea pigs than me. yes they get a lot of clues about the human digestive system from those of mice. But until it is tested out in humans you can't say for sure it is going to happen in humans


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## Talissa (Apr 10, 2004)

not well,Just wanted to clarify that I took paragone to counteract any pathogenic bacterial overgrowth as a result of taking the antibacterial Flagyl without probiotics, I wasn't fighting parasites, that I know of--PG is for both.I'm on a learning curve here with communicating on this bb & I'm realizing how imp it is to be very very clear in what you're saying & how it may be interpreted!Wishing all the best,Talissa


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## Talissa (Apr 10, 2004)

Bonniei,I think you should ask Eric!! As far as I know, surprisingly 90% of the serotonin in the body is normally in the mast cells of the intestines--it's an abnormally higher % in IBS-D & highest in IBS-C.And as far as I know, it's the serotonin in the gut that is one of the factors in motility regulation.It is a bigger problem for those with IBS-C, and I've even read somewhere that IBS-C patients have higher levels of anxiousness because of this.The other q's are good, & I don't fully get that either. I'm sure after the honeymoon, we'll find out. (hopefully it'll be in English







T-


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## Talissa (Apr 10, 2004)

B-Just did a quick search, & I think this may clear it up(3rd para)?"Drugs known as 5HT3 receptor antagonists inhibit the action of serotonin in the gut. Alosetron (Lotronex), the first 5HT3 receptor antagonist developed for IBS, had a rocky start. FDA-approved in 2000, Lotronex relieved symptoms for many women with diarrhea-predominant IBS. (The drug doesnï¿½t work in men.) Constipation was the most common side effect. Several months later, reports of severe complications of constipation that resulted in 44 hospitalizations and 5 deaths prompted the manufacturer to withdraw the drug from the market. These complications included intestinal blockages, extreme inflammation and distention of the large intestine, and compromised blood flow to the colon (ischemic colitis).It was a tremendous disappointment for the many women who benefited from Lotronex. Lobbying by patients and doctors eventually brought this drug back to market in 2002, but only under a tightly controlled prescribing program (for more information, go to www.lotronex.com). A 5HT3 antagonist (cilansetron) is now under study. Preliminary data suggest that this drug offers benefits to both men and women with IBS. _The 5HT4 agonists have the opposite effect of 5HT3 antagonists._ Like Lotronex, the 5HT4 agonist tegaserod (Zelnorm) greatly improves symptoms, but this time for women with constipation-predominant IBS. It, too, is effective only in women. Tegaserod speeds up movement of bowel contents through the colon and reduces sensitivity to intestinal nerve stimulation. As youï¿½d expect, diarrhea is the most common side effect." http://www.hmiworld.org/current/around_ibs.html


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## bonniei (Jan 25, 2001)

Thanks talissa i already know about the 5HT agonists and antagonists. i had already posted this info previously on the thread. like they say lotronex inhibits the action of serotonin and like i said it blocks the release of serotonin. So reducing serotonin in the gut or increasing the uptake into the brain prevents D. But they also say in IBS C they seem to want less serotonin in the gut(you would think if Zelnorm acts in the opposite way to lotronex then you want more serotonin) or more serotonin uptake from the gut in order not to desensitize the receptors in the gut. This seems counterintuitive when you consider the way lotonex acts and consider that Zelnorm acts in the opposite manner.I hope the more knowledgeable members like flux or eric comment on it, if they can.


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## Talissa (Apr 10, 2004)

BI signed off on that & thought, duh, she knows this!! lol It's been a long day.Here's something that WILL help clear it up: "The watery diarrhea is probably attributable to the potentiation of serotonergic signaling in SERT -/- mice, whereas the transient constipation may be caused by episodes of enhanced 5-HT release leading to 5-HT receptor desensitization." http://www.ncbi.nlm.nih.gov/entrez/query.f...8&dopt=Abstract And you're couldn't be more right--regarding serotonin & drugs to treat the problems, Flux & Eric are more knowledgeable. Hands down. This is why I said you should ask Eric.But I'm glad I stayed up later than planned so I could try & "help" you. (We're going to Saba for the day tomorrow & need to get up at about 5 am.)It's been educational.


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## bonniei (Jan 25, 2001)

Thanks talissa. The last article you posted might give me a leadHave fun tomorrow. We will miss your posts on this thread


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## bonniei (Jan 25, 2001)

eric do you see the contradiction in these two quotes below and how do you explain it?""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" " (This above quote is from one of your articles)and"whereas selective serotonin reuptake inhibitors (SSRIs) such as sertraline (Zoloft), * 50 to 150 mg/d, may be more useful in patients with a tendency for constipation."Rakel: Conn's Current Therapy 2004, 56th ed., Copyright ï¿½ 2004 Elsevier Also ,do you see a contradiction in the two quotes below and how do you explain it?"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" and my statement" Zelnorm has the opposite effect of Lotronex and is conducive to more serotonin being there in the gut"


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## bonniei (Jan 25, 2001)

flux could you please address my above post to eric , TIA


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## flux (Dec 13, 1998)

> quote:It's hard for nurtients to be absorbed from cells that are literally flattened


This has *nothing* to do with IBS.


> quote:IBS is classic poor nutrient uptake:


*Nutrient digestion and absorption are both normal in IBS.*


> quote:I'm on a learning curve here


This curve?


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## eric (Jul 8, 1999)

First off, its NOT the mast cells that store the majority of serotonin in the gut, it is the serotonin-containing entero-endocrine cells (EC).although mast cells do release some serotonin, an importantt chemical mast cells release is histimine.How the new drugs work"Serotonin and IBSFrom the Winter 2000 issue of ParticipateHow do the new serotonergically active drugs currently being developed for the treatment of irritable bowel syndrome (IBS) differ from the selective serotonin reuptake inhibitor (SSRI) class of drugs [e.g., fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft)]? The SSRIs have been specifically developed as antidepressant drugs. Serotonin is found in both the brain and the gut, but it is now widely understood that 95% of the serotonin in the body resides in the gut.There are different types of serotonin that are called receptor subtypes, identified as "5-HT" followed by a number. The serotonin found in the gut consists mainly of 5-HT3 and 5-HT4 subtypes. Most of the serotonin found in the brain is of the 5-HT1 and 5-HT2 subtypes; antidepressants tend to work on these subtypes. Nevertheless, they also have some effect on the 5-HT3 and 5-HT4 receptors located mainly in the gut. This effect may explain, in part, why antidepressants can help relieve some IBS symptoms. The newer serotonergically active drugs for treatment of IBS target the serotonin found in the gut. They are not antidepressants and have their major effect on the 5-HT receptors in the gut, not the brain.The newer drugs for treatment of IBS, such as alosetron and tegaserod (which is not yet available for use), target 5-HT3 and 5-HT4 respectively. These drugs are "gut specific" and tend to have minimal effect on brain serotonin. They are not antidepressants. However, these new gut specific drugs and antidepressants will, no doubt, be used in a complementary manner to treat IBS.5-HT, Receptors, and IBS -- From the Fall 1999 issue of ParticipateSerotonin (5-hydroxytryptamine, or 5-HT) is a chemical neurotransmitter (a chemical in the nervous system that helps transmit messages along the nervous system). It is found in three main areas of the body: the intestinal wall, blood vessels, and the central nervous system.Chemical neurotransmitters produce their effects as a consequence of interactions with appropriate receptors. In cell biology, a receptor is a structure on the surface of a cell or inside a cell that selectively receives and binds a specific substance -- such as a hormone or a neurotransmitter.Serotonin (5-HT) interacts with an array of receptors. Approximately 14 types of serotonin receptors have been identified in humans. These receptor sites are numbered. (For example, serotonin receptor site 1 is labeled 5-HT1, site 2 is 5-HT2, etc.) These different receptors act on different areas of the body, such as those affecting smooth muscle relaxation, sleep regulation, cardiovascular function, and gastrointestinal and vascular smooth muscle contraction.An antagonist acts against and blocks an action. An agonist acts like and stimulates an action. Antagonists and agonists are key agents in the chemistry of the human body and in pharmacology-the study and development of drugs.The new generation of drugs being evaluated to treat IBS either block or stimulate the action of serotonin at specific receptor sites that affect the GI tract." http://www.aboutibs.org/Publications/serotonin.html I also have to add that the researchers I talked to in the past are also looking into any impurities of chemical contents in the manufacturing of serotonin, for clues as well.alsoBr J Pharmacol. 2004 Apr;141(8):1285-93. Related Articles, Links Role of serotonin in the pathophysiology of the irritable bowel syndrome.Crowell MD.Mayo Clinic College of Medicine and Mayo Foundation, Scottsdale, AZ, U.S.A.The irritable bowel syndrome (IBS) is a complex disorder that is associated with altered gastrointestinal motility, secretion, and sensation. Serotonin (5-HT) is an important neurotransmitter and paracrine signalling molecule in the gastrointestinal tract. 5-HT release from enterochromaffin (EC) cells initiates peristaltic, secretory, vasodilatory, vagal and nociceptive reflexes. The enteric nervous system (ENS) comprises a semiautonomous effector system that is connected to the central autonomic network. Parasympathetic and sympathetic nerves modulate the ENS via afferent and efferent communications. Ongoing, bidirectional brain-gut interactions involving 5-HT pathways occur that significantly influence the effector systems. Altered 5-HT signalling may lead to both intestinal and extraintestinal symptoms in IBS. 5-HT directly and indirectly affects intestinal motor and secretory function and abnormalities may lead to either constipation or diarrhea. 5-HT modulates sensation and perception of visceral stimulation at peripheral and central sites. Therapeutic agents targeting altered 5-HT signalling may provide new, effective treatments for patients with IBS.British Journal of Pharmacology (2004) 141, 1285-1293. doi:10.1038/sj.bjp.0705762PMID: 15100164when Tal, posted the above."Normal gut physiology is molded by the interaction between the intestinal microbiota and the host's gastrointestinal tissues, including motility, absorption and secretion, and intestinal permeability. ""But this left out sensation, very important."Med Sci Monit. 2004 Mar 23;10(4):RA52-RA62. Epub ahead of print Related Articles, Links Irritable bowel syndrome: a model of the brain-gut interactions.Mulak A, Bonaz B.Department of Gastroenterology and Hepatology, Wroclaw Medical University, Wroclaw, Poland.Brain-gut interactions are increasingly recognized as underlying pathomechanisms of functional gastrointestinal disorders. Bi-directional communication between the central nervous system (CNS) and the enteric nervous system (ENS) occurs both in health and disease. Various CNS- and gut-directed stressors stimulate the brain-gut axis. Processes modulating responsiveness to stressors along the brain-gut axis involve neural pathways, the immunological, and endocrinological mechanisms. Disturbances at every level of neural control of the gastrointestinal tract can affect modulation of gastrointestinal motility, secretion, immune functions as well as perception and emotional response to visceral events. ENS function, central processing, and autonomic regulation play an important role in the brain-gut dialogue. Stress and emotions may trigger neuroimmune and neuroendocrine reactions via the brain-gut axis. Various non-site specific neurotransmitters influence gastrointestinal, endocrine and immune function, as well as human behavior and emotional state, depending on their location. The physiology of the digestive tract, the subjective experience of symptom, health behavior, and treatment outcome are strongly affected by psychosocial factors. Recently, a biopsychosocial model of IBS containing physiological, emotional, cognitive and behavioral components has been proposed. Rapid progress in neurogastroenterology, using new brain imaging techniques, should bring better understanding of the brain-gut axis and open new therapeutic perspectives.PMID: 15039657"Curr Opin Investig Drugs. 2004 Jan;5(1):55-60. Links Enterochromaffin cells and 5-HT signaling in the pathophysiology of disorders of gastrointestinal function.Crowell MD, Shetzline MA, Moses PL, Mawe GM, Talley NJ.Mayo Foundation and Mayo Clinic, GI Physiology & Motility, Division of Gastroenterology & Hepatology, 13400 E Shea Blvd, Scottsdale, AZ 85259, USA. crowell.michael###Mayo.eduDisorders of gastrointestinal function are common and significantly reduce quality-of-life, as well as negatively impacting healthcare costs. Consequently, there is much interest in understanding the pathogenesis of these disorders. Increasing, albeit as yet limited, evidence has implicated alterations in 5-hydroxytryptamine (5-HT) release, and the subsequent interaction of 5-HT with specific 5-HT receptor subtypes, in the altered gut function of patients with irritable bowel syndrome (IBS) and other functional bowel diseases. Alterations to enterochromaffin cells and/or 5-HT signaling can result in gastrointestinal dysmotility, visceral hypersensitivity and secretomotor abnormalities in the gut. Evidence is beginning to link disturbed 5-HT physiology with the pathophysiology of diarrhea and constipation in IBS, and with slow-transit constipation. This review discusses the current evidence on the pathobiology of these systems.PMID: 14983974Gastroenterology. 2004 Mar;126(3):693-702. Links *Activated mast cells in proximity to colonic nerves correlate with abdominal pain in irritable bowel syndrome.* Barbara G, Stanghellini V, De Giorgio R, Cremon C, Cottrell GS, Santini D, Pasquinelli G, Morselli-Labate AM, Grady EF, Bunnett NW, Collins SM, Corinaldesi R.Background & Aims: The mechanisms underlying abdominal pain perception in irritable bowel syndrome (IBS) are poorly understood. Intestinal mast cell infiltration may perturb nerve function leading to symptom perception. We assessed colonic mast cell infiltration, mediator release, and spatial interactions with mucosal innervation and their correlation with abdominal pain in IBS patients. Methods: IBS patients were diagnosed according to Rome II criteria and abdominal pain quantified according to a validated questionnaire. Colonic mucosal mast cells were identified immunohistochemically and quantified with a computer-assisted counting method. Mast cell tryptase and histamine release were analyzed immunoenzymatically. Intestinal nerve to mast cell distance was assessed with electron microscopy. Results: Thirty-four out of 44 IBS patients (77%) showed an increased area of mucosa occupied by mast cells as compared with controls (9.2% +/- 2.5% vs. 3.3 +/- 0.8%, respectively; P 0.001). There was a 150% increase in the number of degranulating mast cells (4.76 +/- 3.18/field vs. 2.42 +/- 2.26/field, respectively; P = 0.026). Mucosal content of tryptase was increased in IBS and mast cells spontaneously released more tryptase (3.22 +/- 3.48 pmol/min/mg vs. 0.87 +/- 0.65 pmol/min/mg, respectively; P = 0.015) and histamine (339.7 +/- 59.0 ng/g vs. 169.3 +/- 130.6 ng/g, respectively; P = 0.015). Mast cells located within 5 microm of nerve fibers were 7.14 +/- 3.87/field vs. 2.27 +/- 1.63/field in IBS vs. controls (P 0.001). Only mast cells in close proximity to nerves were significantly correlated with severity and frequency of abdominal pain/discomfort (P 0.001 and P = 0.003, respectively). Conclusions: Colonic mast cell infiltration and mediator release in proximity to mucosal innervation may contribute to abdominal pain perception in IBS patients.PMID: 14988823Overlapping Upper and Lower Gastrointestinal Symptoms *Overlapping Upper and Lower Gastrointestinal Symptoms * Gastroenterology, November 2003 Journal ScanFromThe American Journal of GastroenterologyNovember (Volume 98, Number 11)Overlapping Upper and Lower Gastrointestinal Symptoms in Irritable Bowel Syndrome Patients With Constipation or DiarrheaTalley NJ, Dennis EH, Schettler-Duncan VA, Lacy BE, Olden KW, Crowell MDThe American Journal of Gastroenterology. 2003;98(11):2454-2459Findings from a number of studies have suggested that patients with irritable bowel syndrome (IBS) may have motor dysfunction that extends beyond the colon to include other parts of the gastrointestinal tract, such as the stomach, esophagus, and small intestine.Indeed, the functional gastrointestinal disorders, including IBS and functional dyspepsia, are currently defined by symptom groupings that seem to cluster together in both clinical practice and population-based studies. However, these symptoms commonly overlap, leading some investigators to question the validity of subdividing the disorders based exclusively on symptom presentation.In this setting, it is recognized that distinguishing between IBS and functional dyspepsia can be diagnostically challenging because of the variations in symptom patterns, which frequently overlap. But this symptom overlap is poorly quantified and defined, and it remains unclear whether symptom patterns differ in subgroups of IBS that have been arbitrarily defined by primary bowel patterns of constipation and diarrhea (Note: The Rome committee has not endorsed subdividing IBS patients according to primary alteration in bowel function because of significant overlap in primary bowel symptoms). Therefore, Talley and colleagues set out to investigate the distribution of upper and lower gastrointestinal symptoms among patients with IBS with constipation and IBS with diarrhea. They hypothesized that IBS with constipation would be associated with more upper gastrointestinal complaints, and would therefore more often overlap with functional dyspepsia.The study involved 121 consecutive patients who presented with a diagnosis of IBS. Patients were grouped according to primary bowel symptoms as either IBS with constipation (58 women and 18 men, mean age 47 ï¿½ 17 years) or IBS with diarrhea (26 women and 19 men, mean age 47 ï¿½ 15 years). All patients completed the Hopkins Bowel Symptom Questionnaire (which includes a brief quality-of-life assessment) and the Hopkins Symptom Checklist. Patients with alternating bowel habits (between constipation and diarrhea) were excluded so as to more accurately assess the overlap between upper and lower gastrointestinal complaints.Overall, results showed that IBS with constipation was associated with more bloating and early satiety; this likely reflects underlying pathophysiologic mechanisms that are distinct from those in IBS with diarrhea. In fact, patients with IBS with constipation reported significantly more overall gastrointestinal symptoms when compared with patients with IBS with diarrhea (6.67 vs 4.62, respectively, P .001). Abdominal pain patterns differed in patients with IBS with constipation vs in patients with IBS with diarrhea (lower abdominal pain: 40.8% vs 24.4%, and upper abdominal pain: 36.8% vs 24.4%, respectively). However, there were no significant differences in personality subscales by IBS subgroup -- but somatization was positively associated with multiple symptom reports and was negatively correlated with quality of life.These findings demonstrated that upper gastrointestinal symptoms consistent with functional dyspepsia were more common among patients with IBS with constipation. Despite considerable overlap of upper and lower gastrointestinal symptoms among patients with IBS with constipation and patients with IBS with diarrhea, the former had more frequent lower abdominal pain and bloating. A better elucidation of the overlap between symptoms in patients with IBS may help guide clinical management of this disorder, which should be targeted at the multiple symptoms in these patients. http://www.medscape.com/viewarticle/465193_4 Sapsman, thanks for the wedding wishes.


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## eric (Jul 8, 1999)

as an aside and I worte this now some time ago, it is on the IBS tales site and this site.The tale of Shawn EricI was just thinking of expressing some of my thoughts on IBS and having it for 30 years. I have pain-predominant IBS and alternating constipation and diarrhea. Although I can say had and really mean it, as I am doing so much better at about 85% and I believe still improving thanks to the IBS self-help group and Mike's hypnotherapy tapes.I believe my IBS started from a trip to Mexico where I swallowed a small amount of chlorinated water out of a swimming pool and a half hour later, I was very sick with amoebic dysentery and spent the next month seriously close to death. No joke. They also pumped tons of penicillin into me at this time. However, amoebic dysentery is known to cause inflammation in the digestive tract. I recovered from that and I don't remember when or how soon I came back from Mexico. I was suffering from severe abdominal pain and alternating constipation and diarrhea. It wasn't too long before they started the first tests on me and that testing would continue on and off for a big part of my life and cost thousands of dollars. The first tests were stool samples and upper GI tests, all negative. The next test was a lower gi, also negative. Blood tests and all the regular tests from a normal MD. I was ten. In those days no one had a clue about IBS and they called it spastic colon or nervous stomach. I missed a lot of school and was always trying to catch up in my school work. Since the good doctors couldn't figure it out, I was sent for therapy and put on librium and told it was psychosomatic. I struggled for years through school, some working and trying to explain to friends why I was in pain a lot and could not do things. Dating was a problem. They thought I had a stomach ache and it would go away and I should just quit being a big baby. Funny because my boss said that to me also, ten years later as well as a lot of coworkers. More testing. Basically the same kinds of tests over again. When you're in your teens and you're seeing some upstate NY MD in a small town in those days testing didn't amount to much. Still no advice from anyone on what to do. My parents were very supportive and my mom is a nurse, which was very helpful and supportive. However, sometimes my mom's own concern bothered me as she could not help and I could see that in her eyes while I lay there in complete agony from the knife jabbing sharp pains coming from my gut. When I got these pains I would hyperventilate and all kinds of thoughts raced through my head. For me this was already establishing itself into my thought patterns on a day-to-day basis and I didn't really know much about living any other way as I hit my late teens. I was having episodes at least two to four times a week. Although I would have some remissions they always came back and for a while my IBS went cyclic and bothered me most in the winter months, but in the summer improved somewhat. But it came back. Meanwhile, I continued to try to figure some of it out for myself, in ways I could manage it or do things to reduce it. Late teens to late twenties. More tests. "Maybe an ulcer, but we don't see it." New drugs, and from there librax, donnatol, prescription tagament, and a few others I don't even remember, but prozac was one as well. No noticeable long term improvement. Mid thirties. I got serious and went to the best GI doc in town and told him to test away on everything we could think of that might be applicable. Also worried it could be something else still, although nothing showed up before he tested me and after he tested me. More drugs. Bentyl and valium. Sent to therapy told to relieve stress. I knew this wasn't the cause and thought because the pain was so severe that something had to be wrong in there, it just couldn't be possible to have this much pain and not have something physically that they could see wrong. I just didn't get it. I did know stress aggravated it but not to the extent I do now or the kinds of stress either environmental, physical, or psychological and at the time I did not know how to reduce it enough with the management techniques I was using and I used a lot of them. I tried all the food aspects and nothing other then some common sense on most things. Although it made sense what was going in had something to do with it, but in reality looking back now, it was common sense issues of eating too much too fast, fat, spices etc etc... There were some weird signals before an attack. My skin would turn whiter, my eyes would twitch and my hands would sweat. Sometimes I would get dizzy. My therapist had migraines and knew nothing about IBS, other then realizing some of the symptoms sounded somewhat like some symptoms she would get with her migraines and that it was not in my head (psychosomatic or crazy) and I should go back to the doctor. It wasn't helping me to see her so I agreed. Although she didn't explain serotonin to me, nor did my doctor take the time to either. I feel if someone would have explained some of the mind-gut connections earlier I could have saved a lot of time and effort. I know some are relatively new, but I think they had some idea and either it was too complicated to explain to me or they just didn't have the time. I think at this point one of the best things a doctor can do is explain some of this to new patients. I didn't have any other issues I was healthy otherwise and was playing soccer for twenty years and going professional until I blew my kneecap out. I believe I personally have a classic case of IBS. For me I believe it is faulty neurotransmitters that are not talking right between my brain and my gut. Just some thoughts and thank god for hypnotherapy, which I want to add some of my thoughts on as a side note. I am drug free and very happy with the results. I want to say something about hypnotherapy in general and what I believe and have seen for myself and these are my own personal comments from my experiences with it. Although, many others feel the same way now. It is the deepest from of relaxation I personally have ever found. It has tremendously reduced the pain for me from severe to very mild. I think this has worked two ways. It has steered my thoughts and attention away from the pain when I want and I also believe the relaxation aspect of it is releasing endorphins to my gut. This has been a big achievement and will save me trips to the ER. When I wake up in the morning I no longer have IBS on my mind first thing. I no longer dwell on it. I don't worry to much about going out or bathrooms any more. I know longer turn white or have my hands sweat. I can relax my gut at will. My whole body is more relaxed in general and I didn't realize how tense it was before. I breathe better and more deeply, which I have found useful if I feel any twinges of a potential problem. I sleep better and more deeply. Day-to-day problems don't bother me like they used to. I can eat things I couldn't before. I feel like I have been rewired so to speak. My BMs have improved substantially. There are symptoms I don't even remember and that is unbelievable. Anyway just some thoughts of an IBSer pondering. I don't know if this helps anyone and I also don't want to say hypnosis is a cure or the only thing people should be doing to manage IBS, but it is one majorly effective tool that isn't understood by a lot of people or used enough by doctors in the IBS world and why I sound like a broken record sometimes. However, I hope no one gets tired of hearing about something that really works for the majority of people with IBS as there are just too few of the things that do. http://www.ibstales.com/male_tales_dh1.htm I was pain predominate IBS with alternating d/c, more on the d side and incomlplete evacuation, rectal sensitivity, sleep problems, back pain problems, emotion and anxiety from the IBS symptoms problems, and I am sure I can think of some more things.


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## bonniei (Jan 25, 2001)

I don't know if i was being clear or not and if that was the reason i didn't get an answer or if eric and flux, you just don't have the answers. I will give it one more try.1) Lotronex blacks the release of serotonin in the gut because serotonin leads to peristalsis2) So if you have D you don't want excess serotonin in the gut and would like the capacity to reuptake serotonin in the gut.3) So if you have C you want the opposite to happen ie you want excess serotonin in the gut to initiate peristalsis4)So you don't want to reupptake serotonin if you have C5) So it is good to have the SERT transporter if you have D and no SERT transporter if you have C6) so this part of the quote-.""findings suggest that patients with constipation and IBS may have a reduced capacity to reuptake serotonin,"This should be good for C7) But it seems it is not good because by the second part of the quote the reduced capacity to uptake serotonin leads " to excess free serotonin and then desensitization of these receptors, thus reducing motor function" Isn't this contadictory to statement 4)?The quotes in this post are from eric's post 5-07-04 10;49 am


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## eric (Jul 8, 1999)

Bonniei, I am going to tell my mom I love her.







But there might be some confusion here.One serotonin does not directly travel to the brain from the gut, but signals nerve fibers to the brain. If this in some way is part of what your thinking. That was confusing to me a while ago, just so you know.I will look at this closer later.You might want to read this also though, maybe its clearer, I am not sure.IBS: Improving Diagnosis, Serotonin Signaling, and Implications for Treatment http://www.medscape.com/viewarticle/463521 "Serotonin Reuptake TransporterThere is likely an evolutionary advantage to having physiologic mechanisms that regulate serotonin levels and activity, because it could be quite harmful without these regulatory mechanisms.3 One of the primary mechanisms the body has for regulating availability of serotonin within the extracellular space is the serotonin reuptake transporter (SERT). SERT is present in the brain and gut. The amount of serotonin reuptake that occurs from the extracellular space is genetically determined and is based on whether there are long, short, or heterozygous polymorphisms in the promoter for synthesis of SERT. For instance, homozygosity for the short variant and presence of the heterozygous variant result in less transcript, less protein expression, and thus, less reuptake of serotonin. SERT activity is obviously an important factor influencing serotonin availability to act on postsynaptic receptors, and would possibly affect the response to serotonergic medications such as SSRIs, in the treatment of depression, and to the novel agents tegaserod and alosetron, for IBS."It sure is very complicated.


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## bonniei (Jan 25, 2001)

no it wasn't really any clearer. it said


> quote: Therefore, a small study of 30 patients (15 women) with IBS with diarrhea was performed in which the patients were given alosetron 1 mg orally twice daily for 6 weeks and their colonic transit measured via scintigraphy at the end of treatment. Only 23 (12 women) of these patients actually submitted blood for analysis, but 8 long homozygous, 4 short homozygous, and 11 heterozygous SERT polymorphisms were identified. When colonic transit was measured, the patients with a long homozygous polymorphism (associated with more serotonin reuptake, ie, there is conceivably less serotonin around to stimulate the gut and peristalsis and therefore gut motility is slowed) had greater slowing of colonic transit with alosetron than heterozygotes.


it seems that people who already have more serotonin reuptake are responsive to lotronex which blacks the release of serotonin. if already they have more serotonin uptake then there won't be excess serotonin floating around so what would lotronex achieve atleast as far as serotonin is concerned. *i suppose i am correct in saying that serotonin blocks the release of serotonin*


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## bonniei (Jan 25, 2001)

i forgot to call my mom to wish her yesterday night. Now it is too late since she is about 12 hours ahead.


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## bonniei (Jan 25, 2001)

Talissa,


> quote:The watery diarrhea is probably attributable to the potentiation of serotonergic signaling in SERT -/- mice


i had to look up the definition of potentiation and it is -" Potentiation is the ability of one chemical to enhance the activity of another chemical to an extent greater than the simple summation of the two expected activities. " Which are these chemicals? And it happens in the mice without the SERT transporter. i wonder what happens in iBS-D where they have SERT transporters. They have been found deficient only in IBS-C.is it possible that a certain amount of serotonin leads to D and more than that to desensitization and C? THat is the only sense I can make of it.


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## bonniei (Jan 25, 2001)

> quote:i suppose i am correct in saying that serotonin blocks the release of serotonin


I meant that* I suppose I am correct in saying that Lotronex blocks the release of serotonin *


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## Jhouston (Nov 9, 2003)

Bonnie, I sure would love to understand Serotonin better. I think SSRI's block the "reuptake" of serotonin so there is more serotonin since the reuptake creates a lesser potent serotonin and takes "time" to turnover. So "blocking" makes more and potent Serotonin? That is my understanding and I could be wrong. Wish I knew more and if it is something that I need to fix. C, sleep distubance, and "foggy" after meals. and how this can exacerbate after antibiotic therapy (In my case)? Joann


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## bonniei (Jan 25, 2001)

SSRI's inhibit the reuptake of serotonin back into the blood so there is more serotonin in the synapses.


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## Talissa (Apr 10, 2004)

From _Digestive Diseases and Nutrition_ (p. 2 & 9): Small but powerful players in tipping the balance towards digestive health or disease are the microorganisms that inhabit the gastrointestinal tract. *These microbes can affect intestinal health in some surprising ways, depending on whether they work with, or against, the cells of their host.* ï¿½GOODï¿½ BACTERIAï¿½HOW DO THEY HELP? ...Interestingly, the resident ï¿½goodï¿½ bacteria in the gut were responsible for directing the Paneth cells to make Ang4. Another research team showed that the ï¿½goodï¿½ bacteria, again working through Paneth cells, had an important role in developing the capillary networks found in the small intestine. *In the absence of (ï¿½goodï¿½) bacteria, these networks--which are important for absorption of nutrientsï¿½-do not form properly.* In addition to providing insights into intestinal infections, this research is paving the way toward improved understanding of how bacteria and cells interact to guide the formation of new blood vesselsï¿½-knowledge that could provide the basis for future experimental therapies for intestinal injury and cancer. The significance of appropriate interactions between intestinal cells and bacteria in creating a healthy intestinal immunity was also demonstrated by this research. With this knowledge, researchers have a better perspective on what goes awry in some intestinal diseases. http://www.niddk.nih.gov/federal/advances/2004/ddn.pdf *This article shows that imbalanced gut flora has already been shown to effect the intestinal cells & their ability to absorb nutrients.* _____________________________________________Even Medscape says more success is found in treating IBS with non-drug alternatives, than with Rx drugs.SUCCESS comes from treating disease, not from treating its symptoms._____________________________________________So you guys keep focusing on the drugs to superficially treat the serotonin & its resulting gut-brain axis problem, while the rest of us can focus on fixing it naturally--from the source of the problemï¿½.imbalanced gut flora.Medscape:It must be emphasized that a simple but comprehensive nonpharmacologic management program is most likely to SUCCEED in practice in terms of achieving the best outcomes in IBS. Drugs should generally remain second-line in IBS until agents with better efficacy and established safety profiles become available. http://www.medscape.com/viewprogram/1893_pnt (also on the bottom of this collection of articles is a picture of Drossman, who incidentally doesnï¿½t look all that healthyï¿½)


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## Talissa (Apr 10, 2004)

**********************************************************************But Iï¿½m glad I focused on serotonin for a bit.In my mind, failure of serotonin(derived from tryptophan--A NUTRIENT from protein, & its transport is reliant on 5 other amino acids-nutrients) to properly assimilate may be the key to why some people with imbalanced gut flora are ï¿½Cï¿½ & others are ï¿½Dï¿½. And the varying degrees of inflammation seem to dictate the differences in severity of symptoms.-my Opinion-







**************************************************************Hope everybody had a nice wkd!Talissa


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## Talissa (Apr 10, 2004)

Bonniei,I was in a rush this am & didn't even see your question--I'm sorry, & it doesn't matter because I don't know the answer anyways!!My layman's take on it is that there is a problem with the SERT(serotonin transporter) in those of us with diarrhea & a problem with the EC/mast cell structure enveloping serotonin in those with constipation...What do you think?Do you have a biology background? T-


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## flux (Dec 13, 1998)

> quote:In the absence of (ï¿½goodï¿½) bacteria, these networks--which are important for absorption of nutrientsï¿½-do not form properly.


Not related to IBS


> quote:This article shows that imbalanced gut flora has already been shown to effect the intestinal cells & their ability to absorb nutrients.


Not related to IBS.Do you have *anything* that is related?


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## kel1059 (Feb 28, 2003)

concerning serotonin acting drugs whether they be for brain or gut, they never get to the root cause.they may help many people -- even save the lives of people on the brink of suicide and ease the suffering of obs-compulsives.--but they don't get to the root cause!!!for people who claim that they help i would have to agree, but i am still convinced that everyone would be better off if their doctors were committed to searching for the root cause.(long term use of these drugs are going to cause problems)***********************in IBS serotonin is an intermediate player


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## Talissa (Apr 10, 2004)

Flux,You didn't read the article!!! It encompasses both IBD & IBS in its scope. Imbalanced gut flora has been found in "many" with IBS, when inflammation plays a factor.Please don't make me post the Medscape articles again which say this!!!Clarity came while I was away--in both the crystalization of how all of these things tie together in the pathenogenesis of IBS, as well as the fact that I don't actually have time for this.I've proven my ideas have merit based on proven studies and seem to be in line with the direction new research on IBS is heading.All this debate was bringing on negative energy for me--I had ENOUGH of that when I was in IBS hell.So, cheers, hope you have a truly good day,Talissa


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## bonniei (Jan 25, 2001)

> quote:My layman's take on it is that there is a problem with the SERT(serotonin transporter) in those of us with diarrhea & a problem with the EC/mast cell structure enveloping serotonin in those with constipation...


The following is an opinion from eric's post


> quote:"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. These 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"


It suggests that there is a problem with SERT immunoreactivity in IBS-C


> quote:"The present results indicate that SERT expressed on platelet membranes of D-IBS patients is characterized by low density and binding affinity "


 http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=14687821 " This suggests fewer SERT transpoorters in IBS-D.Also this "While 5-HT release was not altered in the patient groups relative to control values, the decrease in SERT expression in both IBD and IBS leads to a decrease in the capacity to remove 5-HT from the intracellular space once it is released, thus increasing 5-HT availability."Talissa my background is not in Biology but I have spent a good deal of my time reading scientific papers about my IBS problem. I have not been satisfied with just reading abstracts. I have a Ph D in Math.


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## kel1059 (Feb 28, 2003)

talissa,your information is very good.flux wallows in negativity; it is his life. it is his existance.he is the most negative person i have ever come across.he gets his jollies by being right even if it means that he has to distort and twist every bit of information that comes his way.his punishment for all this negativity is that he must live in all the filth that it creates. it is a vicious cycle for him. the more negativity that he spews -- the more problems he creates in his life and the worse are his problems.you reap what you sow.


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## Talissa (Apr 10, 2004)

Bonniei,That makes more sense. A Phd in math--that explains it--you couldn't hide the fact that all your synapses are connecting just fine!But again, the only thing all of this research on serotonin will lead to is MORE DRUGS.Getting to the source of what is CAUSING the problems with serotonin will normalize its functioning NATURALLY.Btw--I like the 2nd line of your signature!!!


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## kel1059 (Feb 28, 2003)

flux,you have run into a person who does nice research.she is going to make a fool of you if you continue to post your lies. http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15123072 Irritable bowel syndrome.Verdu EF, Collins SM.Intestinal Research Programme, McMaster University, Hamilton, Ont., Canada.The intestinal microbiota interacts with several aspects of gastrointestinal function that may affect the expression or progression of disease. For example, a role for bacterial metabolism of bile acids and food has been linked to colorectal cancer development. Studies have also shown a potential role of the intestinal microbiota in the modulation of inflammation in the intestine and joints. Normal gut physiology is molded by the interaction between the intestinal microbiota and the host's gastrointestinal tissues, including motility, absorption and secretion, and intestinal permeability. Early studies in axenic mice demonstrated gross morphological abnormalities and gut motor dysfunction related to the absence of a normal microflora, raising the possibility that shifts in commensal bacterial populations could play a role in the development of altered motility states including functional disorders of the gut. This chapter concentrates on the experimental evidence for a role of intestinal microbiota and the potential therapeutic value of probiotics in functional diseases such as irritable bowel syndrome.PMID: 15123072 [PubMed]


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## flux (Dec 13, 1998)

> quote: Imbalanced gut flora has been found in "many" with IBS,










What the devil is imbalanced flora?


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## bonniei (Jan 25, 2001)

Also re: Mast cell: " In IBS, 5-HT content is reduced, EC cells are increased " The American Journal of Gastroenterology Volume 98, Issue 9, Supplement 1 , September 2003, Pages S262-S263 doi:10.1016/S0002-9270(03)01562-4 Cite or link using doi Copyright ï¿½ 2003 Am. Coll. of Gastroenterology. Published by Elsevier Science Inc. Abstract Key elements of serotonin signaling are altered in IBD and IBS: support for a molecular basis of the irritable bowel syndrome Peter L. Moses M.D.*, Mathew D. Coates B.S., Christine R. Mahoney B.S., Joanna E. Sampson M.D., David R. Linden Ph.D., Jason J. Chen Ph.D., Eric B. Newton M.D., Keith A. Sharkey Ph.D., Micheal D. Crowell Ph.D., Michael D. Gershon Ph.D. and Gary M. Mawe Ph.D. This suggests Mast cells are increased in both kinds of IBS


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## bonniei (Jan 25, 2001)

Thanks Taliss for your comment on my signature. Hope Khomeini dioes not not abduct me amd show me his version of hell







OH that Khomeini is dead. THank goodness.


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## eric (Jul 8, 1999)

This serotonin information is very important and not just about drug therapy in IBS. For one it is understanding things going wrong in IBS first of all.You can accomplish excellent results with other means when you understand the relationships to serotonin and IBS and mast cells and IBS and the big picture of IBS. For example what does relaxation techniques have to do with serotonin?What does the flood of serotonin after eating ahve to do with the symptoms 15 minutes after eating when the food is still in the throat?There are many more examples like this in IBS.Bonniei, have to work all day today, but look in these articles..Gastrointestinal Disorders of Function: The Therapeutic Potential of Serotonin http://www.medscape.com/viewarticle/418895_3 Irritable Bowel Syndrome (IBS): Examining New Findings and Treatments CME http://www.medscape.com/viewprogram/725?src=search Kels, last post. We know Dr Collins is up to date on the brain gut axis and IBS and they are trying to figure out the roles of these things as they try to figure out all the roles in everything.Here is more from dr collins on post infectious IBS."Post-Infective Irritable Bowel SyndromeAmong many postulated causes of irritable bowel syndrome (IBS), one of the most intriguing is that the syndrome represents sequelae of an acute enteric infection. In fact, such an association is not just an interesting theory. According to Stephen M. Collins, MBBS, FRCP, FRCPC, Professor of Medicine and Director of Gastroenterology at McMaster University in Hamilton, Ontario, Canada, "Acute enteric infection appears to be a significant contributing cause to the development of irritable bowel syndrome." The changes associated with such enteric infection appear to be reversible, introducing the opportunity for new treatment strategies for persons at high risk for irritable bowel syndrome (IBS).Clinical observations have suggested that transient infection in the gut can lead to persistent neuromotor dysfunction, and possible symptom generation in persons with IBS. In a large review, Chaudhary and Truelove found that 33% of persons with IBS reported an acute onset to their symptoms. Indeed, a recent controlled study showed that enteric infection was a strong risk factor for developing IBS.Animal Studies: Neuromuscular Dysfunction Post-InfectionIn one animal study by Tougas, Collins and colleagues infected mice with Trichinella spiralis. The results showed that the infection was accompanied by inflammation, reaching its peak in week 2. By week 3, the parasite had been expelled and inflammation had subsided. However, accompanying muscle hypercontractility persisted for up to 6 weeks' post-infection.In a second study by Tougas, the colons of the infected mice were distended using a small balloon and there was evidence of increased afferent nerve activity not only during the infection, but also 4 to 6 weeks' post-infection. Together, these results suggest that transient infection and subsequent inflammation in the gut can alter muscle contraction and increase sensory activity in the colon, suggesting a possible basis for dysmotility and hyperalgesia that occurs in post-infective IBS. But are these effects reversible?In a third study, animals were infected and allowed to recover. After 3 weeks, a short course of dexamethasone was administered. In the animals treated with steroids, muscle hypercontractility was prevented or reversed by day 28 post-infection. "Post-infective changes appear to be reversible and thus provide a basis for designing new experimental approaches in patients," said Dr. Collins.Clinical Association Between Infection and IBSFive recent studies showed that 7% to 31% of persons having food poisoning-associated bacterial gastroenteritis developed IBS, 3 to 12 months' post-infection. This phenomenon has also been observed with parasitic infection; however, the role of viral gastroenteritis is not yet known. The development of IBS appears to be due to a convergence of infection, inflammatory stimuli, central nervous system stimuli, and psychological factors. "The response to inflammatory stimuli is enhanced under stress, with the timing of the stress in relation tostimuli being important," Dr. Collins explained. Psychological factors, however, do not appear to be the sole determinants of whether someone develops IBS post-infection and other human studies suggest that local alterations in response to inflammatory stimuli may be important; this may be, in part, genetically determined.One study showed that 32% of persons with Salmonella-related gastroenteritis developed IBS symptoms within 2 years' post-infection. Biopsies showed no overt inflammatory presence; however, a semiquantitative approach showed an increase in inflammatory cells in those with IBS. Indeed, there was an increased number of lymphocytes and hyperplasia of the serotonin-containing enterochromaffin cells, a major source of 5-HT in the gut. "It is likely that 5-HT measurements would be increased in this subgroup, affording new therapeutic opportunities for these patients," Dr. Collins said. In addition, other studies have shown a potential role for lumenal factors and for cholestyramine-type factors, especially for diarrhea-dominant disease.ConclusionIn closing, Dr. Collins noted that post-infection effects associated with IBS appear to be reversible, warranting further clinical investigation of anti-inflammatory agents and other innovative therapies for persons at risk for IBS. " http://www.cmecorner.com/macmcm/pcp/pcp2000_01.htm there is an increase in serotonin cells and mast cells after infection, there is no overt inflammation however.and one he wrote onStress and the Gastrointestinal TractIV. Modulation of intestinal inflammation by stress: basic mechanisms and clinical relevance which is extremely important in IBS, in Post infectious IBS. http://ajpgi.physiology.org/cgi/content/full/280/3/G315 One of the things Kel and tal, keep leaving out in all this and it cannot be seperated." it is only recently that the role of stress in modulating intestinal inflammatory processes has received the attention of investigators. The feasibility of considering stress as a modulator of inflammatory processes in the gut arises from the following developments: 1) the understanding that corticosteroids elaborated through activation of the hypothalamic-pituitary-adrenal (HPA) axis by stress are anti-inflammatory and that attenuated HPA responses to stress may predispose to inflammation (22); 2) the recognition that many immune and inflammatory cells recognize and respond to neuropeptides (24); and 3) the knowledge that stress may render an organism susceptible to an inflammatory stimulus by altering intestinal physiology, such as the permeability of the epithelium (10). "


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## kel1059 (Feb 28, 2003)

one thing that needs to be pointed out is that the big pharm companies own many of the IBS researchers.they even grant dr drossman many of his funds.to that extent, much of the research is tainted to paint a picture that supports the role of serotonin in IBS. sure serotonin plays a role in IBS but so do hundreds of others chemicals, hormones, neurotransmitters.heck, manipulation of my prostaglandins and leukotrienes via Ibsacol gave me far better control ove some of my symptoms than any serotonin drug i ever took.but even ibsacol did not get to the root cause of my problems.my recovery is due in large part to addressing dysbiosis.


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## kel1059 (Feb 28, 2003)

> quote: http://ajpgi.physiology.org/cgi/content/full/280/3/G315 One of the things Kel and tal, keep leaving out in all this and it cannot be seperated." it is only recently that the role of stress in modulating intestinal inflammatory processes has received the attention of investigators. The feasibility of considering stress as a modulator of inflammatory processes in the gut arises from the following developments: 1) the understanding that corticosteroids elaborated through activation of the hypothalamic-pituitary-adrenal (HPA) axis by stress are anti-inflammatory and that attenuated HPA responses to stress may predispose to inflammation (22); 2) the recognition that many immune and inflammatory cells recognize and respond to neuropeptides (24); and 3) the knowledge that stress may render an organism susceptible to an inflammatory stimulus by altering intestinal physiology, such as the permeability of the epithelium (10). "


i am not ignoring it. i think it is definitely relevant.however, for you to blantantly ignore evidence of intestinal dysbiosis is just ridiculous.


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## Talissa (Apr 10, 2004)

Flux,Maaan, you're making me do this---"Direct and indirect evidence of altered flora of the large and small intestine has been reported in IBS patients."MEDSCAPE http://www.medscape.com/viewarticle/457728_4 ______________________I think you know what imbalanced gut flora is--beneficial intestinal bacteria lowered by the crazy things we humans do to ourselves, allowing the pathogenic bacteria to come in & over-populate.This causes inflammation in IBS, varying degrees, also in the MEDSCAPE article.Also proven in the Canadian study posted below.Are you for real???Hel-lo?


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## bonniei (Jan 25, 2001)

Well eric from your 2nd link serotonin seems to be interdependent on norepinephrine. I think it is wrong of you to talk solely on serotonin. I don't believe I have ever heard you talk about norepinephrine but I could be mistaken.


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## kel1059 (Feb 28, 2003)

talissa,flux actually believes in the intestinal dysbiosis theory (for some people).why he posted his last statement is beyond me. i guess it is part of his general psychiatric illness. anyone who comes on this forum who knows what s/he is talking about is a threat to flux' turf. what i don't understand is why flux will post things that even he knows are lies??????doesn't he know it makes him look bad?odd! maybe there is some type of sociopathic tendencies within.


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## kel1059 (Feb 28, 2003)

flux (maurice) quit wasting talissa' valuable time or i will call your boss at albert einstein school of medicine and tell him you are wasting tax payer $$$ on this nonsense. maurice you keeping those mainframes in tip top shape







http://groups.google.com/groups?hl=en&lr=&...zation%26ie%3DU TF-8%26oe%3DUTF-8%26hl%3Den%26btnG%3DGoogle%2BSearch[/URL]


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## kel1059 (Feb 28, 2003)

talissa,at some point i want to talk to you about this "energy" thing that we are both interested in.i don't like talking about it here because it is rather esoteric and not well accepted by Western standards but i think it is relevant in many disorders including IBS.also, i have had some interesting experiences with Holosync. http://www.mercola.com/article/neuro_technologies.htm this is a technology that works on the brain and it did some surprising things for me. very narrow in its action. not nearly enough to alter the course of IBS, but still interesting.**********************************i stand by my belief that IBS has a great deal to do with the flora we keep. however, i think that there are other things we can do to help straighten out the mess.--acupuncture--HT--Meditation CD's--many others (fill in the blank)


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## flux (Dec 13, 1998)

> quoteirect and indirect evidence of altered flora of the large and small intestine has been reported in IBS patients."


Didn't they mention this was from IBS patients in







?


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## Talissa (Apr 10, 2004)

Okay, now I got it.You're just trying to push my buttons.Very cute.We'll let Medscape know they're reporting about IBS patients lving on the moon, & lovin' every minute of it!


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## kel1059 (Feb 28, 2003)

Disclosure: Douglas A. Drossman, MD, has disclosed that he has received grants for clinical research and educational activities and has served as an advisor or consultant for Novartis.







i will say though that at least they seem to be making an attempt at covering most of the bases.something tells me that they are unable to put the whole thing together to come up with a satisfactory answer.i am still a little confused as to exactly why i made the turnaround that i did but i believe that it had a lot to do with a multimodal approach.the problem with multimodal approaches is that they don't make for very good scientific experiments. all the variables and tinkering with respect to individual patients screws up any study parameters.oh well.


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## bonniei (Jan 25, 2001)

Well Talissa I looked up the references for


> quoteirect and indirect evidence of altered flora of the large and small intestine has been reported in IBS patients."


They wereBalsari A, Ceccarelli A, Dubini F, et al.: The fecal microbial population in the irritable bowel syndrome. Microbiologica 1982, 5:185-194.Swdsinski A, Khilkin M, Ortner M, et al.: Alteration of bacterial concentration in colonic biopsies from patients with irritable bowel syndrome (IBS). Gastroenterology 1999, 116:A1.Pimentel M, Chow EJ, Lin HC: Normalization of lactulose breath testing correlates with symptom improvement in irritable bowel syndrome: a double-blind, randomized, placebo-controlled study. Am J Gastroenterol 2003, 98:412-419The first reference was for a small group of IBS patients.The second one I was unable to pull off on Pub Med. i wonder why?The third is a very controversial study since Lactulose Breath hydrogen tests are not very reliable to detect SIBO.


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## Talissa (Apr 10, 2004)

kel,I agree. I wish they'd try the antibiotic + probiotic, or probiotic only, trials while also on a specific diet for the individuals. And maybe for the people who don't fully recover, keeping them on the probiotics for long periods to see if they simply needed more time to heal.Also, in my case, I've done yoga throughout the worst of it(that was fun) & through recovery, so I don't know what part that may have played.The answers aren't going to be easy. But you have to start somewhere.Love that you posted Drossman's healthy image here--I think he's been taking too many drugs from those friends of his!T-


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## bonniei (Jan 25, 2001)

Talissa, like I said prior to your last post that direct and indirect evidence of altered flora for IBS patients is on shaky ground, there are quite few papers which suggest that probiotics help IBS'ersSen S, Mullan MM, Parker TJ, et al.: Effect of Lactobacillus plantarum 299v on colonic fermentation and symptoms of irritable bowel syndrome. Dig Dis Sci 2002, 47:2615-2620.Madden JA, Hunter JO: A review of the role of the gut microflora in irritable bowel syndrome and the effects of probiotics. Br J Nutr 2002, 88 (Suppl 1): S67-S72.Marteau PR, de Vrese M, Cellier CJ, et al.: Protection from gastrointestinal diseases with the use of probiotics. Am J Clin Nutr 2001, 73 (Suppl 2): S430-S436Nobaek S, Johansson M-L, Molin G, Ahrne S, Jeppsson B.Alteration of intestinal microflora is associated with reduction inabdominal bloating and pain in patients with irritable bowelsyndrome. Am J Gastroenterol 2000;95:1231ï¿½8. Oï¿½Sullivan MA, Oï¿½Morain CA. Bacterial supplementation in theirritable bowel syndrome. A randomized double-blind placebocontrolledcrossover study. Dig Liver Dis 2000;32:294ï¿½301.


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## Talissa (Apr 10, 2004)

Bonniei,I've worked for a while now at healing my intestines naturally and I'm feeling great now, especially compared to my year+ in purgatory(ended after taking natural antibacterial + probiotics). It's night & day. heaven & hell. I had a bumpy 2 years after that, trying to find my triggers, which taking digestive enzymes helped resolve. But today, I have no triggers. I eat anything that I feel is healthy to eat. And sometimes I sneak some fries or cake. I don't eat anything with hfcs(poison) though, but it's a choice. Freedom.How are you feeling?I'm not posting any more studies on how IBS patients have altered gut flora on this thread, nor how this causes inflammation & the dreadful complications of this.No need.Talissaps-others symptoms that have slowly disappeared--pains in the ass, bloating, pains in the ab region, horrible periods, loud tummy rumbles, social anxiety, & having to buy so much da** toilet paper.


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## bonniei (Jan 25, 2001)

Hi Talissa, with zero fructose I get zero gas and D but I end up with C. So then in the nights when it does not matter I have some fructose and have regular BM's. I don't really have that much gas when I have fructose but there is a problem with my sphincters for which I do biofeedback and Beyond Kegels and my doc was happy enough with my improvement to call me back onlty for maintenace purposes. Thanks for asking


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## kel1059 (Feb 28, 2003)

i guess i would be curious to see studies where they use very high amounts of Human Strain Probiotics for 3 to 6 months.I'm on the fence as far as probiotics are concerned. I think they are very important, but I took about 90 Trillion (trillion not billion) over a 6 month period.it was VSL#3 and each day you are supposed to take a single packet that contains 450 billion live bacteria. i took it for 6 months and that is why it adds up to 90 trillion.they really did not seem to do anything great. i still had problems which prompted me to give the Dr D program a shot. however, the only thing that i really did different with dr d is change over to his human strain probiotics.these allowed me to start gaining weight which rather surprised me because i had so much trouble with that issue -- not being able to put it on.none of it makes a whole lot of sense.i am scratching my head over homeopathy. i know it works but i am not exactly sure as to what it did. the sulphur remedy which is known to be helpful to many people with allergies seemed to work a miracle on me. i may never figure it out.


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## I'll B Snookered (Apr 9, 2004)

Hey Bonniei,You keep saying you are fructose intolerant, which may well be true given that it gives you some gas. How do you know, though, that it isn't the fruit pectin that is allowing you to have the good BMs? I have a suggestion. Why not try Halls Fruit Breezers pectin throat drops. They have 7mg of pectin in them, and they have no HFCS or fructose. They do have glucose syrup, but that shouldn't bother you unless you are glucose intolerant as well. If you try this let me know. I believe that they may have had a slight laxative effect for me, but it's hard to tell when you have a cold. Good luck.


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## Talissa (Apr 10, 2004)

Bonniei,I was fructose intolerant as well. After about two weeks(first one uncomfortable as my body adjusted) on Digestive Advantage-IBS....This is going to sound like an ad, & I keep waiting for it to change, but I can eat fructose again. It's amazing to me.After starting digestive enzymes 3 years+ ago, fructose became my only trigger.Ex's of what I have been eating for over a week with no side effects: raw cucumbers, tomatoes, oranges, apples, honey, eggplant, corn, etc.Usually, w/i 2-3 hours of eating these foods, I'd be making consecutive trips to the bathroom. It may change, but the placebo effect has never worked on me before, and I've tried alot.You never know, it may help you as well.T-


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## SpAsMaN* (May 11, 2002)

Kel,i'm happy of your miracle recovery but in other hands i'm confuse because it seems to comes from Homeopaty.I'm not Homeophobic as Flux but i'm very sceptical.Anyway,what was your kind of IBS?







I never tougth the flora would be so popular!Talissa,i still have Creon25(enzyms tested in labs).Maybe i could try it AFTER a meal rather than before.Because i'm always irritated before a meal.What do you think about that?What was your enzyms brand?


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## I'll B Snookered (Apr 9, 2004)

Yeah, spas, I think you've got the longest currently active thread on this board that isn't on the MP. Congratulations. If I were to pee in a cup and dilute it 1:10000, do you think that would cure my IBS?


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## Talissa (Apr 10, 2004)

Hi Spasman,You started a long one!I use Sedona Lab's "ZymaPro complete enzyme formula" midway through my am protein shake & also at lunch-- after dinner, I take Vitamin World's "mutlt-enzyme formula" with HC1.From what I've read, you should only take enzyme formula's that contain HC1 after eating a largish meal. And with any enzyme, if you've got inflammation, you should take them during or after a meal.So, yeh, I think you might lose the irritation. Disclaimer: we're all different


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## flux (Dec 13, 1998)

> quote:The second one I was unable to pull off on Pub Med. i wonder why?


Probably a DDW submission. They're not entered into Pubmed.


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## bonniei (Jan 25, 2001)

Thanks flux.Snookered i had the fructose intolerance hydrogen breath test done. They gave me pure fructose to ingest. i am unlike most people on the board who say they are fructose intolerant, i actually had the test done.secondly it coould be just the fiber allowing me to have a good BM becauae most fructose filled items are fibrous. However if i have many glasses of fruit juice or tomato juice i get loose stools. i don't know if juice contains pectin. i could try your experiment as well.Hi Talissa I had probiotics over two years ago. VSL#3. It helped me but it got too costly. I prefer diet manipulation to spending money. Diid you have the fructose malabsorption test done?


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## I'll B Snookered (Apr 9, 2004)

Oh, no flux. I'm going to call your boss. Get back to work, you scoundrel. Actually, flux, I'd like to hear you tell a joke. Tell a joke, and I won't call your boss. No pictures, please.


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## bonniei (Jan 25, 2001)

flux actually has quite a nice sense of humor. I too wish he would come up with original jokes other than pics. Although some of his pics are quite humorous if you think of what he had to put in the search engine to come up with them. But flux, you have a good sense of humor, why don't you show that off?


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## I'll B Snookered (Apr 9, 2004)

Bonniei,I don't really believe the whole fiber thing, but I think fruit is good because of fructose, pectin, and vitamin C. I am not fructose intolerant, thank goodness, as I eat at least three servings of fruit per day...helps me go! go! go! Well, maybe I just go.


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## bonniei (Jan 25, 2001)

Fiber is real, snookered. It traps water and gas and helps to bulk up stools. It doesn't work though on people with slow motility. Definitely must be tried for C. Atleast 20 g of fiber.


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## I'll B Snookered (Apr 9, 2004)

I know all that jazz, bonniei. I actually do take fiber everyday. It helps moderate a little in either direction. In fact, I eat lots, but not because I think it helps. I just eat lots of fruit and some cooked veggies. I just don't think fiber's the answer. Fiber doesn't make or break my day. It just makes it a little better.


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## bonniei (Jan 25, 2001)

It is true that it might not help IBS'ers much. Way less than docs make you believe. I recently saw a study that soluble fiber helps IBS'ers more than insoluble fiber but here is the punch line- insoluble fiber does not help significantly more than a placebo.







So I hear you!


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## eric (Jul 8, 1999)

First of all Kel, the UNC just released their Annual report for 2004 on funding and on current research projects, I think you ought to read it before you make accusations about the people there, doing excellent research on IBS and other functional disorders. Yes, they are funded by pharms and so is Mayo and UCLA and every other hospital you can think of and even the Doctors your posting here. *Are you opposed to all drugs for all people?* also, why don't you let people read the information and decide what they want instead of saying serotonin is unimportant! Obviously it is important!!!also do you know what peer reviewed means????secondagain I will say this to you.The whole world of doctors and drug companies are all in a huge conspiracy out to get kel.So they post tons of medical information to the national library of medicine and include it in continuing medical education information to doctors and pass it all on to UCLA, Harvard, UNC, mayo, cleveland clinic, Johns Hospkins and everyone else.Go back to figuring out quantum mechanics and homeopathy, what you do best.But again its wrong. This is the combined research from around the world and from many sources other then drug company money. A lot of this research has also been funded by the National Institute of health and other organizations, not connected to drug companies.It is also basic science research over a broad spectrum of sciences from almost every country and then peer reviewed years now.I am glad you understand this all so well and consider yourself such an expert to make those statements.You have no idea what your taking about. This is not helpful. It was not drug company money that lead to the discovery of serotonin and its role in gut function, it was a Doctor, the worlds leading expert on the enteric nervous sytem and a NIH grant."Next you don't even understand what you say you have? *What kind of Dysbiosis do you have?* *Putrefaction Dysbiosis?* *Lack of fiber Dysbiosis?* *Fermentation Dysbiosis ?* *Diet Dysbiosis?* *Medication Dysbiosis?* *Stress Dysbiosis?* Also Leaky gut is not a disease!!! You don't even understand what you think you have?Guess what folks leaky gut is a functional disorder!If the system is not functioning properly!also Leaky gut is caused by inflammation, that is not seen in IBS, the way people here THINK it is and are portraying it, its not overt inflammation, it is specific cells!!! They do not see it, until they peel back the layers of the digestive system and then it is macroscopic, specific cells, in some IBSers. Second, there is good reason to believe there is abnormal flora, BECAUSE of altered transit in some IBSers for one. The sigmoid colon can contract abnormally anywhere along its length in IBS, this traps foods that ferment which can alter bacterial flora. But there can be many reasons for abnormal flora anyway, diet, meds, enviroment, alcohol and others. So far probiotics do seem to have a role in treatment in IBS. Some for reasons not even mentioned here. Bonniei, "I think it is wrong of you to talk solely on serotonin."Its for a very important reason. *Serotonin intiates the Peristaltic Reflex. * "Irritable bowel syndrome (IBS) is the most common functional bowel disorder and has a strong predominance in women. Recent data suggest that the brain may play an important role in the pathophysiology of IBS in the brain-gut axis. It is strongly suspected that serotonin (5-HT), a neurotransmitter found in the brain and gut, may be related to the pathophysiology of IBS." http://www.mdlinx.com/GILinx/thearts.cfm?a...pecid=13&ok=yes "What causes IBS?Unfortunately in the past, patients with IBS were looked upon as having a psychosomatic condition. Research has shed a new light and shown that the disorder has a real physiologic basis. Not only do patients with IBS seem to have a lower threshold for feeling pain and bloating in the gut, but there also seems to be an alteration in motor activity in the intestine. This increased sensitivity occurs because there is a change in normal communication between the nervous system in the gut (the enteric nervous system) and that in the brain and spinal cord (the central nervous system). The enteric nervous system controls not only the motion of the intestine and the perception of pain, but also the ability of the intestines to secrete various substances involved in digestion via chemicals called neurotransmitters. One of the most important of these chemicals seems to be 5-hydroxytrptamine (5-HT), also known as serotonin. There are currently at least 20 different receptors in the body for serotonin. The ones most related to gut function are the 5-HT 3 and 4 receptors. The receptor determines the function that serotonin will have in the gut. Serotonin seems to be particularly important in IBS. Studies indicate that patients with diarrhea-predominant IBS secrete more serotonin after a meal than patients without IBS. This high level of serotonin is thought to stimulate increased movement of the intestine. Further evidence for this difference in processing neurotransmitters in patients with IBS and normal patients lies in the area of Functional MRIs (magnetic resonance imaging studies). Studies show that when a balloon is distended in the intestine of IBS patients there is increased blood flow to areas of the brain that process the emotional response to pain. ""2. What is serotonin and what role does it play in IBS?Serotonin, or 5-hydroxytryptamine (5-HT), is a peptide that is found throughout the body. Approximately 96% of serotonin is located in the gastrointestinal tract, 2% in platelets, and 2% in the CNS. More than 20 types of serotonin receptors at various locations in the human body have been described, but the receptors that seem to be most important in the gastrointestinal tract in general and in IBS in particular are the 5-HT3 and 5-HT4 receptors.Because the structure of the receptor determines the function of the peptide, serotonin has slightly different functions when paired with each different receptor. Generally, these receptors are involved in controlling the motility of and secretions in the gut and the perception of abdominal pain. Typically, 5-HT3 and 5-HT4 receptor agonists promote motility and the antagonists decrease motility. Although the exact mechanism is not known, these receptors do not function properly in IBS." *It also is a clue as to why there is D IBS, C IBS, and alternating D and C IBS. *It may also be a clue to what they see in the brain in emotions and pain. In fact with lotronex, they studied just that.although it did not correalate completely to specific abnormalities of the brain seen in other studies, the ACC."BETHESDA, MARYLAND (September 30, 2002) - The October issue of the journal Gastroenterology includes two studies focusing on how drugs affect the central nervous systemï¿½s control of the gut.Lotronex May Improve IBS by Attenuating Activity in Brain Regions Responsible for EmotionResearchers studying this drug to treat IBS found that it acts in part on the portion of the brain responsible for control of the gut and expression of emotion in the body. These findings substantiate the previously unconfirmed belief of a mind-gut connection in IBS.In the study, 49 non-constipated IBS patients received brain scans before a randomized, placebo-controlled three-week trial with Lotronex. Patients were given rectal and sigmoid distensions, a procedure that inflates the rectum and sigmoid colon with a computer-controlled barostat device. Brain scans assessed patientsï¿½ blood flow to the limbic (emotional) motor system and the pain processing regions of the brain before and during distension.Compared to placebo, Lotronex improved IBS symptoms and reduced blood flow in areas of the brainï¿½s emotional motor system, but not in areas previously reported as being activated by pain. Reduction in blood flow to the emotional motor system was greatest when patients were in a resting state, anticipating distension, and was partially reversed during the actual distension."These findings suggest that Lotronex, in addition to its documented peripheral effect on the enteric nervous system in the gut, may act in part by regulating activity in limbic brain regions, which may be overactive in many patients with IBS," said Emeran A. Mayer, MD, professor of medicine and physiology, UCLA School of Medicine."They knew there were problems in the limbic system in IBS. It is important to realize it maybe just one really important player in the whole picture, it maybe the abnormallities in serotonin transport, also give rise to other system abnormalities.Like dominoes perhaps. This is not fully clear yet of course and there is a lot of research to be done for sure.Second, the treatments work for some people with the new drugs, third, many other studies support the brain gut axis roles and four a whole lot of people get better, with treatments, even relaxtion techniques that modulate serotonin regulation. also, there are sleep problems in IBS and appetite problems for example.Serotonin helps regulate, mood, emotion, sleep and appetite, and gastrointestinal function.The fact is they do not have the whole picture in IBS yet, but many clues already.Two important cells in IBS are enterochromaffin cells, that store the majority of serotonin. And Mast cells.I just want to add to bonniei also, both of these cells are increased in Post infectious IBS. It is also important that Post infectious IBS, leads to IBS it seems, it is the early stages of full blown IBS after the intial inflammation and infection has resolved.It is also important then to understand that stress plays and important role at the time of infection and then very importantly the role chronic stress plays in full blown IBS after the intial infection has resolved. It is also very imortant again to understand the communication between the gut brain and the brain and back, the brain gut axis, again not a theory but systems that very much interact with each other. There is also a difference between the brain gut axis in all humans, and the brain gut connection in IBS. There needs to be more work also on the brain, to see what is really happening there in regards to all IBS. Do IBSers process pain differently from signals from the gut, or is there a speciffic problem in the brain ect ect. However, the brain and the gut are both operational to cause the symptoms. of IBS, that is already known. For one all pain is processed in the brain.Also before this is taken as nothing but drug talk understanding it will lead to natural therapies and treatments.This is what I have been saying for years here now, about the researchers saying a HOLISTIC approach based on what they know now can help most IBSers and why education on complex issues is very important for people to learn and understand as much as possible.Two important systems in IBSthe serotonin systemand the hpa axis systemPREVALENCE AND EPIDEMIOLOGYIrritable bowel syndrome (IBS) is the most commonfunctional gastrointestinal (GI) disorder with worldwideprevalence rates ranging from 9-23%. Functionaldisorders are conditions where there is an absence ofanatomical or biochemical abnormalities on diagnostictests which could explain symptoms. IBS is a chronicfunctional bowel disorder characterized by abdominal painor discomfort and alterations in bowel habits. It is the mostcommon disorder diagnosed by gastroenterologists andaccounts for up to 12% of total visits to primary careproviders Gender appears to play an important role in IBS.Two-thirds of individuals with IBS are female with anestimated prevalence in women ranging from 14-24%. Ofthose who seek healthcare services including tertiary andambulatory care for IBS and other functional boweldisorders, women lead men by a ratio of 2-2.5:1 whileothers estimate the rate to be higher at 3-4:1. However, thegender distribution appears to be less than 2:1 among IBSnon-patients (individuals with symptoms of IBS but whohave not sought health care) in the community. It is notknown if this increased female prevalence represents areporting bias, i.e. if female patients are more willing thanmen to disclose that they have IBS-related symptoms, or ifit represents a biological difference. Not all individuals with IBS symptoms seek medical carefor their symptoms. Based on different epidemiologicalstudies performed in different countries, 20-75% ofindividuals meeting symptom criteria for IBS will seekmedical care for their symptoms at some point in theirlives. There are between 2.4 and 3.5 million annualphysician visits for IBS in the United States, during which2.2 million prescriptions are written. The cost to society interms of direct medical expenses and indirect costsassociated with loss of productivity and work absenteeismis considerable. It has been estimated that the total cost ofIBS is 30 billion dollars per year which includes 20 billiondollars for indirect costs and 10 billion dollars for directcosts.SYMPTOMS OF IBSGastrointestinal (GI) symptoms.The hallmark symptomsof IBS are chronic abdominal pain and/or discomfort andalterations in bowel habits, such as diarrhea, constipationor alternating diarrhea and constipation. Abdominal painhas been reported as primarily crampy or as a generalizedache with superimposed periods of abdominal cramps,although sharp, dull, gas-like, or nondescript pains are alsocommon. The intensity and location of abdominal pain inIBS are highly variable, even at different times within asingle patient. The abdominal pain and/or discomfortexperienced by IBS patients is often severe enough tointerfere with daily activities. Several factors exacerbate orreduce the pain of IBS. Many IBS patients reportincreased symptoms during periods of stress or emotionalupset such as job or marital difficulties. Defecation mayprovide temporary relief from the abdominal pain of IBS,whereas ingestion of food may exacerbate the discomfortin a subset of patients. Based on bowel habits, patients are commonly sub-classified into those having mainly diarrhea, mainlyconstipation, and those alternating between the twopatterns. IBS patients with constipation may experienceinfrequent bowel movements (3/week), hard stools,straining, and sensation of incomplete evacuation. IBSpatients with primarily diarrhea report frequent bowelmovements (3/day), loose and/or watery stools frequent,and urgency. The prevalence of the difference subgroupsbased on bowel habits is similar. Other common IBSsymptoms include bloating, visible abdominal distension,and mucus in the stool.Upper gastrointestinal symptoms are commonly reportedby IBS patients with 25% to 50% of patients reportingheartburn, early satiety, nausea, abdominal fullness, andbloating. Up to 87% have reported intermittent upperabdominal discomfort or pain (dyspepsia) byapproximately 40% of patients. Extra-intestinal symptoms and overlap with othercommon pain syndromes.Many IBS patients also reportextra-intestinal (non-gastrointestinal) symptoms such asfatigue, muscle pain, sleep disturbances, and sexualdysfunction. Up to two-thirds of IBS patients report extra-intestinal symptoms compared to less than 15% of healthyindividuals. These extra-intestinal symptoms may be dueto IBS co-morbidity with other stress-related syndromessuch as fibromyalgia, chronic fatigue syndrome, andinterstitial cystitis. Epidemiological studies have confirmedthe clinical impression that IBS frequently overlaps withthese other conditions in the same patient, suggestingshared pathophysiologic mechanisms. Psychological symptoms.Some IBS patients also havepsychological distress symptoms such as anxiety anddepression particularly in those with severe symptoms andhealth care seeking behavior. Somatization, anxiety anddepressive disorders are also more commonly seen in IBSpatients than in healthy controls. Psychosocial trauma andearly adverse life events (e.g., parental separation orphysical/verbal/sexual abuse history) may profoundlyaffect symptom severity, daily function, and healthoutcome. Although these adverse events such as abusemay be quite prevalent in IBS patients, a significantnumber have not discussed this with anyone and a smallernumber will actually inform their physicians.DIAGNOSIS OF IBSThe diagnosis of IBS is based on identifying characteristicsymptoms and excluding organic disease. An earlyconfident diagnosis permits tests to be minimized andreassures the patient that there is no lethal disease. Thereare no physical findings or diagnostic tests that confirm thediagnosis of IBS. Therefore, diagnosis of IBS involvesidentifying certain symptoms consistent with the disorderand excluding other medical conditions which may have asimilar clinical presentation. The symptom-based Rome IIdiagnostic criteria for IBS (Table 1) emphasize a ï¿½positivediagnosisï¿½ rather than exhaustive tests to exclude otherdiseases. A validation study of the Rome criteria afterexcluding patients with symptoms suggestive of othermedical conditions other than IBS (ï¿½alarm signsï¿½ e.g.bloody stools, weight loss, family history of colon cancer,refractory and severe diarrhea) showed that 100% ofindividuals who met the diagnosis of IBS based on theRome criteria truly had IBS rather than an alternativediagnosis. At 2 years follow-up, none of the IBS patientsrequired a change in diagnosis.Other medical conditions which may present withsymptoms similar to those seen in IBS includeinflammatory bowel disease, GI infections, lactoseintolerance, thyroid disease, microscopic or collagenouscolitis and malabsorption syndromes such as celiac sprue(Table 2). A medical history and physical examination,laboratory and GI tests can help to exclude these otherdiagnoses. These tests include routine blood tests, stoolstudies for infection, and endoscopic procedures such asupper endoscopy, sigmoidoscopy and colonoscopy. Inpatients 50 years of age who meet diagnostic criteria forIBS and have no ï¿½alarm signsï¿½ suggestive of diseases otherthan IBS, initial screening tests such as a complete bloodcount to check for anemia and a chemistry panel can beobtained. Other screening tests to consider are a thyroidtest (TSH) and a blood test for celiac sprue. However,further tests and procedures such as a colonoscopy are notgenerally recommended. Patients 50 years of age withIBS symptoms should undergo a screening colonexamination with either a colonoscopy or flexiblesigmoidoscopy and barium enema if these tests have notbeen done previously, regardless if they have alarm signs(see Figure 1).In some centers, the presence of bacterial overgrowth isoften determined because this condition may causesymptoms similar to those of IBS. It is most commonlydiagnosed by a lactulose hydrogen breath test. Two studiesfrom the same research group found that 78% to 84% ofpatients with IBS had bacterial overgrowth. In patientswith evidence of bacterial overgrowth, those treated withan antibiotic such as neomycin had a greater reduction intheir GI symptoms compared with placebo. Although thesedata are intriguing, there are some methodologiclimitations in these studies and, therefore, the use ofwidespread hydrogen breath testing for bacterialovergrowth is still not generally advocated. PATHOPHYSIOLOGIC MECHANISMS OF IBSAlthough psychological and physiological abnormalitieshave been described, the overall pathophysiology of IBS isnot well understood. Similar to other chronic medicalconditions, a multi-component conceptual model of IBS,which involves genetic, physiologic, emotional, cognitive,and behavioral factors, has been formulated (Figure 2).Although all factors are closely interconnected, theimportance of individual factors in the generation of IBSsymptoms may vary greatly between individuals.Previously, IBS was considered primarily a disorder ofaltered gut motility. Currently, increased bowel sensitivity(visceral hypersensitivity) and altered brain-gutinteractions are felt to play a principal role in thepathophysiology of IBS. Recently, it has been found thatgenetic and environmental factors are important in IBS butfurther studies are needed to understand the importance ofthese factors in the prevalence, symptoms, physiologicresponses and response to treatment in IBS.Altered intestinal motor function.Altered intestinalmotility has been found in IBS, particularly exaggeratedcontractions (motor response) in the lower (sigmoid) colonto psychological stress and food intake. These alterationsmay explain why many IBS patients experience typicalIBS symptoms following meals and develop exacerbationsduring stressful life events. These changes in bowelmotility are likely due to alterations in the autonomicnervous system outflow to the intestine. Increased gut sensitivity.There has been compellingevidence that IBS patients have enhanced perception ofbowel (visceral) stimuli such as food or distensions of thegut wall. The initial clinical observations that led to thehypothesis that patients with IBS have visceralhypersensitivity included the presence of recurringabdominal pain as a principal symptom, the presence oftenderness during palpation of the sigmoid colon (leftlower abdominal area) during physical examination inmany patients, and excessive pain often reported bypatients during endoscopic examination of the sigmoidcolon. Published studies measuring visceral sensitivitysuggest that a variety of abnormal sensations orperceptions in relation to bowel stimuli may be morefrequent in IBS patients. At least two perceptualalterations can be distinguished, a hypervigilance(increased attention or vigilance) towards expectedaversive events arising from the bowel, and hyperalgesia(lowered threshold to pain) which is inducible by sustainedpainful visceral stimulation. These findings are paralleledby similar findings of target system hypersensitivity inother disorders such as fibromyalgia and myofascial paindisorder. In contrast to their enhanced perception ofvisceral pain, most IBS patients have normal or evendecreased pain sensitivity and tolerance for painful coldand mechanical stimulation of somatic (skin and muscle).However, there is a recent study that has demonstratedincreased somatic sensitivity to thermal heat in IBSpatients. Patients with IBS who also have co-existing fibromyalgia have increased somatic sensitivitycomparable to patients with fibromyalgia alone.Increased stress mediators in IBS.There is increasingevidence to support the prominent role of stress in thepathophysiology and in the clinical presentation of IBSsymptoms. There are few published reports on alterationsin stress mediators, such as catecholamines and cortisol tostress or visceral stimulation in IBS. Several studies havereported increased in catecholamines (norepinephrine andepinephrine) and cortisol levels in IBS patients. However,it remains to be determined whether these neuroendocrinealterations play a direct role in gut function and symptomgeneration. Altered brain-gut communication in IBS.A unifyinghypothesis to explain the functional bowel disorders is thatthey result from a dysregulation of the brain-gut axis. Anevolving theory is that normal gastrointestinal functionresults from an integration of intestinal motor, sensory,autonomic and CNS activity and GI symptoms may relateto dysregulation of these systems. Brain imaging studiessuch as functional magnetic resonance imaging (fMRI) andpositron emission tomography (PET) have been performedin IBS patients to measure brain activation patterns tovisceral stimuli. These studies suggest that brainactivation responses to visceral stimuli are distinctlydifferent in IBS patients compared to healthy individuals.IBS patients may have different emotional and cognitiveprocessing of sensory information from the gut comparedto healthy individuals. Post-infectious IBS.Symptoms suggestive of IBS occurin approximately 7-30% of patients following acute GIinfections, often persisting for years following completeresolution of the infection. A large cohort study identifieda self-reported history of acute gastroenteritis as a majorrisk factor for the development of IBS. Reported riskfactors for the development of post-infectious IBS includefemale sex, the duration of the acute diarrheal illness andthe presence of sustained psychosocial stressors around thetime of infection. Post-infectious IBS is not restricted to aparticular organism and has been documented with avariety of bacterial infections (Salmonella, Campylobacterand E. coli) as well as parasitic infection. However, therole of acute viral gastroenteritis in this condition isunknown.In post-infectious IBS, low grade GI inflammation orimmune activation may be a basis for altered motility,and/or nerve and mucosal (lining of bowel) function of thegut in IBS. Recent studies have also shown that in a subsetof unselected IBS patients (no documented history of apreceding gut infection), there is evidence of increasedinflammatory cells in the colon mucosa. It remains to bedetermined if altered gut immune function is a generalcharacteristic of IBS patients. The implication of stressfullife events in the development of post-infectious IBSsuggests a convergence of central (brain) and peripheral (gut) mechanisms in the clinical presentation of thissyndrome.Gender differences.In addition to IBS, many functionalGI disorders and other chronic visceral pain disorders (e.g.interstitial cystitis and chronic pelvic pain) and somaticpain disorders (e.g. fibromyalgia, myofascial paindisorder) are more common in women than in men.Increasing evidence suggests that gender differences existin the symptoms, pathophysiologic responses and responseto certain treatments in IBS. Female IBS patients are morelikely to be constipated, complain of abdominal distensionand certain extra-intestinal symptoms. Studies have alsosupported an influential role of ovarian hormones (e.g.estrogen and progesterone) on bowel function and painsensitivity which can in part explain the gender differencesin IBS. Several investigators have reported a variation inGI symptoms during different phases of the menstrualcycle, particularly increased abdominal pain and loosestools at the perimenstrual (just prior to and at time ofmenses) phase. TREATMENTTreatment of IBS includes both non-pharmacologic andpharmacologic therapies. An important component of non-pharmacologic treatment for IBS is a successful physician-patient relationship. The physician should strive toestablish effective bi-directional communication with thepatient, gain the patientï¿½s confidence with a concise,appropriate medical evaluation and offer reassurance andeducation that IBS is a real medical condition with apotential impact on health related quality of life butwithout significant long/term health risk. Some IBSpatients, especially those presenting with new onset ofsymptoms, express relief that their symptoms are notcaused by a serious condition such as malignancy. Othercomponents of non-pharmacologic treatment of IBSinclude diet recommendations, lifestyle modifications, andpsychosocial intervention if needed. Patients with mild IBS symptoms comprise the mostprevalent group, and are usually treated by primary carepractitioners, rather than specialists. These patients haveless significant functional impairment or psychologicaldisturbance. These patients do not see a clinician veryoften, and usually maintain normal daily activities.Treatment is directed toward education, reassurance, andachievement of a healthier lifestyle and occasionalmedication. Dietary advice may include avoidingoffending foods which can trigger symptoms (e.g. lactoseor fructose products, fatty foods, caffeine, gas-producingfoods). Fiber supplementation has been shown to beeffective for symptoms of constipation. Pharmacologic therapy is best used in IBS patients withmoderate to severe symptoms refractory to physiciancounseling and dietary manipulations. First line treatmenthas traditionally been aimed at treating the mostbothersome symptom because of the lack of effectivetreatment for the overall improvement of multiplesymptoms in IBS patients. However, new therapies forIBS have been recently introduced and have been shown toeffectively treat multiple symptoms of IBS.Anticholinergic/Antispasmodic agents.After fiberpreparations, antispasmodic agents are the next mostcommonly prescribed group of medications for thetreatment of IBS. However, several studies do not providefirm evidence that anticholinergic agents are efficacious inthe IBS population as a whole. Only a few of theseantispasmodics have been shown to be more effective thanplacebo in relieving abdominal pain in high quality clinicalIBS trials but these are not currently available in the U.S. Antidiarrheal agents.In IBS patients with diarrhea,antidiarrheal agents such as loperamide and diphenoxylatecan be effective in decreasing bowel movement frequency,improving stool form by enhancing intestinal water and ionabsorption, and increasing anal sphincter tone at rest.These physiologic actions seem to explain theimprovement in diarrhea, urgency, and fecal soilingobserved in patients with IBS. These medications do nottypically relieve abdominal pain and may causeconstipation.Psychotropic medications.The rationale of using thisclass of drugs in IBS may relate to several factors, such asthe prominent co-morbidity of IBS with psychologicdistress symptoms and the effects of these agents on gutmotility and pain sensation. Among the classes ofantidepressant medications, the tricyclics have been mostextensively evaluated in IBS. At lower doses than thoseusually used to treat depression (starting at 10 mg and upto 75 mg nightly), amitriptyline and desipramine have beenfound to be significantly more effective than placebo inpatients with IBS. Antidepressants have analgesic (painrelief) properties, which may benefit patientsindependently of the psychotropic effects of the drugs.Treatment with tricyclics should begin with low doses(e.g., 10 mg/day) and increased as needed up to fulltherapeutic doses. Selective serotonin reuptake inhibitors(SSRIs, e.g. paroxetine, citalopram) and selective serotoninand noradrenergic reuptake inhibitors (SNRIs, e.g.venlafaxine) have not been well studied for treatment ofIBS, and are more expensive, but have less side effectsthan tricyclics and empirically may help reduce painfulsymptoms and improve general well-being and quality oflife.Novel serotonin agents.The prominent role of serotoninin GI motility and sensation has led to the development ofnovel serotonin agents such as alosetron and tegaserod inthe treatment of IBS. Most of serotonin (also known as 5-HT) in the body resides in the bowel wall withinenterochromaffin cells lining the gut (mucosa) and nervecell bodies. Serotonin is released from theenterochromaffin cells and acts on receptors on the nerveswithin the bowel wall. These nerves may be part of the nervous system which resides completely within the bowelwall, known as the enteric nervous system, or may benerves that transmit painful and non-painful informationby projecting from the bowel to the spinal cord and brain.Activation of these nerves by serotonin leads to the releaseof other neurotransmitters and through their actions, itplays a major role in gut motility, secretion and sensation.Alosetron (Lotronex&#63194







, which is a 5-HT3 antagonist, hasbeen shown to be effective in relieving pain, normalizingbowel frequency, and reducing urgency in non-constipatedIBS female patients. This medication was approved by theFDA last year but was later withdrawn because of theadverse events of constipation and ischemic colitis, thelatter being observed in 0.1%-1% of patients receiving themedication. Future studies are being planned to determineif there is a causal association of alosetron and ischemiccolitis. However, alosetron has recently been re-approvedand now is available for the treatment of women withsevere diarrhea-predominant IBS under the Restricted UseProgram. Alosetron is indicated only for women withsevere diarrhea-predominant IBS who have: chronic IBSsymptoms (generally lasting ≥ 6 months), no evidence ofanatomic or biochemical abnormalities of the GI tractwhich could explain their symptoms, and failed to respondto conventional therapy. IBS is considered severe if itincludes diarrhea and ≥ 1 of the following: frequent andsevere abdominal pain/discomfort, frequent bowel urgencyor fecal incontinence, or disability or restriction of dailyactivities due to IBS. Physicians must enroll in theRestricted Use Program in order to prescribe alosetron.Patients should discuss with their physicians about therisks and benefits of the medication before beingprescribed it. Both should sign the Patient-PhysicianAgreement form. The starting dose of alosetron is now 1mg orally once daily. If the patient does not experiencecomplete relief of their symptoms after 1 month, the dosecan be increased to 1 mg orally twice daily which was theoriginally approved dose. Any patient who experiencesincreased abdominal pain, blood in their stool and/orconstipation should immediately stop their medication andcontact their physician. Tegaserod (Zelnorm&#63194







is a partial 5-HT4agonist, whichhas been shown to be effective in relieving the globalsymptoms of IBS with constipation. It has been recentlyapproved for the treatment of IBS with constipation inwomen. Tegaserod has been shown to accelerate GI transittime in IBS patients and therefore would increase stoolfrequency, and increase electrolyte secretion in the boweland thus improve stool form. In addition to its motilityenhancing properties, tegaserod has been shown to havepain inhibitory properties in animal studies and thereforemay reduce abdominal pain although human studies areneeded to confirm this effect. Unlike other currentlyavailable medications for IBS with constipation, tegaserodappears to be effective in treating the multiple symptomsof IBS. The subjectï¿½s global assessment of relief of IBSsymptoms, change in number of bowel movements, abdominal pain and bloating are all reportedly improved infemale patients with IBS with constipation takingtegaserod as compared to placebo. The only adverse eventswhich were seen at a small but significantly higher rate inpatients taking tegaserod compared to placebo wereheadache and transient diarrhea. Psychological treatments.Referral for psychologicaltreatment can be recommended as part of a multi-component treatment program to help the patient bettermanage the symptoms, or to address psychosocialdifficulties (e.g., abuse, loss) that may be interfere withdaily function and ability to cope with the illness. Ingeneral, these treatments are reserved for patients withmoderate to severe symptoms, particularly if theyexperience psychological distress. However, the patientmust be motivated and see this type of treatment asrelevant to their personal needs. Psychological treatmentsused to treat IBS include psychotherapy (dynamic andcognitive-behavioral therapy), relaxation therapy,hypnotherapy, and biofeedback therapy. Psychologicaltreatments can also be combined. Review of well-designedtreatment studies of IBS supports the superiority ofpsychological treatment over conventional medicaltherapy. Follow-up studies (duration 9-40 months), havedemonstrated that psychological treatment maintainedsuperiority over placebo, indicating that these methodshave lasting value. The choice of treatment will depend onpatient requirements, available resources and theexperience of the therapist. CONCLUSIONSIBS is a common, chronic disorder characterized byexacerbations and remissions, which presents withsymptoms of abdominal pain and/or discomfort and alteredbowel habits. It has a chronic relapsing course and canoverlap with other functional GI (dyspepsia) and non-GI(fibromyalgia) disorders. The clinical diagnosis of IBS is based on identifyingsymptom criteria with a ï¿½positive diagnosisï¿½ and excludingorganic disease with minimal diagnostic evaluation.Clinicians should feel secure with the diagnosis of IBS, ifmade properly, because it is rarely associated with otherexplanations for symptoms. Although there are manyexpensive and sophisticated tests available for theevaluation of IBS symptoms, these are generally notneeded for patients with typical symptoms and no featuressuggestive of organic diseases.An integrated diagnostic and treatment approach firstrequires an effective physician-patient relationship. Acareful history will also identify the need for diagnosticstudies and treatments as determined by the nature andseverity of the predominant symptoms, and the degree andextent of influencing psychosocial and other factors. The fact that definite structural or biochemicalabnormalities for these disorders cannot be detected withconventional diagnostic techniques does not rule out thepossibility that neurobiological alterations will eventuallybe identified to explain fully the symptoms of mostfunctional disorders. Examples of such a shift inperspective from symptom-based disorders withoutdetectable abnormalities to medically treatable diseasesbased on specific neurobiological alterations includeaffective disorders (depression, anxiety) and migraineheadaches. Similar to other chronic illnesses, amulticomponent model that involves physiologic,affective, cognitive, and behavioral factors can beformulated for IBS. Although all factors are closelyinterconnected, the importance of individual factors in thegeneration of IBS symptoms may greatly vary betweenindividuals. Physiologic factors implicated in thegeneration of IBS symptoms include hypersensitivity ofthe GI tract to normal events, autonomic dysfunctionincluding altered intestinal motility response to stress andfood intake, alterations in fluid and electrolyte handling bythe bowel, and alterations in sleep. Many of the traditional therapies have been used to treatspecific IBS symptoms because they have not been shownto significantly relieve global symptoms, which wouldimprove an overall sense of well-being. However, thediscovery of novel serotonergic agents such as tegaserodand alosetron have been shown to be effective in treatingglobal symptoms in patients with IBS compared withplacebo. More recently published studies evaluating theefficacy of antidepressants, such as tricyclics and SSRIs,suggest that these medications may help improve generalwell-being in addition to treating psychological co-morbidity in affected individuals but further studies areneeded. Psychological and behavioral therapies have alsobeen showed to be effective for IBS however it potentiallycan be limited by the availability of experienced therapists.Instituting a multidisciplinary approach using non-pharmacologic and pharmacologic therapeutic modalitiesmay result in the most effective outcome. Future studieswill further enhance our understanding of this conditionand lead to newer, more effective treatments. http://216.109.117.135/search/cache?p=lin+...&yc=15315&icp=1


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## eric (Jul 8, 1999)

oops


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## scottyswotty (Jun 29, 2000)

Now those are two long posts! Come'on guys this is getting nowhere?!! Time to be a bit more mature and declare stalemate.


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## bonniei (Jan 25, 2001)

Well erivc I do understand the importance of serotonin but you were unable to explain the contradiction I came up with. Perhaps you shold have said that you didn't know the answer instead of sendsing me on a wild goose chase. I say wild goose because when I concluded that the balance between serotonin and norepinephrine is important and that is the only thing from your article which explains the contradiction I came up with, it looks like you are not happy with my answer. Well I am not satisfied with your ansswer either. In fact you have no answer for the contradiction I came up with and you might as well admit it instead of expecting me to read another long article.


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## eric (Jul 8, 1999)

oop's"It may also be a clue to what they see in the brain in emotions and pain. In fact with lotronex, they studied just that.although it did not correalate completely to specific abnormalities of the brain seen in other studies, the ACC."The limbic system is part of th ACC.This was back in 97"The most prominent brain region found to be activated in response to intestinal stimulation in healthy subjects was a specific area within the anterior cingulate cortex which forms part of the limbic system. The limbic system, which has also been referred to as the ï¿½visceral cortexï¿½ plays a prominent role in a wide range of functionsï¿½from maintaining homeostasis, to autonomic control of the digestive system, to pain perception to the generation of feelings and emotions, and to memory of past emotional states. The specific area within the anterior cingulate cortex identified in the brain imaging studies plays a prominent role in several aspects relevant to IBS symptoms: 1. It is the ï¿½executive areaï¿½ in the regulation of colonic motility and water absorption which in turn determines the frequency and consistency of bowel movements. 2. It is part of the medial pain system which determines the affective component (i.e. the degree of suffering or unpleasantness) associated with pain perception. Specific regions with the medial pain system play an important role in suppressing the perception of pain by releasing endorphin molecules (the bodyï¿½s own painkillers), while other regions participate in the memory formation of past painful experiences. 3. The brain region identified by the UCLA researchers plays a prominent role in the regulation of maternal behaviors and is crucial for mediating communication between newborns and their mother." http://www.cns.med.ucla.edu/Articles/Patie...eakthroughs.htm "Brain PhysiologyStress reproducibly alters gastrointestinal motility and sensation. The release of corticotropin releasing factor from the hypothalamus may mediate the stress response. Brain centers important in mediating visceral pain include the thalamus (general sensory), insular cortex (visceral sensory), anterior cingulate cortex (general pain awareness), and prefrontal cortex (general pain processing). Visceral pain in IBS is associated with increased prefrontal cortex activation. The normal correlation between subjective pain intensity and activation of the anterior cingulate and insula cortices is lost in IBS. The limbic system is involved in emotion, mood, and visceral autonomic control. Limbic abnormalities are seen in depression and IBS. Thus, this system is a possible site of convergence where emotional disturbance provokes intestinal dysfunction. " http://www.fdhn.org/html/education/gi/ibs_nosology.htm


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## bonniei (Jan 25, 2001)

Was that oops for being a little trigger happy ?


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## eric (Jul 8, 1999)

double post oop's Bonniei







Wasn't trying to ignore the question Bonniei.Although I must admit I have been looking more at the misinformation. And got sidetracked. Although I might not know the answer anyway. LOLThis is very complex and I am still learning here as well.Could you repeat the question for me, something about the serotonin re uptake?Sorry it's been a long day.


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## bonniei (Jan 25, 2001)

Follow the logic hereI don't know if i was being clear or not and if that was the reason i didn't get an answer or if eric and flux, you just don't have the answers. I will give it one more try.1) Lotronex blacks the release of serotonin in the gut because serotonin leads to peristalsis2) So if you have D you don't want excess serotonin in the gut and would like the capacity to reuptake serotonin in the gut.3) So if you have C you want the opposite to happen ie you want excess serotonin in the gut to initiate peristalsis4)So you don't want to reupptake serotonin if you have C5) So it is good to have the SERT transporter if you have D and no SERT transporter if you have C6) so this part of the quote-.""findings suggest that patients with constipation and IBS may have a reduced capacity to reuptake serotonin,"This should be good for C7) But it seems it is not good because by the second part of the quote the reduced capacity to uptake serotonin leads " to excess free serotonin and then desensitization of these receptors, thus reducing motor function" 8) So reduced capacity to reuptake serotonin is not good for IBS-C i.e you want to reuptake serotonin if you have IBS-CNote 8) is in direct contradiction to 4)


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## kel1059 (Feb 28, 2003)

----"Well I am not satisfied with your ansswer either. In fact you have no answer for the contradiction I came up with and you might as well admit it instead of expecting me to read another long article."eric hardly ever has an answer for anything that is why he resorts to long cut and pastes.he is hooked on serotonin because his idols are being PAID by Novartis to overexaggerate its importance. there is big money in SSRI's-- billions in profits.why bother to understand and treat the underlying cause when you can generate millions from the sale of drugs. Symptom supression is big business.eric,i'm a bit hazy on a few details and was wondering if you could clear them up.let's see, at some point you decided to anoint yourself as "IBS-know-it-all"?you pick your "experts" based on whoever comes up with a theory that most closely matches up with your symptoms and experiences?at some point you decided to be the master controlling disperser of all information?you also decided that you --a former cook-- decide on what is correct and incorrect?and you decide on what constitutes an effective treatment and an ineffective treatment?---just nod if all these are correct.***************************************i will tell you again that i think what you did on the Dahlman threads was disgusting. you greatly interfered with the recovery of some of the people all due to your raging ego and twisted thought process.--then you try various public relations stunts (which i won't name) to try and rebuild your image among your 1/2 dozen minions. --all in the name of running a business on this forum (selling tapes, seeking donations for your website, seeking sponsors for your website, and who knows what else). the fact that you have a $$$$$$ financial interest in this whole thing is no excuse for such atrocious behavior.p.s. how do you expect to be taken seriously when your grammar is worse than a 3rd graders?(sorry people for the negativity but eric the businessman needs a wakeup call)


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## eric (Jul 8, 1999)

Bonniei,serotonin intiates peristalsisLotronex is a 5ht 3 antagonist an blocks an action. It blocks the release of serotonin at the 5ht3 receptors."So if you have D you don't want excess serotonin in the gut and would like the capacity to reuptake serotonin in the gut."You want to block the release of serotonin through the 5ht3 receptor, which leads to d.The transporter acts like a sponge. When dimminished it stays around longer in the cells." So if you have C you want the opposite to happen ie you want excess serotonin in the gut to initiate peristalsis"Yes an agonist that stimulates the action through 5ht 4 receptors.5ht3 receptors do not Intiate the peristalsisthe 5ht 4 ones do."So you don't want to reupptake serotonin if you have C"I think its more of a balance, you want more serotonin through the receptor to stimulate the action."In patients with IBS, the study found a significant decrease in serotonin content and significantly higher endocrine cell (EC) populations in patients with IBS compared to controls, *while the release of serotonin from EC cells was not significantly different. In terms of the way the body inactivates serotonin signaling, or the serotonin re-uptake system,* SERT mRNA and SERT immunoreactivity were markedly reduced. This reduction led to a decrease in the capacity to remove serotonin from intracellular space once it was released, thus increasing serotonin availability. ""(SERT). Serotonin transporters are regulatory molecules that control the activity of serotonin within nerve endings in the GI tract to coordinate motility, visceral sensitivity and intestinal secretion.""5) So it is good to have the SERT transporter if you have D and no SERT transporter if you have C"Everyone has SERT transporters." so this part of the quote-.""findings suggest that patients with constipation and IBS may have a reduced capacity to reuptake serotonin,"Through the 5ht4 receptors.I don't have a definitie answer for you yet Bonniei, maybe Flux knows and I am looking into it, but its extremely complex.I am reading also the info like you are and trying to figure some of these things out.This is important to this probaly though."Serotonin Reuptake TransporterThere is likely an evolutionary advantage to having physiologic mechanisms that regulate serotonin levels and activity, because it could be quite harmful without these regulatory mechanisms.[3] One of the primary mechanisms the body has for regulating availability of serotonin within the extracellular space is the serotonin reuptake transporter (SERT). SERT is present in the brain and gut. The amount of serotonin reuptake that occurs from the extracellular space is genetically determined and is based on whether there are long, short, or heterozygous polymorphisms in the promoter for synthesis of SERT. For instance, homozygosity for the short variant and presence of the heterozygous variant result in less transcript, less protein expression, and thus, less reuptake of serotonin. SERT activity is obviously an important factor influencing serotonin availability to act on postsynaptic receptors, and would possibly affect the response to serotonergic medications such as SSRIs, in the treatment of depression, and to the novel agents tegaserod and alosetron, for IBS.Camilleri and colleagues[46] hypothesized that differences in SERT polymorphisms in patients may influence a patient's response to the 5-HT3 antagonist alosetron. It was noted that there were both sex effects and interindividual effects in the way that the medication worked in patients, slowing intestinal transit in some with IBS more than in others. Therefore, a small study of 30 patients (15 women) with IBS with diarrhea was performed in which the patients were given alosetron 1 mg orally twice daily for 6 weeks and their colonic transit measured via scintigraphy at the end of treatment. Only 23 (12 women) of these patients actually submitted blood for analysis, but 8 long homozygous, 4 short homozygous, and 11 heterozygous SERT polymorphisms were identified. When colonic transit was measured, the patients with a long homozygous polymorphism (associated with more serotonin reuptake, ie, there is conceivably less serotonin around to stimulate the gut and peristalsis and therefore gut motility is slowed) had greater slowing of colonic transit with alosetron than heterozygotes. The importance of SERT and its effect on colonic transit response to alosetron on its clinical efficacy, as well as the vulnerability to adverse events associated with the drug, such as constipation and ischemic colitis, need to be examined."Sorry don't have a definitive answer for you on this at the moment. I will try to ask somebody about it though.


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## bonniei (Jan 25, 2001)

Could you please give me a reference for the "Altered Serotonin signaling" paper in your post on 05-07-04 at 10:49 am?. Maybe that has the answer.


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## bonniei (Jan 25, 2001)

Ok I found the reference but it is in a supplemental issue so no details are forthcomingThe American Journal of Gastroenterology Volume 97, Issue 9, Supplement 1 , September 2002, Page S274 Purpose: Serotonin (5-HT) is released from enterochromaffin (EC) cells in response to mechanical and chemical stimulation of the gastrointestinal tract. 5-HT, in turn, activates enteric neural circuitry to initiate peristalsis, and is removed from the interstitial space by the same highly selective 5-HT transporter (SERT) that terminates 5-HT's actions in the brain. Because inflammatory bowel disease (IBD) and disorders of gastrointestinal function, irritable bowel syndrome (IBS), are typically associated with changes in propulsive motility of the colon, we tested the hypothesis that 5-HT signaling is altered in Ulcerative Colitis (UC) and in IBS.Methods: To accomplish this we obtained human rectal biopsies from four groups: normal controls (n=22), ulcerative colitis (UC; N=16), IBS with diarrhea (IBS-D; N=20), IBS with constipation (IBS-C; N=10). Results: SERT-immunoreactivity was much less intense in biopsies from the UC and IBS-C specimens than normal or IBS-D. When the intensity of immunoreactivity was blindly scored on a scale of 0ï¿½3, where 0 was comparable to secondary antiserum controls and 3 represented intense immunoreactivity, the mean scores for the four groups were as follows: control, 2.7ï¿½0.1; IBD, 1.1ï¿½0.2; IBS-D, 2.8ï¿½0.1 and IBS-C, 1.3ï¿½0.3. The intensity values for the IBD and IBS-C groups were significantly lower than the control and IBS-D groups (P<0.001; ANOVA Newman-Keuls comparison test). No differences were detected amongst the groups with regard to the percentage of enteroendocrine cells that were 5-HT-positive.Conclusions: These observations may in part explain the dysmotility seen in patients with IBD and *IBS-C, as these patients may have a decreased capacity for 5-HT re-uptake from the interstitial space, leading to activation and desensitization of 5-HT receptors.* To our knowledge, this is the first report of a reliable histopathologic/immunohistochemical marker of a functional disorder in the GI tract.


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## bonniei (Jan 25, 2001)

HOwever this one says that both IBS C and IBS D have a reduced capacity to reuptake serotonin. The American Journal of Gastroenterology Volume 98, Issue 9, Supplement 1 , September 2003, Pages S262-S263 Abstracts Submitted for the 68th Annual Scientific Meeting of the American College of Gastroenterology doi:10.1016/S0002-9270(03)01562-4 Cite or link using doi Copyright ï¿½ 2003 Am. Coll. of Gastroenterology. Published by Elsevier Science Inc. Abstract Key elements of serotonin signaling are altered in IBD and IBS: support for a molecular basis of the irritable bowel syndrome Peter L. Moses M.D.*, Mathew D. Coates B.S., Christine R. Mahoney B.S., Joanna E. Sampson M.D., David R. Linden Ph.D., Jason J. Chen Ph.D., Eric B. Newton M.D., Keith A. Sharkey Ph.D., Micheal D. Crowell Ph.D., Michael D. Gershon Ph.D. and Gary M. Mawe Ph.D. University of Vermont College of Medicine, Burlington, VT; Columbia University, NY, NY; University of Calgary, Calgary, AB, Canada and Novartis Pharmaceuticals, East Hanover, NJ, USA Available online 3 October 2003. Purpose: Serotonin (5-HT) is a key neurotransmitter and signaling molecule in the gut. 5-HT release from EC cells results in transduction of luminal stimuli initiating peristaltic and secretory reflexes. While the role of 5-HT in UC and IBS is unclear, recent data suggest distinct changes of 5-HT availability in animal models and humans with IBD and IBS. The goal of this study was to determine if IBD and IBS are associated with changes in 5-HT signaling. The following properties were measured from colonic biopsies: 1) 5-HT content; 2) EC cell number; 3) 5-HT release under basal and stimulated conditions; 4) 5-HT transporter (SERT) immunoreactivity and 5) SERT mRNA.Methods: Tissue samples were obtained from individuals who met stringent diagnostic criteria for one of the following groups: 1) control (n=25); 2) UC (n=22); 3) IBS-D (n=16); and 4) IBS-C (n=16). Each large-capacity biopsy was evaluated by immunohistochemical staining, histological assessment, 5-HT content and 5-HT release and the measurement of mRNA encoding SERT.Results: 5-HT was decreased in UC, IBS-C and IBS-D (p less than.001). There was a decrease in EC cell number per mm muscularis mucosa in the UC group, but an increase in the IBS groups (p less than.01). Both IBS groups had significantly higher EC cell populations compared to controls (p less than .05) and ulcerative colitis (p less than .01). No significant changes were detected in the 5-HT release from colonic mucosa relative to control in any of the experimental groups, under basal or stimulated conditions. SERT mRNA levels were significantly reduced in all three experimental groups (p less than .05, p less than .01). In addition, the intensity of SERT immunoreactivity was diminished in all experimental groups ( p less than .001).Conclusions: In IBS, 5-HT content is reduced, EC cells are increased and 5-HT release is not significantly different than controls. SERT mRNA and SERT immunoreactivity are markedly reduced. In UC, 5-HT content and EC cell numbers are reduced in severely inflamed individuals. While 5-HT release was not altered in the patient groups relative to control values,* the decrease in SERT expression in both IBD and IBS leads to a decrease in the capacity to remove 5-HT from the intracellular space once it is released, thus increasing 5-HT availability. *--------------------------------------------------My conclusiom is both IBS C and IBSD have a reduced cap[acity to reuptake serotonin, BUt in IBS it so much more reduced that the excess serotonin it leaves in the synapses desensitizes the receptor.


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## eric (Jul 8, 1999)

Bonniei, I see where your going and I will still try to get some input for you and as you can see its not easy to totally figure out for sure. Here is this link alsoIBS: Improving Diagnosis, Serotonin Signaling, and Implications for Treatment http://www.medscape.com/viewarticle/463521 "Serotonin Reuptake TransporterThere is likely an evolutionary advantage to having physiologic mechanisms that regulate serotonin levels and activity, because it could be quite harmful without these regulatory mechanisms.3 One of the primary mechanisms the body has for regulating availability of serotonin within the extracellular space is the serotonin reuptake transporter (SERT). SERT is present in the brain and gut. The amount of serotonin reuptake that occurs from the extracellular space is genetically determined and is based on whether there are long, short, or heterozygous polymorphisms in the promoter for synthesis of SERT. For instance, homozygosity for the short variant and presence of the heterozygous variant result in less transcript, less protein expression, and thus, less reuptake of serotonin. SERT activity is obviously an important factor influencing serotonin availability to act on postsynaptic receptors, and would possibly affect the response to serotonergic medications such as SSRIs, in the treatment of depression, and to the novel agents tegaserod and alosetron, for IBS."This may also have some useful informationThe Pharmacogenomics Journal 2003, Volume 3, Number 2, Pages 64-66 Irritable bowel syndrome genophenomics: correlation of serotonin-transporter polymorphisms and alosetron responseE Scherl and C L Frissora Division of Gastroenterology and Hepatology, The Weill Medical College of Cornell University, The New York Presbyterian Hospital, New York, USA Abstract "SERT is a transporter protein that is responsible for the reuptake of serotonin from the synaptic space. Therefore, a highly efficient SERT will clear 5-HT from the synapse more rapidly. The more efficient the SERT, the less 5-HT remains in the synapse and the less alosetron is needed to block the 5HT3 receptor. Polymorphisms in the promoter synthesis of SERT (SERT-P) may affect responses to serotonergic medications. Camilleri et al4 investigate the hypothesis that DNA variations of the promoter region for the SERT influence colonic transit in D-IBS patients treated with alosetron, differentiating alosetron responders from nonresponders and improving suboptimal therapeutic response for D-IBS. " http://www.genomica.net/farmagenOMICA/arti.../serotonina.htm This is also interesting in regards to what your talking about.SSRIs in IBS: Sensing a dash of disappointment http://www2.cghjournal.org/scripts/om.dll/...h50023&nav=full


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## bonniei (Jan 25, 2001)

> quote:BUt in IBS it so much more reduced that the excess serotonin it leaves in the synapses desensitizes the receptor.


Oh damn Why don't I ever preview my stuff before posting it?!. I meant


> quote:" BUt in *IBS-C* it so much more reduced that the excess serotonin it leaves in the synapses desensitizes the receptor."










:I will read what you posted and get back to you, eric. It sounds promising.


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## bonniei (Jan 25, 2001)

> quote: The more efficient the SERT, the less 5-HT remains in the synapse and the less alosetron is needed to block the 5HT3 receptor"


I think that this quote from your medscape article says it is relative. Perhaps the efficiency of the SERT is more in D than C , so that the amount of serotonin left in the synapses is enough to cause D but not enough to cause the desensitization which happens in C.Ok I am willing to let is rest at that, eric. Thanks for trying to fill in the gaps


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## Nath (Jan 5, 1999)

I can attest to the too much 5-HT in D's. silly me decided to try some St John's wart, I was in agony for the whole day


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## eric (Jul 8, 1999)

FYISex differences of brain serotonin synthesis in patients with irritable bowel syndrome using a-[11C]methyl-l-tryptophan, positron emission tomography and statistical parametric mappingA Nakai, Y Kumakura, M Boivin, et alBACKGROUND: Irritable bowel syndrome (IBS) is the most common functional bowel disorder and has a strong predominance in women. Recent data suggest that the brain may play an important role in the pathophysiology of IBS in the brain-gut axis. It is strongly suspected that serotonin (5-HT), a neurotransmitter found in the brain and gut, may be related to the pathophysiology of IBS. It is reported that a 5-HT3 antagonist is effective only in female patients with diarrhea-predominant IBS.OBJECTIVE: In the present study, 5-HT synthesis was measured using positron emission tomography, with a-11Cmethyl-l-tryptophan as the tracer, in patients with IBS. The aim of the present study was to compare 5-HT synthesis in the IBS patients with that in the controls, and to compare 5-HT synthesis between male and female IBS patients.METHODS: Six male and six female nonconstipated IBS patients were scanned. Age-matched healthy volunteers were scanned as controls. Eighty minute dynamic scans were performed. Functional 5-HT synthesis images were analyzed using statistical parametric mapping.RESULTS: 5-HT synthesis was greater only in the female IBS patients in the right medial temporal gyrus (multimodal sensory association cortex) compared with the female controls (P<0.001).CONCLUSIONS: The greater brain 5-HT synthesis in the female IBS patients than in the controls may be related to the pathological visceral pain processing of the IBS patients, a larger female predominance of the disorder, and the sex difference of the efficacy of the 5-HT3 antagonist in treatment.Key Words: Irritable bowel syndrome; Positron emission tomography; Serotonin; Sex differences http://www.pulsus.com/Gastro/17_03/naka_ed.htm Serotonin and Its Implication forthe Management of IrritableBowel Syndrome Michael D. Gershon, MD Department of Anatomy and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, NYhttp://216.109.117.135/search/cache?p=sero...ain+and+ibs&d=3 BC7F4982A&c=482&yc=9777&icp=1[/URL]


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## eric (Jul 8, 1999)

Irritable Bowel Syndrome: An Overview By: Lin Chang, M.D., CNS: Center for Neurovisceral Sciences & Womenï¿½s Health; CURE: Digestive Diseases Research Center, Division of Digestive Diseases, UCLA School of Medicine Irritable bowel syndrome (IBS) is a chronic functional bowel disorder characterized by abdominal pain or discomfort and alterations in bowel habits. The clinical diagnosis of IBS is based on identifying symptom criteria with a ï¿½positive diagnosisï¿½ and excluding organic disease with minimal diagnostic evaluation. Although there are many expensive and sophisticated tests available for the evaluation of IBS symptoms, these are generally not needed for patients with typical symptoms and no features suggestive of organic diseases. This article provides a comprehensive overview of the prevalence, symptoms, diagnosis, and treatment options for IBS. "Post Infectious IBS"Symptoms suggestive of IBS occur in approximately 7-30% of patients following acute gi infections, *often persisting for years following complete resolution of the infection.* A large cohort study indentified a self reported history of accuete Gastroenteritis(intestinal infection) as a major risk factor for the development of IBS. *Reported risk factors for the development of post infectious IBS include female sex, duration of the acute diarrheal illness, and the presence of sustainied psychosocial stressors around the time of infection.* *Post infectious IBS is not restricted to a particular organism* and has been documented with a variety of bacterial infections (salmonella, campylobacter and e.coli) as well as parasitic infection.However, the role of accute viral gastroenteritis in this condition is unknown.In Post infectious IBS, low grade GI inflammation, or immune activation, maybe a basis for altered motility, and/or nerve and mucosal(lining of the bowl) function of the gut in IBS. Recent studies have also shown that in a subset of of unselected IBS patients (no documented history of a preceeding gut infection), there is evidence of increased inflammatory cells in the colon mucosa. It remains to be determined if altered gut immune function is a general characteristic of IBS patients. The implication of stressful life events in the development of post infectious IBS suggests a convergence of central (brain) and (peripheral (gut) mechanisms in the clinical presentation of this syndrome. http://www.aboutibs.org/Publications/currentParticipate.html Mast cells are one of the inflammed cells they found and they are linked to chronic stressors and the fight or flight and fighting infection. Chronic stress can re inflame the cells have the intial inflammation has resolved.The cells can be degradulated with out a pathogen through stress.So what does serotonin and mast cells have to do with stress reduction tehniques, what happens to serotonin in the body when you medititate for example?


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## Nath (Jan 5, 1999)

A bit off topic but, while googling for info came across some information linking opioid receptors to 5ht-3 receptors. Which kinda tied into the use of naltrexone etc. http://hatos.ucla.edu/TimHalesfaculty.htm


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## eric (Jul 8, 1999)

Nath, the brain and the ACC and the release of endorphines from the brain back down to the gut is part of the naltrexone strategy.In IBS the ACC's function is different then in controls.This is newGut. 2004 Jun;53(6):829-837. Links Association of distinct alpha(2) adrenoceptor and serotonin transporter polymorphisms with constipation and somatic symptoms in functional gastrointestinal disorders.Kim HJ, Camilleri M, Carlson PJ, Cremonini F, Ferber I, Stephens D, McKinzie S, Zinsmeister AR, Urrutia R.Clinical Enteric Neuroscience Translational and Epidemiological Research (CENTER) Program, Gastroenterology Research Unit, Mayo Clinic College of Medicine, Rochester, Minnesota, USA. Department of Health Sciences Research, Division of Biostatistics, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.BACKGROUND: The role of genetics in the phenotypic manifestations of irritable bowel syndrome (IBS) is unclear. Our aims were: (1) to compare the prevalence of polymorphisms of alpha 2 (alpha(2)) adrenoceptors, norepinephrine transporter, and serotonin transporter protein (soluble carrier protein member 4 (SLC6A4)) promoter in patients with lower functional gastrointestinal disorders (FGID) and in healthy controls; and (2) to test associations of these genetic variations with symptoms of IBS and high somatic symptom scores. METHODS: Validated bowel and somatic symptom questionnaires characterised the phenotype: 90 with IBS constipation (IBS-C), 128 IBS diarrhoea, 38 IBS alternating bowel function, and 20 chronic abdominal pain. Logistic regression analyses assessed associations of different polymorphisms for alpha(2) adrenoceptor and SLC6A4 with IBS or chronic abdominal pain phenotypes and high somatic score. RESULTS: Two distinct polymorphisms independently appeared to be associated with the phenotype IBS-C: alpha(2C) Del 322-325 (odds ratio (OR) 2.48 (95% confidence interval (CI) 0.98, 6.28); p = 0.05) and alpha(2A) -1291 (C--G) (OR 1.66 (95% CI 0.94, 2.92); p = 0.08) relative to wild-type. Overall, the alpha(2C) Del 322-325 polymorphism (alone or combined with other polymorphisms) was also significantly associated with a high somatic symptom score (OR 2.2 (95% CI 1.06, 4.64); p = 0.03). Combinations of polymorphisms were also associated with high somatic scores. CONCLUSION: Functionally distinct alpha(2A) and alpha(2C) adrenoceptor and serotonin transporter polymorphisms are associated with constipation and high somatic symptoms in patients with lower functional gastrointestinal disorders, although the strength of the genetic contribution to the phenotype is unclear.PMID: 15138209


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## eric (Jul 8, 1999)

This is an important study in regards to IBS.Visceral Perception Thresholds After Rectal Thermal and Pressure Stimuli in Irritable Bowel Syndrome PatientsPosted 02/05/2004 Yanqing Li; Yanmei Wang; Xiuli Zuo; Yuting Guo; Haiyan Zhang; Xuefeng Lu; Junman Li; Paul V Desmond Abstract and IntroductionAbstractBackground and Aim: Visceral hypersensitivity has been shown to be present in irritable bowel syndrome (IBS). The current study sought to compare the characteristics of visceral perception thresholds after rectal thermal and pressure stimuli between IBS patients and healthy subjects.Methods: A total of 46 patients with IBS were diagnosed using Rome II criteria. Thirteen healthy individuals participated in the study. Rectal visceral perception thresholds were examined in patients with IBS and in normal controls after thermal and pressure stimuli. Subjects were asked to report the sensation type, location, and spread.Results: Compared with healthy subjects, IBS patients demonstrated significantly initially lower perception thresholds and defecation thresholds to rectal thermal and pressure stimuli, particularly in patients with diarrhea-predominant IBS. Ice stimuli on the abdominal wall had varied effects on symptoms in patients with IBS and did not affect perception thresholds.Conclusions: Visceral perception thresholds were decreased significantly after rectal thermal and pressure stimuli in patients with IBS. Visceral hypersensitivity may be one of the important pathogenic mechanisms in IBS.IntroductionThe irritable bowel syndrome (IBS) is one of the most common disorders seen by gastroenterologists. Patients classically present with chronic abdominal pain and altered bowel habit in the absence of structural or biochemical disorders to account for these symptoms. Though symptoms may be severe,1 the underlying pathophysiology is incompletely understood, and current therapies for the disease are suboptimal.2The pathophysiology of IBS has variously been attributed to deficiency of dietary fiber,3,4 gut infections,5,6 gastrointestinal (GI) dysmotility,7-9 stressful life events,10-12 and psychopathology.13,14 However, none of these factors adequately explains the diverse symptomatology and physiological alterations seen in IBS.15 Abnormal visceral perception has recently been proposed to underly the observed heightened visceral sensitivity in IBS. It is manifested by increased intensity of sensations, lowered thresholds for visceral pain, and/or exaggerated viscerosomatic referral in comparison with control subjects.Several recent reports have indicated that lowered sensory threshold to rectal balloon distension is pre-sent with IBS.16,17 This was not part of generalized hypersensitivity or arousal, as cutaneous sensation was found to be normal and was unrelated to any psychoneuroticism.18Because many patients with IBS complain of worsening of symptoms following a chilled meal or ice on the abdomen, the effect of thermal stimulation on visceral perception has not been studied. The present specific aim was to record visceral perception thresholds after rectal thermal and pressure stimuli in patients with IBS and controls, and to compare them in order to provide more evidence of visceral hypersensitivity in IBS. http://www.medscape.com/viewarticle/466817_2


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## eric (Jul 8, 1999)

World J Gastroenterol. 2003 Dec;9(12):2791-5. Related Articles, Links Visceral hypersensitivity and altered colonic motility after subsidence of inflammation in a rat model of colitis.La JH, Kim TW, Sung TS, Kang JW, Kim HJ, Yang IS.Department of Physiology, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.AIM: Irritable bowel syndrome (IBS) is a functional bowel disorder characterized by visceral hypersensitivity and altered bowel motility. There is increasing evidence suggesting the role of inflammation in the pathogenesis of IBS, which addresses the possibility that formerly established rat model of colitis could be used as an IBS model after the inflammation subsided. METHODS: Colitis was induced by intracolonic instillation of 4% acetic acid in male Sprague-Dawley rats. The extent of inflammation was assessed by histological examination and myeloperoxidase (MPO) activity assay. After subsidence of colitis, the rats were subjected to rectal distension and restraint stress, then the abdominal withdrawal reflex and the number of stress-induced fecal output were measured, respectively. RESULTS: At 2 days post-induction of colitis, the colon showed characteristic inflammatory changes in histology and 8-fold increase in MPO activity. At 7 days post-induction of colitis, the histological features and MPO activity returned to normal. The rats at 7 days post-induction of colitis showed hypersensitive response to rectal distension without an accompanying change in rectal compliance, and defecated more stools than control animals when under stress. CONCLUSION: These results concur largely with the characteristic features of IBS, visceral hypersensitivity and altered defecation pattern in the absence of detectable disease, suggesting that this animal model is a methodologically convenient and useful model for studying a subset of IBS.PMID: 14669335


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## SpAsMaN* (May 11, 2002)

Is there any clinicals trials with natural 5htp like griffonia seed extract or st-John wort for IBS???Naltrexone help some suffers but that dosen't seems to be a cure.


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## Nath (Jan 5, 1999)

Thanks for the info Eric.Id would give St John's wart a try Spasman as it may help people with C. But check it out first as it interacts with certain drugs.I might give the naltrexone another shot in combination with lotronex, the first time I tried it I wasnt taking lotronex.


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## eric (Jul 8, 1999)

your welcome Nath.Spasman, its not the amount of serotonin, its the regulation of it in the body or disregulation.Nath, is right about St Joh's wort, check for interreactions.It may calm your nervous system perhaps.But so does relaxtion techniques, which can be much more effective on IBS and the regulation of serotonin. I did not find a study on it.Spasman, if I were you I would get a sitz marker test done and also check about"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.html Do you have less then three bowel movements a week?


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## SpAsMaN* (May 11, 2002)

I go everyday Portland.It just that the trapped gas are very acidic and mimics temporary C.It is very confusing and it is loose often.When i pop "something normal(6-9inch)" i usually had a bad trapped gas(and C) episode before the work .







The Sitz marker?What is the goal of that?I never tried a long term trial of St-John Wort.It dosen't seems to help when i use that for a week.


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## SpAsMaN* (May 11, 2002)

I just call my G.I.specialist to explain him one more time my abnormal IBS.I will ask him for Opium tincture to overcome the painful trapped gas.I will trade my symptoms for a healthy C if necessary.







He's gonna call me back later.I will ask about the Sitz marker.I hope this is not invasive and complicated.It sound good to drop little rubber.


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## Kathleen M. (Nov 16, 1999)

I would be concerned that the opium might trap the gas worse since it seems to slow down the gut.But what do I know







Sitz marker is mostly non-invasive. You do swallow the markers that they can see in the X-rays they take, but it isn't nearly as invasive as something like a endoscopy.K.


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