Why is it for some people applying heat to the abdomen makes the pain better or go away?Why is it for some people wearing tight pants triggers an attack?Why is it not just bad stress but good stress can trigger an attack?Why is it cold water for some can trigger an attack?Also the symptoms of the "sensation of incomplete evacuation is not needed for and IBS diagnoses, but helps confirm it, because it is not a symptom consistent with a pathogen or enteric infection.IBS is also not contagious, nor does it do more damage to the gi tract?The symptoms in Most IBSers are consitenty the same for many years. Also when using the rome ll diagnoses the diagnoses IS stable and less then five percent are found years later to have an organic condition or major changes in symptoms or red flag or alarm symptoms.
Urgent Suggestion For Eric!
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Capt C, What I have interpreted on this board is Eric is saying There is NO cure because there is No Cause found. That a person may get better but not CURE his/her self ONLY the powers that be are able to Cure (erradicate/ kill) the cause to effect a cure. Also, Eric comes accros to me as saying Well, it does not matter what dysbiosis is going on because if the mind gut was not overreacting then it would "fix" itself. so it would be a moot point to try to put what should be there if in fact what you think should be there is not there since the mind gut has not returned to "normal" whatever that is so get your mind right and then the mind gut will do the rest and hopefully be closer to what it was before all hell broke loose. Is that right? Eric Joann
Capt C, What I have interpreted on this board is Eric is saying There is NO cure because there is No Cause found. That a person may get better but not CURE his/her self ONLY the powers that be are able to Cure (erradicate/ kill) the cause to effect a cure. Also, Eric comes accros to me as saying Well, it does not matter what dysbiosis is going on because if the mind gut was not overreacting then it would "fix" itself. so it would be a moot point to try to put what should be there if in fact what you think should be there is not there since the mind gut has not returned to "normal" whatever that is so get your mind right and then the mind gut will do the rest and hopefully be closer to what it was before all hell broke loose. Is that right? Eric Joann
"What I have interpreted on this board is Eric is saying There is NO cure because there is No Cause found."Basically correct.Funny the use of the words eradicate/kill? It may not be anything needs to be killed or even eradicated, but changed perhaps. Doctors do not use the word "Cure" in IBS for very good reasons. Just like they don't say they can cure migranes or other well know chronic health conditions.When a doctor or someone says they can "cure" IBS, before they have "cured" anyone also may lead to false hope and more anxiety and in IBS that is a major problem, since its very connected to stressors. Not to mention its unethical to say you can cure something you don't know the cause of. Caring doctors may say they can help the symptoms and may say that effective treatment is available and remission might be attainable. But not "cure."They use the word remission for very good reasons.The exact cause of IBS has not been determined yet. Although, they have found many abnormailites in IBS patients, there is still no one specific biological marker in ALL IBS patients yet. IF that is dysbiosis, impairment in brain regions, alter molecular serotonin genes, alter cellular changes in the gi tract or ones not yet discovered. That however does not mean leave out all they have discovered. Honestly some people here are very bias to the cause of IBS to the point of tunnel vision and focus mainly on one idea. Somewhat akin perhaps to foods causing migranes.They may believe the only cause is a bacteria or pathogen, and think mainly in disease STATES but in fact it may or may not be, the evidence so far has implicated a lot and anyone who seriously studies IBS, knows serotonin seems to be majorally implicated and that IBS is already a brain gut axis disorder. Just like they have not been able to "cure" migranes or diabeties or other chronic health problems. You can't "cure" something you do not fully understand the cause of and because the brain gut axis is very complex, there is still a lot of research that needs to be done to figure it all out. There are many issues still needed to be addressed in IBS from cells to neurotransmitters to pathogens and even others.But, suppose for a second that this is true and all IBSers have molecular defects of the SERT gene. The majority of IBSers presenting to gastro clinics effectively demonstarte serotonin dysregulation.Molecular Defect Found for the First Time in IBS Patients http://www.ibsgroup.org/ubb/ultimatebb.php...c;f=10;t=000940 also"The diffuse connections of serotonin allow it to affect many basic psychological functions such as anxiety mechanisms and the regulation of mood, thoughts, aggression, appetite, sex drive and the sleep/wake cycle. Multiple observations suggest that serotonin, one of the most abundant neurotransmitters, plays an important role in the regulation of mood and a key role in the treatment of depression. "Do some of the above look fimilar in non IBS issues, some IBSers have altered REM sleep, others have appetite problems, anxiety problems, depression problems, brain fog, and others.But its a MAJORALLY important neurotransmitter in gut function. The majority of it is stored in the gut, especially in EC cells. EC cells are increase in PI IBS subjects, along with Mast cells, that also release it. In IBS in geneal however it has been majorally implicated. Some people here ignore it or blame it on drug company research. But in fact its peer reviewed research and has to be replicated and observed.How does one go about "curing" molecular defects of cells in the gut that control digestion?Also it is well know in PI IBS patients they have cellular changes in the gi tract with an increase of EC(serotonin) containing cells and mast cells. How does one fix that? Do you use a laser and an electron microscope and surgery to eliminate them? Or maybe there are two little of them, do you then implant them? Maybe in the future that maybe an issue.First however they need to figure it all out.New pathophysiological mechanisms are found and it would not surpprize me at all that even more will be in the future and they are under investigation and each one has to be studied throughly as to cause and effect."Aliment Pharmacol Ther. 2004 Jul;20 Suppl 2:1-9. Related Articles, Links New pathophysiological mechanisms in irritable bowel syndrome.Barbara G, De Giorgio R, Stanghellini V, Cremon C, Salvioli B, Corinaldesi R.Department of Internal Medicine and Gastroenterology, University of Bologna, Italy.Summary Irritable bowel syndrome (IBS) is a functional, multifactorial disease characterized by abdominal pain and erratic bowel habit. Changes in gastrointestinal motor function, enhanced perception of stimuli arising from the gut wall and psychosocial factors are thought to be major contributors for symptom generation. In recent years, several additional factors have been identified and postulated to interact with these classical mechanisms. Reduced ability to expel intestinal gas with consequent gas trapping and bowel distension may contribute to abdominal discomfort/pain and bloating. Abnormal activation of certain brain regions following painful stimulation of the rectum suggests altered processing of afferent signals. An acute gastrointestinal infection is now a recognized aetiological factor for symptom development in a subset of IBS patients (i.e. post-infectious IBS), who are probably unable to down-regulate the initial inflammatory stimulus efficiently. Furthermore, low-grade inflammatory infiltration and activation of mast cells in proximity to nerves in the colonic mucosa may also participate in the frequency and severity of perceived abdominal pain in post-infectious and non-specific IBS. Initial evidence suggests the existence of changes in gut microflora, serotonin metabolism and a genetic contribution in IBS pathophysiology. These novel mechanisms may aid a better understanding of the complex pathophysiology of IBS and to develop new therapies.PMID: 15335408IBS: Improving Diagnosis, Serotonin Signaling, and Implications for Treatment"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.2 http://216.109.117.135/search/cache?p=+ser...&icp=1&.intl=us However, based on what they know now, IBS is treatable for the majority of IBSers. Some methods like CBT and HT for example, maybe hard for the public to understand, why treat the brain for a gut disorder, but HT for example, is statistically and perhaps argueably the most successful treatment to date.They also know now, that a combination of psycological and standard medical thearipies is more effective then standard treatment alone.Because they don't know the exact cause does not mean they don't have research generated insights into effective IBS treatments that help the majority of IBSers to feel better and have less symptoms and even put some into remission, sometimes total remission.Again just because you don't have symptoms, does not been the underlying problems are cured.The history of IBS is important also in the big picture to what they have learned and where things are going. Believe it or not experts in immunology, the enteric nervous sytem, microbiology, neurogastroenterology and many other fields are working on all the issues, they are also combining the information and the shear amount of information the last five to ten years has been very substantial in IBS and they have made a lot of progress.History of Functional DisordersDouglas A. Drossman, MDCenter-Co-DirectorMelissa SwantkowskiNew York UniversityTHE PASTHISTORICAL PRECEDENTSHistorians and physicians have documented the presence of Functional GI disorders throughoutrecorded human history. However, until recently, limited attention has been granted to thesedisorders due to the lack of identifiable pathology and the absence of a conceptual framework tounderstand and categorize them. Systematic investigation of functional GI disorders did notbegin until the middle of the 20th century, and prior to this time, only occasional reports offunctional GI symptoms were published, the first appearing only 200 years ag
ver the past 25 years, scientific attention to understanding and properly caring for patients withfunctional GI disorders has grown progressively. With the understanding comes the rationale foruse of medications directed at intestinal receptors as well as psychopharmacological, behavioral,and psychological forms of treatment. Additionally, there has been an increase in the rate ofscientific publications and greater media exposure to the public through television, radio, andInternet.To understand the historical classification of these disorders, two differing theories relating to theinteraction between the mind and body should be considered.o Holism: a theory built upon the foundation that the mind and body are integratedand utterly inseparable.o Dualism: a theory that proposes a separation between the mind and the body.Greek philosophers Plato, Aristotle, and Hippocrates first proposed the principleof holism about 3,000 years ago, and later in the 12th century; Jewish physicianand philosopher Maimonides reexamined this philosophy. Based on holism, thestudy of medical disease must take into account the whole person rather thanmerely the diseased part. However, societal concepts of illness and diseasedrastically shifted when European philosopher Rene Descartes offered the divergent theory ofdualism in the 17th century. Prior to the notion of dualism, the church discouraged humandissection on the premise that the spirit resided in the body. The acceptance of dualism paved the2way for the emergence of scientific investigation and new medical discoveries by lifting theprohibition of human dissection. This shift in medical thought was congruent with the societalchanges of the 17th century: the shift towards a separation in church and state.IMPLICATIONS FOR FUNCTIONAL GI DISORDERSBased on the concept of dualism, disease was now understood in terms of structuralabnormalities. Therefore, the validity of a disease rested with the observation of morphologicalabnormalities. Medical conditions occurring in the absence of such morphological abnormalitiesand symptoms were not considered legitimate, and were often viewed as psychiatric, consistentwith the concept of dualism. The concept of dualism had other effects with regard to treatment.For example, this would include all the functional GI disorders and other somatic syndromes,such as fibromyalgia. Until the latter part of the 20th century, a medical illness was consideredamenable to scientific inquiry and treatment. However, patients with psychiatric disorders wereinterred in insane asylums and considered to no longer be treatable by medical physicians.Unfortunately this concept leads to a clinical dilemma. Specific diseases explain only about 10%of medical illnesses seen by physicians. Furthermore, people with structural (i.e. organic)diagnosis such as inflammatory bowel disease or cancer show considerable variation in theirsymptom presentation and clinical behavior. Gastroenterologists (as well as other health carepractitioners) are all too familiar with the poor correlation between structural findings onendoscopy and their patient's symptoms.Although efforts to find morphological or even motility etiologies for functional GI disorders inthe latter part of the 20th century were unsuccessful, the assumption that functional GI disordersmust be psychiatric has developed and has permeated current thinking. However, in the face ofcurrent scientific research, this is being seriously challenged. Studies have shown that personswith irritable bowel syndrome who do not seek health care are psychologically much like healthysubjects.THE PRESENTCONCEPTUAL BASES FOR THE STUDY OF FUNCTIONAL GI DISORDERSo The recent acceptance of functional GI disorders as legitimate medical entities isbased on the following three developments The concept of the Biopsychosocial model of illness and diseaseo The development of new investigative methods for studying diseaseo The development of the Rome CriteriaBiopsychosocial ModelIn 1977, the publication of the concept of the Biopsychosocial model by George Engel, and itslater demonstration specifically for gastrointestinal disorders, marked an important change inthinking. A biopsychosocial model of illness and disease provides the needed framework to3understand, categorize, and treat common GI symptoms. These symptoms are the integratedproduct of altered motility, enhanced visceral sensitivity, and brain-gut dysregulation and oftenare influenced by psychosocial factors. Figure 1 illustrates the proposed relationship betweenpsychosocial and physiological factors with functional GI symptoms and the clinical outcome.Early in life, genetics and environmental influences (family attitudes toward bowel training orillness in general, major loss or abuse history or exposure to infection) may affect one'spsychosocial development (susceptibility to life stress, psychological state, coping skills, socialsupport) or the development of gut dysfunction (abnormal motility or visceral hypersensitivity).Additionally, the presence and nature of a functional GI disorder is determined by the interactionof psychosocial factors and altered physiology via the brain-gut axis. In other words, oneindividual afflicted with a bowel disorder but with no psychosocial disturbances, good copingskills and adequate social support may have less severe symptoms and not seek medical care.Another having similar symptoms but with coexistent psychosocial disturbance, high life stress,or poor coping skills may frequent his physician's office and have generally poor outcome.DEVELOPMENT OF NEW INVESTIGATIVE METHODSThe second concurrent process has been the expansion and refinement of investigative methodsthat allow the study of functional GI disorders in terms of biological, cultural, and psychosocial(i.e. brain) influences. These developments include:1. the improvement of motility assessment,2. the standardization of the barostat to measure visceral sensitivity,3. the enhancement of psychometric instruments to determine psychosocialinfluences,4. the introduction of brain imaging (PET, fMRI) to determine CNS contribution tosymptoms, and5. the molecular investigation of brain-gut peptides, which provide insight into howthese symptoms become manifest.In less than ten years, these methods have produced new knowledge of the underlyingpathophysiological features that characterize the age-old symptoms we now define as functionalGI disorders.ROME CRITERIAThe Rome Criteria is an international effort to characterize and classify the functional GIdisorders using a symptom-based classification system. This approach that has its precedentswith classification systems in psychiatry and rheumatology. The rationale for such a system isbased on the premise that patients with functional GI complaints consistently report symptomsthat breed true in their clinical features, yet cannot be classified by any existing structural,physiological or biochemical substrate. The Rome Criteria was built upon the Manning Criteria,which was developed from discriminate function analysis of GI patients.The decision to develop diagnostic criteria by international consensus was introduced as part of alarger effort to address issues within gastroenterology that are not easily resolved by usual4scientific inquiry or literary review. By 1992, several committees had met to discuss the criteria,which ultimately resulted in the publishing of many articles in Gastroenterology Internationaland a book detailing the criteria titled "The Functional Gastrointestinal Disorders (Rome I)".Elaboration of the Rome I criteria led to a second edition of the Rome criteria (titled Rome II) in2000 as well as the publication of a supplement to the journal Gut in 1999. Recently the RomeCoordinating Committee has met to begin Rome III, expected to be published in 2006. To learnmore about the Rome Committees and to see a summary of the Rome II book: go towww.romecriteria.com.PRESENT PATHOPHYSIOLOGICAL OBSERVATIONSDespite differences among the functional gastrointestinal disorders, in location and symptomfeatures, common characteristics are shared with regard to motor and sensory physiology,o central nervous system relationships,o approach to patient care.What follows are the general observations and guidelines.MOTILITYIn healthy subjects, stress can increase motility in the esophagus, stomach, small and largeintestine and colon. Abnormal motility can generate a variety of GI symptoms includingvomiting, diarrhea, constipation, acute abdominal pain, and fecal incontinence. Functional GIpatients have even greater increased motility in response to stressors in comparison to normalsubjects. While abnormal motility plays a vital role in understanding many of the functional GIdisorders and their symptoms, it is not sufficient to explain reports of chronic or recurrentabdominal pain.VISCERAL HYPERSENSITIVITYVisceral hypersensitivity helps to account for disorders associated with chronic or recurrent pain,which are not well correlated with changes in gastrointestinal motility, and in some cases, wheremotility disturbances do not exist. Patients suffering from visceral hypersensitivity have a lowerpain threshold with balloon distension of the bowel or have increased sensitivity to even normalintestinal function. Additionally, there may be an increased or unusual area of somatic referral ofvisceral pain. Recently it has been concluded that visceral hypersensitivity may be induced inresponse to rectal or colonic distension in normal subjects, and to a greater degree, in personswith IBS. Therefore, it is possible that the pain of functional GI disorders may relate tosensitization resulting from chronic abnormal motor hyperactivity, GI infection, or trauma/injuryto the viscera.5BRAIN-GUT AXISThe concept of brain-gut interactions brings together observations relating to motility andvisceral hypersensitivity and their modulation by psychosocial factors. By integrating intestinaland CNS central nervous system activity, the brain-gut axis explains the symptoms relating tofunctional GI disorders. In other words, senses such as vision and smell, as well as enteroceptiveinformation (i.e. emotion and thought) have the capability to affect gastrointestinal sensation,motility, secretion, and inflammation. Conversely, viscerotopic effects reciprocally affect centralpain perception, mood, and behavior. For example, spontaneously induced contractions of thecolon in rats leads to activation of the locus coeruleus in the pons, an area closely connected topain and emotional centers in the brain. Jointly, the increased arousal or anxiety is associatedwith a decrease in the frequency of MMC activity of the small bowel possibly mediated by stresshormones in the brain. Based on these observations, it is no longer rational to try to discriminatewhether physiological or psychological factors produce pain or other bowel symptoms. Instead,the Functional GI disorders are understood in terms of dysregulation of brain-gut function, andthe task is to determine to what degree each is remediable. Therefore, a treatment approachconsistent with the concept of brain-gut dysfunction may focus on the neuropeptides andreceptors that are present in both enteric and central nervous systems.THE ROLE FOR PSYCHOLOGICAL FACTORSAlthough psychological factors do not define these disorders and are not required for diagnosis,they are important modulators of the patient's experience and ultimately, the clinical outcome.Research on the psychosocial aspects of patients with functional GI disorders yields three generalobservations Psychological stress exacerbates gastrointestinal symptoms in patients withfunctional GI disorders and can even produce symptoms in healthy patients (but toa lesser degree).o Psychological disturbances modify the experience of illness and illness behaviorssuch as health care seeking. For example, a history of major psychological trauma(e.g. sexual or physical abuse) is more common among patients seen in referralcenters than in primary care and is associated with a more severe disorder and apoorer clinical outcome. Additionally, psychological trauma may increase painreportingtendency.o Having a functional GI disorder has psychological consequences in terms of one'sgeneral well-being, daily functional status, concerns relating to control oversymptoms, and future implications of the illness (e.g. functioning at work andhome).APPROACH TO TREATMENTThe approach to treatment for all functional GI disorders is founded on a therapeutic physicianpatientrelationship. The basis for implementing a strong physician-patient relationship issupported by evidence that patients with functional GI disorders have anywhere from a 30 to80% placebo response rate regardless of treatment.6Because functional GI disorders are chronic, it is important to determine the immediate reasonsbehind each visit, after which treatment can be based on severity and nature of symptoms,physiological and psychosocial determinants of the patient�s illness behavior, and the degree offunctional impairment.These factors can separate patients into mild, moderate, and severe categories.Patients with mild symptoms usually seen in primary care,o do not have major impairment in function or psychological disturbance ando can maintain normal activity.These patients have concerns about their condition but do not need to make many visits to theirphysician. Regarding treatment, these patients require education about their disorder and itssymptoms as well as information regarding a proper diet and the kinds of medication that canhave adverse effects.Patients with moderate symptoms seen in both primary and secondary care facilities ando experience intermittent disruptions in activity on account of their symptoms.o may identify a close relationship between symptoms and inciting events such asstress, travel, or dietary indiscretion.For these patients, symptom monitoring to record time, severity, and presence of associatedfactors can help to identify inciting factors and give the patient a sense of control over thedisorder. Additionally, pharmacotherapy directed at specific symptoms, particularly those thatimpair daily function, can be helpful, as can psychological treatments (relaxation, hypnosis,cognitive-behavioral therapy, and combination treatments) in reducing anxiety and encouraginghealth promoting behaviors.Patients with severe symptoms have trouble functioning daily,o find their disorder to be disabling and debilitating in nearly every facet of life,o have a high frequency of associated psychological difficulties,o make frequent visits to their physicians , ando may hope for a magical cure.In these cases a long-term physician-patient relationship, which sets realistic treatment goals(such as improved quality of life rather than elimination of all pain) is necessary. The focus forthese patients needs to shift from treating a disease to coping with a chronic disorder, wheremuch of the responsibility is place on the patient, himself. Furthermore, antidepressants haveproven useful to control pain and alleviate associated depressive symptoms.7THE FUTUREFuture studies will identify pathophysiological subgroups, each having its own set ofdeterminants ad treatment. Examples are as follows Some patients will develop their disorders or exacerbate symptoms viasensitization of afferent transmission from infection, enhanced motility, or traumato the gut. They may respond to the newly developing neurotransmitter blockingagents.o Patients with more painful and severe symptoms may prove to have "abnormalperception of normal gut function" rather than abnormal function. Thisdysfunction in the central regulation of incoming visceral signs may be remediedwith a psychopharmacological treatment approach.o The symptoms of some patients could be attributed to genetic factors, which resultin abnormalities in central reactivity to stress, in which case genetic manipulationstrategies would prove beneficial.o Early learning within the familial structure and socio-cultural influences has beendemonstrated to affect symptom perception and illness behavior. Future studiesare also likely to identify psychological and behavioral interventions that aretargeted for this subgroup.While it is likely that there are potent new treatments that will follow our growingpathphysiologic knowledge of these disorders, it is unlikely that they will replace some of thefundamental clinical principles active listening,o careful decision making,o an effective patient-physician relationship, ando patient centered biopsychosocial plan of care. http://www.med.unc.edu/medicine/fgidc/hist...aldisorders.pdf Definition of Health: The World Health Organization."Health is a state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity." Also even based on data from Probiotics studies already done, if they benefit pain and bloating they are worth trying. Gas is a very hard symptoms to treat in IBS and if they were to be shown to help just that great, but they have shown to be even more useful in IBD conditions. On IBS more studies are needed. Not that future studies show more benefits for IBSer. They have also been used on this bb for quite some time now with mixed results. You will hear people say they have cured themselves and you will see some Web advertising "cures" but until all of the above is figured out, there is no "cure" for IBS at this time.Again, I highly recommend getting a copy of this from the IFFGD"In the new IFFGD Digestive Health Matters.Visceral Sensations and Brain-Gut Mechanisms By: Emeran A. Mayer, M.D., Professor of Medicine, Physiology and Psychiatry; Director, Center for Neurovisceral Sciences & Women's Health, David Geffen School of Medicine at UCLA IntroductionOver the past several years, different mechanisms located within the gut, or gut wall have been implicated in as possible pathoophysiologic mechanisms underlying the charecteristic IBS symptoms of abdominal pain and discomfort. The list ranges from altered transit of intestinal gas, alterations in colonic flora, immune cell activation in the gut mucosa, and alterations in serotonin containing enterochromaffin cells lining the gut. For those investigators with a good memory, these novel mechanisms can be added to an older list of proposed pathomechanisms, including altered gut motility('Sapstic Colitus') and alterations in mucus secretion. While the jury is still out, one unique aspect about the gut and its connection to the brain are often forgotten: Our brain gut axis is not designed to generate concious perceptions of every alteration in gut homeostasis and internal enviroment, in particlur when these changes are chronic, and when there is no adaptive behavioral response an affected organism could generate.Evolution has not designed our brain gut axis to experience abdominal pain every time the number of mast cells in our ileum goes up, or the number of our serotonin containing cells goes down. It would be counter productive for an animal with a chronic parasite infestation to experince constant viceral pain, and it wouldn't have any advantage for people living in third world countries with frequent enteric infections to suffer from chronic abdominal pain. It has been suggested that viceral pain maybe a secondary phenomenon of an elaborate system of signaling non painful signals to the brain: hunger and fullness (satiety), well being after a meal, urge to evacuate, ect. At the same time, powerful mechanisms have evolved that keep many other aversive signals out of concious perception: contractions, luminal distension, gas volume, low grade inflammation, ect..The most common symptoms of IBS patients are related to altered perception of sensations, arising from the GI tract, and frequently from sites outside the GI tract, such as the genitourinary system or the musculskeletal system. Sensations of bloating, fullness, gas, incomplete rectal evacuation, and crampy abdominal pain are the most common symptoms patients experience. Numerous reports have demonstarted that a significant percentage of functional bowel disorders (FBD) patients about (60) percent rate experimental distensions of the colon as uncomfortable at lower distension volumes or pressure when compared to healthy control subjects. This finding of an increased perception of viceral signals ("viceral hypersensitvity") has been demonstrated during baloon distension tests of the respective part of the GI tract regarless of where the primary symptoms are- the esophagus, the stomach, or the lower abdomen.In contrast to the current emphasis on mechanisms that may result in sensitization of viceral Afferent pathways in the gut, it may well be that alterations in the way the nervous system normally suppresses the perception of the great majority of sensory activity arising from our viscera are essential for the typical symptom constellation of IBS and other functional disorders to develop."It goes into a lot more detail and I highly recommend people get a copy and read the whole article."SummaryIn summary, it is clear that we still have a long way to go to understand the intricate connections between our digestive system and the brain, and how alterations in this two way communication result in functional bowel disorders symptoms. While more alterations in peripheral mechanisms involved in gut function are being reported, rapid progress has occured in our uunderstanding of the multiple mechanisms by which the brain can increase the concious perception of viceral stimuli, which is normally rarely perceieved." http://www.aboutibs.org/Publications/currentParticipate.html and in regards to dysbiosis and "cure", how does this fit into it all."IBS - 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).
ver the past 25 years, scientific attention to understanding and properly caring for patients withfunctional GI disorders has grown progressively. With the understanding comes the rationale foruse of medications directed at intestinal receptors as well as psychopharmacological, behavioral,and psychological forms of treatment. Additionally, there has been an increase in the rate ofscientific publications and greater media exposure to the public through television, radio, andInternet.To understand the historical classification of these disorders, two differing theories relating to theinteraction between the mind and body should be considered.o Holism: a theory built upon the foundation that the mind and body are integratedand utterly inseparable.o Dualism: a theory that proposes a separation between the mind and the body.Greek philosophers Plato, Aristotle, and Hippocrates first proposed the principleof holism about 3,000 years ago, and later in the 12th century; Jewish physicianand philosopher Maimonides reexamined this philosophy. Based on holism, thestudy of medical disease must take into account the whole person rather thanmerely the diseased part. However, societal concepts of illness and diseasedrastically shifted when European philosopher Rene Descartes offered the divergent theory ofdualism in the 17th century. Prior to the notion of dualism, the church discouraged humandissection on the premise that the spirit resided in the body. The acceptance of dualism paved the2way for the emergence of scientific investigation and new medical discoveries by lifting theprohibition of human dissection. This shift in medical thought was congruent with the societalchanges of the 17th century: the shift towards a separation in church and state.IMPLICATIONS FOR FUNCTIONAL GI DISORDERSBased on the concept of dualism, disease was now understood in terms of structuralabnormalities. Therefore, the validity of a disease rested with the observation of morphologicalabnormalities. Medical conditions occurring in the absence of such morphological abnormalitiesand symptoms were not considered legitimate, and were often viewed as psychiatric, consistentwith the concept of dualism. The concept of dualism had other effects with regard to treatment.For example, this would include all the functional GI disorders and other somatic syndromes,such as fibromyalgia. Until the latter part of the 20th century, a medical illness was consideredamenable to scientific inquiry and treatment. However, patients with psychiatric disorders wereinterred in insane asylums and considered to no longer be treatable by medical physicians.Unfortunately this concept leads to a clinical dilemma. Specific diseases explain only about 10%of medical illnesses seen by physicians. Furthermore, people with structural (i.e. organic)diagnosis such as inflammatory bowel disease or cancer show considerable variation in theirsymptom presentation and clinical behavior. Gastroenterologists (as well as other health carepractitioners) are all too familiar with the poor correlation between structural findings onendoscopy and their patient's symptoms.Although efforts to find morphological or even motility etiologies for functional GI disorders inthe latter part of the 20th century were unsuccessful, the assumption that functional GI disordersmust be psychiatric has developed and has permeated current thinking. However, in the face ofcurrent scientific research, this is being seriously challenged. Studies have shown that personswith irritable bowel syndrome who do not seek health care are psychologically much like healthysubjects.THE PRESENTCONCEPTUAL BASES FOR THE STUDY OF FUNCTIONAL GI DISORDERSo The recent acceptance of functional GI disorders as legitimate medical entities isbased on the following three developments The concept of the Biopsychosocial model of illness and diseaseo The development of new investigative methods for studying diseaseo The development of the Rome CriteriaBiopsychosocial ModelIn 1977, the publication of the concept of the Biopsychosocial model by George Engel, and itslater demonstration specifically for gastrointestinal disorders, marked an important change inthinking. A biopsychosocial model of illness and disease provides the needed framework to3understand, categorize, and treat common GI symptoms. These symptoms are the integratedproduct of altered motility, enhanced visceral sensitivity, and brain-gut dysregulation and oftenare influenced by psychosocial factors. Figure 1 illustrates the proposed relationship betweenpsychosocial and physiological factors with functional GI symptoms and the clinical outcome.Early in life, genetics and environmental influences (family attitudes toward bowel training orillness in general, major loss or abuse history or exposure to infection) may affect one'spsychosocial development (susceptibility to life stress, psychological state, coping skills, socialsupport) or the development of gut dysfunction (abnormal motility or visceral hypersensitivity).Additionally, the presence and nature of a functional GI disorder is determined by the interactionof psychosocial factors and altered physiology via the brain-gut axis. In other words, oneindividual afflicted with a bowel disorder but with no psychosocial disturbances, good copingskills and adequate social support may have less severe symptoms and not seek medical care.Another having similar symptoms but with coexistent psychosocial disturbance, high life stress,or poor coping skills may frequent his physician's office and have generally poor outcome.DEVELOPMENT OF NEW INVESTIGATIVE METHODSThe second concurrent process has been the expansion and refinement of investigative methodsthat allow the study of functional GI disorders in terms of biological, cultural, and psychosocial(i.e. brain) influences. These developments include:1. the improvement of motility assessment,2. the standardization of the barostat to measure visceral sensitivity,3. the enhancement of psychometric instruments to determine psychosocialinfluences,4. the introduction of brain imaging (PET, fMRI) to determine CNS contribution tosymptoms, and5. the molecular investigation of brain-gut peptides, which provide insight into howthese symptoms become manifest.In less than ten years, these methods have produced new knowledge of the underlyingpathophysiological features that characterize the age-old symptoms we now define as functionalGI disorders.ROME CRITERIAThe Rome Criteria is an international effort to characterize and classify the functional GIdisorders using a symptom-based classification system. This approach that has its precedentswith classification systems in psychiatry and rheumatology. The rationale for such a system isbased on the premise that patients with functional GI complaints consistently report symptomsthat breed true in their clinical features, yet cannot be classified by any existing structural,physiological or biochemical substrate. The Rome Criteria was built upon the Manning Criteria,which was developed from discriminate function analysis of GI patients.The decision to develop diagnostic criteria by international consensus was introduced as part of alarger effort to address issues within gastroenterology that are not easily resolved by usual4scientific inquiry or literary review. By 1992, several committees had met to discuss the criteria,which ultimately resulted in the publishing of many articles in Gastroenterology Internationaland a book detailing the criteria titled "The Functional Gastrointestinal Disorders (Rome I)".Elaboration of the Rome I criteria led to a second edition of the Rome criteria (titled Rome II) in2000 as well as the publication of a supplement to the journal Gut in 1999. Recently the RomeCoordinating Committee has met to begin Rome III, expected to be published in 2006. To learnmore about the Rome Committees and to see a summary of the Rome II book: go towww.romecriteria.com.PRESENT PATHOPHYSIOLOGICAL OBSERVATIONSDespite differences among the functional gastrointestinal disorders, in location and symptomfeatures, common characteristics are shared with regard to motor and sensory physiology,o central nervous system relationships,o approach to patient care.What follows are the general observations and guidelines.MOTILITYIn healthy subjects, stress can increase motility in the esophagus, stomach, small and largeintestine and colon. Abnormal motility can generate a variety of GI symptoms includingvomiting, diarrhea, constipation, acute abdominal pain, and fecal incontinence. Functional GIpatients have even greater increased motility in response to stressors in comparison to normalsubjects. While abnormal motility plays a vital role in understanding many of the functional GIdisorders and their symptoms, it is not sufficient to explain reports of chronic or recurrentabdominal pain.VISCERAL HYPERSENSITIVITYVisceral hypersensitivity helps to account for disorders associated with chronic or recurrent pain,which are not well correlated with changes in gastrointestinal motility, and in some cases, wheremotility disturbances do not exist. Patients suffering from visceral hypersensitivity have a lowerpain threshold with balloon distension of the bowel or have increased sensitivity to even normalintestinal function. Additionally, there may be an increased or unusual area of somatic referral ofvisceral pain. Recently it has been concluded that visceral hypersensitivity may be induced inresponse to rectal or colonic distension in normal subjects, and to a greater degree, in personswith IBS. Therefore, it is possible that the pain of functional GI disorders may relate tosensitization resulting from chronic abnormal motor hyperactivity, GI infection, or trauma/injuryto the viscera.5BRAIN-GUT AXISThe concept of brain-gut interactions brings together observations relating to motility andvisceral hypersensitivity and their modulation by psychosocial factors. By integrating intestinaland CNS central nervous system activity, the brain-gut axis explains the symptoms relating tofunctional GI disorders. In other words, senses such as vision and smell, as well as enteroceptiveinformation (i.e. emotion and thought) have the capability to affect gastrointestinal sensation,motility, secretion, and inflammation. Conversely, viscerotopic effects reciprocally affect centralpain perception, mood, and behavior. For example, spontaneously induced contractions of thecolon in rats leads to activation of the locus coeruleus in the pons, an area closely connected topain and emotional centers in the brain. Jointly, the increased arousal or anxiety is associatedwith a decrease in the frequency of MMC activity of the small bowel possibly mediated by stresshormones in the brain. Based on these observations, it is no longer rational to try to discriminatewhether physiological or psychological factors produce pain or other bowel symptoms. Instead,the Functional GI disorders are understood in terms of dysregulation of brain-gut function, andthe task is to determine to what degree each is remediable. Therefore, a treatment approachconsistent with the concept of brain-gut dysfunction may focus on the neuropeptides andreceptors that are present in both enteric and central nervous systems.THE ROLE FOR PSYCHOLOGICAL FACTORSAlthough psychological factors do not define these disorders and are not required for diagnosis,they are important modulators of the patient's experience and ultimately, the clinical outcome.Research on the psychosocial aspects of patients with functional GI disorders yields three generalobservations Psychological stress exacerbates gastrointestinal symptoms in patients withfunctional GI disorders and can even produce symptoms in healthy patients (but toa lesser degree).o Psychological disturbances modify the experience of illness and illness behaviorssuch as health care seeking. For example, a history of major psychological trauma(e.g. sexual or physical abuse) is more common among patients seen in referralcenters than in primary care and is associated with a more severe disorder and apoorer clinical outcome. Additionally, psychological trauma may increase painreportingtendency.o Having a functional GI disorder has psychological consequences in terms of one'sgeneral well-being, daily functional status, concerns relating to control oversymptoms, and future implications of the illness (e.g. functioning at work andhome).APPROACH TO TREATMENTThe approach to treatment for all functional GI disorders is founded on a therapeutic physicianpatientrelationship. The basis for implementing a strong physician-patient relationship issupported by evidence that patients with functional GI disorders have anywhere from a 30 to80% placebo response rate regardless of treatment.6Because functional GI disorders are chronic, it is important to determine the immediate reasonsbehind each visit, after which treatment can be based on severity and nature of symptoms,physiological and psychosocial determinants of the patient�s illness behavior, and the degree offunctional impairment.These factors can separate patients into mild, moderate, and severe categories.Patients with mild symptoms usually seen in primary care,o do not have major impairment in function or psychological disturbance ando can maintain normal activity.These patients have concerns about their condition but do not need to make many visits to theirphysician. Regarding treatment, these patients require education about their disorder and itssymptoms as well as information regarding a proper diet and the kinds of medication that canhave adverse effects.Patients with moderate symptoms seen in both primary and secondary care facilities ando experience intermittent disruptions in activity on account of their symptoms.o may identify a close relationship between symptoms and inciting events such asstress, travel, or dietary indiscretion.For these patients, symptom monitoring to record time, severity, and presence of associatedfactors can help to identify inciting factors and give the patient a sense of control over thedisorder. Additionally, pharmacotherapy directed at specific symptoms, particularly those thatimpair daily function, can be helpful, as can psychological treatments (relaxation, hypnosis,cognitive-behavioral therapy, and combination treatments) in reducing anxiety and encouraginghealth promoting behaviors.Patients with severe symptoms have trouble functioning daily,o find their disorder to be disabling and debilitating in nearly every facet of life,o have a high frequency of associated psychological difficulties,o make frequent visits to their physicians , ando may hope for a magical cure.In these cases a long-term physician-patient relationship, which sets realistic treatment goals(such as improved quality of life rather than elimination of all pain) is necessary. The focus forthese patients needs to shift from treating a disease to coping with a chronic disorder, wheremuch of the responsibility is place on the patient, himself. Furthermore, antidepressants haveproven useful to control pain and alleviate associated depressive symptoms.7THE FUTUREFuture studies will identify pathophysiological subgroups, each having its own set ofdeterminants ad treatment. Examples are as follows Some patients will develop their disorders or exacerbate symptoms viasensitization of afferent transmission from infection, enhanced motility, or traumato the gut. They may respond to the newly developing neurotransmitter blockingagents.o Patients with more painful and severe symptoms may prove to have "abnormalperception of normal gut function" rather than abnormal function. Thisdysfunction in the central regulation of incoming visceral signs may be remediedwith a psychopharmacological treatment approach.o The symptoms of some patients could be attributed to genetic factors, which resultin abnormalities in central reactivity to stress, in which case genetic manipulationstrategies would prove beneficial.o Early learning within the familial structure and socio-cultural influences has beendemonstrated to affect symptom perception and illness behavior. Future studiesare also likely to identify psychological and behavioral interventions that aretargeted for this subgroup.While it is likely that there are potent new treatments that will follow our growingpathphysiologic knowledge of these disorders, it is unlikely that they will replace some of thefundamental clinical principles active listening,o careful decision making,o an effective patient-physician relationship, ando patient centered biopsychosocial plan of care. http://www.med.unc.edu/medicine/fgidc/hist...aldisorders.pdf Definition of Health: The World Health Organization."Health is a state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity." Also even based on data from Probiotics studies already done, if they benefit pain and bloating they are worth trying. Gas is a very hard symptoms to treat in IBS and if they were to be shown to help just that great, but they have shown to be even more useful in IBD conditions. On IBS more studies are needed. Not that future studies show more benefits for IBSer. They have also been used on this bb for quite some time now with mixed results. You will hear people say they have cured themselves and you will see some Web advertising "cures" but until all of the above is figured out, there is no "cure" for IBS at this time.Again, I highly recommend getting a copy of this from the IFFGD"In the new IFFGD Digestive Health Matters.Visceral Sensations and Brain-Gut Mechanisms By: Emeran A. Mayer, M.D., Professor of Medicine, Physiology and Psychiatry; Director, Center for Neurovisceral Sciences & Women's Health, David Geffen School of Medicine at UCLA IntroductionOver the past several years, different mechanisms located within the gut, or gut wall have been implicated in as possible pathoophysiologic mechanisms underlying the charecteristic IBS symptoms of abdominal pain and discomfort. The list ranges from altered transit of intestinal gas, alterations in colonic flora, immune cell activation in the gut mucosa, and alterations in serotonin containing enterochromaffin cells lining the gut. For those investigators with a good memory, these novel mechanisms can be added to an older list of proposed pathomechanisms, including altered gut motility('Sapstic Colitus') and alterations in mucus secretion. While the jury is still out, one unique aspect about the gut and its connection to the brain are often forgotten: Our brain gut axis is not designed to generate concious perceptions of every alteration in gut homeostasis and internal enviroment, in particlur when these changes are chronic, and when there is no adaptive behavioral response an affected organism could generate.Evolution has not designed our brain gut axis to experience abdominal pain every time the number of mast cells in our ileum goes up, or the number of our serotonin containing cells goes down. It would be counter productive for an animal with a chronic parasite infestation to experince constant viceral pain, and it wouldn't have any advantage for people living in third world countries with frequent enteric infections to suffer from chronic abdominal pain. It has been suggested that viceral pain maybe a secondary phenomenon of an elaborate system of signaling non painful signals to the brain: hunger and fullness (satiety), well being after a meal, urge to evacuate, ect. At the same time, powerful mechanisms have evolved that keep many other aversive signals out of concious perception: contractions, luminal distension, gas volume, low grade inflammation, ect..The most common symptoms of IBS patients are related to altered perception of sensations, arising from the GI tract, and frequently from sites outside the GI tract, such as the genitourinary system or the musculskeletal system. Sensations of bloating, fullness, gas, incomplete rectal evacuation, and crampy abdominal pain are the most common symptoms patients experience. Numerous reports have demonstarted that a significant percentage of functional bowel disorders (FBD) patients about (60) percent rate experimental distensions of the colon as uncomfortable at lower distension volumes or pressure when compared to healthy control subjects. This finding of an increased perception of viceral signals ("viceral hypersensitvity") has been demonstrated during baloon distension tests of the respective part of the GI tract regarless of where the primary symptoms are- the esophagus, the stomach, or the lower abdomen.In contrast to the current emphasis on mechanisms that may result in sensitization of viceral Afferent pathways in the gut, it may well be that alterations in the way the nervous system normally suppresses the perception of the great majority of sensory activity arising from our viscera are essential for the typical symptom constellation of IBS and other functional disorders to develop."It goes into a lot more detail and I highly recommend people get a copy and read the whole article."SummaryIn summary, it is clear that we still have a long way to go to understand the intricate connections between our digestive system and the brain, and how alterations in this two way communication result in functional bowel disorders symptoms. While more alterations in peripheral mechanisms involved in gut function are being reported, rapid progress has occured in our uunderstanding of the multiple mechanisms by which the brain can increase the concious perception of viceral stimuli, which is normally rarely perceieved." http://www.aboutibs.org/Publications/currentParticipate.html and in regards to dysbiosis and "cure", how does this fit into it all."IBS - 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)."What I have interpreted on this board is Eric is saying There is NO cure because there is No Cause found."Basically correct.Funny the use of the words eradicate/kill? It may not be anything needs to be killed or even eradicated, but changed perhaps. Doctors do not use the word "Cure" in IBS for very good reasons. Just like they don't say they can cure migranes or other well know chronic health conditions.When a doctor or someone says they can "cure" IBS, before they have "cured" anyone also may lead to false hope and more anxiety and in IBS that is a major problem, since its very connected to stressors. Not to mention its unethical to say you can cure something you don't know the cause of. Caring doctors may say they can help the symptoms and may say that effective treatment is available and remission might be attainable. But not "cure."They use the word remission for very good reasons.The exact cause of IBS has not been determined yet. Although, they have found many abnormailites in IBS patients, there is still no one specific biological marker in ALL IBS patients yet. IF that is dysbiosis, impairment in brain regions, alter molecular serotonin genes, alter cellular changes in the gi tract or ones not yet discovered. That however does not mean leave out all they have discovered. Honestly some people here are very bias to the cause of IBS to the point of tunnel vision and focus mainly on one idea. Somewhat akin perhaps to foods causing migranes.They may believe the only cause is a bacteria or pathogen, and think mainly in disease STATES but in fact it may or may not be, the evidence so far has implicated a lot and anyone who seriously studies IBS, knows serotonin seems to be majorally implicated and that IBS is already a brain gut axis disorder. Just like they have not been able to "cure" migranes or diabeties or other chronic health problems. You can't "cure" something you do not fully understand the cause of and because the brain gut axis is very complex, there is still a lot of research that needs to be done to figure it all out. There are many issues still needed to be addressed in IBS from cells to neurotransmitters to pathogens and even others.But, suppose for a second that this is true and all IBSers have molecular defects of the SERT gene. The majority of IBSers presenting to gastro clinics effectively demonstarte serotonin dysregulation.Molecular Defect Found for the First Time in IBS Patients http://www.ibsgroup.org/ubb/ultimatebb.php...c;f=10;t=000940 also"The diffuse connections of serotonin allow it to affect many basic psychological functions such as anxiety mechanisms and the regulation of mood, thoughts, aggression, appetite, sex drive and the sleep/wake cycle. Multiple observations suggest that serotonin, one of the most abundant neurotransmitters, plays an important role in the regulation of mood and a key role in the treatment of depression. "Do some of the above look fimilar in non IBS issues, some IBSers have altered REM sleep, others have appetite problems, anxiety problems, depression problems, brain fog, and others.But its a MAJORALLY important neurotransmitter in gut function. The majority of it is stored in the gut, especially in EC cells. EC cells are increase in PI IBS subjects, along with Mast cells, that also release it. In IBS in geneal however it has been majorally implicated. Some people here ignore it or blame it on drug company research. But in fact its peer reviewed research and has to be replicated and observed.How does one go about "curing" molecular defects of cells in the gut that control digestion?Also it is well know in PI IBS patients they have cellular changes in the gi tract with an increase of EC(serotonin) containing cells and mast cells. How does one fix that? Do you use a laser and an electron microscope and surgery to eliminate them? Or maybe there are two little of them, do you then implant them? Maybe in the future that maybe an issue.First however they need to figure it all out.New pathophysiological mechanisms are found and it would not surpprize me at all that even more will be in the future and they are under investigation and each one has to be studied throughly as to cause and effect."Aliment Pharmacol Ther. 2004 Jul;20 Suppl 2:1-9. Related Articles, Links New pathophysiological mechanisms in irritable bowel syndrome.Barbara G, De Giorgio R, Stanghellini V, Cremon C, Salvioli B, Corinaldesi R.Department of Internal Medicine and Gastroenterology, University of Bologna, Italy.Summary Irritable bowel syndrome (IBS) is a functional, multifactorial disease characterized by abdominal pain and erratic bowel habit. Changes in gastrointestinal motor function, enhanced perception of stimuli arising from the gut wall and psychosocial factors are thought to be major contributors for symptom generation. In recent years, several additional factors have been identified and postulated to interact with these classical mechanisms. Reduced ability to expel intestinal gas with consequent gas trapping and bowel distension may contribute to abdominal discomfort/pain and bloating. Abnormal activation of certain brain regions following painful stimulation of the rectum suggests altered processing of afferent signals. An acute gastrointestinal infection is now a recognized aetiological factor for symptom development in a subset of IBS patients (i.e. post-infectious IBS), who are probably unable to down-regulate the initial inflammatory stimulus efficiently. Furthermore, low-grade inflammatory infiltration and activation of mast cells in proximity to nerves in the colonic mucosa may also participate in the frequency and severity of perceived abdominal pain in post-infectious and non-specific IBS. Initial evidence suggests the existence of changes in gut microflora, serotonin metabolism and a genetic contribution in IBS pathophysiology. These novel mechanisms may aid a better understanding of the complex pathophysiology of IBS and to develop new therapies.PMID: 15335408IBS: Improving Diagnosis, Serotonin Signaling, and Implications for Treatment"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.2 http://216.109.117.135/search/cache?p=+ser...&icp=1&.intl=us However, based on what they know now, IBS is treatable for the majority of IBSers. Some methods like CBT and HT for example, maybe hard for the public to understand, why treat the brain for a gut disorder, but HT for example, is statistically and perhaps argueably the most successful treatment to date.They also know now, that a combination of psycological and standard medical thearipies is more effective then standard treatment alone.Because they don't know the exact cause does not mean they don't have research generated insights into effective IBS treatments that help the majority of IBSers to feel better and have less symptoms and even put some into remission, sometimes total remission.Again just because you don't have symptoms, does not been the underlying problems are cured.The history of IBS is important also in the big picture to what they have learned and where things are going. Believe it or not experts in immunology, the enteric nervous sytem, microbiology, neurogastroenterology and many other fields are working on all the issues, they are also combining the information and the shear amount of information the last five to ten years has been very substantial in IBS and they have made a lot of progress.History of Functional DisordersDouglas A. Drossman, MDCenter-Co-DirectorMelissa SwantkowskiNew York UniversityTHE PASTHISTORICAL PRECEDENTSHistorians and physicians have documented the presence of Functional GI disorders throughoutrecorded human history. However, until recently, limited attention has been granted to thesedisorders due to the lack of identifiable pathology and the absence of a conceptual framework tounderstand and categorize them. Systematic investigation of functional GI disorders did notbegin until the middle of the 20th century, and prior to this time, only occasional reports offunctional GI symptoms were published, the first appearing only 200 years agver the past 25 years, scientific attention to understanding and properly caring for patients withfunctional GI disorders has grown progressively. With the understanding comes the rationale foruse of medications directed at intestinal receptors as well as psychopharmacological, behavioral,and psychological forms of treatment. Additionally, there has been an increase in the rate ofscientific publications and greater media exposure to the public through television, radio, andInternet.To understand the historical classification of these disorders, two differing theories relating to theinteraction between the mind and body should be considered.o Holism: a theory built upon the foundation that the mind and body are integratedand utterly inseparable.o Dualism: a theory that proposes a separation between the mind and the body.Greek philosophers Plato, Aristotle, and Hippocrates first proposed the principleof holism about 3,000 years ago, and later in the 12th century; Jewish physicianand philosopher Maimonides reexamined this philosophy. Based on holism, thestudy of medical disease must take into account the whole person rather thanmerely the diseased part. However, societal concepts of illness and diseasedrastically shifted when European philosopher Rene Descartes offered the divergent theory ofdualism in the 17th century. Prior to the notion of dualism, the church discouraged humandissection on the premise that the spirit resided in the body. The acceptance of dualism paved the2way for the emergence of scientific investigation and new medical discoveries by lifting theprohibition of human dissection. This shift in medical thought was congruent with the societalchanges of the 17th century: the shift towards a separation in church and state.IMPLICATIONS FOR FUNCTIONAL GI DISORDERSBased on the concept of dualism, disease was now understood in terms of structuralabnormalities. Therefore, the validity of a disease rested with the observation of morphologicalabnormalities. Medical conditions occurring in the absence of such morphological abnormalitiesand symptoms were not considered legitimate, and were often viewed as psychiatric, consistentwith the concept of dualism. The concept of dualism had other effects with regard to treatment.For example, this would include all the functional GI disorders and other somatic syndromes,such as fibromyalgia. Until the latter part of the 20th century, a medical illness was consideredamenable to scientific inquiry and treatment. However, patients with psychiatric disorders wereinterred in insane asylums and considered to no longer be treatable by medical physicians.Unfortunately this concept leads to a clinical dilemma. Specific diseases explain only about 10%of medical illnesses seen by physicians. Furthermore, people with structural (i.e. organic)diagnosis such as inflammatory bowel disease or cancer show considerable variation in theirsymptom presentation and clinical behavior. Gastroenterologists (as well as other health carepractitioners) are all too familiar with the poor correlation between structural findings onendoscopy and their patient's symptoms.Although efforts to find morphological or even motility etiologies for functional GI disorders inthe latter part of the 20th century were unsuccessful, the assumption that functional GI disordersmust be psychiatric has developed and has permeated current thinking. However, in the face ofcurrent scientific research, this is being seriously challenged. Studies have shown that personswith irritable bowel syndrome who do not seek health care are psychologically much like healthysubjects.THE PRESENTCONCEPTUAL BASES FOR THE STUDY OF FUNCTIONAL GI DISORDERSo The recent acceptance of functional GI disorders as legitimate medical entities isbased on the following three developments The concept of the Biopsychosocial model of illness and diseaseo The development of new investigative methods for studying diseaseo The development of the Rome CriteriaBiopsychosocial ModelIn 1977, the publication of the concept of the Biopsychosocial model by George Engel, and itslater demonstration specifically for gastrointestinal disorders, marked an important change inthinking. A biopsychosocial model of illness and disease provides the needed framework to3understand, categorize, and treat common GI symptoms. These symptoms are the integratedproduct of altered motility, enhanced visceral sensitivity, and brain-gut dysregulation and oftenare influenced by psychosocial factors. Figure 1 illustrates the proposed relationship betweenpsychosocial and physiological factors with functional GI symptoms and the clinical outcome.Early in life, genetics and environmental influences (family attitudes toward bowel training orillness in general, major loss or abuse history or exposure to infection) may affect one'spsychosocial development (susceptibility to life stress, psychological state, coping skills, socialsupport) or the development of gut dysfunction (abnormal motility or visceral hypersensitivity).Additionally, the presence and nature of a functional GI disorder is determined by the interactionof psychosocial factors and altered physiology via the brain-gut axis. In other words, oneindividual afflicted with a bowel disorder but with no psychosocial disturbances, good copingskills and adequate social support may have less severe symptoms and not seek medical care.Another having similar symptoms but with coexistent psychosocial disturbance, high life stress,or poor coping skills may frequent his physician's office and have generally poor outcome.DEVELOPMENT OF NEW INVESTIGATIVE METHODSThe second concurrent process has been the expansion and refinement of investigative methodsthat allow the study of functional GI disorders in terms of biological, cultural, and psychosocial(i.e. brain) influences. These developments include:1. the improvement of motility assessment,2. the standardization of the barostat to measure visceral sensitivity,3. the enhancement of psychometric instruments to determine psychosocialinfluences,4. the introduction of brain imaging (PET, fMRI) to determine CNS contribution tosymptoms, and5. the molecular investigation of brain-gut peptides, which provide insight into howthese symptoms become manifest.In less than ten years, these methods have produced new knowledge of the underlyingpathophysiological features that characterize the age-old symptoms we now define as functionalGI disorders.ROME CRITERIAThe Rome Criteria is an international effort to characterize and classify the functional GIdisorders using a symptom-based classification system. This approach that has its precedentswith classification systems in psychiatry and rheumatology. The rationale for such a system isbased on the premise that patients with functional GI complaints consistently report symptomsthat breed true in their clinical features, yet cannot be classified by any existing structural,physiological or biochemical substrate. The Rome Criteria was built upon the Manning Criteria,which was developed from discriminate function analysis of GI patients.The decision to develop diagnostic criteria by international consensus was introduced as part of alarger effort to address issues within gastroenterology that are not easily resolved by usual4scientific inquiry or literary review. By 1992, several committees had met to discuss the criteria,which ultimately resulted in the publishing of many articles in Gastroenterology Internationaland a book detailing the criteria titled "The Functional Gastrointestinal Disorders (Rome I)".Elaboration of the Rome I criteria led to a second edition of the Rome criteria (titled Rome II) in2000 as well as the publication of a supplement to the journal Gut in 1999. Recently the RomeCoordinating Committee has met to begin Rome III, expected to be published in 2006. To learnmore about the Rome Committees and to see a summary of the Rome II book: go towww.romecriteria.com.PRESENT PATHOPHYSIOLOGICAL OBSERVATIONSDespite differences among the functional gastrointestinal disorders, in location and symptomfeatures, common characteristics are shared with regard to motor and sensory physiology,o central nervous system relationships,o approach to patient care.What follows are the general observations and guidelines.MOTILITYIn healthy subjects, stress can increase motility in the esophagus, stomach, small and largeintestine and colon. Abnormal motility can generate a variety of GI symptoms includingvomiting, diarrhea, constipation, acute abdominal pain, and fecal incontinence. Functional GIpatients have even greater increased motility in response to stressors in comparison to normalsubjects. While abnormal motility plays a vital role in understanding many of the functional GIdisorders and their symptoms, it is not sufficient to explain reports of chronic or recurrentabdominal pain.VISCERAL HYPERSENSITIVITYVisceral hypersensitivity helps to account for disorders associated with chronic or recurrent pain,which are not well correlated with changes in gastrointestinal motility, and in some cases, wheremotility disturbances do not exist. Patients suffering from visceral hypersensitivity have a lowerpain threshold with balloon distension of the bowel or have increased sensitivity to even normalintestinal function. Additionally, there may be an increased or unusual area of somatic referral ofvisceral pain. Recently it has been concluded that visceral hypersensitivity may be induced inresponse to rectal or colonic distension in normal subjects, and to a greater degree, in personswith IBS. Therefore, it is possible that the pain of functional GI disorders may relate tosensitization resulting from chronic abnormal motor hyperactivity, GI infection, or trauma/injuryto the viscera.5BRAIN-GUT AXISThe concept of brain-gut interactions brings together observations relating to motility andvisceral hypersensitivity and their modulation by psychosocial factors. By integrating intestinaland CNS central nervous system activity, the brain-gut axis explains the symptoms relating tofunctional GI disorders. In other words, senses such as vision and smell, as well as enteroceptiveinformation (i.e. emotion and thought) have the capability to affect gastrointestinal sensation,motility, secretion, and inflammation. Conversely, viscerotopic effects reciprocally affect centralpain perception, mood, and behavior. For example, spontaneously induced contractions of thecolon in rats leads to activation of the locus coeruleus in the pons, an area closely connected topain and emotional centers in the brain. Jointly, the increased arousal or anxiety is associatedwith a decrease in the frequency of MMC activity of the small bowel possibly mediated by stresshormones in the brain. Based on these observations, it is no longer rational to try to discriminatewhether physiological or psychological factors produce pain or other bowel symptoms. Instead,the Functional GI disorders are understood in terms of dysregulation of brain-gut function, andthe task is to determine to what degree each is remediable. Therefore, a treatment approachconsistent with the concept of brain-gut dysfunction may focus on the neuropeptides andreceptors that are present in both enteric and central nervous systems.THE ROLE FOR PSYCHOLOGICAL FACTORSAlthough psychological factors do not define these disorders and are not required for diagnosis,they are important modulators of the patient's experience and ultimately, the clinical outcome.Research on the psychosocial aspects of patients with functional GI disorders yields three generalobservations Psychological stress exacerbates gastrointestinal symptoms in patients withfunctional GI disorders and can even produce symptoms in healthy patients (but toa lesser degree).o Psychological disturbances modify the experience of illness and illness behaviorssuch as health care seeking. For example, a history of major psychological trauma(e.g. sexual or physical abuse) is more common among patients seen in referralcenters than in primary care and is associated with a more severe disorder and apoorer clinical outcome. Additionally, psychological trauma may increase painreportingtendency.o Having a functional GI disorder has psychological consequences in terms of one'sgeneral well-being, daily functional status, concerns relating to control oversymptoms, and future implications of the illness (e.g. functioning at work andhome).APPROACH TO TREATMENTThe approach to treatment for all functional GI disorders is founded on a therapeutic physicianpatientrelationship. The basis for implementing a strong physician-patient relationship issupported by evidence that patients with functional GI disorders have anywhere from a 30 to80% placebo response rate regardless of treatment.6Because functional GI disorders are chronic, it is important to determine the immediate reasonsbehind each visit, after which treatment can be based on severity and nature of symptoms,physiological and psychosocial determinants of the patient�s illness behavior, and the degree offunctional impairment.These factors can separate patients into mild, moderate, and severe categories.Patients with mild symptoms usually seen in primary care,o do not have major impairment in function or psychological disturbance ando can maintain normal activity.These patients have concerns about their condition but do not need to make many visits to theirphysician. Regarding treatment, these patients require education about their disorder and itssymptoms as well as information regarding a proper diet and the kinds of medication that canhave adverse effects.Patients with moderate symptoms seen in both primary and secondary care facilities ando experience intermittent disruptions in activity on account of their symptoms.o may identify a close relationship between symptoms and inciting events such asstress, travel, or dietary indiscretion.For these patients, symptom monitoring to record time, severity, and presence of associatedfactors can help to identify inciting factors and give the patient a sense of control over thedisorder. Additionally, pharmacotherapy directed at specific symptoms, particularly those thatimpair daily function, can be helpful, as can psychological treatments (relaxation, hypnosis,cognitive-behavioral therapy, and combination treatments) in reducing anxiety and encouraginghealth promoting behaviors.Patients with severe symptoms have trouble functioning daily,o find their disorder to be disabling and debilitating in nearly every facet of life,o have a high frequency of associated psychological difficulties,o make frequent visits to their physicians , ando may hope for a magical cure.In these cases a long-term physician-patient relationship, which sets realistic treatment goals(such as improved quality of life rather than elimination of all pain) is necessary. The focus forthese patients needs to shift from treating a disease to coping with a chronic disorder, wheremuch of the responsibility is place on the patient, himself. Furthermore, antidepressants haveproven useful to control pain and alleviate associated depressive symptoms.7THE FUTUREFuture studies will identify pathophysiological subgroups, each having its own set ofdeterminants ad treatment. Examples are as follows Some patients will develop their disorders or exacerbate symptoms viasensitization of afferent transmission from infection, enhanced motility, or traumato the gut. They may respond to the newly developing neurotransmitter blockingagents.o Patients with more painful and severe symptoms may prove to have "abnormalperception of normal gut function" rather than abnormal function. Thisdysfunction in the central regulation of incoming visceral signs may be remediedwith a psychopharmacological treatment approach.o The symptoms of some patients could be attributed to genetic factors, which resultin abnormalities in central reactivity to stress, in which case genetic manipulationstrategies would prove beneficial.o Early learning within the familial structure and socio-cultural influences has beendemonstrated to affect symptom perception and illness behavior. Future studiesare also likely to identify psychological and behavioral interventions that aretargeted for this subgroup.While it is likely that there are potent new treatments that will follow our growingpathphysiologic knowledge of these disorders, it is unlikely that they will replace some of thefundamental clinical principles active listening,o careful decision making,o an effective patient-physician relationship, ando patient centered biopsychosocial plan of care. http://www.med.unc.edu/medicine/fgidc/hist...aldisorders.pdf Definition of Health: The World Health Organization."Health is a state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity." Also even based on data from Probiotics studies already done, if they benefit pain and bloating they are worth trying. Gas is a very hard symptoms to treat in IBS and if they were to be shown to help just that great, but they have shown to be even more useful in IBD conditions. On IBS more studies are needed. Not that future studies show more benefits for IBSer. They have also been used on this bb for quite some time now with mixed results. You will hear people say they have cured themselves and you will see some Web advertising "cures" but until all of the above is figured out, there is no "cure" for IBS at this time.Again, I highly recommend getting a copy of this from the IFFGD"In the new IFFGD Digestive Health Matters.Visceral Sensations and Brain-Gut Mechanisms By: Emeran A. Mayer, M.D., Professor of Medicine, Physiology and Psychiatry; Director, Center for Neurovisceral Sciences & Women's Health, David Geffen School of Medicine at UCLA IntroductionOver the past several years, different mechanisms located within the gut, or gut wall have been implicated in as possible pathoophysiologic mechanisms underlying the charecteristic IBS symptoms of abdominal pain and discomfort. The list ranges from altered transit of intestinal gas, alterations in colonic flora, immune cell activation in the gut mucosa, and alterations in serotonin containing enterochromaffin cells lining the gut. For those investigators with a good memory, these novel mechanisms can be added to an older list of proposed pathomechanisms, including altered gut motility('Sapstic Colitus') and alterations in mucus secretion. While the jury is still out, one unique aspect about the gut and its connection to the brain are often forgotten: Our brain gut axis is not designed to generate concious perceptions of every alteration in gut homeostasis and internal enviroment, in particlur when these changes are chronic, and when there is no adaptive behavioral response an affected organism could generate.Evolution has not designed our brain gut axis to experience abdominal pain every time the number of mast cells in our ileum goes up, or the number of our serotonin containing cells goes down. It would be counter productive for an animal with a chronic parasite infestation to experince constant viceral pain, and it wouldn't have any advantage for people living in third world countries with frequent enteric infections to suffer from chronic abdominal pain. It has been suggested that viceral pain maybe a secondary phenomenon of an elaborate system of signaling non painful signals to the brain: hunger and fullness (satiety), well being after a meal, urge to evacuate, ect. At the same time, powerful mechanisms have evolved that keep many other aversive signals out of concious perception: contractions, luminal distension, gas volume, low grade inflammation, ect..The most common symptoms of IBS patients are related to altered perception of sensations, arising from the GI tract, and frequently from sites outside the GI tract, such as the genitourinary system or the musculskeletal system. Sensations of bloating, fullness, gas, incomplete rectal evacuation, and crampy abdominal pain are the most common symptoms patients experience. Numerous reports have demonstarted that a significant percentage of functional bowel disorders (FBD) patients about (60) percent rate experimental distensions of the colon as uncomfortable at lower distension volumes or pressure when compared to healthy control subjects. This finding of an increased perception of viceral signals ("viceral hypersensitvity") has been demonstrated during baloon distension tests of the respective part of the GI tract regarless of where the primary symptoms are- the esophagus, the stomach, or the lower abdomen.In contrast to the current emphasis on mechanisms that may result in sensitization of viceral Afferent pathways in the gut, it may well be that alterations in the way the nervous system normally suppresses the perception of the great majority of sensory activity arising from our viscera are essential for the typical symptom constellation of IBS and other functional disorders to develop."It goes into a lot more detail and I highly recommend people get a copy and read the whole article."SummaryIn summary, it is clear that we still have a long way to go to understand the intricate connections between our digestive system and the brain, and how alterations in this two way communication result in functional bowel disorders symptoms. While more alterations in peripheral mechanisms involved in gut function are being reported, rapid progress has occured in our uunderstanding of the multiple mechanisms by which the brain can increase the concious perception of viceral stimuli, which is normally rarely perceieved." http://www.aboutibs.org/Publications/currentParticipate.html and in regards to dysbiosis and "cure", how does this fit into it all."IBS - 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).
ver the past 25 years, scientific attention to understanding and properly caring for patients withfunctional GI disorders has grown progressively. With the understanding comes the rationale foruse of medications directed at intestinal receptors as well as psychopharmacological, behavioral,and psychological forms of treatment. Additionally, there has been an increase in the rate ofscientific publications and greater media exposure to the public through television, radio, andInternet.To understand the historical classification of these disorders, two differing theories relating to theinteraction between the mind and body should be considered.o Holism: a theory built upon the foundation that the mind and body are integratedand utterly inseparable.o Dualism: a theory that proposes a separation between the mind and the body.Greek philosophers Plato, Aristotle, and Hippocrates first proposed the principleof holism about 3,000 years ago, and later in the 12th century; Jewish physicianand philosopher Maimonides reexamined this philosophy. Based on holism, thestudy of medical disease must take into account the whole person rather thanmerely the diseased part. However, societal concepts of illness and diseasedrastically shifted when European philosopher Rene Descartes offered the divergent theory ofdualism in the 17th century. Prior to the notion of dualism, the church discouraged humandissection on the premise that the spirit resided in the body. The acceptance of dualism paved the2way for the emergence of scientific investigation and new medical discoveries by lifting theprohibition of human dissection. This shift in medical thought was congruent with the societalchanges of the 17th century: the shift towards a separation in church and state.IMPLICATIONS FOR FUNCTIONAL GI DISORDERSBased on the concept of dualism, disease was now understood in terms of structuralabnormalities. Therefore, the validity of a disease rested with the observation of morphologicalabnormalities. Medical conditions occurring in the absence of such morphological abnormalitiesand symptoms were not considered legitimate, and were often viewed as psychiatric, consistentwith the concept of dualism. The concept of dualism had other effects with regard to treatment.For example, this would include all the functional GI disorders and other somatic syndromes,such as fibromyalgia. Until the latter part of the 20th century, a medical illness was consideredamenable to scientific inquiry and treatment. However, patients with psychiatric disorders wereinterred in insane asylums and considered to no longer be treatable by medical physicians.Unfortunately this concept leads to a clinical dilemma. Specific diseases explain only about 10%of medical illnesses seen by physicians. Furthermore, people with structural (i.e. organic)diagnosis such as inflammatory bowel disease or cancer show considerable variation in theirsymptom presentation and clinical behavior. Gastroenterologists (as well as other health carepractitioners) are all too familiar with the poor correlation between structural findings onendoscopy and their patient's symptoms.Although efforts to find morphological or even motility etiologies for functional GI disorders inthe latter part of the 20th century were unsuccessful, the assumption that functional GI disordersmust be psychiatric has developed and has permeated current thinking. However, in the face ofcurrent scientific research, this is being seriously challenged. Studies have shown that personswith irritable bowel syndrome who do not seek health care are psychologically much like healthysubjects.THE PRESENTCONCEPTUAL BASES FOR THE STUDY OF FUNCTIONAL GI DISORDERSo The recent acceptance of functional GI disorders as legitimate medical entities isbased on the following three developments The concept of the Biopsychosocial model of illness and diseaseo The development of new investigative methods for studying diseaseo The development of the Rome CriteriaBiopsychosocial ModelIn 1977, the publication of the concept of the Biopsychosocial model by George Engel, and itslater demonstration specifically for gastrointestinal disorders, marked an important change inthinking. A biopsychosocial model of illness and disease provides the needed framework to3understand, categorize, and treat common GI symptoms. These symptoms are the integratedproduct of altered motility, enhanced visceral sensitivity, and brain-gut dysregulation and oftenare influenced by psychosocial factors. Figure 1 illustrates the proposed relationship betweenpsychosocial and physiological factors with functional GI symptoms and the clinical outcome.Early in life, genetics and environmental influences (family attitudes toward bowel training orillness in general, major loss or abuse history or exposure to infection) may affect one'spsychosocial development (susceptibility to life stress, psychological state, coping skills, socialsupport) or the development of gut dysfunction (abnormal motility or visceral hypersensitivity).Additionally, the presence and nature of a functional GI disorder is determined by the interactionof psychosocial factors and altered physiology via the brain-gut axis. In other words, oneindividual afflicted with a bowel disorder but with no psychosocial disturbances, good copingskills and adequate social support may have less severe symptoms and not seek medical care.Another having similar symptoms but with coexistent psychosocial disturbance, high life stress,or poor coping skills may frequent his physician's office and have generally poor outcome.DEVELOPMENT OF NEW INVESTIGATIVE METHODSThe second concurrent process has been the expansion and refinement of investigative methodsthat allow the study of functional GI disorders in terms of biological, cultural, and psychosocial(i.e. brain) influences. These developments include:1. the improvement of motility assessment,2. the standardization of the barostat to measure visceral sensitivity,3. the enhancement of psychometric instruments to determine psychosocialinfluences,4. the introduction of brain imaging (PET, fMRI) to determine CNS contribution tosymptoms, and5. the molecular investigation of brain-gut peptides, which provide insight into howthese symptoms become manifest.In less than ten years, these methods have produced new knowledge of the underlyingpathophysiological features that characterize the age-old symptoms we now define as functionalGI disorders.ROME CRITERIAThe Rome Criteria is an international effort to characterize and classify the functional GIdisorders using a symptom-based classification system. This approach that has its precedentswith classification systems in psychiatry and rheumatology. The rationale for such a system isbased on the premise that patients with functional GI complaints consistently report symptomsthat breed true in their clinical features, yet cannot be classified by any existing structural,physiological or biochemical substrate. The Rome Criteria was built upon the Manning Criteria,which was developed from discriminate function analysis of GI patients.The decision to develop diagnostic criteria by international consensus was introduced as part of alarger effort to address issues within gastroenterology that are not easily resolved by usual4scientific inquiry or literary review. By 1992, several committees had met to discuss the criteria,which ultimately resulted in the publishing of many articles in Gastroenterology Internationaland a book detailing the criteria titled "The Functional Gastrointestinal Disorders (Rome I)".Elaboration of the Rome I criteria led to a second edition of the Rome criteria (titled Rome II) in2000 as well as the publication of a supplement to the journal Gut in 1999. Recently the RomeCoordinating Committee has met to begin Rome III, expected to be published in 2006. To learnmore about the Rome Committees and to see a summary of the Rome II book: go towww.romecriteria.com.PRESENT PATHOPHYSIOLOGICAL OBSERVATIONSDespite differences among the functional gastrointestinal disorders, in location and symptomfeatures, common characteristics are shared with regard to motor and sensory physiology,o central nervous system relationships,o approach to patient care.What follows are the general observations and guidelines.MOTILITYIn healthy subjects, stress can increase motility in the esophagus, stomach, small and largeintestine and colon. Abnormal motility can generate a variety of GI symptoms includingvomiting, diarrhea, constipation, acute abdominal pain, and fecal incontinence. Functional GIpatients have even greater increased motility in response to stressors in comparison to normalsubjects. While abnormal motility plays a vital role in understanding many of the functional GIdisorders and their symptoms, it is not sufficient to explain reports of chronic or recurrentabdominal pain.VISCERAL HYPERSENSITIVITYVisceral hypersensitivity helps to account for disorders associated with chronic or recurrent pain,which are not well correlated with changes in gastrointestinal motility, and in some cases, wheremotility disturbances do not exist. Patients suffering from visceral hypersensitivity have a lowerpain threshold with balloon distension of the bowel or have increased sensitivity to even normalintestinal function. Additionally, there may be an increased or unusual area of somatic referral ofvisceral pain. Recently it has been concluded that visceral hypersensitivity may be induced inresponse to rectal or colonic distension in normal subjects, and to a greater degree, in personswith IBS. Therefore, it is possible that the pain of functional GI disorders may relate tosensitization resulting from chronic abnormal motor hyperactivity, GI infection, or trauma/injuryto the viscera.5BRAIN-GUT AXISThe concept of brain-gut interactions brings together observations relating to motility andvisceral hypersensitivity and their modulation by psychosocial factors. By integrating intestinaland CNS central nervous system activity, the brain-gut axis explains the symptoms relating tofunctional GI disorders. In other words, senses such as vision and smell, as well as enteroceptiveinformation (i.e. emotion and thought) have the capability to affect gastrointestinal sensation,motility, secretion, and inflammation. Conversely, viscerotopic effects reciprocally affect centralpain perception, mood, and behavior. For example, spontaneously induced contractions of thecolon in rats leads to activation of the locus coeruleus in the pons, an area closely connected topain and emotional centers in the brain. Jointly, the increased arousal or anxiety is associatedwith a decrease in the frequency of MMC activity of the small bowel possibly mediated by stresshormones in the brain. Based on these observations, it is no longer rational to try to discriminatewhether physiological or psychological factors produce pain or other bowel symptoms. Instead,the Functional GI disorders are understood in terms of dysregulation of brain-gut function, andthe task is to determine to what degree each is remediable. Therefore, a treatment approachconsistent with the concept of brain-gut dysfunction may focus on the neuropeptides andreceptors that are present in both enteric and central nervous systems.THE ROLE FOR PSYCHOLOGICAL FACTORSAlthough psychological factors do not define these disorders and are not required for diagnosis,they are important modulators of the patient's experience and ultimately, the clinical outcome.Research on the psychosocial aspects of patients with functional GI disorders yields three generalobservations Psychological stress exacerbates gastrointestinal symptoms in patients withfunctional GI disorders and can even produce symptoms in healthy patients (but toa lesser degree).o Psychological disturbances modify the experience of illness and illness behaviorssuch as health care seeking. For example, a history of major psychological trauma(e.g. sexual or physical abuse) is more common among patients seen in referralcenters than in primary care and is associated with a more severe disorder and apoorer clinical outcome. Additionally, psychological trauma may increase painreportingtendency.o Having a functional GI disorder has psychological consequences in terms of one'sgeneral well-being, daily functional status, concerns relating to control oversymptoms, and future implications of the illness (e.g. functioning at work andhome).APPROACH TO TREATMENTThe approach to treatment for all functional GI disorders is founded on a therapeutic physicianpatientrelationship. The basis for implementing a strong physician-patient relationship issupported by evidence that patients with functional GI disorders have anywhere from a 30 to80% placebo response rate regardless of treatment.6Because functional GI disorders are chronic, it is important to determine the immediate reasonsbehind each visit, after which treatment can be based on severity and nature of symptoms,physiological and psychosocial determinants of the patient�s illness behavior, and the degree offunctional impairment.These factors can separate patients into mild, moderate, and severe categories.Patients with mild symptoms usually seen in primary care,o do not have major impairment in function or psychological disturbance ando can maintain normal activity.These patients have concerns about their condition but do not need to make many visits to theirphysician. Regarding treatment, these patients require education about their disorder and itssymptoms as well as information regarding a proper diet and the kinds of medication that canhave adverse effects.Patients with moderate symptoms seen in both primary and secondary care facilities ando experience intermittent disruptions in activity on account of their symptoms.o may identify a close relationship between symptoms and inciting events such asstress, travel, or dietary indiscretion.For these patients, symptom monitoring to record time, severity, and presence of associatedfactors can help to identify inciting factors and give the patient a sense of control over thedisorder. Additionally, pharmacotherapy directed at specific symptoms, particularly those thatimpair daily function, can be helpful, as can psychological treatments (relaxation, hypnosis,cognitive-behavioral therapy, and combination treatments) in reducing anxiety and encouraginghealth promoting behaviors.Patients with severe symptoms have trouble functioning daily,o find their disorder to be disabling and debilitating in nearly every facet of life,o have a high frequency of associated psychological difficulties,o make frequent visits to their physicians , ando may hope for a magical cure.In these cases a long-term physician-patient relationship, which sets realistic treatment goals(such as improved quality of life rather than elimination of all pain) is necessary. The focus forthese patients needs to shift from treating a disease to coping with a chronic disorder, wheremuch of the responsibility is place on the patient, himself. Furthermore, antidepressants haveproven useful to control pain and alleviate associated depressive symptoms.7THE FUTUREFuture studies will identify pathophysiological subgroups, each having its own set ofdeterminants ad treatment. Examples are as follows Some patients will develop their disorders or exacerbate symptoms viasensitization of afferent transmission from infection, enhanced motility, or traumato the gut. They may respond to the newly developing neurotransmitter blockingagents.o Patients with more painful and severe symptoms may prove to have "abnormalperception of normal gut function" rather than abnormal function. Thisdysfunction in the central regulation of incoming visceral signs may be remediedwith a psychopharmacological treatment approach.o The symptoms of some patients could be attributed to genetic factors, which resultin abnormalities in central reactivity to stress, in which case genetic manipulationstrategies would prove beneficial.o Early learning within the familial structure and socio-cultural influences has beendemonstrated to affect symptom perception and illness behavior. Future studiesare also likely to identify psychological and behavioral interventions that aretargeted for this subgroup.While it is likely that there are potent new treatments that will follow our growingpathphysiologic knowledge of these disorders, it is unlikely that they will replace some of thefundamental clinical principles active listening,o careful decision making,o an effective patient-physician relationship, ando patient centered biopsychosocial plan of care. http://www.med.unc.edu/medicine/fgidc/hist...aldisorders.pdf Definition of Health: The World Health Organization."Health is a state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity." Also even based on data from Probiotics studies already done, if they benefit pain and bloating they are worth trying. Gas is a very hard symptoms to treat in IBS and if they were to be shown to help just that great, but they have shown to be even more useful in IBD conditions. On IBS more studies are needed. Not that future studies show more benefits for IBSer. They have also been used on this bb for quite some time now with mixed results. You will hear people say they have cured themselves and you will see some Web advertising "cures" but until all of the above is figured out, there is no "cure" for IBS at this time.Again, I highly recommend getting a copy of this from the IFFGD"In the new IFFGD Digestive Health Matters.Visceral Sensations and Brain-Gut Mechanisms By: Emeran A. Mayer, M.D., Professor of Medicine, Physiology and Psychiatry; Director, Center for Neurovisceral Sciences & Women's Health, David Geffen School of Medicine at UCLA IntroductionOver the past several years, different mechanisms located within the gut, or gut wall have been implicated in as possible pathoophysiologic mechanisms underlying the charecteristic IBS symptoms of abdominal pain and discomfort. The list ranges from altered transit of intestinal gas, alterations in colonic flora, immune cell activation in the gut mucosa, and alterations in serotonin containing enterochromaffin cells lining the gut. For those investigators with a good memory, these novel mechanisms can be added to an older list of proposed pathomechanisms, including altered gut motility('Sapstic Colitus') and alterations in mucus secretion. While the jury is still out, one unique aspect about the gut and its connection to the brain are often forgotten: Our brain gut axis is not designed to generate concious perceptions of every alteration in gut homeostasis and internal enviroment, in particlur when these changes are chronic, and when there is no adaptive behavioral response an affected organism could generate.Evolution has not designed our brain gut axis to experience abdominal pain every time the number of mast cells in our ileum goes up, or the number of our serotonin containing cells goes down. It would be counter productive for an animal with a chronic parasite infestation to experince constant viceral pain, and it wouldn't have any advantage for people living in third world countries with frequent enteric infections to suffer from chronic abdominal pain. It has been suggested that viceral pain maybe a secondary phenomenon of an elaborate system of signaling non painful signals to the brain: hunger and fullness (satiety), well being after a meal, urge to evacuate, ect. At the same time, powerful mechanisms have evolved that keep many other aversive signals out of concious perception: contractions, luminal distension, gas volume, low grade inflammation, ect..The most common symptoms of IBS patients are related to altered perception of sensations, arising from the GI tract, and frequently from sites outside the GI tract, such as the genitourinary system or the musculskeletal system. Sensations of bloating, fullness, gas, incomplete rectal evacuation, and crampy abdominal pain are the most common symptoms patients experience. Numerous reports have demonstarted that a significant percentage of functional bowel disorders (FBD) patients about (60) percent rate experimental distensions of the colon as uncomfortable at lower distension volumes or pressure when compared to healthy control subjects. This finding of an increased perception of viceral signals ("viceral hypersensitvity") has been demonstrated during baloon distension tests of the respective part of the GI tract regarless of where the primary symptoms are- the esophagus, the stomach, or the lower abdomen.In contrast to the current emphasis on mechanisms that may result in sensitization of viceral Afferent pathways in the gut, it may well be that alterations in the way the nervous system normally suppresses the perception of the great majority of sensory activity arising from our viscera are essential for the typical symptom constellation of IBS and other functional disorders to develop."It goes into a lot more detail and I highly recommend people get a copy and read the whole article."SummaryIn summary, it is clear that we still have a long way to go to understand the intricate connections between our digestive system and the brain, and how alterations in this two way communication result in functional bowel disorders symptoms. While more alterations in peripheral mechanisms involved in gut function are being reported, rapid progress has occured in our uunderstanding of the multiple mechanisms by which the brain can increase the concious perception of viceral stimuli, which is normally rarely perceieved." http://www.aboutibs.org/Publications/currentParticipate.html and in regards to dysbiosis and "cure", how does this fit into it all."IBS - 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 response to Flux�s questions on how flora species are ID�d if not cultured--found these articles by microbiologists (the experts/heroes)~~Laboratory of Microbiology, Wageningen University, The Netherlands2002 Aug�GI-tract ecology has been experiencing a revival due to the development of molecular techniques, especially those based on 16S RNA (zRNA) genes. A richer ecosystem than previously imagined of novel species is being discovered that is significantly influenced by our host genotype. Special attention has been focused on the bifidobacteria and the lactic acid bacterial (LAB) populations, both those that are naturally present within this complex ecosystem and those that are ingested as probiotics in functional foods. Overall this interest stems from a increasing awareness of interplay between microflora, diet and the health of the host, and is further stimulated by an increasing incidence of gastrointestinal illnesses, and atopy. �Recent advances in molecular technologies, including high-throughput genomics-based approaches, can significantly advance our understanding of the microbe--diet--host interactions and offer valuable information for design and application of health-targeted microbes.� http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12369201 Eur J Clin Nutr. 2002 �Analysis of the intestinal microflora using molecular methods.��A large and complex bacterial community inhabits the distal intestinal tract of humans. This collection, known as the intestinal microflora, is dominated numerically by obligately anaerobic bacterial species. Many of these species have never been cultivated under laboratory conditions...Nucleic acid-based techniques now permit, however, the analysis of even the non-cultivable members of the bacterial community. Polymerase chain reaction (PCR) coupled with denaturing gradient gel electrophoresis (DGGE) provides a useful technique for comparisons of the composition of faecal or intestinal microfloras...This research is important because treatment with oral antibiotics during the first 2 y of life has been identified as a predictor of subsequent atopic disease. The treatment of young children with broad spectrum oral antibiotics might produce perturbations in the composition of the intestinal microflora such that bacteria important in promoting Th1 mechanisms are depleted at a crucial age. � http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12556947 Br J Nutr. 2002 �Molecular methods for exploring the intestinal ecosystem.��Molecular methods have provided renewed impetus for the analysis of the composition of the intestinal microflora in health and disease. The polymerase chain reaction coupled with denaturing gradient gel electrophoresis provides a method whereby the bacterial communities in large numbers of samples can be compared efficiently and effectively. Altered bacterial populations associated with disease states can then be targeted for further investigation. In the long-term, an 'abnormal microflora' might be rectified by the use of probiotics or prebiotics.� http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12088519 Others~~ http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12704557 http://www.ncbi.nlm.nih.gov/entrez/query.f...t&holding=f1000 http://www.ncbi.nlm.nih.gov/books/bv.fcgi?...brk.chapter.622
In response to Flux�s questions on how flora species are ID�d if not cultured--found these articles by microbiologists (the experts/heroes)~~Laboratory of Microbiology, Wageningen University, The Netherlands2002 Aug�GI-tract ecology has been experiencing a revival due to the development of molecular techniques, especially those based on 16S RNA (zRNA) genes. A richer ecosystem than previously imagined of novel species is being discovered that is significantly influenced by our host genotype. Special attention has been focused on the bifidobacteria and the lactic acid bacterial (LAB) populations, both those that are naturally present within this complex ecosystem and those that are ingested as probiotics in functional foods. Overall this interest stems from a increasing awareness of interplay between microflora, diet and the health of the host, and is further stimulated by an increasing incidence of gastrointestinal illnesses, and atopy. �Recent advances in molecular technologies, including high-throughput genomics-based approaches, can significantly advance our understanding of the microbe--diet--host interactions and offer valuable information for design and application of health-targeted microbes.� http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12369201 Eur J Clin Nutr. 2002 �Analysis of the intestinal microflora using molecular methods.��A large and complex bacterial community inhabits the distal intestinal tract of humans. This collection, known as the intestinal microflora, is dominated numerically by obligately anaerobic bacterial species. Many of these species have never been cultivated under laboratory conditions...Nucleic acid-based techniques now permit, however, the analysis of even the non-cultivable members of the bacterial community. Polymerase chain reaction (PCR) coupled with denaturing gradient gel electrophoresis (DGGE) provides a useful technique for comparisons of the composition of faecal or intestinal microfloras...This research is important because treatment with oral antibiotics during the first 2 y of life has been identified as a predictor of subsequent atopic disease. The treatment of young children with broad spectrum oral antibiotics might produce perturbations in the composition of the intestinal microflora such that bacteria important in promoting Th1 mechanisms are depleted at a crucial age. � http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12556947 Br J Nutr. 2002 �Molecular methods for exploring the intestinal ecosystem.��Molecular methods have provided renewed impetus for the analysis of the composition of the intestinal microflora in health and disease. The polymerase chain reaction coupled with denaturing gradient gel electrophoresis provides a method whereby the bacterial communities in large numbers of samples can be compared efficiently and effectively. Altered bacterial populations associated with disease states can then be targeted for further investigation. In the long-term, an 'abnormal microflora' might be rectified by the use of probiotics or prebiotics.� http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12088519 Others~~ http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12704557 http://www.ncbi.nlm.nih.gov/entrez/query.f...t&holding=f1000 http://www.ncbi.nlm.nih.gov/books/bv.fcgi?...brk.chapter.622
Probiotics are foods that contain live bacteria. It is the bacteria and metabolites which they produce that give these probiotics their health promoting properties.Prebiotics are foods or nutrients that are used by specific bacteria and that can be added to the diet to increase the chances of these particular bacteria growing and thriving in the intestine.One commonly used prebiotic is fructo ologosacharide (FOS). It occurs naturally in things like onions and even wheat in very small amounts. I avoid it -- it causes too much gas and bloat. It was snuck into our food supply back in the 90s when Coors Brewing filed a Generally Regarded As Safe (GRAS) document with the FDA. At the time, the health food industry was chosen as the initial market for it. Cheap forms of it have been used extensively in all kinds of foods in Japan for a couple of decades - not really as a prebiotic but as a cheap alternative sweetener. A better form of FOS has been manufactured in the Netherlands from chicory and is used in some commercial yogurt and kefir. It's sometimes listed on the label as inulin/FOS. Apparently, the human body cannot diegest and metabilize FOS but the beneficial bacteria in the colon can. Of course, prebiotics are as controversial as probiotics, if not more so.
Probiotics are foods that contain live bacteria. It is the bacteria and metabolites which they produce that give these probiotics their health promoting properties.Prebiotics are foods or nutrients that are used by specific bacteria and that can be added to the diet to increase the chances of these particular bacteria growing and thriving in the intestine.One commonly used prebiotic is fructo ologosacharide (FOS). It occurs naturally in things like onions and even wheat in very small amounts. I avoid it -- it causes too much gas and bloat. It was snuck into our food supply back in the 90s when Coors Brewing filed a Generally Regarded As Safe (GRAS) document with the FDA. At the time, the health food industry was chosen as the initial market for it. Cheap forms of it have been used extensively in all kinds of foods in Japan for a couple of decades - not really as a prebiotic but as a cheap alternative sweetener. A better form of FOS has been manufactured in the Netherlands from chicory and is used in some commercial yogurt and kefir. It's sometimes listed on the label as inulin/FOS. Apparently, the human body cannot diegest and metabilize FOS but the beneficial bacteria in the colon can. Of course, prebiotics are as controversial as probiotics, if not more so.
For more info, this is a pretty good article re: prebiotics: http://www.findarticles.com/p/articles/mi_...170/ai_78576180
For more info, this is a pretty good article re: prebiotics: http://www.findarticles.com/p/articles/mi_...170/ai_78576180
FYIEditorial April 2000Volume 95, Number 4Pages 862-863 -------------------------------------------------------------------------------- Symptom Expression in Pain-Predominant Functional Bowel Syndrome: Is Visceral Hyperalgesia the Whole Truth? Michael S. Shapiro, M.D.a and Kevin W. Olden, M.D.a --------------------------------------------------------------------------------Ever increasing socioeconomic pressures have elevated cost-effective management of patients with irritable bowel syndrome (IBS) and related functional disorders as a high priority in gastroenterology practice. The illness of these patients produces an enormous cost to society related to absenteeism and use of medical resources (1). Although most individuals with IBS go about their daily lives without need for medical care, about 30% of IBS sufferers seek assistance for their disorder (2). IBS patients pursue consultation mainly because of their abdominal pain (3). The severity of abdominal pain reported by patients with functional bowel syndrome to their physician often drives the aggressiveness of a workup in the attempt to identify "serious disease." This results in higher risk to the patient and greater expense. However, what is uncertain is whether, in IBS patients, painful symptoms directly reflect pathophysiological mechanisms involved in pain production such as visceral hyperalgesia, or whether they are a consequence of psychosocial factors. In this issue of the Journal, Drossman et al. address the question of what factors influence severity of the pain reported in pain-predominant functional bowel disorders (4). Patients considered in this study were sufferers of moderate to severe painful functional bowel syndrome as identified by a validated Functional Bowel Severity Index. A total of 83.3% of subjects in the study fulfilled standard Rome criteria for IBS. Psychosocial and behavioral parameters were compared between moderate and severe groups. Psychological factors were considered as potential modulators of pain expression based on the high prevalence of psychiatric disturbance detected in patients who present with functional bowel complaints, in the range of 42-61% (1). Visceral hyperalgesia also is considered to be a major mechanism involved in symptom production in functional bowel syndrome, and can be demonstrated in up to 94% of IBS patients by rectal distention (5). For this study, visceral hypersensitivity was assessed by barostat balloon rectal distention to detect differences in pain perception. The results show compelling evidence that psychosocial and behavioral elements are the crucial and predominant factors that distinguish moderate from severe functional bowel syndrome. Major factors associated significantly with the severe pain-predominant group included depression, reduced perception of quality of life, impaired coping skills, and increased health care use. Of 19 psychosocial variables entered into a regression model to predict pain severity, four factors were identified as highly predictive of severe functional pain: physical dysfunction, eating dysfunction, days in bed for GI symptoms, and number of times the physician was called for GI symptoms. These factors are characteristic of "learned illness behavior" (6), in which patients are preoccupied with multiple somatic complaints and adopt a behavioral pattern to reflect this preoccupation. Although heighted visceral hypersensitivity was suggested in the severe pain-predominant group, the differences between this group and the moderate group were not substantial, and regression analysis did not find sensitivity to rectal distention to be a good predictor of pain severity. This study illustrates the crucial role of psychosocial and behavioral disturbance in how pain is perceived and reported in IBS and other painful functional GI disorders. Visceral hypersensitivity has been the focus of intense investigation as a possible mechanism of symptom generation in IBS and the functional GI disorders (2, 7). Although the data of Drossman et al. do not reject a role for visceral hypersensitivity in painful functional bowel syndrome, they suggest that visceral hyperalgesia alone is not sufficient to explain how pain is communicated by patients with functional GI disorders. In particular, somatization disorder has been found to correlate with reduced pain threshold (8) in IBS and is prevalent in functional bowel syndrome sufferers who seek medical care (6). The mechanism by which psychological factors modulate pain reporting and perception is not known. Some attention has been directed to chronic stress as a factor, which is highly prevalent in patients with functional bowel syndrome (9) and is associated with increased intensity of symptoms reported (10, 11). Stress may influence the threshold to painful distention (8). A possible biochemical basis for these effects may involve, at some level, corticotropin-releasing factor, which is an important player in the stress response and which has been demonstrated to influence symptoms in IBS (12). Whitehead and Palsson have proposed a model of pain perception and reporting in IBS that incorporates a dynamic interplay of physiological and psychosocial factors leading to how symptoms ultimately are described by the patient (8). Illness behavior plays a pivotal part in this model and is directly linked to health care use. The results of Drossman et al., appearing in this issue of the Journal, lend support to the "biopsychosocial" model of functional GI disorder. Their findings also emphasize the importance of modification of illness behavior patterns as the most effective means of enacting a favorable outcome for these most challenging patients. How can these findings be applied? There is a need to heighten awareness of the clinician involved in the care of these patients regarding the recognition of important psychosocial factors in functional bowel patients. Symptoms must be interpreted as a complex manifestation of brain-gut interaction and not merely as gut dysfunction. Establishing an effective patient-physician relationship is a crucial step in successfully sorting out such patient issues (1). Once contributing psychological features are identified, effective therapy can be offered, which may include use of psychotropic drugs, cognitive-behavioral therapy, dynamic psychotherapy, hypnotherapy, or other behavioral techniques that have been shown to benefit these patients (1). Thus, we are reminded that effective medical care for these patients requires a thoughtful blend of art and science, based on insightful interview, knowledge of the complexity of factors involved in symptom expression, and the ability to persuade, with sensitivity, patients as to the most helpful intervention. --------------------------------------------------------------------------------aDivision of Gastroenterology and Hepatology, Mayo Clinic Scottsdale, Scottsdale, Arizona http://www-east.elsevier.com/ajg/issues/9504/ajg1973edi.htm
FYIEditorial April 2000Volume 95, Number 4Pages 862-863 -------------------------------------------------------------------------------- Symptom Expression in Pain-Predominant Functional Bowel Syndrome: Is Visceral Hyperalgesia the Whole Truth? Michael S. Shapiro, M.D.a and Kevin W. Olden, M.D.a --------------------------------------------------------------------------------Ever increasing socioeconomic pressures have elevated cost-effective management of patients with irritable bowel syndrome (IBS) and related functional disorders as a high priority in gastroenterology practice. The illness of these patients produces an enormous cost to society related to absenteeism and use of medical resources (1). Although most individuals with IBS go about their daily lives without need for medical care, about 30% of IBS sufferers seek assistance for their disorder (2). IBS patients pursue consultation mainly because of their abdominal pain (3). The severity of abdominal pain reported by patients with functional bowel syndrome to their physician often drives the aggressiveness of a workup in the attempt to identify "serious disease." This results in higher risk to the patient and greater expense. However, what is uncertain is whether, in IBS patients, painful symptoms directly reflect pathophysiological mechanisms involved in pain production such as visceral hyperalgesia, or whether they are a consequence of psychosocial factors. In this issue of the Journal, Drossman et al. address the question of what factors influence severity of the pain reported in pain-predominant functional bowel disorders (4). Patients considered in this study were sufferers of moderate to severe painful functional bowel syndrome as identified by a validated Functional Bowel Severity Index. A total of 83.3% of subjects in the study fulfilled standard Rome criteria for IBS. Psychosocial and behavioral parameters were compared between moderate and severe groups. Psychological factors were considered as potential modulators of pain expression based on the high prevalence of psychiatric disturbance detected in patients who present with functional bowel complaints, in the range of 42-61% (1). Visceral hyperalgesia also is considered to be a major mechanism involved in symptom production in functional bowel syndrome, and can be demonstrated in up to 94% of IBS patients by rectal distention (5). For this study, visceral hypersensitivity was assessed by barostat balloon rectal distention to detect differences in pain perception. The results show compelling evidence that psychosocial and behavioral elements are the crucial and predominant factors that distinguish moderate from severe functional bowel syndrome. Major factors associated significantly with the severe pain-predominant group included depression, reduced perception of quality of life, impaired coping skills, and increased health care use. Of 19 psychosocial variables entered into a regression model to predict pain severity, four factors were identified as highly predictive of severe functional pain: physical dysfunction, eating dysfunction, days in bed for GI symptoms, and number of times the physician was called for GI symptoms. These factors are characteristic of "learned illness behavior" (6), in which patients are preoccupied with multiple somatic complaints and adopt a behavioral pattern to reflect this preoccupation. Although heighted visceral hypersensitivity was suggested in the severe pain-predominant group, the differences between this group and the moderate group were not substantial, and regression analysis did not find sensitivity to rectal distention to be a good predictor of pain severity. This study illustrates the crucial role of psychosocial and behavioral disturbance in how pain is perceived and reported in IBS and other painful functional GI disorders. Visceral hypersensitivity has been the focus of intense investigation as a possible mechanism of symptom generation in IBS and the functional GI disorders (2, 7). Although the data of Drossman et al. do not reject a role for visceral hypersensitivity in painful functional bowel syndrome, they suggest that visceral hyperalgesia alone is not sufficient to explain how pain is communicated by patients with functional GI disorders. In particular, somatization disorder has been found to correlate with reduced pain threshold (8) in IBS and is prevalent in functional bowel syndrome sufferers who seek medical care (6). The mechanism by which psychological factors modulate pain reporting and perception is not known. Some attention has been directed to chronic stress as a factor, which is highly prevalent in patients with functional bowel syndrome (9) and is associated with increased intensity of symptoms reported (10, 11). Stress may influence the threshold to painful distention (8). A possible biochemical basis for these effects may involve, at some level, corticotropin-releasing factor, which is an important player in the stress response and which has been demonstrated to influence symptoms in IBS (12). Whitehead and Palsson have proposed a model of pain perception and reporting in IBS that incorporates a dynamic interplay of physiological and psychosocial factors leading to how symptoms ultimately are described by the patient (8). Illness behavior plays a pivotal part in this model and is directly linked to health care use. The results of Drossman et al., appearing in this issue of the Journal, lend support to the "biopsychosocial" model of functional GI disorder. Their findings also emphasize the importance of modification of illness behavior patterns as the most effective means of enacting a favorable outcome for these most challenging patients. How can these findings be applied? There is a need to heighten awareness of the clinician involved in the care of these patients regarding the recognition of important psychosocial factors in functional bowel patients. Symptoms must be interpreted as a complex manifestation of brain-gut interaction and not merely as gut dysfunction. Establishing an effective patient-physician relationship is a crucial step in successfully sorting out such patient issues (1). Once contributing psychological features are identified, effective therapy can be offered, which may include use of psychotropic drugs, cognitive-behavioral therapy, dynamic psychotherapy, hypnotherapy, or other behavioral techniques that have been shown to benefit these patients (1). Thus, we are reminded that effective medical care for these patients requires a thoughtful blend of art and science, based on insightful interview, knowledge of the complexity of factors involved in symptom expression, and the ability to persuade, with sensitivity, patients as to the most helpful intervention. --------------------------------------------------------------------------------aDivision of Gastroenterology and Hepatology, Mayo Clinic Scottsdale, Scottsdale, Arizona http://www-east.elsevier.com/ajg/issues/9504/ajg1973edi.htm
From above"How can these findings be applied? There is a need to heighten awareness of the clinician involved in the care of these patients regarding the recognition of important psychosocial factors in functional bowel patients. Symptoms must be interpreted as a complex manifestation of brain-gut interaction and not merely as gut dysfunction."
From above"How can these findings be applied? There is a need to heighten awareness of the clinician involved in the care of these patients regarding the recognition of important psychosocial factors in functional bowel patients. Symptoms must be interpreted as a complex manifestation of brain-gut interaction and not merely as gut dysfunction."
Arch Intern Med. 2004 Sep 13;164(16):1773-80. Related Articles, Links Clinical determinants of health-related quality of life in patients with irritable bowel syndrome.Spiegel BM, Gralnek IM, Bolus R, Chang L, Dulai GS, Mayer EA, Naliboff B.Division of Gastroenterology, the VA Greater Los Angeles Healthcare System, the Division of Digestive Diseases.BACKGROUND: Current guidelines recommend routine assessment of health-related quality of life (HRQOL) in patients with irritable bowel syndrome (IBS). However, physicians rarely have the time to measure HRQOL with the appropriate methodological rigor, and data suggest that HRQOL in patients with IBS is often estimated using inaccurate clinical gestalt. The identification of predictive factors could allow physicians to better assess HRQOL without using misleading clinical clues. We, therefore, sought to identify determinants of HRQOL in patients with IBS. METHODS: We examined 770 patients, 18 years or older, with IBS at a university-based referral center. Subjects completed a symptom questionnaire, the Symptoms Checklist-90 items psychometric checklist, and the 36-Item Short-Form Health Survey. The main outcome was HRQOL as measured by the mental and physical component scores of the 36-Item Short-Form Health Survey. We first developed a list of hypothesis-driven HRQOL predictors, and then performed multivariate regression analysis to measure the independent association of each predictor with HRQOL. RESULTS: Seven factors (r(2) = 0.39) independently predicted physical HRQOL: (1) more than 5 physician visits per year, (2) tiring easily, (3) low in energy, (4) severe symptoms, (5) predominantly painful symptoms, (6) the feeling that there is "something seriously wrong with body," and (7) symptom flares for longer than 24 hours. Eight factors (r(2) = 0.36) independently predicted mental HRQOL: (1) feeling tense, (2) feeling nervous, (3) feeling hopeless, (4) difficulty sleeping, (5) tiring easily, (6) low sexual interest, (7) IBS symptom interference with sexual function, and (8) low energy. CONCLUSIONS: Health-related quality of life in patients with IBS is primarily related to extraintestinal symptoms rather than traditionally elicited gastrointestinal symptoms. These findings suggest that rather than focusing on physiological epiphenomena (stool characteristics and subtype of IBS) and potentially misleading clinical factors (age and disease duration), physicians might be better served to gauge global symptom severity, address anxiety, and eliminate factors contributing to chronic stress in patients with IBS. PMID: 15364671Webmedjust fyiMind-Body-Pain Connection: How Does It Work?By Michael Henry JosephWebMD Live Events Transcript Archive Event Date: 05/11/2000.Moderator: Welcome to WebMD Live's World Watch and Health News Auditorium. Today we are discussing "The Mind-Body-Pain Connection: How Does It Work?" with Brenda Bursch, Ph.D., Michael Joseph, M.D., and Lonnie Zeltzer, M.D.Brenda Bursch, Ph.D., is the Associate Director of the Pediatric Pain Program, Co-Director of Pediatric Chronic Pain Clinical Service and Assistant Clinical Professor of Psychiatry & Biobehavioral Sciences at UCLA Department of Pediatrics in the School of Medicine. She has written about asthma, developmental & behavioral pediatrics, emergency medicine, AIDS education and prevention, chronic digestive diseases and pediatric bowel disorders. She has membership in the American Pain Society, American Psychological Association, Munchausen Syndrome by Proxy Network, and the UCLA Center for the Study of Organizational and Group Dynamics. Michael Henry Joseph, MD, is an assistant professor of pediatrics and co-director of Chronic Pain Services at the University of California at Los Angeles Children's Hospital. He is a recipient of the Golden Apple Award for Excellence in Teaching. Lonnie Zeltzer, M.D., is an expert in the field of pediatric pain. She is a former president of the Society for Adolescent Medicine and member of the National Institute of Health?s Human Development Study Section. She is currently a Professor of Pediatrics and Anesthesiology at the UCLA School of Medicine. She is Director of the UCLA Pediatric Pain Program and Associate Director of the Patients & Survivors Section, Cancer Prevention and Control Research Branch of the UCLA Jonsson Comprehensive Cancer Center. She has well over one hundred scientific publications, reviews and chapters in medical journals, and has lectured internationally. Moderator: Doctors, welcome back to WebMD Live.Dr. Bursch: Thank you.Dr. Joseph: Thank you.Dr. Zeltzer: Thank you.Dr. Zeltzer: As you know, the mind-body pain connection is the basis upon which our pediatric pain program at UCLA operates, both in terms of how it conceptually views pain and its approach to treatment. I would like to begin by discussing the physiology that is underlying a lot of our functional definitions of pain and our basic philosophy and our mind-body connection model.Dr. Joseph: I'd like to say the differentiation into components is a fallacy. Your brain and nervous system communicate with the rest of your body just like all other organ systems. All work together. Pain is not a simple entity in which it's like pulling on a string and ringing a little bell in your head. It's more dynamic than that, in which you do have nerve input from fingers and toes and organs that goes to spinal column and then to your brain. You also have nerve pathways that are coming from your brain down your spinal column. There are many factors that change the way we actually perceive pain and can make pain more intense or less intense depending on the situation. This is also true for other symptoms. This connection between your central nervous system and your brain communicates with your peripheral nervous system so nerves coming from organs, arms and legs, and all symptoms that you may be feeling can be altered by your nervous system either increased or decreased. That's true of nausea or difficulty breathing or any symptom you might be feeling. In fact, it's true of all of your senses. Your sense of hearing, smell, taste, vision are also all interpreted perceptions. Different factors that can alter your perception specifically when it comes to pain include how much attention you pay to the symptom, what the meaning of the symptom is. For some people, pain is a good thing such as when you've been working out and you're waiting to feel that burn and the burn has a good context, as opposed to if you pull a muscle, you may have exactly the same amount of tissue damage but the way you perceive the pain is very different. Memory can affect perception of pain. When we are awake, it takes much less stimulus to cause pain than when we are asleep. If we were in a coma, it would take even more, possibly we don't even experience pain.Dr. Bursch: As Dr. Joseph just described, the nature of perception of pain, each individual is different not only in pre-existing neurology but also in their experiences that would contribute to their memories of pain, to their arousal, due to circumstances and their experiences and the meanings they attribute. Also, there are different points at which they would become distressed by the signaling. From a physiologic standpoint, people have different levels at which sensory nerves that carry pain information will send those signals. Some people have the ability to have a lot of stimulation before the signals are sent, and some people are very sensitive and a very little stimulation sends the signal. People with irritable bowel syndrome are known through many studies to have a very low threshold for sensory info sent from their intestine to their brain.Dr. Zeltzer: People can learn different coping skills and ways of blocking out the sensation so they experience them, but it doesn't have to distress them. Since you describe the physiologic basis for how pain becomes pain -- how different tissue injury turns into pain -- maybe you can talk about the body's natural pain control system, from a mind-body perspective?Dr. Joseph: The body has a number of ways of controlling pain throughout different organ systems. The most direct is pathways, nerve pathways, that travel from your brain back down your spinal column and they signal directly to those same nerves that are sending pain signals to your brain. They interrupt those pain signals on their way up. These nerve pathways are activated by a number of factors. The easiest one to recognize is fear. A good example of this is, say you're in a dark parking lot and you accidentally shut your finger in the car door. It hurts a lot. You start hearing footsteps behind you. All of a sudden your finger stops hurting. There's no difference in the amount of tissue damage between when you heard the footsteps and when you didn't, but your brain has sent signals to your body that it is time to run away as opposed to time to feel pain. There are subtle ways that your body controls pain, as well. Your brain makes chemicals called endorphins and enkephalins. These molecules are very similar to drugs such as morphine, which everybody recognizes as a pain fighting drug. Interestingly, not only your brain makes these chemicals but also your immune system. B-lymphocytes actually make these chemicals as well. When you have inflamed or infected areas and sending pain signals, even your immune systems can go to those areas, release pain modulating chemicals into that area and decrease the pain right then, if it's something the person needs to have happen at that time. There are many ways pain can be increased or decreased depending on the needs of the individual at each time.Dr. Bursch: Based on the earlier model that Dr. Joseph presented that delineated the relationship of memory, attention and arousal on the pain system, there are a number of behavioral or cognitive strategies that one can engage in order to impact perception of pain, things as simple as engaging in relaxing activities, using distraction so that you're focusing on something else. It could be using visualization techniques which is similar to distraction technique. You can use your mind and you can use your body in ways that the actual pain perception can be altered if you can alter your arousal or your attention or your memory, or memory you have about the pain. You can change your experience of that symptom.Dr. Zeltzer: It is always amazing to me how powerful the mind is at having actual physical effects on the body, and it always reconfirms my belief (and that of most clinicians and researchers in pain) that the mind and body are tightly linked. It is always amazing that one can have extreme pain and that thinking about something or having a different emotion, like anxiety, joy and happiness, can alter the experience of that pain, and if one were looking through PET (positron emission tomography) scans at brain metabolic activity or if you looked at the signals of the nervous system, one would see actual physical changes going on during these thinkings and emotional events. Maybe you might want to talk a little bit about the role of some of the complementary therapies focusing on the mind-body connection in treating pain?Dr. Joseph: I would love to. We do utilize a number of therapies that work specifically on a mind/body connection, the most obvious of which is biofeedback. Biofeedback is a technique in which sensors are placed on the body to measure either the tension in muscles or they can measure skin temperature or heart rate. These measures are displayed for the patient on a screen with lights, sounds and numbers. The patient is then taught ways and taught skills on how to use their mind to alter different physiologic factors within their bodies such as their muscle tension or their pulse rate. They're taught ways to relax and as they do this, the read out on the computer actually shows them how much success they're having which then reinforces ability of the mind to interact and control what the body is doing. Quite often, a number of pain syndromes are reinforced by ongoing muscle tension. Muscle tension may or may not be cause of pain, but it certainly continues the pain for longer periods of time or makes the pain worse. Learning ways to control how your body reacts to the pain and to stress in general assists the patient in learning control and reducing the overall pain signaling. Other therapies that focus on mind/body reaction include hypnotherapy. It involves state of focused concentration in which patient can use their mind to control a host of physiologic factors including perception of nausea, amount of constriction in their lungs if they have asthma and effectively control perception of pain to the extent where they can turn down pain signaling Additionally, therapies such as movement therapy or integration of the body back to the mind can actually work in the reverse direction, whereby getting your body to move in ways that it is not used to sends signals to the brain that improve pain signaling, or can turn down perception of other symptoms as well. Therapies can be targeted brain to body, or body to brain. Again, operating from the direction of altering perception of symptoms, from the position of arousal and attention, individual psychotherapies, group therapy or family therapy can be helpful. At an individual level, distressing events and increased overall body arousal can contribute to ongoing pain as well as other ongoing symptoms, and addressing those distressing things in one's life can lead to less body arousal and less experience of symptoms.Dr. Bursch: When coping with symptoms and self management of symptoms, this can be addressed through learning of skills focused on relaxation, or how one interprets those signals cognitively, and what they do with the signals once they perceive them. One person might feel body sensations and interpret those as fatal and drive their symptoms higher, or they might understand through education and they might understand the symptoms they're experiencing are really symptoms of panic and they are not going to lead to death. If it is true, rather than having these symptoms lead to catastrophic thinking, it can be a signal for engaging in relaxation techniques. At a family level, parents and siblings can be taught techniques so they don't contribute to arousal or excessive attention to the symptoms. If you are sitting at your computer and very engrossed in a computer game, you might not be paying attention to your abdominal pain. If someone walks into the room and says how is your abdominal pain, your attention will shift from the computer to the abdomen and then you will perceive it and feel pain. Concerned family members often in their attempt to be supportive, contribute to increased perceptions of pain by frequently asking about symptoms. That's an example of how education and changes in behavior can affect pain perception and coping with pain.Dr. Zeltzer: Brenda, you brought up the neural peptides and the role that they play in pain, especially in the development of chronic pain. I assume you mean examples such as serotonin. Would you like to talk more about that?Dr. Bursch: Sure. In my initial discussion of physiology I left out some of the specifics about which neuropeptides and neurotransmitters were involved with chronic pain development. I think that they're interesting for a few reasons, mainly because I think that it's relatively well accepted that neurotransmitters work in your nervous system. Serotonin is involved in pathways that are functional with depression as well as anxiety. There are other neurotransmitters, such as substance P, which is major transmitter of pain, or nociception, which is the nerve signaling portion of pain. I think the truly interesting fact is that many organs other than your nervous system also have receptors for these same neuropeptides, such as substance P not only signals pain but it also causes dilation of blood vessels. That seems somewhat interesting but when you've been injured, not only do you want to tell your brain there's a site of injury but you also want to increase blood flow to that same area because you want the bloods cells that initiate healing to go there. There's the concept that the entire existence of pain evolved to signal the individual that there is some form of tissue injury and you need to stop and begin the healing process. Separate from pain, there are also other neurotransmitters that affect organs. The easiest ones to understand are neurotransmitters such as adrenaline or epinephrine. These signals cause a whole host of both emotional changes as well as physiologic changes. In addition, other neurotransmitters cause various changes in organ function. Quite often when you have different emotional states, that same neuro signaling causes differences in your organ functioning as well. People who are depressed have activated and disregulation in their immune system, as well as alterations in their liver, etc. It's no wonder that quite often chronic physical diseases are also associated with psychological illness, further indications that there is no separation between what we consider the mind and body. Both systems are continually monitoring each other. There is also research that demonstrates that behavioral interventions that increase one's sense of a mastery over a task can improve one's immune functioning. Again, this idea that it works both ways is an important one to remember.Dr. Zeltzer: Given that certain neurotransmitters play a role in both chronic pain and in other emotional states and conditions such as anxiety and depression, maybe you would like to explain why certain antidepressants that are used for treating both anxiety and depression are also useful in treating chronic pain?Dr. Joseph: The medications that we have found useful for treating pain, other than the medications such as opioids that we know have been used to treat pain for eons, have been in the realm of anti-anxiety medications or antidepressants. Ones that are useful are medications such as the tricyclic antidepressants. These medications work through a number of neurotransmitters, specifically norepinephrine and epinephrine. These medications make the specific neurotransmitters available to the nerves for longer periods of time. Not only do they help in depression, but they have been found to be very useful in decreasing pain signaling.Dr. Bursch: Other medications such as Mellaril (thioridazine hydrochloride), which is not an antidepressant but was developed to treat severe anxiety and even psychosis, is active through a different neurotransmitter pathway and is also very effective at decreasing pain signaling, as well as assisting the mind in distracting from the pain and decreasing pain perception. For these reasons, when children come to our pediatric pain clinic with chronic pain, we typically use a variety of treatments that may include medications such as those that Michael described, as well as helping the child and family to change their belief systems about the pain and the controllability of the pain, as well as function, as well as incorporating many alternative and complementary therapies such as biofeedback, acupuncture, massage, and others.Dr. Zeltzer: Certainly, because of the mind-body connection, when pain becomes chronic, it recruits so many different parts of the body -- the mind, the emotions, and the neurochemistry -- that a multi-modal (meaning many different components) approach is needed to treat the pain and help the child be able to go back to school, sleep, and do other activities.Dr. Bursch: I would like to emphasize what Dr. Zeltzer presented and underscore the importance of education.Dr. Zeltzer: Many children coming to us have been placed on drugs, even some of the same drugs we might recommend, but without the other components and because of the mind-body connection, the various components must be addressed, otherwise the drugs alone will not be effective.Dr. Bursch: Many people who have chronic pain spend much time, money, and energy attempting to find that part of their body that is broken, and while it's reasonable to have a thorough evaluation, often one's pain has been going on for a while. It is very difficult or impossible to find the source of that pain. As we've described, the reason for that is because it is a pain signaling issue that can go on, even if the initial reason for the pain has gone away. If you start to treat your pain without an understanding of this, you could spend a lot of time in search for the cause when you will never find one and, of course, be quite distressed in the meantime which can contribute to the pain itself. If you're spending a lot of time in the diagnostic part of this, then you might not be spending time on treatment and getting better. So cognitively understanding how the various systems interact to help pain continue long after the reason for pain has gone away can actually help somebody get better and refrain from causing themselves more distress and more pain.Moderator: Doctors, as we near the end of our time, would you care to offer some closing remarks?Dr. Joseph: I think I would like to reiterate the fact that your mind and your body do communicate with each other on an intimate basis. Your mind is your body and your body is your mind. Those systems are not separate. When we are dealing with chronic illness or chronic pain, what has happened is a discommunication of those normally functioning pathways. Instead of mind and body being one, they become separated and it leads to chronic stress. By learning techniques and reintegrating healthy communication, that communication enables the body and person as a whole to heal and become healthy again.Dr. Zeltzer: Certainly, I would like to provide the phone number for anybody who has a child with a chronic pain problem and would like further information about our pain clinic: It's UCLA, (310) 825 0731.Dr. Zeltzer: Thank you, Brenda and Mike, for participating.Dr. Joseph: Thank you, Dr. Zeltzer, for having us.Dr. Bursch: Thank you. http://my.webmd.com/content/article/1/1700_50465
Arch Intern Med. 2004 Sep 13;164(16):1773-80. Related Articles, Links Clinical determinants of health-related quality of life in patients with irritable bowel syndrome.Spiegel BM, Gralnek IM, Bolus R, Chang L, Dulai GS, Mayer EA, Naliboff B.Division of Gastroenterology, the VA Greater Los Angeles Healthcare System, the Division of Digestive Diseases.BACKGROUND: Current guidelines recommend routine assessment of health-related quality of life (HRQOL) in patients with irritable bowel syndrome (IBS). However, physicians rarely have the time to measure HRQOL with the appropriate methodological rigor, and data suggest that HRQOL in patients with IBS is often estimated using inaccurate clinical gestalt. The identification of predictive factors could allow physicians to better assess HRQOL without using misleading clinical clues. We, therefore, sought to identify determinants of HRQOL in patients with IBS. METHODS: We examined 770 patients, 18 years or older, with IBS at a university-based referral center. Subjects completed a symptom questionnaire, the Symptoms Checklist-90 items psychometric checklist, and the 36-Item Short-Form Health Survey. The main outcome was HRQOL as measured by the mental and physical component scores of the 36-Item Short-Form Health Survey. We first developed a list of hypothesis-driven HRQOL predictors, and then performed multivariate regression analysis to measure the independent association of each predictor with HRQOL. RESULTS: Seven factors (r(2) = 0.39) independently predicted physical HRQOL: (1) more than 5 physician visits per year, (2) tiring easily, (3) low in energy, (4) severe symptoms, (5) predominantly painful symptoms, (6) the feeling that there is "something seriously wrong with body," and (7) symptom flares for longer than 24 hours. Eight factors (r(2) = 0.36) independently predicted mental HRQOL: (1) feeling tense, (2) feeling nervous, (3) feeling hopeless, (4) difficulty sleeping, (5) tiring easily, (6) low sexual interest, (7) IBS symptom interference with sexual function, and (8) low energy. CONCLUSIONS: Health-related quality of life in patients with IBS is primarily related to extraintestinal symptoms rather than traditionally elicited gastrointestinal symptoms. These findings suggest that rather than focusing on physiological epiphenomena (stool characteristics and subtype of IBS) and potentially misleading clinical factors (age and disease duration), physicians might be better served to gauge global symptom severity, address anxiety, and eliminate factors contributing to chronic stress in patients with IBS. PMID: 15364671Webmedjust fyiMind-Body-Pain Connection: How Does It Work?By Michael Henry JosephWebMD Live Events Transcript Archive Event Date: 05/11/2000.Moderator: Welcome to WebMD Live's World Watch and Health News Auditorium. Today we are discussing "The Mind-Body-Pain Connection: How Does It Work?" with Brenda Bursch, Ph.D., Michael Joseph, M.D., and Lonnie Zeltzer, M.D.Brenda Bursch, Ph.D., is the Associate Director of the Pediatric Pain Program, Co-Director of Pediatric Chronic Pain Clinical Service and Assistant Clinical Professor of Psychiatry & Biobehavioral Sciences at UCLA Department of Pediatrics in the School of Medicine. She has written about asthma, developmental & behavioral pediatrics, emergency medicine, AIDS education and prevention, chronic digestive diseases and pediatric bowel disorders. She has membership in the American Pain Society, American Psychological Association, Munchausen Syndrome by Proxy Network, and the UCLA Center for the Study of Organizational and Group Dynamics. Michael Henry Joseph, MD, is an assistant professor of pediatrics and co-director of Chronic Pain Services at the University of California at Los Angeles Children's Hospital. He is a recipient of the Golden Apple Award for Excellence in Teaching. Lonnie Zeltzer, M.D., is an expert in the field of pediatric pain. She is a former president of the Society for Adolescent Medicine and member of the National Institute of Health?s Human Development Study Section. She is currently a Professor of Pediatrics and Anesthesiology at the UCLA School of Medicine. She is Director of the UCLA Pediatric Pain Program and Associate Director of the Patients & Survivors Section, Cancer Prevention and Control Research Branch of the UCLA Jonsson Comprehensive Cancer Center. She has well over one hundred scientific publications, reviews and chapters in medical journals, and has lectured internationally. Moderator: Doctors, welcome back to WebMD Live.Dr. Bursch: Thank you.Dr. Joseph: Thank you.Dr. Zeltzer: Thank you.Dr. Zeltzer: As you know, the mind-body pain connection is the basis upon which our pediatric pain program at UCLA operates, both in terms of how it conceptually views pain and its approach to treatment. I would like to begin by discussing the physiology that is underlying a lot of our functional definitions of pain and our basic philosophy and our mind-body connection model.Dr. Joseph: I'd like to say the differentiation into components is a fallacy. Your brain and nervous system communicate with the rest of your body just like all other organ systems. All work together. Pain is not a simple entity in which it's like pulling on a string and ringing a little bell in your head. It's more dynamic than that, in which you do have nerve input from fingers and toes and organs that goes to spinal column and then to your brain. You also have nerve pathways that are coming from your brain down your spinal column. There are many factors that change the way we actually perceive pain and can make pain more intense or less intense depending on the situation. This is also true for other symptoms. This connection between your central nervous system and your brain communicates with your peripheral nervous system so nerves coming from organs, arms and legs, and all symptoms that you may be feeling can be altered by your nervous system either increased or decreased. That's true of nausea or difficulty breathing or any symptom you might be feeling. In fact, it's true of all of your senses. Your sense of hearing, smell, taste, vision are also all interpreted perceptions. Different factors that can alter your perception specifically when it comes to pain include how much attention you pay to the symptom, what the meaning of the symptom is. For some people, pain is a good thing such as when you've been working out and you're waiting to feel that burn and the burn has a good context, as opposed to if you pull a muscle, you may have exactly the same amount of tissue damage but the way you perceive the pain is very different. Memory can affect perception of pain. When we are awake, it takes much less stimulus to cause pain than when we are asleep. If we were in a coma, it would take even more, possibly we don't even experience pain.Dr. Bursch: As Dr. Joseph just described, the nature of perception of pain, each individual is different not only in pre-existing neurology but also in their experiences that would contribute to their memories of pain, to their arousal, due to circumstances and their experiences and the meanings they attribute. Also, there are different points at which they would become distressed by the signaling. From a physiologic standpoint, people have different levels at which sensory nerves that carry pain information will send those signals. Some people have the ability to have a lot of stimulation before the signals are sent, and some people are very sensitive and a very little stimulation sends the signal. People with irritable bowel syndrome are known through many studies to have a very low threshold for sensory info sent from their intestine to their brain.Dr. Zeltzer: People can learn different coping skills and ways of blocking out the sensation so they experience them, but it doesn't have to distress them. Since you describe the physiologic basis for how pain becomes pain -- how different tissue injury turns into pain -- maybe you can talk about the body's natural pain control system, from a mind-body perspective?Dr. Joseph: The body has a number of ways of controlling pain throughout different organ systems. The most direct is pathways, nerve pathways, that travel from your brain back down your spinal column and they signal directly to those same nerves that are sending pain signals to your brain. They interrupt those pain signals on their way up. These nerve pathways are activated by a number of factors. The easiest one to recognize is fear. A good example of this is, say you're in a dark parking lot and you accidentally shut your finger in the car door. It hurts a lot. You start hearing footsteps behind you. All of a sudden your finger stops hurting. There's no difference in the amount of tissue damage between when you heard the footsteps and when you didn't, but your brain has sent signals to your body that it is time to run away as opposed to time to feel pain. There are subtle ways that your body controls pain, as well. Your brain makes chemicals called endorphins and enkephalins. These molecules are very similar to drugs such as morphine, which everybody recognizes as a pain fighting drug. Interestingly, not only your brain makes these chemicals but also your immune system. B-lymphocytes actually make these chemicals as well. When you have inflamed or infected areas and sending pain signals, even your immune systems can go to those areas, release pain modulating chemicals into that area and decrease the pain right then, if it's something the person needs to have happen at that time. There are many ways pain can be increased or decreased depending on the needs of the individual at each time.Dr. Bursch: Based on the earlier model that Dr. Joseph presented that delineated the relationship of memory, attention and arousal on the pain system, there are a number of behavioral or cognitive strategies that one can engage in order to impact perception of pain, things as simple as engaging in relaxing activities, using distraction so that you're focusing on something else. It could be using visualization techniques which is similar to distraction technique. You can use your mind and you can use your body in ways that the actual pain perception can be altered if you can alter your arousal or your attention or your memory, or memory you have about the pain. You can change your experience of that symptom.Dr. Zeltzer: It is always amazing to me how powerful the mind is at having actual physical effects on the body, and it always reconfirms my belief (and that of most clinicians and researchers in pain) that the mind and body are tightly linked. It is always amazing that one can have extreme pain and that thinking about something or having a different emotion, like anxiety, joy and happiness, can alter the experience of that pain, and if one were looking through PET (positron emission tomography) scans at brain metabolic activity or if you looked at the signals of the nervous system, one would see actual physical changes going on during these thinkings and emotional events. Maybe you might want to talk a little bit about the role of some of the complementary therapies focusing on the mind-body connection in treating pain?Dr. Joseph: I would love to. We do utilize a number of therapies that work specifically on a mind/body connection, the most obvious of which is biofeedback. Biofeedback is a technique in which sensors are placed on the body to measure either the tension in muscles or they can measure skin temperature or heart rate. These measures are displayed for the patient on a screen with lights, sounds and numbers. The patient is then taught ways and taught skills on how to use their mind to alter different physiologic factors within their bodies such as their muscle tension or their pulse rate. They're taught ways to relax and as they do this, the read out on the computer actually shows them how much success they're having which then reinforces ability of the mind to interact and control what the body is doing. Quite often, a number of pain syndromes are reinforced by ongoing muscle tension. Muscle tension may or may not be cause of pain, but it certainly continues the pain for longer periods of time or makes the pain worse. Learning ways to control how your body reacts to the pain and to stress in general assists the patient in learning control and reducing the overall pain signaling. Other therapies that focus on mind/body reaction include hypnotherapy. It involves state of focused concentration in which patient can use their mind to control a host of physiologic factors including perception of nausea, amount of constriction in their lungs if they have asthma and effectively control perception of pain to the extent where they can turn down pain signaling Additionally, therapies such as movement therapy or integration of the body back to the mind can actually work in the reverse direction, whereby getting your body to move in ways that it is not used to sends signals to the brain that improve pain signaling, or can turn down perception of other symptoms as well. Therapies can be targeted brain to body, or body to brain. Again, operating from the direction of altering perception of symptoms, from the position of arousal and attention, individual psychotherapies, group therapy or family therapy can be helpful. At an individual level, distressing events and increased overall body arousal can contribute to ongoing pain as well as other ongoing symptoms, and addressing those distressing things in one's life can lead to less body arousal and less experience of symptoms.Dr. Bursch: When coping with symptoms and self management of symptoms, this can be addressed through learning of skills focused on relaxation, or how one interprets those signals cognitively, and what they do with the signals once they perceive them. One person might feel body sensations and interpret those as fatal and drive their symptoms higher, or they might understand through education and they might understand the symptoms they're experiencing are really symptoms of panic and they are not going to lead to death. If it is true, rather than having these symptoms lead to catastrophic thinking, it can be a signal for engaging in relaxation techniques. At a family level, parents and siblings can be taught techniques so they don't contribute to arousal or excessive attention to the symptoms. If you are sitting at your computer and very engrossed in a computer game, you might not be paying attention to your abdominal pain. If someone walks into the room and says how is your abdominal pain, your attention will shift from the computer to the abdomen and then you will perceive it and feel pain. Concerned family members often in their attempt to be supportive, contribute to increased perceptions of pain by frequently asking about symptoms. That's an example of how education and changes in behavior can affect pain perception and coping with pain.Dr. Zeltzer: Brenda, you brought up the neural peptides and the role that they play in pain, especially in the development of chronic pain. I assume you mean examples such as serotonin. Would you like to talk more about that?Dr. Bursch: Sure. In my initial discussion of physiology I left out some of the specifics about which neuropeptides and neurotransmitters were involved with chronic pain development. I think that they're interesting for a few reasons, mainly because I think that it's relatively well accepted that neurotransmitters work in your nervous system. Serotonin is involved in pathways that are functional with depression as well as anxiety. There are other neurotransmitters, such as substance P, which is major transmitter of pain, or nociception, which is the nerve signaling portion of pain. I think the truly interesting fact is that many organs other than your nervous system also have receptors for these same neuropeptides, such as substance P not only signals pain but it also causes dilation of blood vessels. That seems somewhat interesting but when you've been injured, not only do you want to tell your brain there's a site of injury but you also want to increase blood flow to that same area because you want the bloods cells that initiate healing to go there. There's the concept that the entire existence of pain evolved to signal the individual that there is some form of tissue injury and you need to stop and begin the healing process. Separate from pain, there are also other neurotransmitters that affect organs. The easiest ones to understand are neurotransmitters such as adrenaline or epinephrine. These signals cause a whole host of both emotional changes as well as physiologic changes. In addition, other neurotransmitters cause various changes in organ function. Quite often when you have different emotional states, that same neuro signaling causes differences in your organ functioning as well. People who are depressed have activated and disregulation in their immune system, as well as alterations in their liver, etc. It's no wonder that quite often chronic physical diseases are also associated with psychological illness, further indications that there is no separation between what we consider the mind and body. Both systems are continually monitoring each other. There is also research that demonstrates that behavioral interventions that increase one's sense of a mastery over a task can improve one's immune functioning. Again, this idea that it works both ways is an important one to remember.Dr. Zeltzer: Given that certain neurotransmitters play a role in both chronic pain and in other emotional states and conditions such as anxiety and depression, maybe you would like to explain why certain antidepressants that are used for treating both anxiety and depression are also useful in treating chronic pain?Dr. Joseph: The medications that we have found useful for treating pain, other than the medications such as opioids that we know have been used to treat pain for eons, have been in the realm of anti-anxiety medications or antidepressants. Ones that are useful are medications such as the tricyclic antidepressants. These medications work through a number of neurotransmitters, specifically norepinephrine and epinephrine. These medications make the specific neurotransmitters available to the nerves for longer periods of time. Not only do they help in depression, but they have been found to be very useful in decreasing pain signaling.Dr. Bursch: Other medications such as Mellaril (thioridazine hydrochloride), which is not an antidepressant but was developed to treat severe anxiety and even psychosis, is active through a different neurotransmitter pathway and is also very effective at decreasing pain signaling, as well as assisting the mind in distracting from the pain and decreasing pain perception. For these reasons, when children come to our pediatric pain clinic with chronic pain, we typically use a variety of treatments that may include medications such as those that Michael described, as well as helping the child and family to change their belief systems about the pain and the controllability of the pain, as well as function, as well as incorporating many alternative and complementary therapies such as biofeedback, acupuncture, massage, and others.Dr. Zeltzer: Certainly, because of the mind-body connection, when pain becomes chronic, it recruits so many different parts of the body -- the mind, the emotions, and the neurochemistry -- that a multi-modal (meaning many different components) approach is needed to treat the pain and help the child be able to go back to school, sleep, and do other activities.Dr. Bursch: I would like to emphasize what Dr. Zeltzer presented and underscore the importance of education.Dr. Zeltzer: Many children coming to us have been placed on drugs, even some of the same drugs we might recommend, but without the other components and because of the mind-body connection, the various components must be addressed, otherwise the drugs alone will not be effective.Dr. Bursch: Many people who have chronic pain spend much time, money, and energy attempting to find that part of their body that is broken, and while it's reasonable to have a thorough evaluation, often one's pain has been going on for a while. It is very difficult or impossible to find the source of that pain. As we've described, the reason for that is because it is a pain signaling issue that can go on, even if the initial reason for the pain has gone away. If you start to treat your pain without an understanding of this, you could spend a lot of time in search for the cause when you will never find one and, of course, be quite distressed in the meantime which can contribute to the pain itself. If you're spending a lot of time in the diagnostic part of this, then you might not be spending time on treatment and getting better. So cognitively understanding how the various systems interact to help pain continue long after the reason for pain has gone away can actually help somebody get better and refrain from causing themselves more distress and more pain.Moderator: Doctors, as we near the end of our time, would you care to offer some closing remarks?Dr. Joseph: I think I would like to reiterate the fact that your mind and your body do communicate with each other on an intimate basis. Your mind is your body and your body is your mind. Those systems are not separate. When we are dealing with chronic illness or chronic pain, what has happened is a discommunication of those normally functioning pathways. Instead of mind and body being one, they become separated and it leads to chronic stress. By learning techniques and reintegrating healthy communication, that communication enables the body and person as a whole to heal and become healthy again.Dr. Zeltzer: Certainly, I would like to provide the phone number for anybody who has a child with a chronic pain problem and would like further information about our pain clinic: It's UCLA, (310) 825 0731.Dr. Zeltzer: Thank you, Brenda and Mike, for participating.Dr. Joseph: Thank you, Dr. Zeltzer, for having us.Dr. Bursch: Thank you. http://my.webmd.com/content/article/1/1700_50465
as I have stated before the HPA axis is part of fighting infection and IS the fight or flight system, the system directly effects gut function in IBS and IBSers are sensitive to stress and the mast cell in the gut is connected to the system. also when the brain is calm it is the result of serotonin. To much causes anxiety and the right amount relaxation.But""Psychophysiological arousal is at the core of treating functional GI disorders. There is so much distress, anxiety, antisipatory anxiety, and negative reaction to symptoms, that calming the Mind and body often makes a significant difference in symptoms."and anology is this article on going to the doctors office and as you can see the fight or flight is triggered by threats either real or perceieved, either conciously or unconciously.Does anyone see a connection?The key to being relatively calm in the dentist�s chair begins wellbefore the actual visit. I say relatively calm because if you�resuffering from dental phobia and have been for a while, it�s unlikelythat you will feel "perfectly" comfortable your first or second visit.Each of us must take an active part in overcoming our fears. Peopledon�t get over their fear of heights for instance, in an flash. It takespractice - practice changing your thoughts. Long before thedreaded event you must take charge of your thinking. If youconsciously make an effort at being more calm, you will be morecalm. Let�s create a mental picture. You�re sitting at your desk and glanceat the calendar. You notice your dental appointment is only twoweeks from today. Immediately your mind kicks into overdrive. "Iknow it�s going to be terrible. What if I get nauseous while I�m in thechair? What if the anesthetic doesn�t take hold quickly enough? Iknow it�s going to hurt. I�m grateful I found a new dentist whoadvertises gentle procedures, but can I trust him to be gentle withmy mouth? Oh I remember that awful antiseptic stench from when Iwas a youngster. I wonder if they�ve found anyway to correct that?"As you think about the upcoming visit, your body begins respondingto your fear thoughts. Physical sensations can range from mild tosevere depending on how vivid a scene you�ve painted in your mind,and how long you engage in the working up process. Yourshoulders and neck may feel tense. Your jaw may start to hurtbecause you�ve got it got your teeth clamped together so tightly.You may find yourself short of breath or a headache may belooming on the horizon. Your stomach may be churning and yourinsides trembling.Actually these body signals can be viewed as good instead of bad.They are a sure sign that you are thinking fear and a signal for youto take action. You see the body doesn�t know the differencebetween an imagined experience and a real one. How can that beyou say! If you doubt my words, think about a frightful dream youexperienced, one where someone or something was chasing you.You awaken from the dream feeling as though your heart ispounding out of your chest, perhaps even perspiring. Your bodywas reacting to an imagined fear, thoughts you were having in adream state. The character in your dream was not reality, yet yourbody responded as if he were genuine.Each and every time you catch yourself anxious about yourupcoming appointment, stop and W.A.I.T. Stop and ask yourself:What Am I Thinking? Rather than letting your thoughts control you,take the time to control your thoughts. Consciously toss out theunhealthy fear thoughts and replace them with healthy secure andrealistic thoughts. Using the picture we created earlier, here are a few ways toreprogram what�s going on in your mind. The original thoughts are initalic, followed by the replacement thought(s).Your dental appointment is only two weeks from today You can view that fact insecurely, the appointment is onlytwo weeks away, or securely - the appointment is still twoweeks away. I know it�s going to be terrible You really don�t know how uncomfortable it�s going to be.The anticipation is always worse than the actual event. What if I get nauseous while I�m in the chair? Feeling nauseous is uncomfortable, but doesn�t necessarilymean that anything worse is going to happen. Feelingnauseous is distressing, but it is not dangerous. Feelingsand sensations will rise, fall and run their course if wedon�t attach danger to them. Take away the fear (danger)and your stomach will quiet down on it�s own accord. What if the anesthetic doesn�t take hold quickly enough? If you feel the first poke of a dental instrument, speak up.Tell the doctor it hurts. If you begin to feel pain while thedrilling�s going on, hold up your hand as a signal to thedoc. You may not be able to speak clearly with theposition you�re mouth is in, but you can make some kind ofsound, Grunt if you need to.- but do show some sign thatyou�re feeling pain. Remember your pain receptors are inyour body. Even though the dentists fingers are in yourmouth, he has no clue of what you�re feeling unless you lethim know. Do not suffer in silence. And if you�re concernedabout sounding a bit odd, don�t. Dentists, assistants andhygienists are used to hearing us "talk with our mouths full."I know it�s going to hurt The replacement thought here is simply: I don�t know if it�sgoing to hurt - because you really don�t know! None of uscan predict the future. I�m grateful I found a new dentist who advertises gentleprocedures, but can I trust him to be gentle with my mouth? Realistically there is no guarantee. But in all probability theman or woman is more compassionate and caring than thedentists of long ago. Oh I remember that awful antiseptic stench from when I was ayoungster. I wonder if they�ve found anyway to correct that? Most probably they have. New technology dentistry nowincludes pleasant flavors for the things they place in ourmouths. If the flavors have improved, so have the scents.Everything on the patient end of dentistry Is moreuser-friendly these days. And all those physical sensations you experience two weeks beforeyour appointment are the direct result of your fear thoughts - theytoo are distressing, but they are not dangerous.Practice in reprogramming thoughts has two beneficial effects. Itcalms down the anticipatory fear you have before your visit, andmakes it easier to calm yourself down at the office. It�s much easierto recall secure and realistic thoughts if you�ve taken the time to usethem before. You can have them at your fingertips or the tip of yourtongue, ready to use while you�re in the chair.Another excellent method for stopping racing thoughts is objectivity- the process of thinking of something measurable and verifiable.This is a great technique to use, when you�re stuck "in the chair."Think about your automobile and picture every detail - interior andexterior colors, number of doors, the shape of the door handles, allthe indicators on the dashboard, the type of fabric on the seats.The list is endless. If you don�t own an automobile, think of aspecific room in your home. Think about the size of the room -length, width, height of the ceiling, how the furniture is placed, thecolors, lamps and all other accessories. It�s a fact that we can onlyhave a single thought in a single instant. Describing in your mind(thinking about) an object or objects that are familiar to you doesn�tgive the mind a chance to harbor racing, upsetting thoughts. Fearthoughts are persistent and they will try to sneak back in. Whenthey do, simply bring your attention (your thoughts) back todescribing your chosen object or place.When you have a fear of dentists you really have the choice of twodiscomforts -the actual discomfort you may feel during theappointment (notice I said "may" have), or you have the discomfortof not going and having the needed work done and beating yourselfup for giving into your fear. The dialogue goes like this: I�m such acoward. But I can�t help it. I�m scared. But I can�t admit it toanyone.Every act of self-control produces a sense of self-respect. Alongwith the relief you feel for having the dental procedure behind youinstead of staring you in the face, I guarantee you that when youface your fear you will gain a realistic sense of self-pride. This nextstep is important whether you do it immediately after you leave theoffice or later on in the day - take time to give yourself a mental paton the back. You deserve it! No one else needs to be aware of it. Itwas your effort that got you through. It�s your victory and you canbe proud of it.Whether your fear is dentists or tax audits, driving or diving, theabove tactics will work at reducing anxiety. If your anxiety hasgrown into a full blown phobia, it�s merely going to take more ofyour effort. The key as with any life skill is do put to use whatyou�ve learned. Changing thoughts is the first step in taking backcontrol of your life.Print this article and carry it with you for easy reference. Memorizeand use the phrase "distressing but not dangerous." Do whatever ittakes to help you be an active participant in reprogramming yourmind.It�s true - Change your thoughts and change your life.1998 Rose VanSickleAuthor - Peace of Body, Peace of Mind
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