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Eric, I have an urgent suggestion for you regarding these questions you raised on the other thread (Talissa's):
quote:Eric wrote:So tell me what are the little critters (abnormal gut flora) doing if not causing inflammation or infection or Alarm symptoms, because pain and discomfort is a must for the diagnoses of IBS. And alarm symptoms would suggest something other then IBS.Nor is it likely that gut flora is passing the brain barrier, so it woould have to be a messeger (neurotransmitters) of some sort that can access and have access to the brain. Most infections or patogens cause d, as the body trys to dispel them.
And-
quote:Eric wrote: Considering how many people have taken them (antibiotics) in the general population, how come everyone does not have IBS with altered gut flora?
Now, it seems obvious that you are suggesting that because of the clearly demonstrated abnormalities in the brain-gut axis of IBS patients as reported by the IBS experts/researchers, you believe that dysbiosis itself cannot possibly be the "cause" of IBS. This is because these abnormalities occur in such places as the brain, and in the nerve systems controlling the gut, while dysbiosis is inside the colon itself, in the flora, and so you feel that can't possibly be causing those other abnormalites because they are in different places. And furthermore, you are suggesting that if dysbiosis (from antibiotics, for instance) were the cause of IBS, why doesn't everyone with dysbiosis have IBS? (Please correct me if I'm misinterpreting anything you are saying).Now I'd like to reference this recent study which you posted earlier: Intestinal microecology and quality of life in irritable bowel syndrome patients And from that study, this particular quote from the "Discussion" section of the study:
quote: "Further studies are still needed. However, there was dysbacteriosis (dysbiosis) in IBS patients. Whether it is the effect or just cause of IBS remains unclear"
Now clearly, these IBS experts are suggesting that dysbacteriosis MAY possibly be the cause of IBS. And obviously, on the other side of the coin, they are also suggesting that dysbacteriosis MAY NOT be the cause of IBS. As they say, more studies are needed to resolve this. But at this point in time, they are clearly stating that there is not enough evidence to either "rule out", or to "rule in" dysbacteriosis as the cause of IBS.Now what I'd like to explore with you, my friend Eric, is the fact that these people believe that dysbacteriosis MAY be the cause of IBS. We have to keep in mind of course, that these are IBS experts who conducted this medical study which you originally posted, so I'm sure you must hold them in high esteem and trust them and believe in their conclusions. And of course, as modern IBS experts, they must be fully aware of the other medical studies you have posted here showing that there are abnormalities in the brain-gut axis of IBS patients. And also, as IBS experts, they must be fully aware that, as you pointed out, there are people who do have dysbacteriosis, yet don't have IBS. Nevertheless, despite this knowledge, these IBS experts have NOT ruled out the possibility that dysbacteriosis could be the cause of of IBS. So they must believe that there are possible explanations for those aspects you have brought up.However, amazingly, it's clear from your quotes at the beginning of this message that somehow you yourself HAVE ruled out dysbacteriosis as the cause of IBS, so you do NOT agree with these IBS experts in this conclusion of theirs! What is it that you know that they do not, my friend? Just as you feel you must aggressively "correct" anyone here who happens to suggest that dysbiosis may be the cause of IBS, by posing such questions as those at the start of this message, you certainly must also feel an urgent need to correct the "misinformation" being propogated by these IBS experts in their study when they suggest the very same thing, musn't you? Following is my urgent suggestion to you. You stated this in the other thread:
quote:Eric wrote:I am very good freinds with many of the top researchers on IBS and have been for years.
I don't know if that happens to include the IBS experts who conducted this study, but regardless, I'm sure you must feel you need to contact them ASAP about their wayward conclusions. Please do share your superior knowledge with them, and correct them in their misguided ways! Since you are already very good friends with many top IBS researchers, I'm sure you'll have no trouble commanding the attention of these experts, even if you are not already personally acquainted with them. I'm sure they will amend their study and give you many thanks and full credit for setting them straight!Here is their contact information, from the top of the study:Correspondence to: Professor Jian-Min Si, Department of Gastroenterology, Sir Run Run Shaw Affiliated Hospital of Zhejiang University, Hangzhou 310016, Zhejiang Province, China. Email: sijm###163.net And please Eric, post their reply here on this bulletin board ASAP, I'm sure it will prove to be most interesting!Sincerely,Captain Colon
 

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I'm not sure he knows which end is up concerning IBS. He posts information from Dr Esther Sternberg that claims that the brain is on the receiving end of intestinal dysbiosis, but then the next day he claims that this has nothing to do with it.His experts are of two persuasions:1. IBS is psychosomatic...2. IBS is due to defective neurotransmitters... (keep in mind that the drug companies are paying them big bucks to chase down this blind alley)Dr Drossman was past president of the American Psychosomatic Society. i think these are the same people who used to blame a mother's aloof emotional state for a child's autism. I think they are also the same people who used to think that ulcers were caused by too much stress.to be fair, i think that it is safe to say that it would be foolish to completely ignore the emotional aspect of illness. I don't have a problem with a little HT or some other neurotechnology, but to ignore the gut flora is just plain foolish.
 

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I'm not sure he knows which end is up concerning IBS. He posts information from Dr Esther Sternberg that claims that the brain is on the receiving end of intestinal dysbiosis, but then the next day he claims that this has nothing to do with it.His experts are of two persuasions:1. IBS is psychosomatic...2. IBS is due to defective neurotransmitters... (keep in mind that the drug companies are paying them big bucks to chase down this blind alley)Dr Drossman was past president of the American Psychosomatic Society. i think these are the same people who used to blame a mother's aloof emotional state for a child's autism. I think they are also the same people who used to think that ulcers were caused by too much stress.to be fair, i think that it is safe to say that it would be foolish to completely ignore the emotional aspect of illness. I don't have a problem with a little HT or some other neurotechnology, but to ignore the gut flora is just plain foolish.
 

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quote: However, there was dysbacteriosis (dysbiosis) in IBS patients.
How is dysbacteriosis defined? Since most of the flora can't even be identified let alone grown in culture easily, how can ever know what's normal and abnormal in the gut?What makes the sheer number of the bacteria a valid measure for dysbacteriosis? Even we allow for the numbers of bacteria and the numbers of these bacteria to count for dysbacteriosis, how do we know the difference they found is actually meaningful? While the means may be different, there could be patients whose bacterial counts overlap with the controls.
quote: Now clearly, these IBS experts
They are?
quote:1. IBS is psychosomatic...
Who says that?
 

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quote: However, there was dysbacteriosis (dysbiosis) in IBS patients.
How is dysbacteriosis defined? Since most of the flora can't even be identified let alone grown in culture easily, how can ever know what's normal and abnormal in the gut?What makes the sheer number of the bacteria a valid measure for dysbacteriosis? Even we allow for the numbers of bacteria and the numbers of these bacteria to count for dysbacteriosis, how do we know the difference they found is actually meaningful? While the means may be different, there could be patients whose bacterial counts overlap with the controls.
quote: Now clearly, these IBS experts
They are?
quote:1. IBS is psychosomatic...
Who says that?
 

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"? While the means may be different, there could be patients whose bacterial counts overlap with the controls."Why would you even raise this point? So what if there are some patients who might match the controls with respect to various bacteria. Focusing on ridiculous points tells me that you are more interested in dismissing evidence and tearing things down than being hopeful about what they are discovering.Have you ever wondered if the overwhelming amount of negativity in your life plays a role...It is like your mind is permanently stuck on negative.----------------------------------------------"Since most of the flora can't even be identified let alone grown in culture easily, how can ever know what's normal and abnormal in the gut?"This may be true, but it does not mean that they should not try and learn more about it.At one time they knew very little about h. pylori
 

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"? While the means may be different, there could be patients whose bacterial counts overlap with the controls."Why would you even raise this point? So what if there are some patients who might match the controls with respect to various bacteria. Focusing on ridiculous points tells me that you are more interested in dismissing evidence and tearing things down than being hopeful about what they are discovering.Have you ever wondered if the overwhelming amount of negativity in your life plays a role...It is like your mind is permanently stuck on negative.----------------------------------------------"Since most of the flora can't even be identified let alone grown in culture easily, how can ever know what's normal and abnormal in the gut?"This may be true, but it does not mean that they should not try and learn more about it.At one time they knew very little about h. pylori
 

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Captain C.Because you have to be able to read the article carefully for one and not cherry pick what a person wants to hear or believe.becausethe conclusion was"CONCLUSION: There are intestinal flora disorders in IBS patients, which may be involved in triggering the IBS-like symptoms. IBS patients experience significant impairment in QoL, however, the impairment is not caused directly by enteric symptoms."I find it odd this is always left out when this abstarct is posted? Thats bias. In triggering the symptoms,, but it does not say cause and its well known bacteria can trigger symptoms, like eating leftovers out of the fridge, or a high fiber diet that can change gut flora, but the colon reacts to ALL stimulus for one.But the improvements were also in quality of life impairment and those improvements were not directly related to enteric symptoms.Also many thngs can cause altered gut flora, including stress and altered transit of food material in the colon, not to mention the questions Flux is bringing up, that are very valid. There are already many impairments known about IBS, not just altered gut flora, even though some here only foucus and believe in this, it is much much more complex then then the cherry picking on dysbiosis. One article a couple of you have picked out in the thousands of articles on IBS explaining problems in IBS.also what does this mean from the above study"There was no significant difference in gut flora between two subgroups"When real dysbiosis studies, explain rectal hypersensitvity, all variations of bowel patterns, why there are higher stress hormones, why there is higher levels of serotonin in the gi tract after eating in women, why there is viceral hypersensitvity, why more women then men get IBS, why a bacteria or parasite or may now even a virus can later LEAD to IBS, after the infection has RESOLVED and why their is autonomic and CNS impairments and more then we will see. Bacteria can only cause so many problems. They study bacteria a lot in other conditions such as IBD and MC and other conditions and compare the info to functional disorders ect., and they have been studdying bacteria in IBS for many many years now and still are for their role in IBS.The study above did not elaborate on what they already know about PI IBS leading to IBS and that information and research is extensive and much is already known.Further more the study has references, but I don't see references to either major US or UK IBS researchers, so its hard to say what collaboration they have with the rest of the world.Also when you read that abstart there are all kinds of thing they are nt discussing in the bigger picture of IBS.On the thread you took my quotes off, I have tried to explain things they alreay have found, but some people here totally ignore, like the years and years of research on all the above impairments don't exist.They have also not shown how gut flora or any particular organisms becomes pathogenic in IBS to cause the multiply cluster of symptoms, other then real pathogens, that cause enteric infection and inflammation when they become out of control, lkie C Diff or ameobic dysentary. The role of gut flora, remains at this point speculative at best. Also the treatment of gut flora with probiotics to reestablish gut flora colonies, has to date only shown limited results on bloating and pain. This may have tyo do with gas and pressure sensitve cells lining the gi tract that fire neruotransmitters to signal the brain and cause pain.It also has not explain why IBSers have lost the filter that filters information to the brain so you don't perceive concious feeling and sensations in the gut.I highly suggest Capt Colon, you get the UNC "Digest" and the new IFFGD "Digestive Health matters" and in the later read this.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 Kel, falls pray to her own beliefs."psychosomatic SYLLABICATION: psy�cho�so�mat�ic PRONUNCIATION: AUDIO: sk-s-mtk KEY ADJECTIVE: 1. Of or relating to a disorder having physical symptoms but originating from mental or emotional causes. 2. Relating to or concerned with the influence of the mind on the body, and the body on the mind, especially with respect to disease: psychosomatic medicine. "In IBS the second applies. " Relating to or concerned with the influence of the mind on the body, and the body on the mind, especially with respect to disease: psychosomatic medicine. "Nobody who studies serious IBS research believes anymore IBS is "all in the head" they have found many physical abnormalities, just not specific biological markers in all IBSers yet.Kel, left out, and these are the kinds of things that do not help and that is Dr Drossman is the chairman to diagnose IBS and collaberates with most all big IBS intitutions around the world and they share information. Or that Dr Drossman is a regognized world leader in IBS and GI disorders of function, which is a new classification for the functional disorders. Functional disorders, (How the System Functions)!!!"Douglas A. Drossman, MDCo-Director of the UNC Center for Functional GI & Motility Disorders Dr. Drossman is Professor of Medicine and Psychiatry at the UNC School of Medicine, Division of Gastroenterology & Hepatology. He has had a long-standing interest in the research and evaluation of difficult to diagnose and treat GI disorders. He established a program of research in functional GI disorders at UNC more than 25 years ago and has published more than 350 books, articles and abstracts relating to epidemiology, psychosocial and quality of life assessment, design of treatment trials, and outcomes of research in GI disorders. He has also published two books, a GI procedures manual, and a textbook on FGIDs (Rome I and Rome II editions).Dr. Drossman received his MD degree from Albert Einstein College of Medicine in 1970, and completed his medical residency at the University of North Carolina School of Medicine and New York University-Bellevue Medical Center. After his residency, he sub-specialized in psychosocial (psychosomatic) medicine at the University of Rochester School of Medicine and in gastroenterology at the University of North Carolina in 1976-1978.As the Medical Director of the UNC Center for Functional GI & Motility Disorders, Dr. Drossman sees patients in the functional GI and motility clinic. He also precepts GI fellows and visiting gastroenterologists to develop their clinical skills in treating patients. And, he facilitates the learning of medical faculty, psychiatry residents and medical students with regard to the biopsychosocial care of patients with functional GI disorders. In 2004, Dr. Drossman received the AGA Distinguished Educator Award, recognizing an individual for achievements as an outstanding educator over a lifelong career. Dr. Drossman�s educational and clinical interests in the psychosocial/behavioral aspects of patient care have led to the development of a series of videotapes to teach physicians and other healthcare professionals how to conduct an effective patient interview, carry out a psychosocial assessment, and enhance patient-doctor communication. He has taught numerous US and international workshops on this topic and was chair of the ACG Physician-Patient Relations Committee from 1994-1996. He is also a charter fellow of the American Academy on Physicians and Patients, a consortium of doctors teaching these skills to medical school faculty.Dr. Drossman has an active research program that relates to the clinical, epidemiological, psychosocial, and treatment aspects of irritable bowel syndrome. He has developed and validated several assessment measures that are used worldwide for clinical research. Recently, he began looking at brain imaging (fMRI) in functional bowel disorders to determine if reported changes in the brain were responsive to treatment. He also consults with pharmaceutical companies and government agencies regarding treatment trials. In 1999, Dr. Drossman received the Janssen Award for Clinical Research in Digestive Diseases. In 2003, he received the Research Scientist Award for Clinical Research presented by the Functional Brain-Gut Research Group (FBG) during Digestive Diseases Week.In addition to his clinical care, research and teaching responsibilities associated with the UNC School of Medicine and the Center for Functional GI & Motility Disorders, Dr. Drossman has numerous involvements with leading national and international organizations: Chair of the Executive Committee (since 1989) and President (since 2003) of the Rome Foundation Editor of Rome II: The Functional Gastrointestinal Disorders, 2nd edition; senior editor for Rome III to be published in 2006 Member of the Board of Directors, Chair of the Scientific Advisory Board, and Chair of the Awards Committee of the International Foundation for Functional GI Disorders (IFFGD) Since 2003, chair of the Nerve-Gut Section of the AGA Council Founder and past chair of the Functional Brain-Gut Research Group (FBG) special interest section within the American Gastroenterological Association (AGA) 1999 Chair of the Digestive Health Initiative on Functional GI Disorders sponsored by the American Digestive Health Foundation Past-president of the American Psychosomatic Society Fellow of the American College of Physicians (ACP) Fellow of the American College of Gastroenterology (ACG) Charter fellow of the American Academy of Physician and Patient Since 2001, Associate Editor of Gastroenterology, the official journal of the AGA Author of the AGA Clinical Teaching Project on IBS � Unit 13 (1997) Author of the AGA Gastroenterology Teaching Project (2003) Editor of the Manual on GI Procedures (now in its fourth edition) On the board of the medical website Medscape Gastroenterology Gastroenterology Section editor of the Merck Manual Dr. Drossman is considered a world authority in the field of functional GI disorders and physician-patient communication. He presents at numerous national and international meetings throughout the year." http://www.med.unc.edu/medicine/fgidc/drossman.htm Funny when you read mayos site or UNC or UCLA, IFFGD, and others on the big picture, you almost never if ever see the word dysbiosis. You do see intestinal permeability and its relationship to the intial enteric infection in PI IBS.Dysbiosis and quite a few other things, are words use on this site very liberally by a few people, many who do not have a strong education on the big picture of IBS and all the abnormalities and even the basic functions of the digestive tract. As well as being careful to interpret the wording of the studies, which are worded very specifically for a lot of reasons.The conclusions of the above study is only the need to study more in depth gut flora in IBS and this is being done for its roles. But they are also studying it in general as well, and there is a ton they don't know on them. Just because there are higher and lower levels, does not automatically mean they have become pathogenic, maybe just influnce the issues.Most people who do get abnormal pathogen bacteria or parasites or viruses, get d, and usally a fever for some or weight loss for some the body is trying to expel them, hence the d.But in IBS they can already partly explain the D and C and d/c in conjuntion with IBS already.Its already known that serotonin is majorally implicated in IBS also. Kel, just disregards it and blames it on drug companies. But for some those drugs do work and do help and for others many other methods do work and do help, just diet and stress reduction work and help in IBS.There is also mild moderate and severe IBS to take into account, so do those people have mild moderate and severe alterations in gut flora? There is also a lot of information on why there is mild, moderate, and severe IBS.And some mild people take fiber and get better?Its also important to look at the past and see why treatments have really helped the majority of IBS patients on singular symptoms and global symptoms.So far no gut flora changes studies have shown major improvements in motility or global symptoms of IBS, only in part pain and bloating. IBS is also already regonized as a brain gut axis dysfunction around the world and many people still do not understand this and some refuse to believe it. Probably in part, because then they believe it means its all in the head, but that is a misinterpretation of what it really means.Brain-Gut Interaction in Irritable Bowel Syndrome: New Findings of a Multicomponent Disease Symposium Mexico and Israel http://216.109.117.135/search/cache?p=brai...&icp=1&.intl=us So explain some things to me Capt Colon, because the last time I asked you some of these questions you just diappeared and did not answer them.Remember this is from the Chairman of Rome and an world regonized expert in IBS and functional disorders of which there is some thrity of them and they frequently overlap, like functional Abdominal pain syndrome or functional d or functional c, and explain how altered gut flora cause these conditions and how they overlap or how in different people they cause only d or only pain or only c. Some people only look at IBS and do not look at it in regards to the overlapping of other gi disorders of function?But in 2001Annu Rev Med. 2001;52:319-38. Related Articles, Links Irritable bowel syndrome.Ringel Y, Sperber AD, Drossman DA.UNC Center for Functional GI and Motility Disorders, Division of Digestive Diseases and Nutrition, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599-7080, USA. ringel###med.unc.eduThe irritable bowel syndrome (IBS) is a functional gastrointestinal disorder whose hallmark is abdominal pain or discomfort associated with a change in the consistency or frequency of stools. In the western world, 8% to 23% of adults have IBS and its socioeconomic cost is substantial. Research-generated insights have led to the understanding of IBS as a disorder of brain-gut regulation. The experience of symptoms derives from dysregulation of the bidirectional communication system between the gastrointestinal tract and the brain, mediated by neuroendocrine and immunological factors and modulated by psychosocial factors. The biopsychosocial model integrates the various physical and psychosocial factors that contribute to the patient's illness. This model and the recently revised symptom-based criteria (i.e. the "Rome II criteria") form the basis for establishing a comprehensive and effective approach for the diagnosis and management of the disorder.Publication Types: Review Review, Academic PMID: 11160782 so please explain to me know"Research-generated insights have led to the understanding of IBS as a disorder of brain-gut regulation. The experience of symptoms derives from dysregulation of the bidirectional communication system between the gastrointestinal tract and the brain, mediated by neuroendocrine and immunological factors and modulated by psychosocial factors."what research generated insights have lead to this understanding of IBS as a disorder of the brain gut axis dysregulation.and how the symptoms derives from this dysregulation in the communication between the gut brain and the brain and how it is mediated by neuroendocrine and immunological factors and modulated by psychosocial factors."because these are things I am trying to help explain on this bb to people, and I have to say with a lot of hostility, by a few members.So go for it. If you want you can also show how changes in gut flora accomplish and are part of the big picture of brain gut axis dysregulation.And yes everything is not known, but that does not mean leave out what is already known. In stead of loonking at just one problem, ie. gut flora, try studying the whole picture starting with the basics and importantly how the system works in the first place. For example, many eople do not know the digestive system is lined with pressure sensitive ec cells that release serotonin when there is distension from food or stress or other reasons and why this is important is sensations in general and in IBS hypersensivity and Hyperalgesia: Lowered threshold to pain.Or even the importantance in IBS to "Hypervigilance: Increased vigilance. An intensified state of paying attention to or focusing on specific things. May severely limit a person's ability to focus on specific tasks or engage in reflective thinking when their focus is on scanning for threatening stimuli. A person with a functional GI disorder or incontinence may be hypervigilant when their focus is on scanning for bodily sensations or indications that signal symptom onset. "as some examples
 

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Captain C.Because you have to be able to read the article carefully for one and not cherry pick what a person wants to hear or believe.becausethe conclusion was"CONCLUSION: There are intestinal flora disorders in IBS patients, which may be involved in triggering the IBS-like symptoms. IBS patients experience significant impairment in QoL, however, the impairment is not caused directly by enteric symptoms."I find it odd this is always left out when this abstarct is posted? Thats bias. In triggering the symptoms,, but it does not say cause and its well known bacteria can trigger symptoms, like eating leftovers out of the fridge, or a high fiber diet that can change gut flora, but the colon reacts to ALL stimulus for one.But the improvements were also in quality of life impairment and those improvements were not directly related to enteric symptoms.Also many thngs can cause altered gut flora, including stress and altered transit of food material in the colon, not to mention the questions Flux is bringing up, that are very valid. There are already many impairments known about IBS, not just altered gut flora, even though some here only foucus and believe in this, it is much much more complex then then the cherry picking on dysbiosis. One article a couple of you have picked out in the thousands of articles on IBS explaining problems in IBS.also what does this mean from the above study"There was no significant difference in gut flora between two subgroups"When real dysbiosis studies, explain rectal hypersensitvity, all variations of bowel patterns, why there are higher stress hormones, why there is higher levels of serotonin in the gi tract after eating in women, why there is viceral hypersensitvity, why more women then men get IBS, why a bacteria or parasite or may now even a virus can later LEAD to IBS, after the infection has RESOLVED and why their is autonomic and CNS impairments and more then we will see. Bacteria can only cause so many problems. They study bacteria a lot in other conditions such as IBD and MC and other conditions and compare the info to functional disorders ect., and they have been studdying bacteria in IBS for many many years now and still are for their role in IBS.The study above did not elaborate on what they already know about PI IBS leading to IBS and that information and research is extensive and much is already known.Further more the study has references, but I don't see references to either major US or UK IBS researchers, so its hard to say what collaboration they have with the rest of the world.Also when you read that abstart there are all kinds of thing they are nt discussing in the bigger picture of IBS.On the thread you took my quotes off, I have tried to explain things they alreay have found, but some people here totally ignore, like the years and years of research on all the above impairments don't exist.They have also not shown how gut flora or any particular organisms becomes pathogenic in IBS to cause the multiply cluster of symptoms, other then real pathogens, that cause enteric infection and inflammation when they become out of control, lkie C Diff or ameobic dysentary. The role of gut flora, remains at this point speculative at best. Also the treatment of gut flora with probiotics to reestablish gut flora colonies, has to date only shown limited results on bloating and pain. This may have tyo do with gas and pressure sensitve cells lining the gi tract that fire neruotransmitters to signal the brain and cause pain.It also has not explain why IBSers have lost the filter that filters information to the brain so you don't perceive concious feeling and sensations in the gut.I highly suggest Capt Colon, you get the UNC "Digest" and the new IFFGD "Digestive Health matters" and in the later read this.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 Kel, falls pray to her own beliefs."psychosomatic SYLLABICATION: psy�cho�so�mat�ic PRONUNCIATION: AUDIO: sk-s-mtk KEY ADJECTIVE: 1. Of or relating to a disorder having physical symptoms but originating from mental or emotional causes. 2. Relating to or concerned with the influence of the mind on the body, and the body on the mind, especially with respect to disease: psychosomatic medicine. "In IBS the second applies. " Relating to or concerned with the influence of the mind on the body, and the body on the mind, especially with respect to disease: psychosomatic medicine. "Nobody who studies serious IBS research believes anymore IBS is "all in the head" they have found many physical abnormalities, just not specific biological markers in all IBSers yet.Kel, left out, and these are the kinds of things that do not help and that is Dr Drossman is the chairman to diagnose IBS and collaberates with most all big IBS intitutions around the world and they share information. Or that Dr Drossman is a regognized world leader in IBS and GI disorders of function, which is a new classification for the functional disorders. Functional disorders, (How the System Functions)!!!"Douglas A. Drossman, MDCo-Director of the UNC Center for Functional GI & Motility Disorders Dr. Drossman is Professor of Medicine and Psychiatry at the UNC School of Medicine, Division of Gastroenterology & Hepatology. He has had a long-standing interest in the research and evaluation of difficult to diagnose and treat GI disorders. He established a program of research in functional GI disorders at UNC more than 25 years ago and has published more than 350 books, articles and abstracts relating to epidemiology, psychosocial and quality of life assessment, design of treatment trials, and outcomes of research in GI disorders. He has also published two books, a GI procedures manual, and a textbook on FGIDs (Rome I and Rome II editions).Dr. Drossman received his MD degree from Albert Einstein College of Medicine in 1970, and completed his medical residency at the University of North Carolina School of Medicine and New York University-Bellevue Medical Center. After his residency, he sub-specialized in psychosocial (psychosomatic) medicine at the University of Rochester School of Medicine and in gastroenterology at the University of North Carolina in 1976-1978.As the Medical Director of the UNC Center for Functional GI & Motility Disorders, Dr. Drossman sees patients in the functional GI and motility clinic. He also precepts GI fellows and visiting gastroenterologists to develop their clinical skills in treating patients. And, he facilitates the learning of medical faculty, psychiatry residents and medical students with regard to the biopsychosocial care of patients with functional GI disorders. In 2004, Dr. Drossman received the AGA Distinguished Educator Award, recognizing an individual for achievements as an outstanding educator over a lifelong career. Dr. Drossman�s educational and clinical interests in the psychosocial/behavioral aspects of patient care have led to the development of a series of videotapes to teach physicians and other healthcare professionals how to conduct an effective patient interview, carry out a psychosocial assessment, and enhance patient-doctor communication. He has taught numerous US and international workshops on this topic and was chair of the ACG Physician-Patient Relations Committee from 1994-1996. He is also a charter fellow of the American Academy on Physicians and Patients, a consortium of doctors teaching these skills to medical school faculty.Dr. Drossman has an active research program that relates to the clinical, epidemiological, psychosocial, and treatment aspects of irritable bowel syndrome. He has developed and validated several assessment measures that are used worldwide for clinical research. Recently, he began looking at brain imaging (fMRI) in functional bowel disorders to determine if reported changes in the brain were responsive to treatment. He also consults with pharmaceutical companies and government agencies regarding treatment trials. In 1999, Dr. Drossman received the Janssen Award for Clinical Research in Digestive Diseases. In 2003, he received the Research Scientist Award for Clinical Research presented by the Functional Brain-Gut Research Group (FBG) during Digestive Diseases Week.In addition to his clinical care, research and teaching responsibilities associated with the UNC School of Medicine and the Center for Functional GI & Motility Disorders, Dr. Drossman has numerous involvements with leading national and international organizations: Chair of the Executive Committee (since 1989) and President (since 2003) of the Rome Foundation Editor of Rome II: The Functional Gastrointestinal Disorders, 2nd edition; senior editor for Rome III to be published in 2006 Member of the Board of Directors, Chair of the Scientific Advisory Board, and Chair of the Awards Committee of the International Foundation for Functional GI Disorders (IFFGD) Since 2003, chair of the Nerve-Gut Section of the AGA Council Founder and past chair of the Functional Brain-Gut Research Group (FBG) special interest section within the American Gastroenterological Association (AGA) 1999 Chair of the Digestive Health Initiative on Functional GI Disorders sponsored by the American Digestive Health Foundation Past-president of the American Psychosomatic Society Fellow of the American College of Physicians (ACP) Fellow of the American College of Gastroenterology (ACG) Charter fellow of the American Academy of Physician and Patient Since 2001, Associate Editor of Gastroenterology, the official journal of the AGA Author of the AGA Clinical Teaching Project on IBS � Unit 13 (1997) Author of the AGA Gastroenterology Teaching Project (2003) Editor of the Manual on GI Procedures (now in its fourth edition) On the board of the medical website Medscape Gastroenterology Gastroenterology Section editor of the Merck Manual Dr. Drossman is considered a world authority in the field of functional GI disorders and physician-patient communication. He presents at numerous national and international meetings throughout the year." http://www.med.unc.edu/medicine/fgidc/drossman.htm Funny when you read mayos site or UNC or UCLA, IFFGD, and others on the big picture, you almost never if ever see the word dysbiosis. You do see intestinal permeability and its relationship to the intial enteric infection in PI IBS.Dysbiosis and quite a few other things, are words use on this site very liberally by a few people, many who do not have a strong education on the big picture of IBS and all the abnormalities and even the basic functions of the digestive tract. As well as being careful to interpret the wording of the studies, which are worded very specifically for a lot of reasons.The conclusions of the above study is only the need to study more in depth gut flora in IBS and this is being done for its roles. But they are also studying it in general as well, and there is a ton they don't know on them. Just because there are higher and lower levels, does not automatically mean they have become pathogenic, maybe just influnce the issues.Most people who do get abnormal pathogen bacteria or parasites or viruses, get d, and usally a fever for some or weight loss for some the body is trying to expel them, hence the d.But in IBS they can already partly explain the D and C and d/c in conjuntion with IBS already.Its already known that serotonin is majorally implicated in IBS also. Kel, just disregards it and blames it on drug companies. But for some those drugs do work and do help and for others many other methods do work and do help, just diet and stress reduction work and help in IBS.There is also mild moderate and severe IBS to take into account, so do those people have mild moderate and severe alterations in gut flora? There is also a lot of information on why there is mild, moderate, and severe IBS.And some mild people take fiber and get better?Its also important to look at the past and see why treatments have really helped the majority of IBS patients on singular symptoms and global symptoms.So far no gut flora changes studies have shown major improvements in motility or global symptoms of IBS, only in part pain and bloating. IBS is also already regonized as a brain gut axis dysfunction around the world and many people still do not understand this and some refuse to believe it. Probably in part, because then they believe it means its all in the head, but that is a misinterpretation of what it really means.Brain-Gut Interaction in Irritable Bowel Syndrome: New Findings of a Multicomponent Disease Symposium Mexico and Israel http://216.109.117.135/search/cache?p=brai...&icp=1&.intl=us So explain some things to me Capt Colon, because the last time I asked you some of these questions you just diappeared and did not answer them.Remember this is from the Chairman of Rome and an world regonized expert in IBS and functional disorders of which there is some thrity of them and they frequently overlap, like functional Abdominal pain syndrome or functional d or functional c, and explain how altered gut flora cause these conditions and how they overlap or how in different people they cause only d or only pain or only c. Some people only look at IBS and do not look at it in regards to the overlapping of other gi disorders of function?But in 2001Annu Rev Med. 2001;52:319-38. Related Articles, Links Irritable bowel syndrome.Ringel Y, Sperber AD, Drossman DA.UNC Center for Functional GI and Motility Disorders, Division of Digestive Diseases and Nutrition, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599-7080, USA. ringel###med.unc.eduThe irritable bowel syndrome (IBS) is a functional gastrointestinal disorder whose hallmark is abdominal pain or discomfort associated with a change in the consistency or frequency of stools. In the western world, 8% to 23% of adults have IBS and its socioeconomic cost is substantial. Research-generated insights have led to the understanding of IBS as a disorder of brain-gut regulation. The experience of symptoms derives from dysregulation of the bidirectional communication system between the gastrointestinal tract and the brain, mediated by neuroendocrine and immunological factors and modulated by psychosocial factors. The biopsychosocial model integrates the various physical and psychosocial factors that contribute to the patient's illness. This model and the recently revised symptom-based criteria (i.e. the "Rome II criteria") form the basis for establishing a comprehensive and effective approach for the diagnosis and management of the disorder.Publication Types: Review Review, Academic PMID: 11160782 so please explain to me know"Research-generated insights have led to the understanding of IBS as a disorder of brain-gut regulation. The experience of symptoms derives from dysregulation of the bidirectional communication system between the gastrointestinal tract and the brain, mediated by neuroendocrine and immunological factors and modulated by psychosocial factors."what research generated insights have lead to this understanding of IBS as a disorder of the brain gut axis dysregulation.and how the symptoms derives from this dysregulation in the communication between the gut brain and the brain and how it is mediated by neuroendocrine and immunological factors and modulated by psychosocial factors."because these are things I am trying to help explain on this bb to people, and I have to say with a lot of hostility, by a few members.So go for it. If you want you can also show how changes in gut flora accomplish and are part of the big picture of brain gut axis dysregulation.And yes everything is not known, but that does not mean leave out what is already known. In stead of loonking at just one problem, ie. gut flora, try studying the whole picture starting with the basics and importantly how the system works in the first place. For example, many eople do not know the digestive system is lined with pressure sensitive ec cells that release serotonin when there is distension from food or stress or other reasons and why this is important is sensations in general and in IBS hypersensivity and Hyperalgesia: Lowered threshold to pain.Or even the importantance in IBS to "Hypervigilance: Increased vigilance. An intensified state of paying attention to or focusing on specific things. May severely limit a person's ability to focus on specific tasks or engage in reflective thinking when their focus is on scanning for threatening stimuli. A person with a functional GI disorder or incontinence may be hypervigilant when their focus is on scanning for bodily sensations or indications that signal symptom onset. "as some examples
 

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Sorry for butting in here Capt C, but flux, you�ve GOT to be kidding me.
quote:flux wrote:Since most of the flora can't even be identified let alone grown in culture easily, how can ever know what's normal and abnormal in the gut?
If this were true, why use antibiotics or antifungals? How could doctors use anything but broad spectrum if its all just guess-work?If that were true, how could they find the following in IBS patients? ~~Markers of Cl. perfringens, Cl. difficile, Enterococcus, Streptomyces, Enterobacterial, Klebsiella, E. coli, Peptostreptococcus, Candida Albicans, genus of Streptococcus, of Staphylococcus, of Fusobacterium sp and others microorganisms were revealed. http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=11565126 Or this~~The mucosal surface of the human gastrointestinal (GI) tract is about 200�300 m2 and is colonized by 1013�14 bacteria of 400 different species and subspecies. Savage has defined and categorized the gastrointestinal microflora into two types, autochthonous flora (indigenous flora) and allochthonous flora (transient flora). Autochthonous microorganisms colonize particular habitats, i.e., physical spaces in the GI tract, whereas allochthonous microorganisms cannot colonize particular habitats except under abnormal conditions. Most pathogens are allochthonous microorganisms; nevertheless, some pathogens can be autochthonous to the ecosystem and normally live in harmony with the host, except when the system is disturbe http://biomed.humanapress.com/ChapterDetai...59259-766-1:491 Here�s just a small snipet of what�s known in re: to human probiotics within the intestinal tract~~Bifidobacteria, called probiotics, are a natural part of the bacterial flora in the human body(in the colon) and have a symbiotic bacteria-host relationship with humans. B. longum promotes good digestion, boosts the immune system, and produces lactic and acetic acid that controls intestinal pH. These bacteria also inhibit the growth of Candida albicans, E. coli, and other bacteria that have more pathogenic qualities than Bifidobacteria.Genome StructureThe circular chromosome of Bifidobacterium longum has a genome approximately 2,260,000 bp in length with a 60% G-C content. More research is being done on sequencing other species of Bifidobacterium, especially to understand its probiotic qualities. Cell Structure and MetabolismBifidobacterium is a Gram-positive, anaerobic, branched rod-shaped bacterium. In the intestines, they ferment sugars to produce lactic acid. The B. longum genome codes for many proteins specialized for the catabolism of oligosaccharides. This bacterium also is able to use so-called "nondigestible" plant polymers or host-derived glycoproteins and glcoconjugates; it is thought that Bifidobacterium's ability to compete with other gastrointestinal bacteria and occupy a large percentage in the bacterial flora of the gastrointestinal region might be partly due to the large variety of molecules that it is able to use for energy (Schell et al. 2002). Bifidobacteria have a unique hexose metabolism that occurs through a phosphoketolase pathway. This pathway, called the bifid shunt, uses the key enzyme frutose-6-phosphate phosphoketolase (F6PPK) and is the generally used as a diagnostic test for this Bifidobacteria because it's not found in other gram-positive intestinal bacteria. http://biology.kenyon.edu/Microbial_Biorea...dobacterium.htm The gastrointestinal tract represents a complex ecosystem in which a delicate balance exists between the intestinal microflora and the host. The microflora are principally comprised of facultative anaerobes and obligate anaerobes. Approximately 95% of the intestinal bacterial population in humans is comprised of obligate anaerobes, including Bifidobacterium, Clostridium, Eubacterium, Fusobacterium, Peptococcus, Peptostreptococcus and Bacteroides. Approximately 1% to 10% of the intestinal population is comprised of facultative anaerobes, including Lactobacillus, Escherichia coli, Klebsiella, Streptococcus, Staphylococcus and Bacillus. Aerobic organisms are not present in the intestinal tract of healthy individuals with the exception of Pseudomonas, which is present in very small amounts. Most of the bacteria are present in the colon where the bacterial concentration ranges between 1011 to 1012 colony-forming units (CPU) per milliliter.The intestinal microflora are important for maturation of the immune system, the development of normal intestinal morphology and in order to maintain a chronic and immunologically balanced inflammatory response. The microflora reinforce the barrier function of the intestinal mucosa, helping in the prevention of the attachment of pathogenic microorganisms and the entry of allergens. Some members of the microflora may contribute to the body's requirements for certain vitamins, including biotin, pantothenic acid and vitamin B12. Alteration of the microbial flora of the intestine, such as may occur with antibiotic use, disease and aging, can negatively affect its beneficial role. http://www.gettingwell.com/drug_info/nmdru.../pro_0034.shtml
 

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Sorry for butting in here Capt C, but flux, you�ve GOT to be kidding me.
quote:flux wrote:Since most of the flora can't even be identified let alone grown in culture easily, how can ever know what's normal and abnormal in the gut?
If this were true, why use antibiotics or antifungals? How could doctors use anything but broad spectrum if its all just guess-work?If that were true, how could they find the following in IBS patients? ~~Markers of Cl. perfringens, Cl. difficile, Enterococcus, Streptomyces, Enterobacterial, Klebsiella, E. coli, Peptostreptococcus, Candida Albicans, genus of Streptococcus, of Staphylococcus, of Fusobacterium sp and others microorganisms were revealed. http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=11565126 Or this~~The mucosal surface of the human gastrointestinal (GI) tract is about 200�300 m2 and is colonized by 1013�14 bacteria of 400 different species and subspecies. Savage has defined and categorized the gastrointestinal microflora into two types, autochthonous flora (indigenous flora) and allochthonous flora (transient flora). Autochthonous microorganisms colonize particular habitats, i.e., physical spaces in the GI tract, whereas allochthonous microorganisms cannot colonize particular habitats except under abnormal conditions. Most pathogens are allochthonous microorganisms; nevertheless, some pathogens can be autochthonous to the ecosystem and normally live in harmony with the host, except when the system is disturbe http://biomed.humanapress.com/ChapterDetai...59259-766-1:491 Here�s just a small snipet of what�s known in re: to human probiotics within the intestinal tract~~Bifidobacteria, called probiotics, are a natural part of the bacterial flora in the human body(in the colon) and have a symbiotic bacteria-host relationship with humans. B. longum promotes good digestion, boosts the immune system, and produces lactic and acetic acid that controls intestinal pH. These bacteria also inhibit the growth of Candida albicans, E. coli, and other bacteria that have more pathogenic qualities than Bifidobacteria.Genome StructureThe circular chromosome of Bifidobacterium longum has a genome approximately 2,260,000 bp in length with a 60% G-C content. More research is being done on sequencing other species of Bifidobacterium, especially to understand its probiotic qualities. Cell Structure and MetabolismBifidobacterium is a Gram-positive, anaerobic, branched rod-shaped bacterium. In the intestines, they ferment sugars to produce lactic acid. The B. longum genome codes for many proteins specialized for the catabolism of oligosaccharides. This bacterium also is able to use so-called "nondigestible" plant polymers or host-derived glycoproteins and glcoconjugates; it is thought that Bifidobacterium's ability to compete with other gastrointestinal bacteria and occupy a large percentage in the bacterial flora of the gastrointestinal region might be partly due to the large variety of molecules that it is able to use for energy (Schell et al. 2002). Bifidobacteria have a unique hexose metabolism that occurs through a phosphoketolase pathway. This pathway, called the bifid shunt, uses the key enzyme frutose-6-phosphate phosphoketolase (F6PPK) and is the generally used as a diagnostic test for this Bifidobacteria because it's not found in other gram-positive intestinal bacteria. http://biology.kenyon.edu/Microbial_Biorea...dobacterium.htm The gastrointestinal tract represents a complex ecosystem in which a delicate balance exists between the intestinal microflora and the host. The microflora are principally comprised of facultative anaerobes and obligate anaerobes. Approximately 95% of the intestinal bacterial population in humans is comprised of obligate anaerobes, including Bifidobacterium, Clostridium, Eubacterium, Fusobacterium, Peptococcus, Peptostreptococcus and Bacteroides. Approximately 1% to 10% of the intestinal population is comprised of facultative anaerobes, including Lactobacillus, Escherichia coli, Klebsiella, Streptococcus, Staphylococcus and Bacillus. Aerobic organisms are not present in the intestinal tract of healthy individuals with the exception of Pseudomonas, which is present in very small amounts. Most of the bacteria are present in the colon where the bacterial concentration ranges between 1011 to 1012 colony-forming units (CPU) per milliliter.The intestinal microflora are important for maturation of the immune system, the development of normal intestinal morphology and in order to maintain a chronic and immunologically balanced inflammatory response. The microflora reinforce the barrier function of the intestinal mucosa, helping in the prevention of the attachment of pathogenic microorganisms and the entry of allergens. Some members of the microflora may contribute to the body's requirements for certain vitamins, including biotin, pantothenic acid and vitamin B12. Alteration of the microbial flora of the intestine, such as may occur with antibiotic use, disease and aging, can negatively affect its beneficial role. http://www.gettingwell.com/drug_info/nmdru.../pro_0034.shtml
 

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Er, do you even know what "enteric symptoms" are?I don't think you do, based on your saying this~
quote:But the improvements were also in quality of life impairment and those improvements were not directly related to enteric symptoms.
It's info from a questionnaire~~"IBS patients were evaluated by enteric symptom questionnaire-9" http://www.wjgnet.com/1007-9327/10/1802.asp Just FYI~"The interactions between the mucosal immune systems and the enteric microflora maintain the physiologically normal state of inflammation or activation of gut-associated lymphoid tissue (Peyer's patches, lymphoid follicles, lymphocytes, and mesenteric lymph node cells) throughout life [6]. It is becoming increasingly evident in gastrointestinal disorders that colonic bacterial flora are implicated in the initiation and maintenance of intestinal dysfunction, such as inflammatory bowel diseases and irritable bowel syndrome." http://www.biomedcentral.com/1523-3820/5/183
 

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Er, do you even know what "enteric symptoms" are?I don't think you do, based on your saying this~
quote:But the improvements were also in quality of life impairment and those improvements were not directly related to enteric symptoms.
It's info from a questionnaire~~"IBS patients were evaluated by enteric symptom questionnaire-9" http://www.wjgnet.com/1007-9327/10/1802.asp Just FYI~"The interactions between the mucosal immune systems and the enteric microflora maintain the physiologically normal state of inflammation or activation of gut-associated lymphoid tissue (Peyer's patches, lymphoid follicles, lymphocytes, and mesenteric lymph node cells) throughout life [6]. It is becoming increasingly evident in gastrointestinal disorders that colonic bacterial flora are implicated in the initiation and maintenance of intestinal dysfunction, such as inflammatory bowel diseases and irritable bowel syndrome." http://www.biomedcentral.com/1523-3820/5/183
 

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Capt colon, also take into account, that most IBSers, do not have nocturnal symtoms, that the majority have pain on the left side and that up to 80 percent have rectal hypersensitivity."Enteric nervous system (ENS): Autonomic nervous system within the walls of the digestive tract. The ENS regulates digestion and the muscle contractions that eliminate solid waste."otherwise known as the "brain in the gut.""The gastrointestinal system functions independently of the rest of the body, and we can digest our food without thinking. Messages between the brain and gut alert us to gastrointestinal malfunction (pain), and conditions such as stress aggravate the IBS symptoms of diarrhea and constipation."graph http://www.fda.gov/fdac/features/2001/ibsside.html Gut Thoughtsby Maia SzalavitzPosted February 1, 2002 � Issue 119 --------------------------------------------------------------------------------AbstractThough few know about it, humans have a second brain that handles most of the body's digestive functions. Study of the enteric nervous system is a rapidly growing specialty, offering insight into malfunctions of the "gut brain" as well as the more complex cranial brain.--------------------------------------------------------------------------------Digestion is such a prosaic function that most people prefer not to think about it. Fortunately, they don't have to - at least not with the brain in their heads. Though few know about it, humans (and other animals) have a second brain that handles most digestive functions.Deep in your gut lies a complex self-contained nervous system containing more nerve cells than the spinal cord, and indeed more neurons than all the rest of the peripheral nervous system. There are over 100 million nerve cells in the human small intestine alone.Malfunctions of this "gut brain" may be involved in irritable bowel syndrome (IBS), a condition that affects an estimated 20 percent of the U.S. population and is believed to be responsible for $8 billion in health care costs alone in the United States each year, according to the International Foundation for Functional Gastrointestinal Disorders. Patients with IBS suffer bouts of chronic diarrhea, constipation, or sometimes both alternately. IBS is the most common diagnosis made by gastroenterologists.The study of the enteric nervous system is a rapidly growing specialty known as neurogastroenterology."What the gut has to do is extremely complicated," says Michael Gershon, chair of the department of anatomy and cell biology at the Columbia University College of Physicians and Surgeons and author of The Second Brain (Harper Perennial, 1999). "If the brain had to control that, it would have to run huge cables and have a huge number of cells devoted solely to that purpose. It makes great evolutionary sense to separate these functions and essentially use a microcomputer that is independent rather than a central processing unit."In fact, researchers believe that the gut brain evolved first - because digestion came before locomotion in multicellular creatures. In mammals, the two systems originate near each other in the outer layer of the early embryo.Like many poorly understood organs, the gut brain was discovered by classical anatomists in the 19th century and then ignored. "No one knew what it did," says David Wingate, emeritus professor of gastrointestinal science at Queen Mary, University of London. "When you'd ask what it was for in medical school, they'd say, 'Let's move on.'"In 1899, physiologists studying dogs found that unlike any other reflex, the continuous push of material through the digestive system (now called the peristaltic reflex) continued when nerves linking the brain to the intestines were cut.By the 1970s, a society for the study of gastrointestinal motility had been set up - but how this motility was controlled remained unclear. The vagus nerve, for example, sends some fibers from the brain to the gut; however, it connects directly with only a tiny minority of cells there.In 1965, Gershon published a paper in Science suggesting that serotonin might act as a neurotransmitter in the gut. At the time, acetylcholine and norepinephrine were accepted as transmitters in the peripheral nervous system, but serotonin was seen as a centrally acting transmitter used by some nerves to modulate the action of others.The peripheral nervous system wasn't supposed to use such controls - only the brain and spinal cord were believed to process information through "interneurons" such as those containing serotonin.At a meeting of the Society for Neuroscience in 1981, however, Gershon and others marshaled enough data to finally convince skeptics that serotonin was indeed a key transmitter in the gut.In fact, it is now known that 95% of the body's serotonin is used by the gut - and the enteric nervous system contains every neurotransmitter and neuromodulator found so far in the brain."We now know quite a lot about the library of programs run by the gut brain]," says Jackie Wood, professor of physiology and cell biology and of internal medicine at Ohio State University. "For example, when the bowel is empty, one particular program runs." Called the migrating motor complex (MMC), this involves a series of movements running from the stomach to the end of the small intestine, which is believed to function in keeping the potentially dangerous bacteria stored in the colon from moving upwards rather than out.At least 500 different species of deadly bacteria have been found to inhabit a person's colon at any given time; "traveler's diarrhea" often results when this mix is changed through exposure to new pathogens. If this happens, the gut runs a program designed to expel as much of its contents as quickly as possible - unpleasant for the vacationer, but much better than a fatal infection."Another program involves a flood of serotonin throughout the entire circuit, which produces the digestive pattern that mixes and stirs the contents," says Wood.Because the gut brain is smaller and more accessible than the brain itself, understanding it could offer insights about how to parse the more complex organ. "That idea was what lead me to begin my research when I was a fledgling neuroscientist," says Gershon. "I looked at the brain and found it daunting, and I still do, so I looked for a simpler nervous system to study." He adds, "'Simple nervous system,' of course, turned out to be an oxymoron."Unlike the cranial brain, however, the gut brain doesn't seem to be conscious - or at least, in health, it doesn't impinge much on consciousness. "The gut is not an organ from which you like to receive frequent progress reports," says Gershon. For most digestive processes, no news is good news.The problem in IBS, in fact, may be that the enteric nervous system becomes overly sensitive to normal functioning and reports to the brain when it shouldn't. Or, the brain may overreact to normal bowel signals.Normally, the brain may avoid conscious awareness of most gut activity. But in IBS, says Wingate, one theory is that "the barrier to information being projected into consciousness is lowered."As in many heterogeneous conditions defined by symptoms rather than specific pathology, different subgroups of patients may have different causes or varying levels of contributions by different factors.In some cases, IBS may be an autoimmune problem - something like multiple sclerosis of the gut, where immune cells attack nervous tissue. "If you catch it early enough," says Wood, "You can use steroids to treat it in such cases." High doses of steroids shut down immune activity and prevent immune cells from causing harm, but they don't help once damage has been done.The gut is, in fact, a major immune organ, containing more immune cells than the rest of the body combined. The enteric nervous system interacts intimately with the immune system, and can affect mood and behavior by signaling the central nervous system.Further, the gut brain may in fact be the only system that can refuse central signals. Says Gershon, "The gut brain can say no to the big brain, absolutely. In fact, there are nerve fibers that project towards the CNS, and if the bowel doesn't like the message, it can turn it off or cancel it."Indeed, the vagus nerve mostly carries information from the enteric nervous system to the brain - for every one message sent by the brain to the gut, about nine are sent in the other direction. And recent research has found that stimulating this nerve can have antidepressant and even learning-enhancing effects - so "gut feelings" could genuinely be more than just a metaphor.The similarities between the two nervous systems may also mean that they are vulnerable to similar toxins and disease processes. For example, in both Parkinson's disease and Alzheimer's, the degenerative processes seen in brain nerve cells are also seen in the neurons of the enteric system.This link could also help explain the connection between psychological problems and gut problems - and could put to rest the myth that problems such as IBS are simply "neuroses" because they so often occur in people with other psychological disorders.It may be that the real reason that bowel disorders often accompany psychological problems is that both brain and gut neurons are suffering simultaneously - in addition to the fact that having to spend a significant portion of one's life attending to bathroom functions is in itself depressing.Simultaneous effects of drugs on both systems also account for the gastrointestinal "side effects" of Prozac and other drugs that act on serotonin metabolism - which actually may have more effect on the bowel than on the brain, because serotonin predominates in the bowel and the drug moves through the digestive system before reaching the brain.Fortunately, in most people, the bowel quickly develops tolerance to these drugs, and gastrointestinal side effects usually subside within a few days or weeks of the start of treatment. In fact, low doses of SSRI (selective serotonin reuptake inhibitor) drugs may actually help patients with IBS. And since different serotonin receptors predominate in the brain and in the gut, new drugs may be developed to affect certain subtypes but not others."What's exciting," says Wingate, "is getting away from essentially anecdotal ways of categorizing patients by symptoms and being able to study their problems in a very systematic biological way."Maia Szalavitz is a health/science journalist who has written for the New York Times, the Washington Post, Newsday, New York Magazine, Salon, and other major publications. http://www.vaccinationnews.com/DailyNews/F...02/GutBrain.htm The gut has a mind of its ownOperating like the cranial brain and looking uncannily similar to it, the gut brain is continuously active, whether we're aware of it or no, writes CHANTAL OUIMETBy CHANTAL OUIMETSpecial to The Globe and MailTuesday, December 31, 2002 � Print Edition, Page R7 Ever wonder why you get cramps when you're stressed? Or why you get "butterflies" in your stomach before a job interview? And why your gut tells you not to trust a certain person?Scientists say it's because the body has two brains -- the familiar one encased in our skull and another more obscure one in our gut. This "second brain," known as the enteric nervous system, is located in our digestive tract and holds about 100-million nerve cells -- more than in our spinal cord.Less complex and smaller than our cranial brain, this "second brain," which contains between 70 to 85 per cent of the body's immune cells, is an independent data-processing centre handling a complicated circuitry of neurons, neuromodulators and neurotransmitters."Every neurotransmitter that exists in our brain, also exists in the gut without exception. The brain in the gut is simply the brain gone south," says Dr. Michael Gershon, author of The Second Brain, and chairman of the department of anatomy and cell biology at Columbia University College of Physicians and Surgeons.In 1899, anatomists and physiologists studying dogs found that, unlike any other reflex, the continuous push of material through the digestive system continued after nerves linking the brain to the intestines were severed. In other words, they discovered the gut had a mind of its own.Operating like our brain and looking uncannily similar to it, the gut brain responds to stimulus and is continuously active whether we're aware of it or not. But it doesn't think or feel. Feeling is held in the cerebral cortex of the brain. This "second brain" performs a different role."The brain in the head deals with the finer things in life: religion, philosophy, appreciation of art and music, creativity, etc.," says Dr. Gershon. "Whereas the brain in the gut deals with this dirty, messy and disgusting business of digestion. The brain in the head doesn't have to get its hands dirty with that kind of thing since it has delegated the job."They may have different roles but our two brains are interconnected. One thousand to 2,000 nerve fibres connect them and enable the two to talk. When one gets upset, the other one does too."I don't think we could have made that statement a few years ago. . . . We've been finding out that the nerves in the gut independently regulate gut function, but do so in a dialogue with the nerves in our head. It's a nerve-to-nerve discussion," says Keith Sharkey, physiology and biophysics professor at the University of Calgary.Interest in the gut brain resurfaced in the early 1980s after new technology became available."For the first time, we were able to see in elegant and exquisite detail the specific way that nerves went from A to B," explains Prof. Sharkey. "That gives you a chance to ask questions that could not or had not been asked before."There are approximately 250 research laboratories now studying the enteric nervous system around the world. This new breed of neuroscientists is not only fuelling the present renaissance in the field of neurogastroenterology (study of the nerves entrenched in the lining of the esophagus, stomach, small intestine and colon), but offering insights into malfunctions of both brains.Scientists have discovered that the gut brain may be involved in gastrointestinal disorders like ulcerative colitis, Crohn's disease and irritable bowel syndrome -- a condition that affects between 15 and 20 per cent of the population."Back in the days when . . . I was a medical student, I was taught that these diseases were psychosomatic. . . . But they're a real thing. Your gut can literately drive your brain crazy," notes Dr. Gershon. "If you are walking around with a burning sensation in your upper belly and it feels terrible, you can get pretty anxious. Likewise, if you've got aches and you're on the toilet with diarrhea every five minutes, it can change your personality. But it's more than that."For many years, individuals (mostly women) with irritable bowel syndrome, a functional disorder characterized by abdominal pain, bloating, flatulence, diarrhea and/or constipation, suffered in silence. Doctors believed the illness was imagined -- all in the head."We now know IBS is not psychosomatic. There is an element of the brain controlling the gut which has to be born in the mind. But we now understand that there is also an organic and physiological basis for the functional changes in the little brain," declares Prof. Sharkey.Dr. Nicholas Diamant, a gastroenterologist at Toronto Western Hospital and an emeritus professor of medicine and physiology at the University of Toronto, agrees that both brains are involved in the disorder."The brain sends signals down to the little brain via the spinal cord which acts as a gate for the pain signals," Dr. Diamant says. "The brain may not be closing this gate adequately to modulate and regulate the signals coming up from the gut. Therefore, the brain is letting more signals come up than it normally would."A study by the Mayo Foundation published this August in Gastroenterology, the official journal of the American Gastroenterological Association, suggested there is genetic determinant that predicts the response to medication of IBS patients with diarrhea-predominant symptoms."It has to do with how the body inactivates the [neuro]transmitter serotonin. In some patients, the body inactivation is more efficient and the patient therefore responds better to the medication," explains Dr. Michael Carmilleri, professor of medicine and physiology at the Mayo Clinic in Rochester and one of the authors of the report."It's a landmark paper. . . . We are starting to relate changes in the signalling in the 'second brain' to real diseases based not only on functional changes but on genetic studies as well," says Prof. Sharkey.This July, a drug came on the Canadian market to treat patients (women only) with constipation-predominant IBS. Experts say Tegaserod, known commercially as Zelnorm, is only effective in 60 to 65 per cent of people."IBS is defined by a series of symptoms," says Prof. Sharkey. "It's a multiple disease entity. . . . We don't understand it well enough to ever consider a miracle-type cure because it's too complicated for that."In the case of Crohn's disease and ulcerative colitis (both autoimmune diseases), Dr. Carmilleri says the gut brain may play a role. "There is some interaction between the immune cells in the intestines and the 'second brain.' "The discovery of the brain-gut connection also allowed scientists to learn what is at the heart of the most visceral human emotions. A gut feeling, for example, isn't just a poetic image used to convey intuition. It arises from the interplay between our two brains."It's a "body loop" which is activated every time we are being challenged or stressed. From a lifetime of activating this "body loop" during good or bad situations, we learn to interpret this preverbal feedback as good or bad," says Emeran Mayer, professor of medicine and physiology at the University of California -- Los Angeles.Butterflies are minor indicators of pain and another example of this close relationship. Prof. Mayer says when one is faced with an anxiety-ridden situation, the brain in our skull sends urgent messages to our "second brain" and throws it off balance. "The big brain also becomes more sensitive to signals from the gut and amplifies them to unpleasant conscious sensations," he wrote. Therefore, one reads this response as gurgling or "butterflies" in the belly.Stomach cramps, heartburn, diarrhea or constipation due to stress are again an illustration of the gut rising to the level of conscious perception. "The dialogue between the brain in our head and the brain in our gut sometimes goes awry. . . . in such a way that the brain in our gut responds inappropriately to stimulus," says Prof. Sharkey. In turn, the nerves tell the muscles to contract more or less or make the glands secrete more or less fluid.Not all of the signals sent from the "second brain" to the cranial brain are bad news. "Some of the information that is being sent from the gut to the brain can establish how well the brain in the head works. . . . Your gut doesn't think for you but if it's behaving well, it can contribute to your mood being good," says Dr. Gershon. As a result, this interaction plays a role in dictating behavior and in creating human joy as well as sadness.Scientists affirm the brain constantly communicates and listens to our "second brain." Its functions are then taken over by the brain with respect to the activation of major emotions such as fear, anxiety, anger, sadness or happiness. There is no direct proof but a lot of suggestive evidence."Chemicals released from cells within the 'second brain' . . . can activate vagal sensory neurons (cells high in the neck) which signal back to the brain. These vagal sensory neurons play a prominent role in many emotional processes and it is certainly conceivable that such signals play a role in generating happiness or a sense of well-being. The newborn gets its first sense of well-being from stimulation of the gut and release of chemicals through milk," wrote Prof. Mayer.Dr. Diamant, a specialist in the mind-body connection, says each person's "second brain" reacts differently. "If you think everybody feels the same thing when the gut does something, you are in deep trouble. You have to consider the whole person and all the baggage they carry. The gut's reaction may be based on many experiences as well as the individual's genetic makeup."It's an exciting time for scientists because research in the field of neurogastroenterology is still evolving. Even medical students are generally shocked by the "second brain's" complexity. "That hasn't really made it to the textbooks yet," says Prof. Sharkey. "It takes a few years for emerging knowledge to become dogma." http://ibs.med.ucla.edu/Articles/PatientArticle001.htm The mind and the immune system-------------------------------------------------------------------------------- FYIHarvard Health"The Mind and the Immune System�Part IOne of the standing mysteries of medicine is the relationship between the mind and physical health�how feelings, thoughts, attitudes, and behavior are related to physical illness, how psychological and social stress affect the likelihood of developing a disease or the ability to resist it, and how counseling for emotional problems can aid recovery from illness. One of the clues to this mystery lies in the immune system, the network that defends us against microbes and other invaders. Interest in the connections between the brain and the immune system has given birth to the discipline of psychoneuroimmunology. These systems communicate through the sympathetic nervous system and the endocrine glands, especially the hypothalamic-pituitary-adrenal (HPA) axis. Like the immune system, both are dedicated to the defense of the body against stress and danger, and both are directed from the same part of the brain, the hypothalamus. All three�the immune system, sympathetic nervous system, and HPA axis�respond to some of the same transmitter chemicals. The sympathetic nervous system is part of the autonomic nervous system, which controls involuntary functions like heart rate, digestion, and breathing. The sympathetic nerves serve as an emergency response network, heightening the body�s readiness to accept a challenge or escape in the face of danger. The sympathetic nerves are connected to various organs of the immune system, such as the thymus gland, the bone marrow, the spleen, and lymph nodes. Immune cells, including T cells, monocytes, and B cells, have receptors for the neurotransmitters released by sympathetic nerves. Damage to the hypothalamus and loss of sympathetic transmitters impairs the functioning of the immune system. An injection of antigens (foreign substances that activate the immune system) affects the concentration of sympathetic neurotransmitters in the brain. Immune LearningAnimal experiments show that the immune system can �learn� by association. In one experiment, rats drank sweetened water containing a drug that causes nausea and depresses the immune system. They became so sick that they avoided sweetened water for some time after the drug was removed. That behavioral conditioning eventually was extinguished (wore off), and they returned to drinking the water�only to start developing infections at an abnormally high rate. Apparently, by association with the immunosuppressant drug, sugared water was provoking a conditioned response that continued to suppress the rats� immune systems even when it no longer affected their behavior. Another experiment involved mice bred to be genetically vulnerable to an autoimmune disease (one in which an overactive immune system attacks the body�s own tissues). They were given a flavored solution containing a drug that suppresses the immune system, delaying the onset of the disease. Then most of the drug was removed, but as long as the flavor remained, the rats continued to drink the liquid and resist the disease. The immune system had learned by association to suppress itself when the animals recognized that taste. Conditioned learning can also enhance immune function, as another experiment showed. Mice were repeatedly forced to smell camphor while they were injected with a substance that stimulated the activity of natural killer (NK) cells, a type of white blood cell. When they were exposed to the smell of camphor without the injection, the activity of their NK cells still increased. Hormonal EffectsThe HPA axis regulates the body�s activity through the circulation of the blood rather than directly through neural connections. The hypothalamus directs the pituitary gland to produce hormones that travel in the blood to the adrenal glands, where they cause the release of cortisol and other steroids as well as epinephrine (adrenaline) and its chemical relative norepinephrine (both of which also serve as neurotransmitters in the sympathetic system). These stress hormones influence the immune reaction through receptors on immune cells. Adrenaline, which prepares the body for immediate action, stimulates the immune system. One function of cortisol and related hormones (glucocorticoids) is to serve as a feedback mechanism that conserves energy by tuning down the emergency reaction when it is no longer needed. Rising cortisol levels signal the brain to shut down an immune response that threatens to become overactive. There�s evidence that stress is associated with depressed immune function in one or another part of the system. In one study, the activity of NK cells declined in medical students preparing for an examination. Those who felt calmer and had a slower heart rate also showed fewer immune changes. In another study, unemployment slowed the multiplication of white blood cells in response to antigens. A survey found that unhappily married women had lower numbers of certain immune cells than women with happy marriages. Elderly people caring for relatives with Alzheimer�s disease have higher than average levels of cortisol and low levels of antibody response to influenza vaccine. Stress delays the production of antibodies in mice infected with influenza virus and suppresses the activity of NK cells in animals inoculated with herpes simplex virus. Social stress can be even more damaging than physical stress. In a report published last year, some mice were put into a cage with a highly aggressive mouse two hours a day for six days. Other mice were kept in tiny cages without food and water for long periods. Both groups of mice were exposed to a bacterial toxin, and the socially stressed animals were twice as likely to die. Severe depression resembles a chronic stress response, and depressed patients often lack the normal daily variation in the production of cortisol. Depressed patients seem to have lower NK cell activity than healthy controls, possibly because of high cortisol levels. In one study, the lymphocytes (a type of white blood cell) of depressed and bereaved persons responded sluggishly to the substances that normally stimulate them to proliferate. Isolation can also suppress immune function. Infant monkeys separated from their mothers, especially if they are caged alone rather than in groups, generate fewer lymphocytes in response to antigens and fewer antibodies in response to viruses. Some studies have found lower NK cell activity in separated and divorced than in married men. NK cell activity also has been found to be lower in medical students who say they are lonely. In a year-long study of people caring for husbands or wives with Alzheimer�s disease, changes in immune function were greatest in those who had the fewest friends and least outside help. In general, good social support is associated with better immune function in the elderly, even after correction for health habits, depression, anxiety, and life stress. The effect of traumatic stress on the immune system has been studied occasionally. According to one report, four months after the passage of Hurricane Andrew in Florida, people in the most heavily damaged neighborhoods showed red uced activity in four out of five immune functions. Similar results were found in a study of hospital employees after an earthquake in Los Angeles. And a report published last year suggested that men with a history of posttraumatic stress disorder (PTSD), even long after apparent recovery, had lower numbers of various immune cells and lower levels of immune activity�possibly indicating a long-lasting suppression of the system. Another study found lower lymphocyte activity in abused women. But it�s not easy to generalize about the effect of stress hormones and sympathetic nervous system activity on immune functioning. Much depends on the individual, the timing, the kind of stress, and the part of the immune system under consideration. The results of studies on depression, for example, are conflicting; it does not consistently suppress any part of the immune system except NK cells. Animal experiments suggest that the nervous system responds differently to acute and chronic stress. The acute stress reaction is often a healthy response to a challenge. But chronic stress may cause the feedback controls to fail, turning the emergency response into a condition that persists when it no longer has any use. Stress hormones and sympathetic activity remain at high levels, suppressing immune function and possibly promoting illness. The immune systems of people who are under chronic stress may also respond abnormally to acute stress. The Difference it MakesWhat matters most is whether the mind�s influence on the immune system has the power to raise or lower the risk of illness or injury. On that issue only a little evidence is available. Healing of injuries. One study found that the wound from a biopsy healed more slowly in women under high emotional stress. In another experiment, a wound healed more slowly in students when it was inflicted before an examination rather than just before vacation. Slow healing has also been found in people caring for Alzheimer�s patients. Colds and flu. Both observation and experiments suggest that stress makes people more susceptible to colds and other respiratory infections. In a one-year study, researchers asked 100 people to keep a diary recording their feelings and events in their lives. They were examined periodically for bacteria in throat cultures and virus antibodies in the blood. Stressful events were four times more likely to come before rather than after new infections. And people who developed a cold or other infection had often been feeling more angry and tense than usual. In an English study published in 1991, 420 people were given nose drops containing a cold virus after answering questions about their personality, health practices, and behavior. They were asked about feelings of frustration, nervousness, anxiety, and depression and about events such as loss of a job or deaths in the family. When the subjects were quarantined and monitored for nine days, those under greater stress were more likely to catch a cold. Researchers have continued to confirm this connection. In a study conducted in the late 1990s at the University of Pittsburgh, 276 healthy adults were given nose drops containing a cold virus. The symptoms were most severe in those who reported a high level of stress in their lives�but only when it was prolonged stress caused by such problems as unemployment and troubled marriages. Resistance to the virus was correlated with strong social support, especially a variety of contacts with family, neighbors, friends, workmates, and fellow members of voluntary organizations. This effect was independent of smoking, alcohol consumption, and quality of sleep. People with the weakest (least diverse) social ties were four times more susceptible to colds than those with the strongest ties. Stress can also interfere with the response to a vaccine. In one study, flu shots were given to 32 people under high stress and 32 under low stress, matched for age, sex, and social class. The vaccine produced higher levels of antibodies in the low-stress group, and the high-stress people were more likely to become infected. The University of Pittsburgh researchers found a close association between difficulties in coping with stress, flu symptoms, and a specific immune response. Fifty-five volunteers were given nose drops containing a flu virus after answering questions about their ability to handle stress in their lives. The people with the most stress-related problems produced higher concentrations of interleukin-6, a chemical messenger that attracts immune cells to the site of an infection. They also produced more mucus (had stuffier noses) and generally developed more serious symptoms in direct proportion to the rise in their interleukin-6 levels. "www.health.harvard.edu/hh....do?id=537
 

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Capt colon, also take into account, that most IBSers, do not have nocturnal symtoms, that the majority have pain on the left side and that up to 80 percent have rectal hypersensitivity."Enteric nervous system (ENS): Autonomic nervous system within the walls of the digestive tract. The ENS regulates digestion and the muscle contractions that eliminate solid waste."otherwise known as the "brain in the gut.""The gastrointestinal system functions independently of the rest of the body, and we can digest our food without thinking. Messages between the brain and gut alert us to gastrointestinal malfunction (pain), and conditions such as stress aggravate the IBS symptoms of diarrhea and constipation."graph http://www.fda.gov/fdac/features/2001/ibsside.html Gut Thoughtsby Maia SzalavitzPosted February 1, 2002 � Issue 119 --------------------------------------------------------------------------------AbstractThough few know about it, humans have a second brain that handles most of the body's digestive functions. Study of the enteric nervous system is a rapidly growing specialty, offering insight into malfunctions of the "gut brain" as well as the more complex cranial brain.--------------------------------------------------------------------------------Digestion is such a prosaic function that most people prefer not to think about it. Fortunately, they don't have to - at least not with the brain in their heads. Though few know about it, humans (and other animals) have a second brain that handles most digestive functions.Deep in your gut lies a complex self-contained nervous system containing more nerve cells than the spinal cord, and indeed more neurons than all the rest of the peripheral nervous system. There are over 100 million nerve cells in the human small intestine alone.Malfunctions of this "gut brain" may be involved in irritable bowel syndrome (IBS), a condition that affects an estimated 20 percent of the U.S. population and is believed to be responsible for $8 billion in health care costs alone in the United States each year, according to the International Foundation for Functional Gastrointestinal Disorders. Patients with IBS suffer bouts of chronic diarrhea, constipation, or sometimes both alternately. IBS is the most common diagnosis made by gastroenterologists.The study of the enteric nervous system is a rapidly growing specialty known as neurogastroenterology."What the gut has to do is extremely complicated," says Michael Gershon, chair of the department of anatomy and cell biology at the Columbia University College of Physicians and Surgeons and author of The Second Brain (Harper Perennial, 1999). "If the brain had to control that, it would have to run huge cables and have a huge number of cells devoted solely to that purpose. It makes great evolutionary sense to separate these functions and essentially use a microcomputer that is independent rather than a central processing unit."In fact, researchers believe that the gut brain evolved first - because digestion came before locomotion in multicellular creatures. In mammals, the two systems originate near each other in the outer layer of the early embryo.Like many poorly understood organs, the gut brain was discovered by classical anatomists in the 19th century and then ignored. "No one knew what it did," says David Wingate, emeritus professor of gastrointestinal science at Queen Mary, University of London. "When you'd ask what it was for in medical school, they'd say, 'Let's move on.'"In 1899, physiologists studying dogs found that unlike any other reflex, the continuous push of material through the digestive system (now called the peristaltic reflex) continued when nerves linking the brain to the intestines were cut.By the 1970s, a society for the study of gastrointestinal motility had been set up - but how this motility was controlled remained unclear. The vagus nerve, for example, sends some fibers from the brain to the gut; however, it connects directly with only a tiny minority of cells there.In 1965, Gershon published a paper in Science suggesting that serotonin might act as a neurotransmitter in the gut. At the time, acetylcholine and norepinephrine were accepted as transmitters in the peripheral nervous system, but serotonin was seen as a centrally acting transmitter used by some nerves to modulate the action of others.The peripheral nervous system wasn't supposed to use such controls - only the brain and spinal cord were believed to process information through "interneurons" such as those containing serotonin.At a meeting of the Society for Neuroscience in 1981, however, Gershon and others marshaled enough data to finally convince skeptics that serotonin was indeed a key transmitter in the gut.In fact, it is now known that 95% of the body's serotonin is used by the gut - and the enteric nervous system contains every neurotransmitter and neuromodulator found so far in the brain."We now know quite a lot about the library of programs run by the gut brain]," says Jackie Wood, professor of physiology and cell biology and of internal medicine at Ohio State University. "For example, when the bowel is empty, one particular program runs." Called the migrating motor complex (MMC), this involves a series of movements running from the stomach to the end of the small intestine, which is believed to function in keeping the potentially dangerous bacteria stored in the colon from moving upwards rather than out.At least 500 different species of deadly bacteria have been found to inhabit a person's colon at any given time; "traveler's diarrhea" often results when this mix is changed through exposure to new pathogens. If this happens, the gut runs a program designed to expel as much of its contents as quickly as possible - unpleasant for the vacationer, but much better than a fatal infection."Another program involves a flood of serotonin throughout the entire circuit, which produces the digestive pattern that mixes and stirs the contents," says Wood.Because the gut brain is smaller and more accessible than the brain itself, understanding it could offer insights about how to parse the more complex organ. "That idea was what lead me to begin my research when I was a fledgling neuroscientist," says Gershon. "I looked at the brain and found it daunting, and I still do, so I looked for a simpler nervous system to study." He adds, "'Simple nervous system,' of course, turned out to be an oxymoron."Unlike the cranial brain, however, the gut brain doesn't seem to be conscious - or at least, in health, it doesn't impinge much on consciousness. "The gut is not an organ from which you like to receive frequent progress reports," says Gershon. For most digestive processes, no news is good news.The problem in IBS, in fact, may be that the enteric nervous system becomes overly sensitive to normal functioning and reports to the brain when it shouldn't. Or, the brain may overreact to normal bowel signals.Normally, the brain may avoid conscious awareness of most gut activity. But in IBS, says Wingate, one theory is that "the barrier to information being projected into consciousness is lowered."As in many heterogeneous conditions defined by symptoms rather than specific pathology, different subgroups of patients may have different causes or varying levels of contributions by different factors.In some cases, IBS may be an autoimmune problem - something like multiple sclerosis of the gut, where immune cells attack nervous tissue. "If you catch it early enough," says Wood, "You can use steroids to treat it in such cases." High doses of steroids shut down immune activity and prevent immune cells from causing harm, but they don't help once damage has been done.The gut is, in fact, a major immune organ, containing more immune cells than the rest of the body combined. The enteric nervous system interacts intimately with the immune system, and can affect mood and behavior by signaling the central nervous system.Further, the gut brain may in fact be the only system that can refuse central signals. Says Gershon, "The gut brain can say no to the big brain, absolutely. In fact, there are nerve fibers that project towards the CNS, and if the bowel doesn't like the message, it can turn it off or cancel it."Indeed, the vagus nerve mostly carries information from the enteric nervous system to the brain - for every one message sent by the brain to the gut, about nine are sent in the other direction. And recent research has found that stimulating this nerve can have antidepressant and even learning-enhancing effects - so "gut feelings" could genuinely be more than just a metaphor.The similarities between the two nervous systems may also mean that they are vulnerable to similar toxins and disease processes. For example, in both Parkinson's disease and Alzheimer's, the degenerative processes seen in brain nerve cells are also seen in the neurons of the enteric system.This link could also help explain the connection between psychological problems and gut problems - and could put to rest the myth that problems such as IBS are simply "neuroses" because they so often occur in people with other psychological disorders.It may be that the real reason that bowel disorders often accompany psychological problems is that both brain and gut neurons are suffering simultaneously - in addition to the fact that having to spend a significant portion of one's life attending to bathroom functions is in itself depressing.Simultaneous effects of drugs on both systems also account for the gastrointestinal "side effects" of Prozac and other drugs that act on serotonin metabolism - which actually may have more effect on the bowel than on the brain, because serotonin predominates in the bowel and the drug moves through the digestive system before reaching the brain.Fortunately, in most people, the bowel quickly develops tolerance to these drugs, and gastrointestinal side effects usually subside within a few days or weeks of the start of treatment. In fact, low doses of SSRI (selective serotonin reuptake inhibitor) drugs may actually help patients with IBS. And since different serotonin receptors predominate in the brain and in the gut, new drugs may be developed to affect certain subtypes but not others."What's exciting," says Wingate, "is getting away from essentially anecdotal ways of categorizing patients by symptoms and being able to study their problems in a very systematic biological way."Maia Szalavitz is a health/science journalist who has written for the New York Times, the Washington Post, Newsday, New York Magazine, Salon, and other major publications. http://www.vaccinationnews.com/DailyNews/F...02/GutBrain.htm The gut has a mind of its ownOperating like the cranial brain and looking uncannily similar to it, the gut brain is continuously active, whether we're aware of it or no, writes CHANTAL OUIMETBy CHANTAL OUIMETSpecial to The Globe and MailTuesday, December 31, 2002 � Print Edition, Page R7 Ever wonder why you get cramps when you're stressed? Or why you get "butterflies" in your stomach before a job interview? And why your gut tells you not to trust a certain person?Scientists say it's because the body has two brains -- the familiar one encased in our skull and another more obscure one in our gut. This "second brain," known as the enteric nervous system, is located in our digestive tract and holds about 100-million nerve cells -- more than in our spinal cord.Less complex and smaller than our cranial brain, this "second brain," which contains between 70 to 85 per cent of the body's immune cells, is an independent data-processing centre handling a complicated circuitry of neurons, neuromodulators and neurotransmitters."Every neurotransmitter that exists in our brain, also exists in the gut without exception. The brain in the gut is simply the brain gone south," says Dr. Michael Gershon, author of The Second Brain, and chairman of the department of anatomy and cell biology at Columbia University College of Physicians and Surgeons.In 1899, anatomists and physiologists studying dogs found that, unlike any other reflex, the continuous push of material through the digestive system continued after nerves linking the brain to the intestines were severed. In other words, they discovered the gut had a mind of its own.Operating like our brain and looking uncannily similar to it, the gut brain responds to stimulus and is continuously active whether we're aware of it or not. But it doesn't think or feel. Feeling is held in the cerebral cortex of the brain. This "second brain" performs a different role."The brain in the head deals with the finer things in life: religion, philosophy, appreciation of art and music, creativity, etc.," says Dr. Gershon. "Whereas the brain in the gut deals with this dirty, messy and disgusting business of digestion. The brain in the head doesn't have to get its hands dirty with that kind of thing since it has delegated the job."They may have different roles but our two brains are interconnected. One thousand to 2,000 nerve fibres connect them and enable the two to talk. When one gets upset, the other one does too."I don't think we could have made that statement a few years ago. . . . We've been finding out that the nerves in the gut independently regulate gut function, but do so in a dialogue with the nerves in our head. It's a nerve-to-nerve discussion," says Keith Sharkey, physiology and biophysics professor at the University of Calgary.Interest in the gut brain resurfaced in the early 1980s after new technology became available."For the first time, we were able to see in elegant and exquisite detail the specific way that nerves went from A to B," explains Prof. Sharkey. "That gives you a chance to ask questions that could not or had not been asked before."There are approximately 250 research laboratories now studying the enteric nervous system around the world. This new breed of neuroscientists is not only fuelling the present renaissance in the field of neurogastroenterology (study of the nerves entrenched in the lining of the esophagus, stomach, small intestine and colon), but offering insights into malfunctions of both brains.Scientists have discovered that the gut brain may be involved in gastrointestinal disorders like ulcerative colitis, Crohn's disease and irritable bowel syndrome -- a condition that affects between 15 and 20 per cent of the population."Back in the days when . . . I was a medical student, I was taught that these diseases were psychosomatic. . . . But they're a real thing. Your gut can literately drive your brain crazy," notes Dr. Gershon. "If you are walking around with a burning sensation in your upper belly and it feels terrible, you can get pretty anxious. Likewise, if you've got aches and you're on the toilet with diarrhea every five minutes, it can change your personality. But it's more than that."For many years, individuals (mostly women) with irritable bowel syndrome, a functional disorder characterized by abdominal pain, bloating, flatulence, diarrhea and/or constipation, suffered in silence. Doctors believed the illness was imagined -- all in the head."We now know IBS is not psychosomatic. There is an element of the brain controlling the gut which has to be born in the mind. But we now understand that there is also an organic and physiological basis for the functional changes in the little brain," declares Prof. Sharkey.Dr. Nicholas Diamant, a gastroenterologist at Toronto Western Hospital and an emeritus professor of medicine and physiology at the University of Toronto, agrees that both brains are involved in the disorder."The brain sends signals down to the little brain via the spinal cord which acts as a gate for the pain signals," Dr. Diamant says. "The brain may not be closing this gate adequately to modulate and regulate the signals coming up from the gut. Therefore, the brain is letting more signals come up than it normally would."A study by the Mayo Foundation published this August in Gastroenterology, the official journal of the American Gastroenterological Association, suggested there is genetic determinant that predicts the response to medication of IBS patients with diarrhea-predominant symptoms."It has to do with how the body inactivates the [neuro]transmitter serotonin. In some patients, the body inactivation is more efficient and the patient therefore responds better to the medication," explains Dr. Michael Carmilleri, professor of medicine and physiology at the Mayo Clinic in Rochester and one of the authors of the report."It's a landmark paper. . . . We are starting to relate changes in the signalling in the 'second brain' to real diseases based not only on functional changes but on genetic studies as well," says Prof. Sharkey.This July, a drug came on the Canadian market to treat patients (women only) with constipation-predominant IBS. Experts say Tegaserod, known commercially as Zelnorm, is only effective in 60 to 65 per cent of people."IBS is defined by a series of symptoms," says Prof. Sharkey. "It's a multiple disease entity. . . . We don't understand it well enough to ever consider a miracle-type cure because it's too complicated for that."In the case of Crohn's disease and ulcerative colitis (both autoimmune diseases), Dr. Carmilleri says the gut brain may play a role. "There is some interaction between the immune cells in the intestines and the 'second brain.' "The discovery of the brain-gut connection also allowed scientists to learn what is at the heart of the most visceral human emotions. A gut feeling, for example, isn't just a poetic image used to convey intuition. It arises from the interplay between our two brains."It's a "body loop" which is activated every time we are being challenged or stressed. From a lifetime of activating this "body loop" during good or bad situations, we learn to interpret this preverbal feedback as good or bad," says Emeran Mayer, professor of medicine and physiology at the University of California -- Los Angeles.Butterflies are minor indicators of pain and another example of this close relationship. Prof. Mayer says when one is faced with an anxiety-ridden situation, the brain in our skull sends urgent messages to our "second brain" and throws it off balance. "The big brain also becomes more sensitive to signals from the gut and amplifies them to unpleasant conscious sensations," he wrote. Therefore, one reads this response as gurgling or "butterflies" in the belly.Stomach cramps, heartburn, diarrhea or constipation due to stress are again an illustration of the gut rising to the level of conscious perception. "The dialogue between the brain in our head and the brain in our gut sometimes goes awry. . . . in such a way that the brain in our gut responds inappropriately to stimulus," says Prof. Sharkey. In turn, the nerves tell the muscles to contract more or less or make the glands secrete more or less fluid.Not all of the signals sent from the "second brain" to the cranial brain are bad news. "Some of the information that is being sent from the gut to the brain can establish how well the brain in the head works. . . . Your gut doesn't think for you but if it's behaving well, it can contribute to your mood being good," says Dr. Gershon. As a result, this interaction plays a role in dictating behavior and in creating human joy as well as sadness.Scientists affirm the brain constantly communicates and listens to our "second brain." Its functions are then taken over by the brain with respect to the activation of major emotions such as fear, anxiety, anger, sadness or happiness. There is no direct proof but a lot of suggestive evidence."Chemicals released from cells within the 'second brain' . . . can activate vagal sensory neurons (cells high in the neck) which signal back to the brain. These vagal sensory neurons play a prominent role in many emotional processes and it is certainly conceivable that such signals play a role in generating happiness or a sense of well-being. The newborn gets its first sense of well-being from stimulation of the gut and release of chemicals through milk," wrote Prof. Mayer.Dr. Diamant, a specialist in the mind-body connection, says each person's "second brain" reacts differently. "If you think everybody feels the same thing when the gut does something, you are in deep trouble. You have to consider the whole person and all the baggage they carry. The gut's reaction may be based on many experiences as well as the individual's genetic makeup."It's an exciting time for scientists because research in the field of neurogastroenterology is still evolving. Even medical students are generally shocked by the "second brain's" complexity. "That hasn't really made it to the textbooks yet," says Prof. Sharkey. "It takes a few years for emerging knowledge to become dogma." http://ibs.med.ucla.edu/Articles/PatientArticle001.htm The mind and the immune system-------------------------------------------------------------------------------- FYIHarvard Health"The Mind and the Immune System�Part IOne of the standing mysteries of medicine is the relationship between the mind and physical health�how feelings, thoughts, attitudes, and behavior are related to physical illness, how psychological and social stress affect the likelihood of developing a disease or the ability to resist it, and how counseling for emotional problems can aid recovery from illness. One of the clues to this mystery lies in the immune system, the network that defends us against microbes and other invaders. Interest in the connections between the brain and the immune system has given birth to the discipline of psychoneuroimmunology. These systems communicate through the sympathetic nervous system and the endocrine glands, especially the hypothalamic-pituitary-adrenal (HPA) axis. Like the immune system, both are dedicated to the defense of the body against stress and danger, and both are directed from the same part of the brain, the hypothalamus. All three�the immune system, sympathetic nervous system, and HPA axis�respond to some of the same transmitter chemicals. The sympathetic nervous system is part of the autonomic nervous system, which controls involuntary functions like heart rate, digestion, and breathing. The sympathetic nerves serve as an emergency response network, heightening the body�s readiness to accept a challenge or escape in the face of danger. The sympathetic nerves are connected to various organs of the immune system, such as the thymus gland, the bone marrow, the spleen, and lymph nodes. Immune cells, including T cells, monocytes, and B cells, have receptors for the neurotransmitters released by sympathetic nerves. Damage to the hypothalamus and loss of sympathetic transmitters impairs the functioning of the immune system. An injection of antigens (foreign substances that activate the immune system) affects the concentration of sympathetic neurotransmitters in the brain. Immune LearningAnimal experiments show that the immune system can �learn� by association. In one experiment, rats drank sweetened water containing a drug that causes nausea and depresses the immune system. They became so sick that they avoided sweetened water for some time after the drug was removed. That behavioral conditioning eventually was extinguished (wore off), and they returned to drinking the water�only to start developing infections at an abnormally high rate. Apparently, by association with the immunosuppressant drug, sugared water was provoking a conditioned response that continued to suppress the rats� immune systems even when it no longer affected their behavior. Another experiment involved mice bred to be genetically vulnerable to an autoimmune disease (one in which an overactive immune system attacks the body�s own tissues). They were given a flavored solution containing a drug that suppresses the immune system, delaying the onset of the disease. Then most of the drug was removed, but as long as the flavor remained, the rats continued to drink the liquid and resist the disease. The immune system had learned by association to suppress itself when the animals recognized that taste. Conditioned learning can also enhance immune function, as another experiment showed. Mice were repeatedly forced to smell camphor while they were injected with a substance that stimulated the activity of natural killer (NK) cells, a type of white blood cell. When they were exposed to the smell of camphor without the injection, the activity of their NK cells still increased. Hormonal EffectsThe HPA axis regulates the body�s activity through the circulation of the blood rather than directly through neural connections. The hypothalamus directs the pituitary gland to produce hormones that travel in the blood to the adrenal glands, where they cause the release of cortisol and other steroids as well as epinephrine (adrenaline) and its chemical relative norepinephrine (both of which also serve as neurotransmitters in the sympathetic system). These stress hormones influence the immune reaction through receptors on immune cells. Adrenaline, which prepares the body for immediate action, stimulates the immune system. One function of cortisol and related hormones (glucocorticoids) is to serve as a feedback mechanism that conserves energy by tuning down the emergency reaction when it is no longer needed. Rising cortisol levels signal the brain to shut down an immune response that threatens to become overactive. There�s evidence that stress is associated with depressed immune function in one or another part of the system. In one study, the activity of NK cells declined in medical students preparing for an examination. Those who felt calmer and had a slower heart rate also showed fewer immune changes. In another study, unemployment slowed the multiplication of white blood cells in response to antigens. A survey found that unhappily married women had lower numbers of certain immune cells than women with happy marriages. Elderly people caring for relatives with Alzheimer�s disease have higher than average levels of cortisol and low levels of antibody response to influenza vaccine. Stress delays the production of antibodies in mice infected with influenza virus and suppresses the activity of NK cells in animals inoculated with herpes simplex virus. Social stress can be even more damaging than physical stress. In a report published last year, some mice were put into a cage with a highly aggressive mouse two hours a day for six days. Other mice were kept in tiny cages without food and water for long periods. Both groups of mice were exposed to a bacterial toxin, and the socially stressed animals were twice as likely to die. Severe depression resembles a chronic stress response, and depressed patients often lack the normal daily variation in the production of cortisol. Depressed patients seem to have lower NK cell activity than healthy controls, possibly because of high cortisol levels. In one study, the lymphocytes (a type of white blood cell) of depressed and bereaved persons responded sluggishly to the substances that normally stimulate them to proliferate. Isolation can also suppress immune function. Infant monkeys separated from their mothers, especially if they are caged alone rather than in groups, generate fewer lymphocytes in response to antigens and fewer antibodies in response to viruses. Some studies have found lower NK cell activity in separated and divorced than in married men. NK cell activity also has been found to be lower in medical students who say they are lonely. In a year-long study of people caring for husbands or wives with Alzheimer�s disease, changes in immune function were greatest in those who had the fewest friends and least outside help. In general, good social support is associated with better immune function in the elderly, even after correction for health habits, depression, anxiety, and life stress. The effect of traumatic stress on the immune system has been studied occasionally. According to one report, four months after the passage of Hurricane Andrew in Florida, people in the most heavily damaged neighborhoods showed red uced activity in four out of five immune functions. Similar results were found in a study of hospital employees after an earthquake in Los Angeles. And a report published last year suggested that men with a history of posttraumatic stress disorder (PTSD), even long after apparent recovery, had lower numbers of various immune cells and lower levels of immune activity�possibly indicating a long-lasting suppression of the system. Another study found lower lymphocyte activity in abused women. But it�s not easy to generalize about the effect of stress hormones and sympathetic nervous system activity on immune functioning. Much depends on the individual, the timing, the kind of stress, and the part of the immune system under consideration. The results of studies on depression, for example, are conflicting; it does not consistently suppress any part of the immune system except NK cells. Animal experiments suggest that the nervous system responds differently to acute and chronic stress. The acute stress reaction is often a healthy response to a challenge. But chronic stress may cause the feedback controls to fail, turning the emergency response into a condition that persists when it no longer has any use. Stress hormones and sympathetic activity remain at high levels, suppressing immune function and possibly promoting illness. The immune systems of people who are under chronic stress may also respond abnormally to acute stress. The Difference it MakesWhat matters most is whether the mind�s influence on the immune system has the power to raise or lower the risk of illness or injury. On that issue only a little evidence is available. Healing of injuries. One study found that the wound from a biopsy healed more slowly in women under high emotional stress. In another experiment, a wound healed more slowly in students when it was inflicted before an examination rather than just before vacation. Slow healing has also been found in people caring for Alzheimer�s patients. Colds and flu. Both observation and experiments suggest that stress makes people more susceptible to colds and other respiratory infections. In a one-year study, researchers asked 100 people to keep a diary recording their feelings and events in their lives. They were examined periodically for bacteria in throat cultures and virus antibodies in the blood. Stressful events were four times more likely to come before rather than after new infections. And people who developed a cold or other infection had often been feeling more angry and tense than usual. In an English study published in 1991, 420 people were given nose drops containing a cold virus after answering questions about their personality, health practices, and behavior. They were asked about feelings of frustration, nervousness, anxiety, and depression and about events such as loss of a job or deaths in the family. When the subjects were quarantined and monitored for nine days, those under greater stress were more likely to catch a cold. Researchers have continued to confirm this connection. In a study conducted in the late 1990s at the University of Pittsburgh, 276 healthy adults were given nose drops containing a cold virus. The symptoms were most severe in those who reported a high level of stress in their lives�but only when it was prolonged stress caused by such problems as unemployment and troubled marriages. Resistance to the virus was correlated with strong social support, especially a variety of contacts with family, neighbors, friends, workmates, and fellow members of voluntary organizations. This effect was independent of smoking, alcohol consumption, and quality of sleep. People with the weakest (least diverse) social ties were four times more susceptible to colds than those with the strongest ties. Stress can also interfere with the response to a vaccine. In one study, flu shots were given to 32 people under high stress and 32 under low stress, matched for age, sex, and social class. The vaccine produced higher levels of antibodies in the low-stress group, and the high-stress people were more likely to become infected. The University of Pittsburgh researchers found a close association between difficulties in coping with stress, flu symptoms, and a specific immune response. Fifty-five volunteers were given nose drops containing a flu virus after answering questions about their ability to handle stress in their lives. The people with the most stress-related problems produced higher concentrations of interleukin-6, a chemical messenger that attracts immune cells to the site of an infection. They also produced more mucus (had stuffier noses) and generally developed more serious symptoms in direct proportion to the rise in their interleukin-6 levels. "www.health.harvard.edu/hh....do?id=537
 

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Best Pract Res Clin Gastroenterol. 2004 Aug;18(4):747-71. Related Articles, Links Alterations of sensori-motor functions of the digestive tract in the pathophysiology of irritable bowel syndrome.Delvaux M.Department of Internal Medicine and Digestive Pathology, CHU de Brabois, F-54511 Vandoeuvre-les-Nancy, France.Pathophysiology of irritable bowel syndrome (IBS) is based upon multiple factors that have been organised in a comprehensive model centred around the brain-gut axis. The brain-gut axis encompasses nerve pathways linking the enteric and the central nervous systems and contains a large proportion of afferent fibres. Functionally and anatomically, visceral nerves are divided in to two categories: the parasympathetic pathways distributing to the upper gut through the vagi and to the hindgut, through the pelvic and pudendal nerves, and the sympathetic pathways, arising form the spinal cord and distributing to the midgut via the paravertebral ganglia. Several abnormalities of gut sensori-motor function have been described in patients with IBS. Abnormal motility patterns have been described at the intestinal and colonic levels. Changes in colonic motility are mainly related to bowel disturbances linked to IBS but do not correlate with pain. More recently, visceral hypersensitivity has been recognised as a main characteristic of patients with IBS. It is defined by an exaggerated perception of luminal distension of various segments of the gut and related to peripheral changes in the processing of visceral sensations as well as modulation of perception by centrally acting factors including mood and stress. Viscero-visceral reflexes link the two edges of the brain-gut axis and may account for the origin of symptoms in some pathological conditions. Recent advances in the understanding of the role of myenteric plexus allowed recognition of several neurotransmitters involved at the level of both the afferent and efferent pathways. Targeting the receptors of these neurotransmitters is a promising way for development of new treatments for IBS.PMID: 15324712 Eur J Pain. 2004 Oct;8(5):451-463. Related Articles, Links Sex-based differences in gastrointestinal pain.Mayer EA, Berman S, Chang L, Naliboff BD.Departments of Medicine, Psychiatry and Biobehavioral Sciences, CNS: Center for Neurovisceral Sciences and Women's Health, UCLA Division of Digestive Diseases, UCLA and VA GLAHS, Bldg. 115/CURE, WLA VA Medical Center, 11301 Wilshire Blvd., Room 213, Los Angeles, CA 90073, USA.Recent interest has focused on sex-related differences in irritable bowel syndrome (IBS) physiology and treatment responsiveness to novel pharmacologic therapies. Similar to a variety of other chronic pain conditions and certain affective disorders, IBS is more prevalent amongst women, both in population-based studies as well as in clinic-based surveys. Non-painful gastrointestinal symptoms, constipation and somatic discomfort are more commonly reported by female IBS patients. While perceptual differences to rectosigmoid stimulation are only observed following repeated noxious stimulation of the gut, sex-related differences in certain sympathetic nervous system (SNS) responses to rectosigmoid stimulation are consistently seen. Consistent with experimental findings in animals, current evidence is consistent with a pathophysiological model which emphasizes sex-related differences in autonomic and antinociceptive responses to certain visceral stimuli. PMID: 15324776 This was the VSL# study"But Dr. Fedorak cautioned that "we don't know how they work. They appear to strengthen the mucosal barrier of the bowel and improve immune function. And we don't know which probiotics to use or in what combination.""also this was a newer VSL 3 study" Aliment Pharmacol Ther. 2003 Apr 1;17(7):895-904. Related Articles, Links A randomized controlled trial of a probiotic, VSL#3, on gut transit and symptoms in diarrhoea-predominant irritable bowel syndrome.Kim HJ, Camilleri M, McKinzie S, Lempke MB, Burton DD, Thomforde GM, Zinsmeister AR.Clinical Enteric Neuroscience Translational & Epidemiological Research Program, Mayo Clinic and Mayo Foundation, Rochester, MN 55905, USA.AIM: To investigate the effects of a probiotic formulation, VSL#3, on gastrointestinal transit and symptoms of patients with Rome II irritable bowel syndrome with predominant diarrhoea. METHODS: Twenty-five patients with diarrhoea-predominant irritable bowel syndrome were randomly assigned to receive VSL#3 powder (450 billion lyophilized bacteria/day) or matching placebo twice daily for 8 weeks after a 2-week run-in period. Pre- and post-treatment gastrointestinal transit measurements were performed in all patients. Patients recorded their bowel function and symptoms daily in a diary during the 10-week study, which was powered to detect a 50% change in the primary colonic transit end-point. RESULTS: There were no significant differences in mean gastrointestinal transit measurements, bowel function scores or satisfactory global symptom relief between the two treatment groups, pre- or post-therapy. Differences in abdominal bloating scores between treatments were borderline significant (P = 0.09, analysis of covariance). Further analysis revealed that abdominal bloating was reduced (P = 0.046) with VSL#3 mean post- minus pre-treatment score, - 13.7; 95% confidence interval (CI), - 2.5 to - 24.9, but not with placebo (P = 0.54) (mean post- minus pre-treatment score, - 1.7; 95% CI, 7.1 to - 10.4). With the exception of changes in abdominal bloating, VSL#3 had no effect on other individual symptoms: abdominal pain, gas and urgency. All patients tolerated VSL#3 well. CONCLUSION: VSL#3 appears to be promising in the relief of abdominal bloating in patients with diarrhoea-predominant irritable bowel syndrome. This is unrelated to an alteration in gastrointestinal or colonic transit.Publication Types: Clinical Trial Randomized Controlled Trial PMID: 12656692Med Sci Monit. 2004 Jun;10(6):RA125-31. Epub 2004 Jun 01. Related Articles, Links The brain-gut axis in irritable bowel syndrome--clinical aspects.Mach T.Department of Infectious Diseases and Hepatology, Jagiellonian University School of Medicine, ul. Sniadeckich 10, 31-153 Krakow, Poland. mstmach###cyf-kr.edu.plIrritable bowel syndrome (IBS) is the most common chronic gastrointestinal (GI) disorder, affecting about 20% of the world's population. Chronic abdominal pain or discomfort relieved by defecation and associated with altered bowel habits are the mainstay in diagnosis. The pathophysiology of IBS remains unknown. This biopsychosocial disorder involves dysregulation of the nervous system, altered intestinal motility, and increased visceral sensitivity. All of these result from dysregulation of the bidirectional communication between the gut with its enteric nervous system and the brain (the brain-gut axis), modulated by various psychosocial and environmental factors (e.g. infection, inflammation). Numerous neurotransmitters are found in the brain and gut that regulate GI activities, including 5-hydroxytryptamine (5-HT, serotonin) and its 5-HT3 and 5-HT4 receptors. The current approach to IBS patients is based on a positive diagnosis of the symptom complex, exclusion of underlying organic disease, and institution of a therapeutic trial. Traditional symptomatic treatment has included antidiarrheals, laxatives and bulking agents/fiber, low-dose tricyclic antidepressants, antispasmodics for pain, and "alternative" therapies (e.g. psychotherapy, hypnotherapy). The scientific evidence supporting this therapy is limited. Novel approaches include visceral analgesics and serotonin agonists and antagonists. In patients with severe diarrhea, 5-HT3 receptor antagonists (e.g. alosetron) and selective M3-type anticholinergics are indicated, in constipation 5-HT4 agonists (e.g. tegaserod), and in pain alfa2-adrenergics (e.g. clonidine), cholecystokinin antagonists, kappa-opioid agonists (e.g. fedotozine), and neurokinin antagonists; some of these agents are still being investigated. Understanding the brain-gut axis is crucial in the development of effective therapies for IBS.Publication Types: Review Review, Tutorial PMID: 15173682Irritable Bowel Syndrome (IBS), which is classified as a functional gastrointestinal disorder, is a chronic condition of the lower gastrointestinal tract (Figure 1) that affects as many as 15% of adults in the United States. Not easily characterized by structural abnormalities, infection, or metabolic disturbances, the underlying mechanisms of IBS have for many years remained unclear. Recent research, however, has lead to an increased understanding of IBS. As a result, IBS is now considered an organic and, most likely, neurologic bowel disorder. IBS is often referred to as spastic, nervous or irritable colon. Its hallmark is abdominal pain or discomfort associated with a change in the consistency and/or frequency of bowel movements. Although the causes of IBS have not to date been fully elucidated, it is believed that symptoms can occur as a result of a combination of factors, including visceral hypersensitivity, altered bowel motility, neurotransmitters imbalance, infection and psychosocial factors (Figure 2). " http://hopkins-gi.nts.jhu.edu/pages/latin/...se=43&lang_id=1 Rome"Irritable Bowel Syndrome: How far do you go in the Workup?Douglas A. Drossman, M.D.Professor of Medicine and PsychiatryCo-Director, UNC Center for Functional GI and Motility DisordersDivision of Digestive DiseasesUniversity of North Carolina at Chapel Hill"For example, there is a subgroup of patients, called "post-infectious IBS" who appear to respond to an enteric infection such as campylobactor jejuni with an increased inflammatory cell response (22). This is associated with activating enterochromaffin cells to produce 5HT, and CD3 cells to produce cytokines, which in turn leads to enhanced motility and lowered visceral sensation thresholds (22;23). But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it. All patients with active celiac disease have microscopic inflammation, but a large proportion do not have abdominal pain, and patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds (24) . In individuals with these disorders, there may be central nervous system counter-regulatory measures responding to the peripheral pain/inflammatory processes that increase pain thresholds. With regard to IBS, the gut-related effects of microscopic inflammation may be only one component of a dysfunctional brain-gut system. In addition, and often in response to stress, there may be a failure to activate descending pain inhibitory systems that enable the clinical experience of pain and other symptoms that typify this disorder (25). In one prospective study of post-infectious IBS, it was found that those who retained their symptoms 3-months after an enteric infection had not only increased mucosal cellularity, but also had increased psychosocial distress at the time of the infection. Furthermore, lowered visceral sensation thresholds and increased motility were present after the infection regardless of whether or not the patients retained their symptoms (26). Therefore, the microscopic inflammation and its physiological effects on motility and sensation contribute to, but are not always sufficient for the clinical expression of IBS pain. At least for post-infectious IBS this provides some evidence that psychological distress alters brain pain regulatory pathways to amplify incoming visceral signals leading to the full clinical expression of this syndrome " http://www.romecriteria.org/reading1.html So it does not seem to be caused ONLY by inflammation and infection and the inflammation seen are specific cells called mast cells and they are very connected to stress and fighting infection. Hence why there is a big already known correlation between gut infection and being stressed at the time of infection leading to IBS in PI IBS after the RESOLUTION of the Initial INFECTION. Probiotics have shown to reduce gas pain and bloating in some studies, but this is at the level of the gut and for some reasons they are alreay aware of, because the colon has pressure senisive cells, thats how the colon works and I don't think you have study the basics of this fact at all. What probiotics and I am not agasint them in the slightest haven't shown is any effect on the impairments and resolution of those impairments of pain in the brain of IBS patients yet. They have shown they help at the gut level somewhat, but only on bloating and pain, probably through gas reduction and possibly on some immune function which in turn would help pain at the gut level, so as not to signal pain to the brain.But there is still impairment of certain brain centers they have found in IBS and not control subjects which they have a ton of information on to implicate in IBS symptoms. Even that chrnoic stressors are contributing to if not causing the inflammation of those mast cells without a pathogen.and Robin Spiller is a leading expert on Inflammtion and IBS and on PI IBS."Best Pract Res Clin Gastroenterol. 2004 Aug;18(4):641-61. Related Articles, Links Inflammation as a basis for functional GI disorders.Spiller RC.Division of Gastroenterology, The Wolfson Digestive Disease Centre, University Hospital, Nottingham NG7 2UH, UK.The term 'Functional diseases' implies symptoms arising from an organ without overt pathology. However this is more apparent than real since inflammation often leaves changes in nerves and mucosal function only apparent with specialised techniques. Acute onset functional dyspepsia accounts for around 1/5 of functional dyspepsia and is characterised by early satiety, nausea, vomiting and weight loss. Impaired postcibal fundal accommodation may underlie some of these symptoms. Post infectious gastroparesis is much rarer and is associated with markedly delayed gastric emptying and antral hypomotility. Approximately 1/10 of IBS cases describe a post infectious onset. Post infectious IBS is typically of the diarrhoea-predominant type. Post inflammatory functional diseases tend to be associated with less psychological abnormalities and have a better prognosis than other functional diseases. There are isolated anecdotal reports of symptom response to anti-inflammatory treatments but larger controlled trials are needed.PMID: 15324705 "Gastroenterology. 2003 Dec;125(6):1651-9. Related Articles, Links Relative importance of enterochromaffin cell hyperplasia, anxiety, and depression in postinfectious IBS.Dunlop SP, Jenkins D, Neal KR, Spiller RC.Wolfson Digestive Diseases Centre, University Hospital, Nottingham, England.BACKGROUND & AIMS: Both psychological and mucosal changes (increased enterochromaffin EC cells and T lymphocytes) have been associated with postinfectious irritable bowel syndrome (PI-IBS). However, previous studies have been underpowered to determine the relative importance of these changes in predicting the development of PI-IBS. Our aim was to prospectively determine the relative importance of both psychological and histologic factors in the development of PI-IBS after Campylobacter infection. METHODS: Questionnaires detailing psychological and bowel symptoms were sent to 1977 patients 3 months after infection. Twenty-eight patients with new-onset PI-IBS, 28 age- and sex-matched patient controls who were asymptomatic after infection, and 34 healthy volunteers underwent rectal biopsy, which was assessed for serotonin-containing EC cells, mast cells, and lamina propria T lymphocytes. RESULTS: PI-IBS, predominantly of the diarrhea-predominant subtype, occurred in 103 of 747 (13.8%) of those infected. EC cell counts per high-power field (hpf) were higher in patients with PI-IBS (35.8 +/- 1.2) compared with patient controls (30.6 +/- 1.9; P = 0.022) and volunteers (29.1 +/- 1.8; P = 0.006). Lamina propria T lymphocytes per hpf were higher in patients with PI-IBS (127.1 +/- 8.7) and patient controls (113.4 +/- 6.2) in contrast to healthy volunteers (97.1 +/- 5.7) (P = 0.006 and P = 0.058, respectively). Anxiety, depression, and fatigue were significantly increased in patients with PI-IBS compared with patient controls. Multivariate analysis indicated that increased EC cell counts and depression were equally important predictors of developing PI-IBS (relative risk, 3.8 and 3.2 for each standard deviation increase in respective values). CONCLUSIONS: Both increased EC cells and depression are important independent predictors of developing PI-IBS. PMID: 14724817EC cells store the majority of serotonin in the gut. Serotonin is majorally implicated in IBS!!!!"Am J Gastroenterol. 2003 Jul;98(7):1578-83. Related Articles, Links Distinctive clinical, psychological, and histological features of postinfective irritable bowel syndrome.Dunlop SP, Jenkins D, Spiller RC.Division of Divisions of Gastroenterology, University Hospital, Nottingham, United Kingdom.OBJECTIVE: Irritable bowel syndrome after gastroenteritis is well recognized. Our aim was to determine whether postinfective IBS (PI-IBS) has histological or clinical features that are distinct from those of IBS patients with no history of preceding infection. METHODS: A total of 75 consecutive IBS outpatients and 36 healthy control subjects completed a questionnaire detailing symptoms, mode of onset, and previous psychiatric history. All underwent a full diagnostic workup including rectal biopsy, which included immunostaining and quantification for lamina propria or intraepithelial T lymphocytes, serotonin-containing enterochromaffin (EC), and mast cells. Patients were divided according to onset of symptoms into PI-IBS (n = 23) or non-PI-IBS (n = 52) patients. RESULTS: Diarrhea predominance occurred more frequently in PI-IBS (70%) than in non-PI-IBS (42%) patients (p = 0.03). A history of previous treatment for anxiety or depression was present in 26% of PI-IBS patients compared to 54% of non-PI-IBS (p = 0.02). Biopsy results for all patients were normal using conventional criteria; however, quantification revealed that PI-IBS showed increased EC cells compared to those of non-PI-IBS patients (p = 0.017) and controls (p = 0.02). Lamina propria T lymphocytes were increased in PI-IBS (p = 0.026) and non-PI-IBS (p = 0.011) patients compared to controls. Mast cells were increased in non-PI-IBS patients (p = 0.054) compared to controls. CONCLUSIONS: Individuals with PI-IBS are a clinically distinct subgroup characterized by diarrheal symptoms, less psychiatric illness, and increased serotonin-containing EC cells compared to those with non-PI-IBS.PMID: 12873581 ""Curr Treat Options Gastroenterol. 2003 Aug;6(4):329-337. Related Articles, Links Treatment of Irritable Bowel Syndrome.Spiller RC.Department of Gastroenterology, University Hospital, Derby Road, Nottingham NG7 2UH, UK. robin.spiller###nottingham.ac.ukIrritable bowel syndrome (IBS) is an extremely common cause of consultation, and at present is diagnosed on the basis of symptoms and a few simple exclusion tests. Exclusion diets can be successful, but many patients have already attempted and failed such treatments before consulting. Anxiety and somatization may be an important driver of consultation. Patients' concerns should be understood and addressed. Those with prominent psychiatric disease may benefit from psychotherapy. Hypnotherapy benefits symptoms in those without psychologic disturbance, but its availability is limited. Antidepressants are effective in improving both mood and IBS symptoms globally, and the evidence is particularly good for tricyclic antidepressants. Although antispasmodics are currently the most commonly prescribed drugs, most responses (75%) are due to the placebo effect and not specific to the drug. Bulk laxatives such as ispaghula can increase stool frequency and help pain, but bloating may be aggravated. Loperamide is effective treatment for urgency and loose stools, but less effective for bloating and pain. 5-HT(3) antagonists such as alosetron improve urgency, stool consistency, and pain in diarrhea-predominant-IBS. The 5-HT(4) agonist tegaserod shows modest benefit in constipation-predominant IBS, improving stool frequency, consistency, and bloating as well as global improvement. There are many new drugs, such as cholecystokinin, neurokinin, and corticotropin receptor antagonists, in development."Gastroenterology. 2003 May;124(6):1662-71. Related Articles, Links Postinfectious irritable bowel syndrome.Spiller RC.Division of Gastroenterology, University Hospital, Nottingham, United Kingdom. robin.spiller###noittingham.ac.ukA small but significant subgroup of patients with irritable bowel syndrome (IBS) report a sudden onset of their IBS symptoms after a bout of gastroenteritis. Population-based surveys show that although a history of neurotic and psychologic disorders, pain-related diseases, and gastroenteritis are all risk factors for developing IBS, gastroenteritis is the most potent. More toxigenic organisms increase the risk 11-fold, as does an initial illness lasting more than 3 weeks. Hypochondriasis and adverse life events double the risk for postinfective (PI)-IBS and may account for the increased proportion of women who develop this syndrome. PI-IBS is associated with modest increases in mucosal T lymphocytes and serotonin-containing enteroendocrine cells. Animal models and some preliminary human data suggest this leads to excessive serotonin release from the mucosa. Both the histologic changes and symptoms in humans may last for many years with only 40% recovering over a 6-year follow-up. Celiac disease, microscopic colitis, lactose intolerance, early stage Crohn's disease, and bile salt malabsorption should be excluded, as should colon cancer in those over the age of 45 years or in those with a positive family history. Treatment with Loperamide, low-fiber diets, and bile salt- binding therapy may help some patients. Serotonin antagonists are logical treatments but have yet to be evaluated.Publication Types: Review Review, Tutorial PMID: 12761724and this was a comment from him when other doctors suggested"Full-thickness biopsy of the jejunum reveals inflammation and enteric neuropathy in irritable bowel syndrome."he respondedEditorialsNeuropathology of IBS?Robin C. Spiller [MEDLINE LOOKUP] http://www2.us.elsevierhealth.com/scripts/...004857&nav=full and some of this information is from 2002 and they know more about it all since then and a lot of them all share resources and studies and peer reviews.hence theFrom - Report on the 5th International Symposium on Functional Gastrointestinal DisordersApril 4, 2003 to April 7, 2003 Milwaukee, Wisconsin By: Douglas A. Drossman, M.D ., UNC Center for Functional GI and Motility Disorders at Chapel Hill, and William F. Norton, IFFGDBasic Principles -- Brain-Gut Moderators: Emeran Mayer MD; Robin Spiller MD. Panel: Robin Spiller MD; Jackie Wood PhD; George Chrousos MD; Yvette Tach� PhD; Lisa Goehler PhD; G.F. Gebhart PhD; Emeran Mayer MD. Click on Titles to View Other TopicsIntroductionOutcomes of Pediatric Functional GI Disorders Epidemiology/Genetic/Behavioral Factors Brain Imaging Emerging Techniques to Evaluate and Treat Functional GI and Motility Disorders Clinical Applications of Diagnosis and Treatment Functional GI DisordersGeneral Principles of TreatmentPharmacological Treatment Psychological Treatment IFFGD Research AwardsThe brain-gut axis refers to the continuous back and forth interactions of information and feedback that take place between the gastrointestinal tract, and the brain and spinal cord (which together comprise the central nervous system). These interrelated feedback circuits can influence brain processes and bowel functions -- affecting pain perception, thoughts and one's appraisal of symptoms, gut sensitivity, secretions, inflammatory responses, and motility. The brain-gut circuits can be activated by an external or internal factor or stimulus that makes a demand on the system, such as a stressful event, an injury, an emotional thought or feeling, or even the ingestion of food. Symptoms of functional GI disorders may result from a maladaptive response to stimuli at some point within the complex interactions that take place along the brain-gut axis. Basic science is the fundamental approach to understanding how systems work. Basic research takes place in the laboratory and often involves the study of molecules and cells. From this body of knowledge is drawn the means to investigate practical applications and to formulate clinical practices. Translational science converts basic science discoveries into the practical applications that benefit people. One of the more exciting areas of recent research relates to the basic and translational aspects of the effects of stress on inflammation, cytokine and immune modulation, and pain. (Cytokines are a type of protein released by cells of the immune system, which act through specific cell receptors to regulate immune responses.) This series of presentations address three important research areas in the field of functional GI disorders, which have recently attracted considerable attention: the role of immune activation in the gut and the interactions of the gut immune and nervous systems; the role of the central nervous system in the regulation (modulation) of pain perception (nociception); and the emerging field of animal models with relevance for functional GI disorder research. This section demonstrates the rapid progress seen in the last few years in better understanding of basic mechanisms, in particular the neuroimmune interactions underlying symptom generation in patients with "functional" GI disorders. There are immune responses to infections. To defend itself from a foreign substance or invader, such as a bacterium or virus, the body mounts an immune response controlled by the brain. There needs to be a balance between infection and the body's immune response; the immune system needs to turn on and turn off at the right times to destroy the invader but not to the degree that it may harm healthy tissue. Robin Spiller, University Hospital, Nottingham, England began the session by noting the difficulty in separating disorders of structure ("organic") from disorders of function. He noted, "The difference is based on how high the power of your microscope is." This was elaborated upon in his presentation on Post-infectious Functional GI Disorders. It has been observed that IBS-like symptoms, that persist for 6 months to a year or longer, may appear after a bout with an acute infection in the gastrointestinal tract (e.g., food-poisoning). This is termed, "post-infectious IBS." A study by Gwee et al showed that the presence of unusual or amplified life stress at the time of onset of infection increased the chances of developing IBS symptoms. Inflammation persisted in patients with IBS-like symptoms but did not in patients whose symptoms resolved. This suggests that the brain's management of certain stressful stimuli (i.e., psychologic distress) affects the brain-gut system's ability to inhibit inflammation. It has frequently been observed that some individuals with more severe symptoms of IBS have coexisting psychologic distress. Stress has been thought to influence health-care seeking behavior, either by increasing motility, visceral hypersensitivity or inflammation, or by enhancing one's perception of gut symptoms, all of which lead to a greater need to seek care for them. The concept of post-infectious IBS suggests that in some circumstances stress (the biological process by which the body adapts in response to a stimuli) may influence symptoms. Persistence of the underlying inflammatory response may lead to post-infectious disorders of function. A variety of neuroimmune responses can lead to intestinal over-responsiveness (sensitization) and other clinical effects. These responses include direct toxicity to nerves that influence intestinal contractions, alteration in gut immune activation, abnormalities of serotonin metabolism, and persisting low-grade inflammation. IBS developing after infective gastroenteritis is associated with subtle increases in enteroendocrine and chronic inflammatory cells in the gut mucosa. The net effect may be to increase serotonin availability in the gut and enhance secretion and propulsive motility patterns. Serotonin antagonists may be beneficial in such patients Notably, the concept of "post-infectious IBS" has grown to include studies of their application in post-infectious gastroparesis and dyspepsia. 1Major inflammatory responses have not been observed in most IBS patients. However, in some studies subtle changes associated with inflammation have been noticed, such as increased presence of mast cells (a type of immune system cell present in blood and tissue). Jackie Wood, Ohio State University College of Medicine discussed the Effects of Inflammation on the Gut Enteric Nervous System, specifically noting the importance of mast cell degranulation (the release from within the cell of granules, or small sacs, containing chemicals that can digest microorganisms and fight infection). In tissue mast cells accumulate around nerve endings of nerves that contain the neurotransmitter serotonin. The release of substances that can induce activity in excitable tissue (i.e., histamine, Interleukin-1 (IL-1), and bradykinin) by mast cells can affect receptor and neurotransmitter function in the enteric nervous system - the part of the autonomic nervous system that controls function of the gastrointestinal tract. In other words, when mast cells in the intestinal lining empty their contents in response to an infection, they activate nearby nerve endings. In a subgroup of patients, this can have significance in terms of resulting clinical consequences of diarrhea and abdominal discomfort. 2----------------------------------------------side notehistimine is released in the gut by stress and effects mast cellsalso"Jack Wood, PhDProfessor of Physiology and Internal MedicineChairman Emeritus, Department of PhysiologyThe Ohio State University College of Medicine Dr. Wood was the first to use microelectrodes to record the electrical and synaptic behavior of neurons in the enteric nervous system. He coined the term "brain-in-the-gut" in view of emerging evidence that the enteric nervous system had neurophysiological properties like the brain and spinal cord. In recent years he has focused on signaling interactions between the enteric immune system and the brain-in-the-gut during infectious enteritis and food allergy. In this lecture he shows how the central nervous system, enteric nervous system and intestinal immune system are integrated during physical and emotional stress to produce irritable bowel symptoms of diarrhea and abdominal pain and discomfort. " http://www.conference-cast.com/ibs/Lecture...dRegLecture.cfm -------------------------------------------------Yvette Tach�, University of California Los Angeles discussed Stress and Inflammation. The experience of stress is an adaptive behavior common to all living organisms. The activation of corticotropin releasing factor (CRF) signaling pathway, is the major mediating mechanism involved with the body's stress response system in which gastric emptying is inhibited (with possible loss of appetite) while colonic motor activity is stimulated (producing a loose stool or a sensation of bowel urgency). There is growing evidence that activation of this CRF pathways impacts on inflammation, autonomic nervous system function, immunity, and clinical behavior or illness, all of which may be linked to the pathophysiology of the functional gastrointestinal disorders. While we often talk about how the brain -- influenced for example by arousal and/or psychosocial factors -- can affect immune function, the reverse is also true. Immune activation, following infection for example, can influence brain function. Lisa Goehler, University of Virginia discussed Cytokines and Vagal Afferents: Immune Signaling to the Brain. Cytokines are substances that are produced by white blood cells to regulate certain functions during inflammatory and immune responses. The vagus is a nerve made of both sensory and motor fibers that innervates nearly every internal organ. The gastrointestinal (GI) tract, along with the lungs and liver, is an area of tissue that most commonly comes in contact with microorganisms (pathogens), such as bacteria or viruses, capable of activating an immune response. Cytokine mediators activate neurons that convey messages from tissue to the brain (afferent neurons) through the vagus nerve. The GI tract is richly supplied with vagal afferents that can signal immune activation in the tissue. This process may underlie the mechanism that causes individuals to feel sick. The concept of "sickness symptoms" is not always recognized. The cytokine inflammatory and immune mediators distributed throughout the body (peripheral), which appear to interact through vagal pathways, have systemic effects that manifest as symptoms in the body. (Mediators are substances released from cells to regulate immune responses.) Such symptoms include fever, increased sensitivity to pain, loss of appetite, and decreased desire for social interaction. The process may provide the basis for a role of the vagus as an interface between the site of the immune response and the brain that results in symptoms of altered mood, including anxiety or depression, that are sometimes associated with gastrointestinal disease. 4 Jerry Gebhart, The University of Iowa discussed the CNS Modulation of Visceral Nociceptive Responses. The central nervous system (CNS) is composed of the brain and spinal cord. The brain interprets and influences our perceptions of the pain sensation signals transmitted from the gut (visceral nociceptive responses) to the spinal cord and then to higher centers. Several structures in the brain (periaqueductal gray, dorsolateral pons, and rostroventral medulla) can facilitate or inhibit signals sent to the CNS and influence the perceived discomfort, or even whether the signals are experienced as pain. Inflammation of the bowel can produce increased sensitivity to pain or enhanced intensity of pain sensation (hyperalgesia) via increased activity of certain cells (for example, those that contain nNOS) in these higher brain modulatory centers. 5 To close the Brain-Gut sessions, Emeran Mayer, University of California Los Angeles discussed Evolving Animal Models of Visceral Hypersensitivity. In contrast to most other disorders of the digestive system, functional disorders of the gut continue to be defined by symptom criteria rather than by biological markers. Realistic animal models of functional gastrointestinal (GI) disorders in which to test hypotheses have not been available until recently. While it is unlikely that there will ever be an animal model to replicate all complexities of the human functional GI disorders, animal research is likely to help us understand some of the key underlying mechanisms responsible for symptom generation. This includes over-responsiveness of central stress circuits to visceral and psychological stimuli, resulting in altered autonomic responses (motility, secretion), increased pain sensitivity (visceral hypersensitivity) and possibly altered immune function of the gut. Future studies with genetically altered (i.e., transgenic) mice that become models for studying specific human diseases and their treatments may further increase our understanding of these mechanisms" http://www.iffgd.org/symposium2003brain-gut.html From - Report on the 5th International Symposium onFunctional Gastrointestinal DisordersApril 4, 2003 to April 7, 2003 Milwaukee, Wisconsin By: Douglas A. Drossman, M.D., UNC Center for Functional GI and Motility Disorders at Chapel Hill, and William F. Norton, IFFGDBrain Imaging Moderator: Reza Shaker MD. Panel: Reza Shaker MD; Bruce Naliboff PhD; David Thompson MD. "Central activation -- the rapid short-term biophysical and biochemical changes in neurons that make possible such activities as thought, perception, and voluntary movement -- appears to increase as intensity of stimulus increases. However, repeated exposure can lead to adaptation, as the brain adjusts to the stimuli, with decreased central activation. In studies, IBS patients are differentiated from healthy controls by showing greater activation of an area of the brain essential for conscious pain (the anterior mid-cingulate component of the anterior cingulate cortex). It is in this region in the brain where the systems concerned with emotion or feeling, attention, and working memory interact. On the other hand, controls (and also patients with inflammatory bowel disease who have adapted to the visceral signals) show greater activation of the descending pain inhibitory pathways in areas of the brain involved in the suppression of pain (in the brain stem in the region of the periaqueductal gray). " From - Report on the 5th International Symposium onFunctional Gastrointestinal DisordersApril 4, 2003 to April 7, 2003 Milwaukee, Wisconsin By: Douglas A. Drossman, M.D., UNC Center for Functional GI and Motility Disorders at Chapel Hill, and William F. Norton, IFFGDEpidemiology/Genetic/Behavioral Factors This is very important also to the big picture. http://www.iffgd.org/symposium2003factors.html ""But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it."
 

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Best Pract Res Clin Gastroenterol. 2004 Aug;18(4):747-71. Related Articles, Links Alterations of sensori-motor functions of the digestive tract in the pathophysiology of irritable bowel syndrome.Delvaux M.Department of Internal Medicine and Digestive Pathology, CHU de Brabois, F-54511 Vandoeuvre-les-Nancy, France.Pathophysiology of irritable bowel syndrome (IBS) is based upon multiple factors that have been organised in a comprehensive model centred around the brain-gut axis. The brain-gut axis encompasses nerve pathways linking the enteric and the central nervous systems and contains a large proportion of afferent fibres. Functionally and anatomically, visceral nerves are divided in to two categories: the parasympathetic pathways distributing to the upper gut through the vagi and to the hindgut, through the pelvic and pudendal nerves, and the sympathetic pathways, arising form the spinal cord and distributing to the midgut via the paravertebral ganglia. Several abnormalities of gut sensori-motor function have been described in patients with IBS. Abnormal motility patterns have been described at the intestinal and colonic levels. Changes in colonic motility are mainly related to bowel disturbances linked to IBS but do not correlate with pain. More recently, visceral hypersensitivity has been recognised as a main characteristic of patients with IBS. It is defined by an exaggerated perception of luminal distension of various segments of the gut and related to peripheral changes in the processing of visceral sensations as well as modulation of perception by centrally acting factors including mood and stress. Viscero-visceral reflexes link the two edges of the brain-gut axis and may account for the origin of symptoms in some pathological conditions. Recent advances in the understanding of the role of myenteric plexus allowed recognition of several neurotransmitters involved at the level of both the afferent and efferent pathways. Targeting the receptors of these neurotransmitters is a promising way for development of new treatments for IBS.PMID: 15324712 Eur J Pain. 2004 Oct;8(5):451-463. Related Articles, Links Sex-based differences in gastrointestinal pain.Mayer EA, Berman S, Chang L, Naliboff BD.Departments of Medicine, Psychiatry and Biobehavioral Sciences, CNS: Center for Neurovisceral Sciences and Women's Health, UCLA Division of Digestive Diseases, UCLA and VA GLAHS, Bldg. 115/CURE, WLA VA Medical Center, 11301 Wilshire Blvd., Room 213, Los Angeles, CA 90073, USA.Recent interest has focused on sex-related differences in irritable bowel syndrome (IBS) physiology and treatment responsiveness to novel pharmacologic therapies. Similar to a variety of other chronic pain conditions and certain affective disorders, IBS is more prevalent amongst women, both in population-based studies as well as in clinic-based surveys. Non-painful gastrointestinal symptoms, constipation and somatic discomfort are more commonly reported by female IBS patients. While perceptual differences to rectosigmoid stimulation are only observed following repeated noxious stimulation of the gut, sex-related differences in certain sympathetic nervous system (SNS) responses to rectosigmoid stimulation are consistently seen. Consistent with experimental findings in animals, current evidence is consistent with a pathophysiological model which emphasizes sex-related differences in autonomic and antinociceptive responses to certain visceral stimuli. PMID: 15324776 This was the VSL# study"But Dr. Fedorak cautioned that "we don't know how they work. They appear to strengthen the mucosal barrier of the bowel and improve immune function. And we don't know which probiotics to use or in what combination.""also this was a newer VSL 3 study" Aliment Pharmacol Ther. 2003 Apr 1;17(7):895-904. Related Articles, Links A randomized controlled trial of a probiotic, VSL#3, on gut transit and symptoms in diarrhoea-predominant irritable bowel syndrome.Kim HJ, Camilleri M, McKinzie S, Lempke MB, Burton DD, Thomforde GM, Zinsmeister AR.Clinical Enteric Neuroscience Translational & Epidemiological Research Program, Mayo Clinic and Mayo Foundation, Rochester, MN 55905, USA.AIM: To investigate the effects of a probiotic formulation, VSL#3, on gastrointestinal transit and symptoms of patients with Rome II irritable bowel syndrome with predominant diarrhoea. METHODS: Twenty-five patients with diarrhoea-predominant irritable bowel syndrome were randomly assigned to receive VSL#3 powder (450 billion lyophilized bacteria/day) or matching placebo twice daily for 8 weeks after a 2-week run-in period. Pre- and post-treatment gastrointestinal transit measurements were performed in all patients. Patients recorded their bowel function and symptoms daily in a diary during the 10-week study, which was powered to detect a 50% change in the primary colonic transit end-point. RESULTS: There were no significant differences in mean gastrointestinal transit measurements, bowel function scores or satisfactory global symptom relief between the two treatment groups, pre- or post-therapy. Differences in abdominal bloating scores between treatments were borderline significant (P = 0.09, analysis of covariance). Further analysis revealed that abdominal bloating was reduced (P = 0.046) with VSL#3 mean post- minus pre-treatment score, - 13.7; 95% confidence interval (CI), - 2.5 to - 24.9, but not with placebo (P = 0.54) (mean post- minus pre-treatment score, - 1.7; 95% CI, 7.1 to - 10.4). With the exception of changes in abdominal bloating, VSL#3 had no effect on other individual symptoms: abdominal pain, gas and urgency. All patients tolerated VSL#3 well. CONCLUSION: VSL#3 appears to be promising in the relief of abdominal bloating in patients with diarrhoea-predominant irritable bowel syndrome. This is unrelated to an alteration in gastrointestinal or colonic transit.Publication Types: Clinical Trial Randomized Controlled Trial PMID: 12656692Med Sci Monit. 2004 Jun;10(6):RA125-31. Epub 2004 Jun 01. Related Articles, Links The brain-gut axis in irritable bowel syndrome--clinical aspects.Mach T.Department of Infectious Diseases and Hepatology, Jagiellonian University School of Medicine, ul. Sniadeckich 10, 31-153 Krakow, Poland. mstmach###cyf-kr.edu.plIrritable bowel syndrome (IBS) is the most common chronic gastrointestinal (GI) disorder, affecting about 20% of the world's population. Chronic abdominal pain or discomfort relieved by defecation and associated with altered bowel habits are the mainstay in diagnosis. The pathophysiology of IBS remains unknown. This biopsychosocial disorder involves dysregulation of the nervous system, altered intestinal motility, and increased visceral sensitivity. All of these result from dysregulation of the bidirectional communication between the gut with its enteric nervous system and the brain (the brain-gut axis), modulated by various psychosocial and environmental factors (e.g. infection, inflammation). Numerous neurotransmitters are found in the brain and gut that regulate GI activities, including 5-hydroxytryptamine (5-HT, serotonin) and its 5-HT3 and 5-HT4 receptors. The current approach to IBS patients is based on a positive diagnosis of the symptom complex, exclusion of underlying organic disease, and institution of a therapeutic trial. Traditional symptomatic treatment has included antidiarrheals, laxatives and bulking agents/fiber, low-dose tricyclic antidepressants, antispasmodics for pain, and "alternative" therapies (e.g. psychotherapy, hypnotherapy). The scientific evidence supporting this therapy is limited. Novel approaches include visceral analgesics and serotonin agonists and antagonists. In patients with severe diarrhea, 5-HT3 receptor antagonists (e.g. alosetron) and selective M3-type anticholinergics are indicated, in constipation 5-HT4 agonists (e.g. tegaserod), and in pain alfa2-adrenergics (e.g. clonidine), cholecystokinin antagonists, kappa-opioid agonists (e.g. fedotozine), and neurokinin antagonists; some of these agents are still being investigated. Understanding the brain-gut axis is crucial in the development of effective therapies for IBS.Publication Types: Review Review, Tutorial PMID: 15173682Irritable Bowel Syndrome (IBS), which is classified as a functional gastrointestinal disorder, is a chronic condition of the lower gastrointestinal tract (Figure 1) that affects as many as 15% of adults in the United States. Not easily characterized by structural abnormalities, infection, or metabolic disturbances, the underlying mechanisms of IBS have for many years remained unclear. Recent research, however, has lead to an increased understanding of IBS. As a result, IBS is now considered an organic and, most likely, neurologic bowel disorder. IBS is often referred to as spastic, nervous or irritable colon. Its hallmark is abdominal pain or discomfort associated with a change in the consistency and/or frequency of bowel movements. Although the causes of IBS have not to date been fully elucidated, it is believed that symptoms can occur as a result of a combination of factors, including visceral hypersensitivity, altered bowel motility, neurotransmitters imbalance, infection and psychosocial factors (Figure 2). " http://hopkins-gi.nts.jhu.edu/pages/latin/...se=43&lang_id=1 Rome"Irritable Bowel Syndrome: How far do you go in the Workup?Douglas A. Drossman, M.D.Professor of Medicine and PsychiatryCo-Director, UNC Center for Functional GI and Motility DisordersDivision of Digestive DiseasesUniversity of North Carolina at Chapel Hill"For example, there is a subgroup of patients, called "post-infectious IBS" who appear to respond to an enteric infection such as campylobactor jejuni with an increased inflammatory cell response (22). This is associated with activating enterochromaffin cells to produce 5HT, and CD3 cells to produce cytokines, which in turn leads to enhanced motility and lowered visceral sensation thresholds (22;23). But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it. All patients with active celiac disease have microscopic inflammation, but a large proportion do not have abdominal pain, and patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds (24) . In individuals with these disorders, there may be central nervous system counter-regulatory measures responding to the peripheral pain/inflammatory processes that increase pain thresholds. With regard to IBS, the gut-related effects of microscopic inflammation may be only one component of a dysfunctional brain-gut system. In addition, and often in response to stress, there may be a failure to activate descending pain inhibitory systems that enable the clinical experience of pain and other symptoms that typify this disorder (25). In one prospective study of post-infectious IBS, it was found that those who retained their symptoms 3-months after an enteric infection had not only increased mucosal cellularity, but also had increased psychosocial distress at the time of the infection. Furthermore, lowered visceral sensation thresholds and increased motility were present after the infection regardless of whether or not the patients retained their symptoms (26). Therefore, the microscopic inflammation and its physiological effects on motility and sensation contribute to, but are not always sufficient for the clinical expression of IBS pain. At least for post-infectious IBS this provides some evidence that psychological distress alters brain pain regulatory pathways to amplify incoming visceral signals leading to the full clinical expression of this syndrome " http://www.romecriteria.org/reading1.html So it does not seem to be caused ONLY by inflammation and infection and the inflammation seen are specific cells called mast cells and they are very connected to stress and fighting infection. Hence why there is a big already known correlation between gut infection and being stressed at the time of infection leading to IBS in PI IBS after the RESOLUTION of the Initial INFECTION. Probiotics have shown to reduce gas pain and bloating in some studies, but this is at the level of the gut and for some reasons they are alreay aware of, because the colon has pressure senisive cells, thats how the colon works and I don't think you have study the basics of this fact at all. What probiotics and I am not agasint them in the slightest haven't shown is any effect on the impairments and resolution of those impairments of pain in the brain of IBS patients yet. They have shown they help at the gut level somewhat, but only on bloating and pain, probably through gas reduction and possibly on some immune function which in turn would help pain at the gut level, so as not to signal pain to the brain.But there is still impairment of certain brain centers they have found in IBS and not control subjects which they have a ton of information on to implicate in IBS symptoms. Even that chrnoic stressors are contributing to if not causing the inflammation of those mast cells without a pathogen.and Robin Spiller is a leading expert on Inflammtion and IBS and on PI IBS."Best Pract Res Clin Gastroenterol. 2004 Aug;18(4):641-61. Related Articles, Links Inflammation as a basis for functional GI disorders.Spiller RC.Division of Gastroenterology, The Wolfson Digestive Disease Centre, University Hospital, Nottingham NG7 2UH, UK.The term 'Functional diseases' implies symptoms arising from an organ without overt pathology. However this is more apparent than real since inflammation often leaves changes in nerves and mucosal function only apparent with specialised techniques. Acute onset functional dyspepsia accounts for around 1/5 of functional dyspepsia and is characterised by early satiety, nausea, vomiting and weight loss. Impaired postcibal fundal accommodation may underlie some of these symptoms. Post infectious gastroparesis is much rarer and is associated with markedly delayed gastric emptying and antral hypomotility. Approximately 1/10 of IBS cases describe a post infectious onset. Post infectious IBS is typically of the diarrhoea-predominant type. Post inflammatory functional diseases tend to be associated with less psychological abnormalities and have a better prognosis than other functional diseases. There are isolated anecdotal reports of symptom response to anti-inflammatory treatments but larger controlled trials are needed.PMID: 15324705 "Gastroenterology. 2003 Dec;125(6):1651-9. Related Articles, Links Relative importance of enterochromaffin cell hyperplasia, anxiety, and depression in postinfectious IBS.Dunlop SP, Jenkins D, Neal KR, Spiller RC.Wolfson Digestive Diseases Centre, University Hospital, Nottingham, England.BACKGROUND & AIMS: Both psychological and mucosal changes (increased enterochromaffin EC cells and T lymphocytes) have been associated with postinfectious irritable bowel syndrome (PI-IBS). However, previous studies have been underpowered to determine the relative importance of these changes in predicting the development of PI-IBS. Our aim was to prospectively determine the relative importance of both psychological and histologic factors in the development of PI-IBS after Campylobacter infection. METHODS: Questionnaires detailing psychological and bowel symptoms were sent to 1977 patients 3 months after infection. Twenty-eight patients with new-onset PI-IBS, 28 age- and sex-matched patient controls who were asymptomatic after infection, and 34 healthy volunteers underwent rectal biopsy, which was assessed for serotonin-containing EC cells, mast cells, and lamina propria T lymphocytes. RESULTS: PI-IBS, predominantly of the diarrhea-predominant subtype, occurred in 103 of 747 (13.8%) of those infected. EC cell counts per high-power field (hpf) were higher in patients with PI-IBS (35.8 +/- 1.2) compared with patient controls (30.6 +/- 1.9; P = 0.022) and volunteers (29.1 +/- 1.8; P = 0.006). Lamina propria T lymphocytes per hpf were higher in patients with PI-IBS (127.1 +/- 8.7) and patient controls (113.4 +/- 6.2) in contrast to healthy volunteers (97.1 +/- 5.7) (P = 0.006 and P = 0.058, respectively). Anxiety, depression, and fatigue were significantly increased in patients with PI-IBS compared with patient controls. Multivariate analysis indicated that increased EC cell counts and depression were equally important predictors of developing PI-IBS (relative risk, 3.8 and 3.2 for each standard deviation increase in respective values). CONCLUSIONS: Both increased EC cells and depression are important independent predictors of developing PI-IBS. PMID: 14724817EC cells store the majority of serotonin in the gut. Serotonin is majorally implicated in IBS!!!!"Am J Gastroenterol. 2003 Jul;98(7):1578-83. Related Articles, Links Distinctive clinical, psychological, and histological features of postinfective irritable bowel syndrome.Dunlop SP, Jenkins D, Spiller RC.Division of Divisions of Gastroenterology, University Hospital, Nottingham, United Kingdom.OBJECTIVE: Irritable bowel syndrome after gastroenteritis is well recognized. Our aim was to determine whether postinfective IBS (PI-IBS) has histological or clinical features that are distinct from those of IBS patients with no history of preceding infection. METHODS: A total of 75 consecutive IBS outpatients and 36 healthy control subjects completed a questionnaire detailing symptoms, mode of onset, and previous psychiatric history. All underwent a full diagnostic workup including rectal biopsy, which included immunostaining and quantification for lamina propria or intraepithelial T lymphocytes, serotonin-containing enterochromaffin (EC), and mast cells. Patients were divided according to onset of symptoms into PI-IBS (n = 23) or non-PI-IBS (n = 52) patients. RESULTS: Diarrhea predominance occurred more frequently in PI-IBS (70%) than in non-PI-IBS (42%) patients (p = 0.03). A history of previous treatment for anxiety or depression was present in 26% of PI-IBS patients compared to 54% of non-PI-IBS (p = 0.02). Biopsy results for all patients were normal using conventional criteria; however, quantification revealed that PI-IBS showed increased EC cells compared to those of non-PI-IBS patients (p = 0.017) and controls (p = 0.02). Lamina propria T lymphocytes were increased in PI-IBS (p = 0.026) and non-PI-IBS (p = 0.011) patients compared to controls. Mast cells were increased in non-PI-IBS patients (p = 0.054) compared to controls. CONCLUSIONS: Individuals with PI-IBS are a clinically distinct subgroup characterized by diarrheal symptoms, less psychiatric illness, and increased serotonin-containing EC cells compared to those with non-PI-IBS.PMID: 12873581 ""Curr Treat Options Gastroenterol. 2003 Aug;6(4):329-337. Related Articles, Links Treatment of Irritable Bowel Syndrome.Spiller RC.Department of Gastroenterology, University Hospital, Derby Road, Nottingham NG7 2UH, UK. robin.spiller###nottingham.ac.ukIrritable bowel syndrome (IBS) is an extremely common cause of consultation, and at present is diagnosed on the basis of symptoms and a few simple exclusion tests. Exclusion diets can be successful, but many patients have already attempted and failed such treatments before consulting. Anxiety and somatization may be an important driver of consultation. Patients' concerns should be understood and addressed. Those with prominent psychiatric disease may benefit from psychotherapy. Hypnotherapy benefits symptoms in those without psychologic disturbance, but its availability is limited. Antidepressants are effective in improving both mood and IBS symptoms globally, and the evidence is particularly good for tricyclic antidepressants. Although antispasmodics are currently the most commonly prescribed drugs, most responses (75%) are due to the placebo effect and not specific to the drug. Bulk laxatives such as ispaghula can increase stool frequency and help pain, but bloating may be aggravated. Loperamide is effective treatment for urgency and loose stools, but less effective for bloating and pain. 5-HT(3) antagonists such as alosetron improve urgency, stool consistency, and pain in diarrhea-predominant-IBS. The 5-HT(4) agonist tegaserod shows modest benefit in constipation-predominant IBS, improving stool frequency, consistency, and bloating as well as global improvement. There are many new drugs, such as cholecystokinin, neurokinin, and corticotropin receptor antagonists, in development."Gastroenterology. 2003 May;124(6):1662-71. Related Articles, Links Postinfectious irritable bowel syndrome.Spiller RC.Division of Gastroenterology, University Hospital, Nottingham, United Kingdom. robin.spiller###noittingham.ac.ukA small but significant subgroup of patients with irritable bowel syndrome (IBS) report a sudden onset of their IBS symptoms after a bout of gastroenteritis. Population-based surveys show that although a history of neurotic and psychologic disorders, pain-related diseases, and gastroenteritis are all risk factors for developing IBS, gastroenteritis is the most potent. More toxigenic organisms increase the risk 11-fold, as does an initial illness lasting more than 3 weeks. Hypochondriasis and adverse life events double the risk for postinfective (PI)-IBS and may account for the increased proportion of women who develop this syndrome. PI-IBS is associated with modest increases in mucosal T lymphocytes and serotonin-containing enteroendocrine cells. Animal models and some preliminary human data suggest this leads to excessive serotonin release from the mucosa. Both the histologic changes and symptoms in humans may last for many years with only 40% recovering over a 6-year follow-up. Celiac disease, microscopic colitis, lactose intolerance, early stage Crohn's disease, and bile salt malabsorption should be excluded, as should colon cancer in those over the age of 45 years or in those with a positive family history. Treatment with Loperamide, low-fiber diets, and bile salt- binding therapy may help some patients. Serotonin antagonists are logical treatments but have yet to be evaluated.Publication Types: Review Review, Tutorial PMID: 12761724and this was a comment from him when other doctors suggested"Full-thickness biopsy of the jejunum reveals inflammation and enteric neuropathy in irritable bowel syndrome."he respondedEditorialsNeuropathology of IBS?Robin C. Spiller [MEDLINE LOOKUP] http://www2.us.elsevierhealth.com/scripts/...004857&nav=full and some of this information is from 2002 and they know more about it all since then and a lot of them all share resources and studies and peer reviews.hence theFrom - Report on the 5th International Symposium on Functional Gastrointestinal DisordersApril 4, 2003 to April 7, 2003 Milwaukee, Wisconsin By: Douglas A. Drossman, M.D ., UNC Center for Functional GI and Motility Disorders at Chapel Hill, and William F. Norton, IFFGDBasic Principles -- Brain-Gut Moderators: Emeran Mayer MD; Robin Spiller MD. Panel: Robin Spiller MD; Jackie Wood PhD; George Chrousos MD; Yvette Tach� PhD; Lisa Goehler PhD; G.F. Gebhart PhD; Emeran Mayer MD. Click on Titles to View Other TopicsIntroductionOutcomes of Pediatric Functional GI Disorders Epidemiology/Genetic/Behavioral Factors Brain Imaging Emerging Techniques to Evaluate and Treat Functional GI and Motility Disorders Clinical Applications of Diagnosis and Treatment Functional GI DisordersGeneral Principles of TreatmentPharmacological Treatment Psychological Treatment IFFGD Research AwardsThe brain-gut axis refers to the continuous back and forth interactions of information and feedback that take place between the gastrointestinal tract, and the brain and spinal cord (which together comprise the central nervous system). These interrelated feedback circuits can influence brain processes and bowel functions -- affecting pain perception, thoughts and one's appraisal of symptoms, gut sensitivity, secretions, inflammatory responses, and motility. The brain-gut circuits can be activated by an external or internal factor or stimulus that makes a demand on the system, such as a stressful event, an injury, an emotional thought or feeling, or even the ingestion of food. Symptoms of functional GI disorders may result from a maladaptive response to stimuli at some point within the complex interactions that take place along the brain-gut axis. Basic science is the fundamental approach to understanding how systems work. Basic research takes place in the laboratory and often involves the study of molecules and cells. From this body of knowledge is drawn the means to investigate practical applications and to formulate clinical practices. Translational science converts basic science discoveries into the practical applications that benefit people. One of the more exciting areas of recent research relates to the basic and translational aspects of the effects of stress on inflammation, cytokine and immune modulation, and pain. (Cytokines are a type of protein released by cells of the immune system, which act through specific cell receptors to regulate immune responses.) This series of presentations address three important research areas in the field of functional GI disorders, which have recently attracted considerable attention: the role of immune activation in the gut and the interactions of the gut immune and nervous systems; the role of the central nervous system in the regulation (modulation) of pain perception (nociception); and the emerging field of animal models with relevance for functional GI disorder research. This section demonstrates the rapid progress seen in the last few years in better understanding of basic mechanisms, in particular the neuroimmune interactions underlying symptom generation in patients with "functional" GI disorders. There are immune responses to infections. To defend itself from a foreign substance or invader, such as a bacterium or virus, the body mounts an immune response controlled by the brain. There needs to be a balance between infection and the body's immune response; the immune system needs to turn on and turn off at the right times to destroy the invader but not to the degree that it may harm healthy tissue. Robin Spiller, University Hospital, Nottingham, England began the session by noting the difficulty in separating disorders of structure ("organic") from disorders of function. He noted, "The difference is based on how high the power of your microscope is." This was elaborated upon in his presentation on Post-infectious Functional GI Disorders. It has been observed that IBS-like symptoms, that persist for 6 months to a year or longer, may appear after a bout with an acute infection in the gastrointestinal tract (e.g., food-poisoning). This is termed, "post-infectious IBS." A study by Gwee et al showed that the presence of unusual or amplified life stress at the time of onset of infection increased the chances of developing IBS symptoms. Inflammation persisted in patients with IBS-like symptoms but did not in patients whose symptoms resolved. This suggests that the brain's management of certain stressful stimuli (i.e., psychologic distress) affects the brain-gut system's ability to inhibit inflammation. It has frequently been observed that some individuals with more severe symptoms of IBS have coexisting psychologic distress. Stress has been thought to influence health-care seeking behavior, either by increasing motility, visceral hypersensitivity or inflammation, or by enhancing one's perception of gut symptoms, all of which lead to a greater need to seek care for them. The concept of post-infectious IBS suggests that in some circumstances stress (the biological process by which the body adapts in response to a stimuli) may influence symptoms. Persistence of the underlying inflammatory response may lead to post-infectious disorders of function. A variety of neuroimmune responses can lead to intestinal over-responsiveness (sensitization) and other clinical effects. These responses include direct toxicity to nerves that influence intestinal contractions, alteration in gut immune activation, abnormalities of serotonin metabolism, and persisting low-grade inflammation. IBS developing after infective gastroenteritis is associated with subtle increases in enteroendocrine and chronic inflammatory cells in the gut mucosa. The net effect may be to increase serotonin availability in the gut and enhance secretion and propulsive motility patterns. Serotonin antagonists may be beneficial in such patients Notably, the concept of "post-infectious IBS" has grown to include studies of their application in post-infectious gastroparesis and dyspepsia. 1Major inflammatory responses have not been observed in most IBS patients. However, in some studies subtle changes associated with inflammation have been noticed, such as increased presence of mast cells (a type of immune system cell present in blood and tissue). Jackie Wood, Ohio State University College of Medicine discussed the Effects of Inflammation on the Gut Enteric Nervous System, specifically noting the importance of mast cell degranulation (the release from within the cell of granules, or small sacs, containing chemicals that can digest microorganisms and fight infection). In tissue mast cells accumulate around nerve endings of nerves that contain the neurotransmitter serotonin. The release of substances that can induce activity in excitable tissue (i.e., histamine, Interleukin-1 (IL-1), and bradykinin) by mast cells can affect receptor and neurotransmitter function in the enteric nervous system - the part of the autonomic nervous system that controls function of the gastrointestinal tract. In other words, when mast cells in the intestinal lining empty their contents in response to an infection, they activate nearby nerve endings. In a subgroup of patients, this can have significance in terms of resulting clinical consequences of diarrhea and abdominal discomfort. 2----------------------------------------------side notehistimine is released in the gut by stress and effects mast cellsalso"Jack Wood, PhDProfessor of Physiology and Internal MedicineChairman Emeritus, Department of PhysiologyThe Ohio State University College of Medicine Dr. Wood was the first to use microelectrodes to record the electrical and synaptic behavior of neurons in the enteric nervous system. He coined the term "brain-in-the-gut" in view of emerging evidence that the enteric nervous system had neurophysiological properties like the brain and spinal cord. In recent years he has focused on signaling interactions between the enteric immune system and the brain-in-the-gut during infectious enteritis and food allergy. In this lecture he shows how the central nervous system, enteric nervous system and intestinal immune system are integrated during physical and emotional stress to produce irritable bowel symptoms of diarrhea and abdominal pain and discomfort. " http://www.conference-cast.com/ibs/Lecture...dRegLecture.cfm -------------------------------------------------Yvette Tach�, University of California Los Angeles discussed Stress and Inflammation. The experience of stress is an adaptive behavior common to all living organisms. The activation of corticotropin releasing factor (CRF) signaling pathway, is the major mediating mechanism involved with the body's stress response system in which gastric emptying is inhibited (with possible loss of appetite) while colonic motor activity is stimulated (producing a loose stool or a sensation of bowel urgency). There is growing evidence that activation of this CRF pathways impacts on inflammation, autonomic nervous system function, immunity, and clinical behavior or illness, all of which may be linked to the pathophysiology of the functional gastrointestinal disorders. While we often talk about how the brain -- influenced for example by arousal and/or psychosocial factors -- can affect immune function, the reverse is also true. Immune activation, following infection for example, can influence brain function. Lisa Goehler, University of Virginia discussed Cytokines and Vagal Afferents: Immune Signaling to the Brain. Cytokines are substances that are produced by white blood cells to regulate certain functions during inflammatory and immune responses. The vagus is a nerve made of both sensory and motor fibers that innervates nearly every internal organ. The gastrointestinal (GI) tract, along with the lungs and liver, is an area of tissue that most commonly comes in contact with microorganisms (pathogens), such as bacteria or viruses, capable of activating an immune response. Cytokine mediators activate neurons that convey messages from tissue to the brain (afferent neurons) through the vagus nerve. The GI tract is richly supplied with vagal afferents that can signal immune activation in the tissue. This process may underlie the mechanism that causes individuals to feel sick. The concept of "sickness symptoms" is not always recognized. The cytokine inflammatory and immune mediators distributed throughout the body (peripheral), which appear to interact through vagal pathways, have systemic effects that manifest as symptoms in the body. (Mediators are substances released from cells to regulate immune responses.) Such symptoms include fever, increased sensitivity to pain, loss of appetite, and decreased desire for social interaction. The process may provide the basis for a role of the vagus as an interface between the site of the immune response and the brain that results in symptoms of altered mood, including anxiety or depression, that are sometimes associated with gastrointestinal disease. 4 Jerry Gebhart, The University of Iowa discussed the CNS Modulation of Visceral Nociceptive Responses. The central nervous system (CNS) is composed of the brain and spinal cord. The brain interprets and influences our perceptions of the pain sensation signals transmitted from the gut (visceral nociceptive responses) to the spinal cord and then to higher centers. Several structures in the brain (periaqueductal gray, dorsolateral pons, and rostroventral medulla) can facilitate or inhibit signals sent to the CNS and influence the perceived discomfort, or even whether the signals are experienced as pain. Inflammation of the bowel can produce increased sensitivity to pain or enhanced intensity of pain sensation (hyperalgesia) via increased activity of certain cells (for example, those that contain nNOS) in these higher brain modulatory centers. 5 To close the Brain-Gut sessions, Emeran Mayer, University of California Los Angeles discussed Evolving Animal Models of Visceral Hypersensitivity. In contrast to most other disorders of the digestive system, functional disorders of the gut continue to be defined by symptom criteria rather than by biological markers. Realistic animal models of functional gastrointestinal (GI) disorders in which to test hypotheses have not been available until recently. While it is unlikely that there will ever be an animal model to replicate all complexities of the human functional GI disorders, animal research is likely to help us understand some of the key underlying mechanisms responsible for symptom generation. This includes over-responsiveness of central stress circuits to visceral and psychological stimuli, resulting in altered autonomic responses (motility, secretion), increased pain sensitivity (visceral hypersensitivity) and possibly altered immune function of the gut. Future studies with genetically altered (i.e., transgenic) mice that become models for studying specific human diseases and their treatments may further increase our understanding of these mechanisms" http://www.iffgd.org/symposium2003brain-gut.html From - Report on the 5th International Symposium onFunctional Gastrointestinal DisordersApril 4, 2003 to April 7, 2003 Milwaukee, Wisconsin By: Douglas A. Drossman, M.D., UNC Center for Functional GI and Motility Disorders at Chapel Hill, and William F. Norton, IFFGDBrain Imaging Moderator: Reza Shaker MD. Panel: Reza Shaker MD; Bruce Naliboff PhD; David Thompson MD. "Central activation -- the rapid short-term biophysical and biochemical changes in neurons that make possible such activities as thought, perception, and voluntary movement -- appears to increase as intensity of stimulus increases. However, repeated exposure can lead to adaptation, as the brain adjusts to the stimuli, with decreased central activation. In studies, IBS patients are differentiated from healthy controls by showing greater activation of an area of the brain essential for conscious pain (the anterior mid-cingulate component of the anterior cingulate cortex). It is in this region in the brain where the systems concerned with emotion or feeling, attention, and working memory interact. On the other hand, controls (and also patients with inflammatory bowel disease who have adapted to the visceral signals) show greater activation of the descending pain inhibitory pathways in areas of the brain involved in the suppression of pain (in the brain stem in the region of the periaqueductal gray). " From - Report on the 5th International Symposium onFunctional Gastrointestinal DisordersApril 4, 2003 to April 7, 2003 Milwaukee, Wisconsin By: Douglas A. Drossman, M.D., UNC Center for Functional GI and Motility Disorders at Chapel Hill, and William F. Norton, IFFGDEpidemiology/Genetic/Behavioral Factors This is very important also to the big picture. http://www.iffgd.org/symposium2003factors.html ""But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it."
 

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Discussion Starter · #18 ·
quote:Flux wrote:How is dysbacteriosis defined? Since most of the flora can't even be identified let alone grown in culture easily, how can ever know what's normal and abnormal in the gut?
Flux, this is your lucky day! I just happen to know the perfect person to help you out with your confusion about dysbacteriosis. Amazingly, his name is also Flux! His email address is at the link below, you can contact him there. I'm sure you two will get along just fine. Here's his story, in his own words:
quote:Flux #2 wrote:I'm about to receive a radical therapy for flatulence: an attempt will be made to completely sterilize my gut with antibiotics (and then re-inoculate it with ultra-mega doses of probiotics). I'm looking to find out what experiences people have had antibiotics and their flatulence levels, either tried for this problem specifically or incidentally for another condition.From what I have read so far here and elsewhere, good results have come from amoxicillin, cephalexin, and metronidazole. One person, however, reported both good and bad results with a combination of amoxicillin and metronidazole. Interestingly, I don't recall anyone reporting just bad effects.I'm also interested in other therapies tried (but I don't mean things like grossly inffective dietary therapies), such as those with probiotics (especially with details about brand and dosages and length of therapy).
Gassy Guy Flux LinkSee Flux, this other Flux knows all about the difference between "good" and "bad" intestinal bacteria, the very things you're confused about. His chosen "therapy" to get rid of the bad and re-establish the good flora is certainly on the radical side, though. But he's obviously had much personal experience with bad bacteria, poor flatulent fellow. I hope you're never stuck in the same room as him! Wheeeeewwwieeee! So anyway Flux, contact Flux and he'll explain the whole thing to ya!
quote: "Now clearly, these IBS experts" Flux wrote:They are?
Of course they are. Your buddy Eric is the one who originally posted this study on this BB. And you do know that Eric only posts accurate medical information from the IBS experts here, don't you? Just ask him, he'll tell ya! Erics Original Post Of Study Sincerely, Captain Colon
 

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Discussion Starter · #19 ·
quote:Flux wrote:How is dysbacteriosis defined? Since most of the flora can't even be identified let alone grown in culture easily, how can ever know what's normal and abnormal in the gut?
Flux, this is your lucky day! I just happen to know the perfect person to help you out with your confusion about dysbacteriosis. Amazingly, his name is also Flux! His email address is at the link below, you can contact him there. I'm sure you two will get along just fine. Here's his story, in his own words:
quote:Flux #2 wrote:I'm about to receive a radical therapy for flatulence: an attempt will be made to completely sterilize my gut with antibiotics (and then re-inoculate it with ultra-mega doses of probiotics). I'm looking to find out what experiences people have had antibiotics and their flatulence levels, either tried for this problem specifically or incidentally for another condition.From what I have read so far here and elsewhere, good results have come from amoxicillin, cephalexin, and metronidazole. One person, however, reported both good and bad results with a combination of amoxicillin and metronidazole. Interestingly, I don't recall anyone reporting just bad effects.I'm also interested in other therapies tried (but I don't mean things like grossly inffective dietary therapies), such as those with probiotics (especially with details about brand and dosages and length of therapy).
Gassy Guy Flux LinkSee Flux, this other Flux knows all about the difference between "good" and "bad" intestinal bacteria, the very things you're confused about. His chosen "therapy" to get rid of the bad and re-establish the good flora is certainly on the radical side, though. But he's obviously had much personal experience with bad bacteria, poor flatulent fellow. I hope you're never stuck in the same room as him! Wheeeeewwwieeee! So anyway Flux, contact Flux and he'll explain the whole thing to ya!
quote: "Now clearly, these IBS experts" Flux wrote:They are?
Of course they are. Your buddy Eric is the one who originally posted this study on this BB. And you do know that Eric only posts accurate medical information from the IBS experts here, don't you? Just ask him, he'll tell ya! Erics Original Post Of Study Sincerely, Captain Colon
 

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quote:Eric wrote:Because you have to be able to read the article carefully for one and not cherry pick what a person wants to hear or believe.becausethe conclusion was"CONCLUSION: There are intestinal flora disorders in IBS patients, which may be involved in triggering the IBS-like symptoms. IBS patients experience significant impairment in QoL, however, the impairment is not caused directly by enteric symptoms."I find it odd this is always left out when this abstarct is posted? Thats bias.
My, my Eric you really are confused, aren't you? There's no bias. The "Conclusion" you quoted above is simply the very basic summary from the study's Abstract. What I quoted is from the "Discussion" section of the complete article, which contains a much more detailed, in-depth and therefore more accurate explanation of the study's findings. There's no disagreement between the two. What I posted is simply more accurate. They say it all when they state:
quote:"Further studies are still needed. However, there was dysbacteriosis in IBS patients. Whether it is the effect or just cause of IBS remains unclear."
That says everything - They are stating that dysbacteriosis may be an effect of the IBS, OR it may actually be the "just cause" of the IBS - they just can't say for sure one way or the other. I don't see anywhere here where it says what you believe though, that dysbacteriosis DOES NOT cause IBS. Please show me where it clearly says that dysbacteriosis does not cause IBS, where they have unequivocally ruled it out - I just don't see it.The quality of life part in your quote above is also just a basic summary from the study's abstract. Here's a more complete discussion from the full article:
quote:In our study, we also found that IBS patients had significantly lower scores on all SF-36 scales with the exception of physical functioning, when compared with the age and sex-matched control group. Decrements in QoL were most pronounced in general health, role physical and vitality. However, there was no significant correlation between QoL and enteric symptoms, which might be due to the frequent presence of anxiety, depression, fatigue and anorexia in IBS patients.
You get the basic idea. But don't despair, Eric, because in the "Inflammation, Infection, and Irritable Bowel Syndrome (IBS): An Update" article which you posted earlier, there was a study described where IBS patients were given a Bifidobacterium probiotic which significantly improved many of their IBS symptoms, and - "The symptomatic response with Bifidobacterium was associated with parallel improvement in quality of life as assessed by using an IBS-specific instrument. A follow-up 4 weeks after discontinuation of the treatment (washout period) showed that both symptoms and quality of life returned to baseline."So, this shows that as the gut flora is improved with probiotics, the quality of life can go up too, probably in an indirect way, I'd think. As the patient feels better with less pain, the quality of life factors naturally improve due to the more positive mental state.ref.("A Role For Probiotics" section):Inflammation, Infection, and Irritable Bowel Syndrome (IBS): An Update
quote:Eric wrote:also what does this mean from the above study"There was no significant difference in gut flora between two subgroups"
I believe that means that the overall numbers of bacteria in the flora were about the same, but the numbers of some of the various specific strains of bacteria were different (different proportions).Now Eric, you have posted vast numbers of pages here from studies in a seeming attempt to try to convince me of something. But that's a complete waste of your time. Let me remind you that this thread isn't about what I believe. It's about what you believe, and why it differs from what the IBS experts concluded in the study you earlier posted. You do believe they are IBS experts, don't you? Of course you do, because you yourself say that you only post accurate medical information from the world's IBS experts here. So did you email them yet to inform them that they are wrong when they say dysbacteriosis MAY be the "just cause" of IBS? Do hurry, I just can't wait to see their reply! Suggestion - Maybe you could email them the studies you posted here to convince them how wrong they are.... Sincerely,Captain Colon
 
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