Irritable Bowel Syndrome and Digestive Health Support Forum banner
1 - 20 of 44 Posts

· Registered
Joined
·
23,788 Posts
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
 

· Registered
Joined
·
23,788 Posts
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
 

· Registered
Joined
·
23,788 Posts
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."
 

· Registered
Joined
·
23,788 Posts
Just because you don't have symptoms, does not mean a person is "cured."also the word is Chronic" "chronic" comes from the Greek word chronos, meaning time). "In order to fully "cure" something you have to know exactly what causes it, they do not yet fully understand the cause of IBS yet, although they are getting way better. In the four years I have been here a ton of research generated insights on IBS and functional disorders have come to light. Some things they have already found out, IBS is a brain gut axis dysfunction with abnormalities and dysregulation of the serotonin system, and immune system. Nor is this a competition of either the brain or the gut, both are operative to cause the symptoms! Symptoms can be generated from either the gut or the brain. It was twenty years you had IBS Kel, if I am not mistaken. Is that chronic?""Living with a long-lasting health condition (also called a chronic illness) presents a person with new challenges. Learning how to meet those challenges is a process - it doesn't happen right away. But understanding more about your condition, and doing your part to manage it, can help you take health challenges in stride. Many people find that taking an active part in the care of a chronic health condition can help them feel stronger and better equipped to deal with lots of life's trials and tribulations. What Are Chronic Illnesses?There are two types of illnesses: acute and chronic. Acute illnesses (like a cold or the flu) are usually over relatively quickly. Chronic illnesses, though, are long-lasting health conditions (the word "chronic" comes from the Greek word chronos, meaning time). Having a chronic condition doesn't necessarily mean an illness is critical or dangerous - although some chronic illnesses, such as cancer and AIDS, can be life threatening. But chronic illnesses can also include conditions like asthma, arthritis, and diabetes. Although the symptoms of a chronic illness might go away with medical care, usually a person still has the underlying condition - even though their treatments mean they may feel completely healthy and well much of the time.Each health condition has its own symptoms, treatment, and course. Aside from the fact that they are all relatively long lasting, chronic illnesses aren't necessarily alike in other ways. Most people who have a chronic illness don't think of themselves as "having a chronic illness," they think of themselves as having a specific condition - such as asthma, or arthritis, or diabetes, or lupus, or sickle cell anemia, or hemophilia, or leukemia, or whatever ongoing health condition they have. If you're living with a chronic illness, you may feel affected not just physically, but also emotionally, socially, and sometimes even financially. The way a person might be affected by a chronic illness depends on the particular illness and how it affects the body, how severe it is, and the kinds of treatments that might be involved. It takes time to adjust to and accept the realities of a long-term illness, but teens who are willing to learn, seek support from others, and participate actively in the care of their bodies usually get through the coping process.The Coping ProcessMost people go through stages in learning to cope with a chronic illness. A person who has just been diagnosed with a particular health condition may feel a lot of things. Some people feel vulnerable, confused, and worried about their health and the future. Others feel sad or disappointed in their bodies. For some, the situation seems unfair, causing them to feel angry at themselves and the people they love. These feelings are the start of the coping process. Everyone's reaction is different, but they're all completely normal. The next stage in the coping process is learning. Most people living with a long-term illness find that knowledge is power - the more they find out about their condition, the more they feel in control and the less frightening it is. The third stage in coping with a chronic illness is all about taking it in stride. At this stage, people feel comfortable with their treatments and with the tools (like inhalers or shots) they need to use to live a normal life. So a person with diabetes, for example, may feel a range of emotions when his or her condition is first diagnosed. The person may believe he or she will never be able to go through the skin prick tests or injections that may be necessary to manage the condition. But after working with doctors and understanding more about the condition, that person will grow to be more practiced at monitoring and managing insulin levels - and it will stop feeling like such a big deal. Over time, managing diabetes will become second nature to that person. The steps involved will seem like just another way to care for one's body, in much the same way as daily teeth brushing or showering help people stay healthy. There's no definite time limit on the coping process - everybody's process of coming to terms with and accepting a chronic illness is different. In fact, most people will find that emotions surface at all stages in the process. Even if treatments go well, it's natural to feel sad or worried from time to time. Recognizing and being aware of these emotions as they surface is all part of the coping process.Tools for Taking ControlPeople living with chronic illnesses often find that the following actions can help them take control and work through the coping process:Acknowledge feelings. Emotions may not be easy to identify. For example, sleeping or crying a lot or grouchiness may be signs of sadness or depression. It's also very common for people with chronic illnesses to feel stress as they balance the realities of dealing with a health condition and coping with schoolwork, social events, and other aspects of everyday life. Many people living with chronic illnesses find that it helps to line up sources of support to deal with the stress and emotions. Some people choose to talk to a therapist or join a support group specifically for people with their condition. It's also important to confide in those you trust, like close friends and family members. The most important factor when seeking help isn't necessarily finding someone who knows a lot about your illness, but finding someone who is willing to listen when you're depressed, angry, frustrated - or even just plain old happy. Noticing the emotions you have, accepting them as a natural part of what you're going through, and expressing or sharing your emotions in a way that feels comfortable can help you feel better about things.Play an active role in your health care. The best way to learn about your condition and put yourself in control is to ask questions. There's usually a lot of information to absorb when visiting a doctor. You may need to go over specifics more than once or ask a doctor or nurse to repeat things to be sure you understand everything. This may sound basic, but lots of people hesitate to say, "Hey, can you say that again?" because they don't want to sound stupid. But it takes doctors years of medical school and practice to learn the information they're passing on to you in one office visit!If you've just been diagnosed with a particular condition, you may want to write down some questions to ask your doctor. For example, some of the things you might want to know are:How will this condition affect me? What kind of treatment is involved? Will it be painful? How many treatments will I get? Will I miss any school? Will I be able to play sports, play a musical instrument, try out for the school play, or participate in other activities I love? What can I expect - will my condition be cured? Will my symptoms go away? What are the side effects of the treatments and how long will they last? Will these treatments make me sleepy, grumpy, or weak? What happens if I miss a treatment or forget to take my medicine? What if the treatments don't work?Even though your doctor can't exactly predict how you'll respond to treatment because it varies greatly from one person to the next, knowing how some people react may help you prepare yourself mentally, emotionally, and physically. The more you learn about your illness, the more you'll understand about your treatments, your emotions, and the best ways to create a healthy lifestyle based on your individual needs.Understand other people's reactions. You may not be the only one who feels emotional about your illness. Parents often struggle with seeing their children sick because they want to prevent anything bad from happening to their children. Some parents feel guilty or think they've failed their child, others may get mad about how unfair it seems. Everyone else's emotions can seem like an extra burden on people who are sick, when of course it's not their fault. Sometimes it helps to explain to a parent that, when you express anger or fear, you're simply asking for their support - not for them to cure you. Tell your parents you don't expect them to have all the answers, but that it helps if they just listen to how you feel and let you know they understand.Because the teen years are all about fitting in, it can be hard to feel different around friends and classmates. Many people with chronic illnesses are tempted to try to keep their condition secret. Sometimes, though, trying to hide a condition can cause its own troubles as Melissa, who has Crohn's disease, discovered. Some of Melissa's medications made her look puffy, and her classmates started teasing her about gaining weight. When Melissa explained her condition, she was surprised at how accepting her classmates were. When talking to friends about your health condition, it can sometimes help to explain that everyone is made differently. For the same reason some people have blue eyes and others brown, some of us are more vulnerable to certain conditions than others. Depending on the severity of your illness, you may find yourself constantly surrounded by well-meaning adults. Teachers, coaches, and school counselors may all try to help you - perhaps causing you to feel dependent, frustrated, or angry. Talk to these people and explain how you feel. Educating and explaining the facts of your condition can help them understand what you're capable of and allow them to see you as a student or an athlete - not a patient.Keep things in perspective. It's easy for a health condition to become the main focus of a person's life - especially when they first learn about and start dealing with the condition. Many people find that reminding themselves that their condition is only a part of who they are can help put things back in perspective. Keeping up with friends, favorite activities, and everyday things helps a lot. Living With a Health Condition There's no doubt the teen years can be a more challenging time to deal with a health condition. In addition to the social pressures to fit in, it's a time of learning about and understanding our bodies. At a time when it's natural to be concerned with body image, it can seem hard to feel different. It's understandable that people can feel just plain sick and tired of dealing with a chronic illness once in a while.Even teens who have lived with an illness since childhood can feel the pull of wanting to lead a "normal" life in which they don't need medicine, have any limitations, or have to care for themselves in any special way. This is a perfectly natural reaction. Sometimes teens who have learned to manage their illness feel so healthy and strong that they wonder whether they need to keep following their disease management program. A person with diabetes, for example, may wonder if he or she can skip a meal when at the mall or check his or her blood sugar after the game instead of before. Unfortunately, easing up on taking care of yourself can have disastrous results. The best approach is to tell your doctor how you feel. Talk to him or her about what you'd like to be doing and can't - see if there's anything you can work out. This is all part of taking more control and becoming a player in your own medical care. When you're living with a chronic health condition, it can feel hard at times to love your body. But you don't have to have a perfect body to have a great body image. Body image can improve when you care for your body, appreciate its capabilities, and accept its limitations - a fact that's true for everyone, whether they're living with a chronic condition or not. Voicing any frustration or sadness to an understanding ear can help when a person feels sick of being sick. At times like this it's important to think of ways others could help and ask for what you'd like. Some people find they can ease their own sense of loss by reaching out and offering to help someone in need. Lending a hand to someone else can help one's own troubles seem easier to manage.Adjusting to living with a chronic illness takes a little time, patience, support - and willingness to learn and participate. People who deal with unexpected challenges often find an inner resilience they might not have known was there before. Many say that they learn more about themselves through dealing with these challenges and feel they grow to be stronger and more self-aware than they would if they'd never faced their particular challenge. People living with chronic illnesses find that when they take an active role in taking care of their body, they grow to understand and appreciate their strengths - and adapt to their weaknesses - as never before. Reviewed by: D'Arcy Lyness, PhDDate reviewed: January 2004"Next this has been replicated in more studies now."In one interesting experiment, balloon distension of the small intestine in IBS patients caused pain. However, if the patients were mentally distracted during the balloon distension, they did not feel pain. This illustrates a typical brain-gut relationship." Perceptions of colonic activity Patients with IBS may perceive colonic sensations in a way that is different. For example, they may have a feeling of incomplete evacuation even though the rectum is empty. They also may feel that they are distended with gas though there is no sign of increased gas when it is measured. A number of studies have shown that IBS patients have a limited tolerance to distension of a balloon inserted into the rectum. They feel pain at a lower degree of distension of the balloon and also feel greater pain at the same degree of distension as normals. This may relate to a heightened sensitivity of the nerves that go from the colon to the spinal cord, known as visceral hypersensitivity. In one interesting experiment, balloon distension of the small intestine in IBS patients caused pain. However, if the patients were mentally distracted during the balloon distension, they did not feel pain. This illustrates a typical brain-gut relationship. Example In addition to pain sensation, motility of the colon has been measured. IBS patients have an abnormal muscular response to a number of stimuli including stress and eating a fatty meal. This is important in terms of diarrhea and constipation patterns in IBS. Brain scanning in IBS One study used a functional scanning technique called Positron Emission Tomography (PET scan) comparing IBS patients to controls. Using this method, it is possible to map certain areas of the brain that respond to specific stimuli elsewhere in the body. When this technique was applied to IBS patients during balloon distension in the rectum, the pre-frontal cortex was activated. This area of the brain is part of the limbic system, involved in emotional feelings. In contrast, a different area of the brain, possibly more involved in pain control, was activated in controls. Even more interesting was the observation that anticipation of rectal stimulation in IBS also activated the pre-frontal cortex. The last finding indicates a direct connection between emotional stimuli and colonic function. http://www.mindbodydigestive.com/ Nor is that the message from researchers that IBS is untreatable, in fact their message is it is treatable for the majority of IBSers.There is also a big overlap of functional dyspepsia and IBS and FD patients show altered motility and viceral hypersensitvity of the esophagus. Do these patients have gut flora dysbiosis of the esophagus?Is non cardiac chest pain from altered gut flora?There is also a big overlap of FM and CFIS, which in part has to do with autonomic dysfunction and the HPA axis.It is also known now that both parasites and bacteria may lead to PI IBS and very possibly a virus. Food poisoning can lead to PI IBS.I also believe probiotics can have a role in managing some peoples IBS. I have not however seen they have "Cured" anyone yet in control trials, I have seen inconsitent results and the experts saying they need to study them more and find out what each specific strain does. I have also seen a lot of people get better without taking them with IBS.Why do IBSers have specific impairment of certain brain centers that are different then controls and different then people with Inflammatory bowel Disease, who certainly have active overt inflammation in the colon?Also how do we know gut flora issues in IBSers are not from medications, stress, fiber, or envirnmental factors? Maybe its even a comborbid problem or a result of altered transit and motility, that result in food residue trapped in the colon which can alter gut flora?Also how does gut flora signal information to the brain? Nor does intestinal permeability of any pathogens show up in any positive blood samples? It also does not seem to be causing overt inflammation in IBS or alarm symtoms, nor is it out of control like in C Dif, where the symptoms then would rule out IBS. They also know that anxiety is a major factor in generating symptoms and their severity.Anxiety increases IBS severity Anxiety-related hyperactivity of the brain may increase the severity and duration of irritable bowel syndrome, say researchers. Given that IBS severity is highly influenced by psychiatric comorbidity, they suggest that phobic anxiety in IBS patients may influence processing in the frontal brain and visceral sensitivity. Svein Blomhoff, from the National Hospital, Oslo, Norway, and colleagues recruited 11 female patients with IBS and comorbid phobic anxiety and compared them with 22 age-matched female patients with IBS but no comorbidity. The patients' event-related potentials (ERPs) were recorded, along with their reaction to hearing words with emotional significance, barostat-assessed visceral sensitivity thresholds, and symptom thresholds. Patients with comorbid phobic anxiety had a significantly increased first negative (N1) ERP wave to all stimuli, compared with the noncomorbid group, the researchers report. This, they say, indicates an increased use of brain attentional resources. The comorbid group also had an increased visceral threshold for the sensation of gas, and a reduced gas-stool and gas-discomfort tolerance. Examining the data closely, the researchers found that enhanced N1 amplitude and reduced gas-stool tolerance were significantly correlated with subjective gas complaints, which accounted for 47% of the variation in symptoms. The researchers conclude: 'The study suggests an association between information processing in the frontal brain and visceral sensitivity characteristics in IBS patients, and indicates that subjective disease-related symptomatology is predicted by brain perceptual characteristics. 'The findings indicate that an interaction between IBS-related and anxiety-related hyperreactivity in the frontal brain may constitute a psychophysiological mechanism for the contribution of psychiatric comorbidity to severity and duration of the irritable bowel syndrome.' The study is published in Psychosomatic Medicine.Psychosom Med 2001; 63: 959�965 http://www.psychiatrymatters.md/internatio...381678328819444 This isn't because its all in the head either, it is due to very real processes of psychoneuroimmunology.Psychophysiological processes can also alter gut flora?Nor is anyone's gut flora the same as anyone elses.
 

· Registered
Joined
·
23,788 Posts
Let me ask something else, in the world of IBS treatments are there any treatments through numerous clinical and hopefully controlled studies shown to be more effective then probiotics in indivdual symptoms and global symptom relief?
 

· Registered
Joined
·
23,788 Posts
This is old now, because they have done a ton more research on PI IBS and in IBS in general, however, No single bacteric or virus or parasite has been shown to directly cause IBS. In Fact with newer research, it has been found that a bacterial enteritis or parasite can lead to the clinical full blown expression of IBS, After the resolution of the infection. And newer research has implicated viruses as well, but the studies are not conclusive yet. There has also been a ton of research that stress at the time of infection is the highest predictor of who gets IBS after an enteric infection. Which is why some people fully recover from the intial infection and some later go on to PI IBS and still later to IBS.Some however, maybe predisposed to it from birth as a congential birth defect perhaps and there are studying that also.Some others may even get it from surgeries or from shock to the digestive system, they are studying that also."Bacteria and IBSMany have wondered if IBS is caused by an infection. To date, no virus, bacteria, or parasite has been found to directly cause IBS. It has, however, been hypothesized that these microbes may indirectly cause IBS or at least exacerbate its symptoms. Some researchers question whether IBS begins with a common bacterial gastroenteritis. Gastroenteritis is an inflammation of the lining of the stomach and intestinal tract often caused by a bacterial infection. Symptoms may include vomiting, abdominal pain, and diarrhea. Other investigators question whether the number or type of bacteria that normally live in the colon affects symptoms.Some individuals with IBS recall that their symptoms began with a gastroenteritis. The first theory of a "post-infection diarrhea" as a possible link has been explored in greater depth this past year. A post-infection diarrhea is a common, temporary phenomenon resulting from the destruction of intestinal digestive enzymes during an infection. Even after the infection has cleared, certain foods will cause the persistence of loose stools for several weeks until the intestine rebuilds its digestive enzymes.One recent Canadian study looked at the occurrence of IBS in people who travel overseas and acquire a "traveler's diarrhea." These investigators found that 10% of travelers who acquired an infectious gastroenteritis subsequently developed IBS. Those who did develop a traveler's diarrhea, compared to those who did not, had an approximate 6-fold increased risk of developing IBS.Another study from England found that 23% of their patients hospitalized for an infectious gastroenteritis went on to develop IBS. Regardless of whether these individuals developed IBS, they all had increased rectal sensitivity and increased colon movements several weeks after their infection had cleared. However, the researchers also found that the individuals who developed IBS reported more life events suggesting that that there may have been a psychological component to their symptoms in addition to the infectious component.Can bacteria cause IBS without a preceding infection? There are trillions of bacteria that normally reside in the gastrointestinal tract where they help digest nutrients. [Fermentation and intestinal gas are a byproduct of this digestive process.] Some investigators have questioned whether the number or type of bacteria normally present is different in individuals with IBS. A group of German investigators found that the tissue taken from the colons in people with IBS had higher bacterial concentrations than the tissue from individuals without IBS. The researchers believe that this finding suggests that the colons of some people with IBS are colonized by a greater number of bacteria than those without IBS. This may alter how nutrients are fermented in the colons of IBS patients.A group of British investigators also believe that colonic fermentation (gas production) is different in some people with IBS. They confirmed this in one study, which may explain why some individuals respond to dietary restriction and why some do not. The investigators went on to measure gas production in IBS patients before and after antibiotic treatment. The antibiotics appeared to reduce the total volume and rate of hydrogen gas production in the people studied. The investigators felt that this second study provided additional evidence of the role of colonic fermentation in IBS symptoms and supported the use of dietary modification or antibiotics to reduce gas production and improve symptoms in people with IBS.These findings are promising. It is too early however, to say conclusively that bacteria and antibiotics have a role in the development of IBS symptoms and in effective treatment.""Where is the Problem in IBS?The definition of IBS suggests that all routine investigations such as blood tests, endoscopy, and radiological imaging should be normal. The condition is diagnosed on the basis of symptoms, elicited through history and physical examination, in the absence of obvious gut abnormality. So what is the problem?Much work has been done to explain the underlying pathology (disease characteristics or cause) in IBS in the hope that treatment could be directly targeted to an abnormality. This approach could be hugely beneficial compared to available treatments that work symptomatically. In IBS, we know the problem is not only in the gut but is also in the brain-gut axis and the autonomic nervous system. Is the problem in the gut? Increased perception of sensations in the gut, or visceral hypersensitivity, has consistently been observed in IBS. Mertz and colleagues from California checked the discomfort threshold in IBS patients and in a control group. In response to balloon distention of the rectum, almost all (94%) of IBS patients showed lowered pain thresholds. The investigators proposed that increased rectal perception could be used as a reliable biological marker for IBS.Is the problem in the brain?Silverman and colleagues from UCLA used a special brain imaging technique, positron emission tomography (PET), to measure the changes in the pattern of blood flow in the brains IBS patients and a control group in response to balloon distention of the rectum. They found that different areas of the brain were activated in IBS patients when rectal stimuli were delivered. This suggests that the brains of people with IBS process signals from the gut differently.Is the problem in the general autonomic nervous system?Monga and colleagues from London checked bladder and esophageal perception and pain thresholds and found that women with IBS have both lower bladder and esophageal sensory thresholds. They suggested that IBS is part of a generalized disorder of smooth muscles. These women also had "irritable bladders." Francis and colleagues from Manchester, UK found that a higher proportion of patients who are seen in the urology clinic have IBS compared to patients seen in other clinics (dermatology; and ear, nose, and throat). There seems to be increasing evidence that the pathology in IBS is not limited to the gut, brain, or autonomic nervous system only. Rather there may be an involvement of all three systems. Therefore, any potential new therapy should be aiming at this widespread pathology." http://www.aboutibs.org/Publications/resea...ml#anchor143049
 

· Registered
Joined
·
23,788 Posts
Why is it also that a pain attack can come on so fast and sometimes last a 1/2 hour or sometimes last a couple hours or even the whole day or even a couple days, but the pain can also go away as quickly as it came on?Also why is it sometimes described as a charlie horse in the gut?Why is it when some people go an lay down and calm the body and mind the pain can go away?Again why do more women then men have it?Why is it there is mild moderate and svere IBS?Why is it that it can wax and wane for years?Why is it that for some, certain times of the year are when its at its worse? For some it maybe winter and for others it maybe summer or anytime of the year?Why is it for some they can get pain with out a d or c or alternating attack to go with the pain?Why is it that some people have functional d with no pain?or functional c with no pain?Or chronic abnominal pain syndrome with no c or d or c/d?
 

· Registered
Joined
·
23,788 Posts
"What I have interpreted on this board is Eric is saying There is NO cure because there is No Cause found."Basically correct.Funny the use of the words eradicate/kill? It may not be anything needs to be killed or even eradicated, but changed perhaps. Doctors do not use the word "Cure" in IBS for very good reasons. Just like they don't say they can cure migranes or other well know chronic health conditions.When a doctor or someone says they can "cure" IBS, before they have "cured" anyone also may lead to false hope and more anxiety and in IBS that is a major problem, since its very connected to stressors. Not to mention its unethical to say you can cure something you don't know the cause of. Caring doctors may say they can help the symptoms and may say that effective treatment is available and remission might be attainable. But not "cure."They use the word remission for very good reasons.The exact cause of IBS has not been determined yet. Although, they have found many abnormailites in IBS patients, there is still no one specific biological marker in ALL IBS patients yet. IF that is dysbiosis, impairment in brain regions, alter molecular serotonin genes, alter cellular changes in the gi tract or ones not yet discovered. That however does not mean leave out all they have discovered. Honestly some people here are very bias to the cause of IBS to the point of tunnel vision and focus mainly on one idea. Somewhat akin perhaps to foods causing migranes.They may believe the only cause is a bacteria or pathogen, and think mainly in disease STATES but in fact it may or may not be, the evidence so far has implicated a lot and anyone who seriously studies IBS, knows serotonin seems to be majorally implicated and that IBS is already a brain gut axis disorder. Just like they have not been able to "cure" migranes or diabeties or other chronic health problems. You can't "cure" something you do not fully understand the cause of and because the brain gut axis is very complex, there is still a lot of research that needs to be done to figure it all out. There are many issues still needed to be addressed in IBS from cells to neurotransmitters to pathogens and even others.But, suppose for a second that this is true and all IBSers have molecular defects of the SERT gene. The majority of IBSers presenting to gastro clinics effectively demonstarte serotonin dysregulation.Molecular Defect Found for the First Time in IBS Patients http://www.ibsgroup.org/ubb/ultimatebb.php...c;f=10;t=000940 also"The diffuse connections of serotonin allow it to affect many basic psychological functions such as anxiety mechanisms and the regulation of mood, thoughts, aggression, appetite, sex drive and the sleep/wake cycle. Multiple observations suggest that serotonin, one of the most abundant neurotransmitters, plays an important role in the regulation of mood and a key role in the treatment of depression. "Do some of the above look fimilar in non IBS issues, some IBSers have altered REM sleep, others have appetite problems, anxiety problems, depression problems, brain fog, and others.But its a MAJORALLY important neurotransmitter in gut function. The majority of it is stored in the gut, especially in EC cells. EC cells are increase in PI IBS subjects, along with Mast cells, that also release it. In IBS in geneal however it has been majorally implicated. Some people here ignore it or blame it on drug company research. But in fact its peer reviewed research and has to be replicated and observed.How does one go about "curing" molecular defects of cells in the gut that control digestion?Also it is well know in PI IBS patients they have cellular changes in the gi tract with an increase of EC(serotonin) containing cells and mast cells. How does one fix that? Do you use a laser and an electron microscope and surgery to eliminate them? Or maybe there are two little of them, do you then implant them? Maybe in the future that maybe an issue.First however they need to figure it all out.New pathophysiological mechanisms are found and it would not surpprize me at all that even more will be in the future and they are under investigation and each one has to be studied throughly as to cause and effect."Aliment Pharmacol Ther. 2004 Jul;20 Suppl 2:1-9. Related Articles, Links New pathophysiological mechanisms in irritable bowel syndrome.Barbara G, De Giorgio R, Stanghellini V, Cremon C, Salvioli B, Corinaldesi R.Department of Internal Medicine and Gastroenterology, University of Bologna, Italy.Summary Irritable bowel syndrome (IBS) is a functional, multifactorial disease characterized by abdominal pain and erratic bowel habit. Changes in gastrointestinal motor function, enhanced perception of stimuli arising from the gut wall and psychosocial factors are thought to be major contributors for symptom generation. In recent years, several additional factors have been identified and postulated to interact with these classical mechanisms. Reduced ability to expel intestinal gas with consequent gas trapping and bowel distension may contribute to abdominal discomfort/pain and bloating. Abnormal activation of certain brain regions following painful stimulation of the rectum suggests altered processing of afferent signals. An acute gastrointestinal infection is now a recognized aetiological factor for symptom development in a subset of IBS patients (i.e. post-infectious IBS), who are probably unable to down-regulate the initial inflammatory stimulus efficiently. Furthermore, low-grade inflammatory infiltration and activation of mast cells in proximity to nerves in the colonic mucosa may also participate in the frequency and severity of perceived abdominal pain in post-infectious and non-specific IBS. Initial evidence suggests the existence of changes in gut microflora, serotonin metabolism and a genetic contribution in IBS pathophysiology. These novel mechanisms may aid a better understanding of the complex pathophysiology of IBS and to develop new therapies.PMID: 15335408IBS: Improving Diagnosis, Serotonin Signaling, and Implications for Treatment"Over the past 50 years, evolving conceptual mechanisms have been proposed to explain the pathophysiology of IBS. These mechanisms have ranged from a purely psychological disorder to such physiologic conditions as a primary abnormality in gastrointestinal (GI) motility or visceral hypersensitivity. However, recent scientific data have increasingly supported that a dysregulation in brain-gut interactions resulting in alterations in GI motility, secretion, and sensation is the principal pathophysiologic mechanism underlying IBS.1 Brain-gut interactions are mediated largely by the autonomic nervous system, which is comprised of the parasympathetic (vagal and sacral parasympathetic), sympathetic, and enteric nervous systems (ENS). Many factors (both central and peripheral) may contribute to an altered brain-gut axis, including genetic predisposition, chronic stress, inflammation/infection, and environmental parameters.1 These alterations may subsequently lead to disturbances in intestinal motility, visceral sensitivity, and mucosal immune response and permeability. In IBS, these disturbances result in symptoms of abdominal pain or discomfort and altered bowel function, the defining characteristics of this disorder.2 http://216.109.117.135/search/cache?p=+ser...&icp=1&.intl=us However, based on what they know now, IBS is treatable for the majority of IBSers. Some methods like CBT and HT for example, maybe hard for the public to understand, why treat the brain for a gut disorder, but HT for example, is statistically and perhaps argueably the most successful treatment to date.They also know now, that a combination of psycological and standard medical thearipies is more effective then standard treatment alone.Because they don't know the exact cause does not mean they don't have research generated insights into effective IBS treatments that help the majority of IBSers to feel better and have less symptoms and even put some into remission, sometimes total remission.Again just because you don't have symptoms, does not been the underlying problems are cured.The history of IBS is important also in the big picture to what they have learned and where things are going. Believe it or not experts in immunology, the enteric nervous sytem, microbiology, neurogastroenterology and many other fields are working on all the issues, they are also combining the information and the shear amount of information the last five to ten years has been very substantial in IBS and they have made a lot of progress.History of Functional DisordersDouglas A. Drossman, MDCenter-Co-DirectorMelissa SwantkowskiNew York UniversityTHE PASTHISTORICAL PRECEDENTSHistorians and physicians have documented the presence of Functional GI disorders throughoutrecorded human history. However, until recently, limited attention has been granted to thesedisorders due to the lack of identifiable pathology and the absence of a conceptual framework tounderstand and categorize them. Systematic investigation of functional GI disorders did notbegin until the middle of the 20th century, and prior to this time, only occasional reports offunctional GI symptoms were published, the first appearing only 200 years ago_Over the past 25 years, scientific attention to understanding and properly caring for patients withfunctional GI disorders has grown progressively. With the understanding comes the rationale foruse of medications directed at intestinal receptors as well as psychopharmacological, behavioral,and psychological forms of treatment. Additionally, there has been an increase in the rate ofscientific publications and greater media exposure to the public through television, radio, andInternet.To understand the historical classification of these disorders, two differing theories relating to theinteraction between the mind and body should be considered.o Holism: a theory built upon the foundation that the mind and body are integratedand utterly inseparable.o Dualism: a theory that proposes a separation between the mind and the body.Greek philosophers Plato, Aristotle, and Hippocrates first proposed the principleof holism about 3,000 years ago, and later in the 12th century; Jewish physicianand philosopher Maimonides reexamined this philosophy. Based on holism, thestudy of medical disease must take into account the whole person rather thanmerely the diseased part. However, societal concepts of illness and diseasedrastically shifted when European philosopher Rene Descartes offered the divergent theory ofdualism in the 17th century. Prior to the notion of dualism, the church discouraged humandissection on the premise that the spirit resided in the body. The acceptance of dualism paved the2way for the emergence of scientific investigation and new medical discoveries by lifting theprohibition of human dissection. This shift in medical thought was congruent with the societalchanges of the 17th century: the shift towards a separation in church and state.IMPLICATIONS FOR FUNCTIONAL GI DISORDERSBased on the concept of dualism, disease was now understood in terms of structuralabnormalities. Therefore, the validity of a disease rested with the observation of morphologicalabnormalities. Medical conditions occurring in the absence of such morphological abnormalitiesand symptoms were not considered legitimate, and were often viewed as psychiatric, consistentwith the concept of dualism. The concept of dualism had other effects with regard to treatment.For example, this would include all the functional GI disorders and other somatic syndromes,such as fibromyalgia. Until the latter part of the 20th century, a medical illness was consideredamenable to scientific inquiry and treatment. However, patients with psychiatric disorders wereinterred in insane asylums and considered to no longer be treatable by medical physicians.Unfortunately this concept leads to a clinical dilemma. Specific diseases explain only about 10%of medical illnesses seen by physicians. Furthermore, people with structural (i.e. organic)diagnosis such as inflammatory bowel disease or cancer show considerable variation in theirsymptom presentation and clinical behavior. Gastroenterologists (as well as other health carepractitioners) are all too familiar with the poor correlation between structural findings onendoscopy and their patient's symptoms.Although efforts to find morphological or even motility etiologies for functional GI disorders inthe latter part of the 20th century were unsuccessful, the assumption that functional GI disordersmust be psychiatric has developed and has permeated current thinking. However, in the face ofcurrent scientific research, this is being seriously challenged. Studies have shown that personswith irritable bowel syndrome who do not seek health care are psychologically much like healthysubjects.THE PRESENTCONCEPTUAL BASES FOR THE STUDY OF FUNCTIONAL GI DISORDERSo The recent acceptance of functional GI disorders as legitimate medical entities isbased on the following three developments:eek: The concept of the Biopsychosocial model of illness and diseaseo The development of new investigative methods for studying diseaseo The development of the Rome CriteriaBiopsychosocial ModelIn 1977, the publication of the concept of the Biopsychosocial model by George Engel, and itslater demonstration specifically for gastrointestinal disorders, marked an important change inthinking. A biopsychosocial model of illness and disease provides the needed framework to3understand, categorize, and treat common GI symptoms. These symptoms are the integratedproduct of altered motility, enhanced visceral sensitivity, and brain-gut dysregulation and oftenare influenced by psychosocial factors. Figure 1 illustrates the proposed relationship betweenpsychosocial and physiological factors with functional GI symptoms and the clinical outcome.Early in life, genetics and environmental influences (family attitudes toward bowel training orillness in general, major loss or abuse history or exposure to infection) may affect one'spsychosocial development (susceptibility to life stress, psychological state, coping skills, socialsupport) or the development of gut dysfunction (abnormal motility or visceral hypersensitivity).Additionally, the presence and nature of a functional GI disorder is determined by the interactionof psychosocial factors and altered physiology via the brain-gut axis. In other words, oneindividual afflicted with a bowel disorder but with no psychosocial disturbances, good copingskills and adequate social support may have less severe symptoms and not seek medical care.Another having similar symptoms but with coexistent psychosocial disturbance, high life stress,or poor coping skills may frequent his physician's office and have generally poor outcome.DEVELOPMENT OF NEW INVESTIGATIVE METHODSThe second concurrent process has been the expansion and refinement of investigative methodsthat allow the study of functional GI disorders in terms of biological, cultural, and psychosocial(i.e. brain) influences. These developments include:1. the improvement of motility assessment,2. the standardization of the barostat to measure visceral sensitivity,3. the enhancement of psychometric instruments to determine psychosocialinfluences,4. the introduction of brain imaging (PET, fMRI) to determine CNS contribution tosymptoms, and5. the molecular investigation of brain-gut peptides, which provide insight into howthese symptoms become manifest.In less than ten years, these methods have produced new knowledge of the underlyingpathophysiological features that characterize the age-old symptoms we now define as functionalGI disorders.ROME CRITERIAThe Rome Criteria is an international effort to characterize and classify the functional GIdisorders using a symptom-based classification system. This approach that has its precedentswith classification systems in psychiatry and rheumatology. The rationale for such a system isbased on the premise that patients with functional GI complaints consistently report symptomsthat breed true in their clinical features, yet cannot be classified by any existing structural,physiological or biochemical substrate. The Rome Criteria was built upon the Manning Criteria,which was developed from discriminate function analysis of GI patients.The decision to develop diagnostic criteria by international consensus was introduced as part of alarger effort to address issues within gastroenterology that are not easily resolved by usual4scientific inquiry or literary review. By 1992, several committees had met to discuss the criteria,which ultimately resulted in the publishing of many articles in Gastroenterology Internationaland a book detailing the criteria titled "The Functional Gastrointestinal Disorders (Rome I)".Elaboration of the Rome I criteria led to a second edition of the Rome criteria (titled Rome II) in2000 as well as the publication of a supplement to the journal Gut in 1999. Recently the RomeCoordinating Committee has met to begin Rome III, expected to be published in 2006. To learnmore about the Rome Committees and to see a summary of the Rome II book: go towww.romecriteria.com.PRESENT PATHOPHYSIOLOGICAL OBSERVATIONSDespite differences among the functional gastrointestinal disorders, in location and symptomfeatures, common characteristics are shared with regard to:eek: motor and sensory physiology,o central nervous system relationships,o approach to patient care.What follows are the general observations and guidelines.MOTILITYIn healthy subjects, stress can increase motility in the esophagus, stomach, small and largeintestine and colon. Abnormal motility can generate a variety of GI symptoms includingvomiting, diarrhea, constipation, acute abdominal pain, and fecal incontinence. Functional GIpatients have even greater increased motility in response to stressors in comparison to normalsubjects. While abnormal motility plays a vital role in understanding many of the functional GIdisorders and their symptoms, it is not sufficient to explain reports of chronic or recurrentabdominal pain.VISCERAL HYPERSENSITIVITYVisceral hypersensitivity helps to account for disorders associated with chronic or recurrent pain,which are not well correlated with changes in gastrointestinal motility, and in some cases, wheremotility disturbances do not exist. Patients suffering from visceral hypersensitivity have a lowerpain threshold with balloon distension of the bowel or have increased sensitivity to even normalintestinal function. Additionally, there may be an increased or unusual area of somatic referral ofvisceral pain. Recently it has been concluded that visceral hypersensitivity may be induced inresponse to rectal or colonic distension in normal subjects, and to a greater degree, in personswith IBS. Therefore, it is possible that the pain of functional GI disorders may relate tosensitization resulting from chronic abnormal motor hyperactivity, GI infection, or trauma/injuryto the viscera.5BRAIN-GUT AXISThe concept of brain-gut interactions brings together observations relating to motility andvisceral hypersensitivity and their modulation by psychosocial factors. By integrating intestinaland CNS central nervous system activity, the brain-gut axis explains the symptoms relating tofunctional GI disorders. In other words, senses such as vision and smell, as well as enteroceptiveinformation (i.e. emotion and thought) have the capability to affect gastrointestinal sensation,motility, secretion, and inflammation. Conversely, viscerotopic effects reciprocally affect centralpain perception, mood, and behavior. For example, spontaneously induced contractions of thecolon in rats leads to activation of the locus coeruleus in the pons, an area closely connected topain and emotional centers in the brain. Jointly, the increased arousal or anxiety is associatedwith a decrease in the frequency of MMC activity of the small bowel possibly mediated by stresshormones in the brain. Based on these observations, it is no longer rational to try to discriminatewhether physiological or psychological factors produce pain or other bowel symptoms. Instead,the Functional GI disorders are understood in terms of dysregulation of brain-gut function, andthe task is to determine to what degree each is remediable. Therefore, a treatment approachconsistent with the concept of brain-gut dysfunction may focus on the neuropeptides andreceptors that are present in both enteric and central nervous systems.THE ROLE FOR PSYCHOLOGICAL FACTORSAlthough psychological factors do not define these disorders and are not required for diagnosis,they are important modulators of the patient's experience and ultimately, the clinical outcome.Research on the psychosocial aspects of patients with functional GI disorders yields three generalobservations:eek: Psychological stress exacerbates gastrointestinal symptoms in patients withfunctional GI disorders and can even produce symptoms in healthy patients (but toa lesser degree).o Psychological disturbances modify the experience of illness and illness behaviorssuch as health care seeking. For example, a history of major psychological trauma(e.g. sexual or physical abuse) is more common among patients seen in referralcenters than in primary care and is associated with a more severe disorder and apoorer clinical outcome. Additionally, psychological trauma may increase painreportingtendency.o Having a functional GI disorder has psychological consequences in terms of one'sgeneral well-being, daily functional status, concerns relating to control oversymptoms, and future implications of the illness (e.g. functioning at work andhome).APPROACH TO TREATMENTThe approach to treatment for all functional GI disorders is founded on a therapeutic physicianpatientrelationship. The basis for implementing a strong physician-patient relationship issupported by evidence that patients with functional GI disorders have anywhere from a 30 to80% placebo response rate regardless of treatment.6Because functional GI disorders are chronic, it is important to determine the immediate reasonsbehind each visit, after which treatment can be based on severity and nature of symptoms,physiological and psychosocial determinants of the patient�s illness behavior, and the degree offunctional impairment.These factors can separate patients into mild, moderate, and severe categories.Patients with mild symptoms:eek: usually seen in primary care,o do not have major impairment in function or psychological disturbance ando can maintain normal activity.These patients have concerns about their condition but do not need to make many visits to theirphysician. Regarding treatment, these patients require education about their disorder and itssymptoms as well as information regarding a proper diet and the kinds of medication that canhave adverse effects.Patients with moderate symptoms:eek: seen in both primary and secondary care facilities ando experience intermittent disruptions in activity on account of their symptoms.o may identify a close relationship between symptoms and inciting events such asstress, travel, or dietary indiscretion.For these patients, symptom monitoring to record time, severity, and presence of associatedfactors can help to identify inciting factors and give the patient a sense of control over thedisorder. Additionally, pharmacotherapy directed at specific symptoms, particularly those thatimpair daily function, can be helpful, as can psychological treatments (relaxation, hypnosis,cognitive-behavioral therapy, and combination treatments) in reducing anxiety and encouraginghealth promoting behaviors.Patients with severe symptoms:eek: have trouble functioning daily,o find their disorder to be disabling and debilitating in nearly every facet of life,o have a high frequency of associated psychological difficulties,o make frequent visits to their physicians , ando may hope for a magical cure.In these cases a long-term physician-patient relationship, which sets realistic treatment goals(such as improved quality of life rather than elimination of all pain) is necessary. The focus forthese patients needs to shift from treating a disease to coping with a chronic disorder, wheremuch of the responsibility is place on the patient, himself. Furthermore, antidepressants haveproven useful to control pain and alleviate associated depressive symptoms.7THE FUTUREFuture studies will identify pathophysiological subgroups, each having its own set ofdeterminants ad treatment. Examples are as follows:eek: Some patients will develop their disorders or exacerbate symptoms viasensitization of afferent transmission from infection, enhanced motility, or traumato the gut. They may respond to the newly developing neurotransmitter blockingagents.o Patients with more painful and severe symptoms may prove to have "abnormalperception of normal gut function" rather than abnormal function. Thisdysfunction in the central regulation of incoming visceral signs may be remediedwith a psychopharmacological treatment approach.o The symptoms of some patients could be attributed to genetic factors, which resultin abnormalities in central reactivity to stress, in which case genetic manipulationstrategies would prove beneficial.o Early learning within the familial structure and socio-cultural influences has beendemonstrated to affect symptom perception and illness behavior. Future studiesare also likely to identify psychological and behavioral interventions that aretargeted for this subgroup.While it is likely that there are potent new treatments that will follow our growingpathphysiologic knowledge of these disorders, it is unlikely that they will replace some of thefundamental clinical principles:eek: active listening,o careful decision making,o an effective patient-physician relationship, ando patient centered biopsychosocial plan of care. http://www.med.unc.edu/medicine/fgidc/hist...aldisorders.pdf Definition of Health: The World Health Organization."Health is a state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity." Also even based on data from Probiotics studies already done, if they benefit pain and bloating they are worth trying. Gas is a very hard symptoms to treat in IBS and if they were to be shown to help just that great, but they have shown to be even more useful in IBD conditions. On IBS more studies are needed. Not that future studies show more benefits for IBSer. They have also been used on this bb for quite some time now with mixed results. You will hear people say they have cured themselves and you will see some Web advertising "cures" but until all of the above is figured out, there is no "cure" for IBS at this time.Again, I highly recommend getting a copy of this from the IFFGD"In the new IFFGD Digestive Health Matters.Visceral Sensations and Brain-Gut Mechanisms By: Emeran A. Mayer, M.D., Professor of Medicine, Physiology and Psychiatry; Director, Center for Neurovisceral Sciences & Women's Health, David Geffen School of Medicine at UCLA IntroductionOver the past several years, different mechanisms located within the gut, or gut wall have been implicated in as possible pathoophysiologic mechanisms underlying the charecteristic IBS symptoms of abdominal pain and discomfort. The list ranges from altered transit of intestinal gas, alterations in colonic flora, immune cell activation in the gut mucosa, and alterations in serotonin containing enterochromaffin cells lining the gut. For those investigators with a good memory, these novel mechanisms can be added to an older list of proposed pathomechanisms, including altered gut motility('Sapstic Colitus') and alterations in mucus secretion. While the jury is still out, one unique aspect about the gut and its connection to the brain are often forgotten: Our brain gut axis is not designed to generate concious perceptions of every alteration in gut homeostasis and internal enviroment, in particlur when these changes are chronic, and when there is no adaptive behavioral response an affected organism could generate.Evolution has not designed our brain gut axis to experience abdominal pain every time the number of mast cells in our ileum goes up, or the number of our serotonin containing cells goes down. It would be counter productive for an animal with a chronic parasite infestation to experince constant viceral pain, and it wouldn't have any advantage for people living in third world countries with frequent enteric infections to suffer from chronic abdominal pain. It has been suggested that viceral pain maybe a secondary phenomenon of an elaborate system of signaling non painful signals to the brain: hunger and fullness (satiety), well being after a meal, urge to evacuate, ect. At the same time, powerful mechanisms have evolved that keep many other aversive signals out of concious perception: contractions, luminal distension, gas volume, low grade inflammation, ect..The most common symptoms of IBS patients are related to altered perception of sensations, arising from the GI tract, and frequently from sites outside the GI tract, such as the genitourinary system or the musculskeletal system. Sensations of bloating, fullness, gas, incomplete rectal evacuation, and crampy abdominal pain are the most common symptoms patients experience. Numerous reports have demonstarted that a significant percentage of functional bowel disorders (FBD) patients about (60) percent rate experimental distensions of the colon as uncomfortable at lower distension volumes or pressure when compared to healthy control subjects. This finding of an increased perception of viceral signals ("viceral hypersensitvity") has been demonstrated during baloon distension tests of the respective part of the GI tract regarless of where the primary symptoms are- the esophagus, the stomach, or the lower abdomen.In contrast to the current emphasis on mechanisms that may result in sensitization of viceral Afferent pathways in the gut, it may well be that alterations in the way the nervous system normally suppresses the perception of the great majority of sensory activity arising from our viscera are essential for the typical symptom constellation of IBS and other functional disorders to develop."It goes into a lot more detail and I highly recommend people get a copy and read the whole article."SummaryIn summary, it is clear that we still have a long way to go to understand the intricate connections between our digestive system and the brain, and how alterations in this two way communication result in functional bowel disorders symptoms. While more alterations in peripheral mechanisms involved in gut function are being reported, rapid progress has occured in our uunderstanding of the multiple mechanisms by which the brain can increase the concious perception of viceral stimuli, which is normally rarely perceieved." http://www.aboutibs.org/Publications/currentParticipate.html and in regards to dysbiosis and "cure", how does this fit into it all."IBS - Beyond the Bowel: The Meaning of Co-existing Medical ProblemsOlafur S. Palsson, Psy.D., Research Associate William E Whitehead, PhDUNC Center for Functional GI & Motility Disorders Irritable bowel syndrome (IBS) is a disorder that is defined by a specific pattern of gastrointestinal symptoms in the absence of abnormal physical findings. The latest diagnostic criteria for IBS, the Rome II criteria created by an international team of experts, require that the patient has abdominal pain for at least 12 weeks in the past 12 months, and that the pain satisfies two of three criteria: It is relieved after bowel movement, associated with change in change in stool frequency or associated with stool form. It is becoming clear, however that these bowel symptoms do not tell the whole story of symptoms experienced by IBS patients. People with this disorder often have many uncomfortable non-gastrointestinal (non-GI) symptoms and health problems in addition to their intestinal troubles.Symptoms All Over the Body in IBSSeveral research reports have established that IBS patients report non-bowel symptoms more frequently than other GI patients and general medical patients. For example, four studies that have asked IBS patients about a wide variety of body symptoms(1-4) all found headaches (reported by 23-45% of IBS patients), back pain (28-81%) and frequent urination (20-56%) to be unusually common in individuals with IBS compared to other people. Fatigue (36-63%) and bad breath or unpleasant taste in the mouth (16-63%) were found by three of these four studies to be more common among IBS patients. Additionally, a large number of other symptoms have been reported to occur with unusually high frequency in single studies. In our recent systematic review of the medical literature(5), we found a total 26 different symptoms, listed in Table 1, that are reported to be more common in IBS patients than comparison groups in at least one study. Table 1. Non-gastrointestinal symptoms more common in irritable bowel syndrome patients than in comparison groups(5). 1. Headache2. Dizziness3. Heart Palpitations or racing heart4. Back pain5. Shortness of breath6. Muscle ache7. Frequent urinating8. Difficulty urinating9. Sensitivity to heat or cold10. Constant tiredness11. Pain during intercourse (sex)12. Trembling hands13. Sleeping difficulties14. Bad breath/unpleasant taste in mouth15. Grinding your teeth16. Jaw pain17. Flushing of your face and neck18. Dry mouth19. Weak or wobbly legs20. Scratchy throat21. Tightness or pressure in chest22. Low sex drive23. Poor appetite24. Eye pain25. Stiff muscles26. Eye twitchingOverlap with Other Medical ConditionsResults from numerous studies (reviewed by Whitehead, Palsson & Jones, 2002(5)) also indicate that IBS overlaps or co-exists more often than would be expected with other medical conditions that appear to have little logical connection with the gut. The most researched example of such an overlap is the co-existence of IBS with fibromyalgia, a disorder characterized by widespread muscle pain. Fibromyalgia affects an estimated 2% of the general population, but in contrast, 28-65% of IBS patients have the disorder. Similar results are obtained when this overlap is examined the opposite way, by studying fibromyalgia patients and looking for IBS: 32-77% of fibromyalgia patients have IBS.Chronic fatigue syndrome (CFS) is another medical condition that has been found to have many times the expected co-occurrence with IBS. CFS is thought to affect only 0.4% of people in general, but it has been reported to be present in 14% of IBS patients(2), and conversely, 35-92% of chronic fatigue syndrome patients have IBS. Other conditions documented in multiple studies to have excess overlap with IBS are temporomandibular joint disorder (TMJ), found in 16-25% of IBS patients(2,6), and chronic pelvic pain (35% of IBS patients(7). In addition to these well established relationships, many other medical conditions appear (judging from single study reports) to have an excess overlap with IBS, although the frequencies of most of them in IBS are much lower than for the disorders already discussed. In fact, we recently(8) compared the frequencies of a broad range of diagnoses in the medical records of 3153 IBS patients in a large Health Maintenance Organization in the U.S. Northwest to an equal number of non-GI patients in the same HMO, and found that the IBS patients had a higher frequency of almost half of all non-gastrointestinal diagnoses, or 64 of the 136 sampled diagnoses.In summary, non-GI symptoms and co-existing medical problems seen in many IBS patients far exceed what is typical for medical patients or GI patients in general. This raises important questions about what causes this phenomenon, and what the implications of it are for IBS patients.What Explains Non-GI Symptoms and Co-existence of Other Disorders in IBS?There are several possible explanations for the preponderance of general symptoms and disorders in IBS. Our research group is currently conducting several research studies that may help shed some light on this mystery, but it is far too early to come to definite conclusions. We will list here some of the possible explanations, and discuss relevant data coming from work by our team and other investigators.A common physical cause? One rather obvious explanation for the high rates of co-existing symptoms and conditions in IBS patients would be that there is something biologically wrong in IBS that also causes the other symptoms or conditions. There are a number of distinct physiological characteristics or "abnormalities" that are seen in many IBS patients, although none of them are found in all patients. These include heightened pain sensitivity in the gut, increased intestinal contractions (motility) or hyper-reactivity to meals or stress (too much movement of the intestines - this is the reason why IBS was called spastic colon in the past), patterns of dysfunction in the autonomic nervous system (the part of the nervous system that helps regulate our inner body functions) and vague signs of immune activation seen in some IBS patients. Although one can suggest ways in which these physiological abnormalities would play a role in some other disorders that co-exist with IBS, there is little evidence so far of a common pattern of physical abnormality that could link IBS and its most common coexisting conditions and symptoms. Patterns of autonomic dysfunction in IBS are not like the ones seen in fibromyalgia and chronic fatigue syndrome, for example; and fibromyalgia patients do not show the same gut pain sensitivity as IBS patients, and conversely, IBS patients do not show the pain-sensitive tender points that are characteristic of fibromyalgia(9-10). Furthermore, as can be seen from reviewing the symptom list in Table 1, the non-GI symptoms that plague IBS patients are so varied, and cover so many different organ systems, that it would be hard to identify any biological connection between them. On the contrary, it seems like the only overall commonality between these symptoms may be that they are non-specific - they are, in other words, not clear symptoms of any identifiable disease processes or diagnosable disorders. Indeed, the symptoms that are most common among IBS patients are generally those that are also common in the general healthy population - they just tend to occur at an even higher rate in people with IBS.Physical expression of emotional discomfort? Another possible explanation for the high number of non-GI symptoms and disorders in IBS is the tendency to translate strong emotions into physical "symptoms". This is sometimes called somatization ("soma" is the Greek word for "body" and somatization therefore literally means "to express in the body"). All people "somatize" to some degree: It is normal to feel butterflies in your stomach, to blush or go pale, get a lump in your throat, or feel the heart beating in your chest if you get very emotional. Shaky hands, stiff neck or excess sweating are likewise quite ordinary when people are under a great deal of stress. However, some people are more vulnerable than others to letting negative emotions express themselves physically. This is often thought to be an alternative and less healthy way of exhibiting or feeling emotional discomfort. Some people may develop a strong tendency to do this because they have a basic personality style that shies away from interpersonal expressiveness. For others, it could be the result of growing up in the care of strict, repressive or abusive parents or caretakers, where normal expression of negative emotions was not allowed or would have been dangerous: Getting a headache or a stomach ache may be an alternative way to "give voice" to negative emotions under such circumstances. It seems that excessive habitual suppression of ordinary verbal and emotional expression of negative emotions, regardless of the reason for it, may lead to the tendency to somatize. There is evidence that this tendency may be at work in IBS, at least among some women with the disorder. Dr. Brenda Toner has found in two studies(11-12) that women with IBS score higher than depressed women and healthy women on questionnaires measuring of the tendency to avoid expression of negative emotions or views.Learned over-attention to body symptoms and excess disease attribution? All people ignore most of the sensations from their bodies most of the time. This is necessary so that we are not overwhelmed by the vast amount of information our senses supply to our brains every moment of our lives. For example, if you are reading this sitting down, you have probably not been at all aware of the sensations of the seat under your body until right now - nor the feeling in your scalp, etc. Our brains constantly sift through the mass of incoming body information and decide what is important for us to become consciously aware of, based on such things as our past experiences and how likely the information is to indicate threat to our health or well-being. Most minor symptoms (those that might be uncomfortable and bothersome if they would get our attention), are simply dismissed in our busy everyday lives, because other things win out in the moment-to-moment competition for our limited attention resources.More frequent attention to mild physical symptoms can be learned, however, and can become a habit. As with most things, such habitual over-attention is probably most easily learned in childhood. It would seem reasonable, for example that a child would get into the habit of noticing physical symptoms more if his or her parents are always talking about their own symptoms. We have recently found(13) that the more medical problems the parents in the childhood home had, the more general physical symptoms adult IBS patients report.A possible consequence of a childhood where the child grew up with parents or others who were seriously ill, is a tendency to interpret common normal physical sensations as symptoms of serious illness. Such serious view of symptoms can also be modeled after the parents' approach to common illness. Dr. Whitehead and colleagues found in a telephone survey of 832 adults 20 years ago(14) that people whose parents paid more attention to cold or flu symptoms in childhood were more likely to view such symptoms as serious in adulthood and to visit doctors for them. They were also more likely to have IBS diagnosis.Evidence that IBS patients interpret physical sensations differently than others is emerging from brain imaging studies. This type of research takes a "snapshot" of the amount of activity in different parts of the brain in response, using techniques such as PET scans (positron emission tomography) and functional MRI (functional Magnetic Resonance Imaging). By examining which parts of the brain react most to painful sensations, it is possible to deduce to some degree how the brain processes the information. In one such study, by Silverman and colleagues(15) , IBS patients but not control subjects reacted to physical sensations from a painful balloon inflation in the rectum with increased blood flow in the left prefrontal cortex, a part of the brain known to process personally threatening information. In contrast, that study and others(16-17) found that IBS patients do not show activity in the anterior cingulate cortex that is indicative of general discomfort in healthy subjects. IBS patients are also more likely to respond to physical stimuli in the GI tract by activating brain centers that handle emotional events. Collectively, this suggests that IBS patients may process body information associated with bowel sensations (and perhaps other physical sensations as well) differently than other people, interpreting them as personally threatening and more emotionally relevant events rather than ordinary discomfort. Such different interpretations of physical sensations would also explain hyper-attention to such sensations.Faulty neurological filtering? After entering the spine (the information highway from the body to the brain), information destined for the brain about body pain is sent along nerves through gates that control how much of this information passes through. Our brains continually send signals down to these spinal gates to cause them to block signals that are of too low intensity to provide valuable information (you do not want to constantly know about all your minor aches and discomforts from regular body activity). This is one of the ways that the brain uses to limit the vast amounts of information constantly streaming in from millions of nerve sensors throughout our bodies. A current popular hypothesis in the field of IBS research is that an inadequate amount of this "descending inhibition" of incoming pain information is at least partly to blame for the hypersensitivity to intestinal discomfort and pain seen in IBS, and causes signals from pain sensors that would normally be blocked to pass on through to the brain. Some researchers have further suggested that the same kind of slack traffic control could be more widespread in IBS and may explain the observed proneness to headaches, back pain or muscle aches. People who have more open pain gates because of faulty inhibition would theoretically be like the princess in H.C. Andersen's classic story "The Princess and the Pea" who could feel a pea through 20 mattresses. The problem with this as an explanation for symptom overabundance in IBS is, first, that it would explain only excess in pain-type symptoms, which are but one of many types of overabundant symptoms in IBS, and secondly, that there are no direct data on IBS patients yet to show us how valid this view is.Result of greater psychological distress?As was explained above, it is normal for people who are emotionally distressed to experience more physical symptoms. At least half of IBS patients who have consulted doctors have been diagnosed with an affective ("emotional") disorder - typically either depression or an anxiety disorder. Additionally, many people with IBS who have no affective disorder diagnosis have significant symptoms of anxiety and depression. One might therefore ask whether the physical symptoms reported could simply be a side effect of psychological distress. We have addressed this question in two studies presented at this year's Annual Meeting of the American Gastroenterological Association(18-19).
 

· Registered
Joined
·
23,788 Posts
FYIEditorial April 2000Volume 95, Number 4Pages 862-863 -------------------------------------------------------------------------------- Symptom Expression in Pain-Predominant Functional Bowel Syndrome: Is Visceral Hyperalgesia the Whole Truth? Michael S. Shapiro, M.D.a and Kevin W. Olden, M.D.a --------------------------------------------------------------------------------Ever increasing socioeconomic pressures have elevated cost-effective management of patients with irritable bowel syndrome (IBS) and related functional disorders as a high priority in gastroenterology practice. The illness of these patients produces an enormous cost to society related to absenteeism and use of medical resources (1). Although most individuals with IBS go about their daily lives without need for medical care, about 30% of IBS sufferers seek assistance for their disorder (2). IBS patients pursue consultation mainly because of their abdominal pain (3). The severity of abdominal pain reported by patients with functional bowel syndrome to their physician often drives the aggressiveness of a workup in the attempt to identify "serious disease." This results in higher risk to the patient and greater expense. However, what is uncertain is whether, in IBS patients, painful symptoms directly reflect pathophysiological mechanisms involved in pain production such as visceral hyperalgesia, or whether they are a consequence of psychosocial factors. In this issue of the Journal, Drossman et al. address the question of what factors influence severity of the pain reported in pain-predominant functional bowel disorders (4). Patients considered in this study were sufferers of moderate to severe painful functional bowel syndrome as identified by a validated Functional Bowel Severity Index. A total of 83.3% of subjects in the study fulfilled standard Rome criteria for IBS. Psychosocial and behavioral parameters were compared between moderate and severe groups. Psychological factors were considered as potential modulators of pain expression based on the high prevalence of psychiatric disturbance detected in patients who present with functional bowel complaints, in the range of 42-61% (1). Visceral hyperalgesia also is considered to be a major mechanism involved in symptom production in functional bowel syndrome, and can be demonstrated in up to 94% of IBS patients by rectal distention (5). For this study, visceral hypersensitivity was assessed by barostat balloon rectal distention to detect differences in pain perception. The results show compelling evidence that psychosocial and behavioral elements are the crucial and predominant factors that distinguish moderate from severe functional bowel syndrome. Major factors associated significantly with the severe pain-predominant group included depression, reduced perception of quality of life, impaired coping skills, and increased health care use. Of 19 psychosocial variables entered into a regression model to predict pain severity, four factors were identified as highly predictive of severe functional pain: physical dysfunction, eating dysfunction, days in bed for GI symptoms, and number of times the physician was called for GI symptoms. These factors are characteristic of "learned illness behavior" (6), in which patients are preoccupied with multiple somatic complaints and adopt a behavioral pattern to reflect this preoccupation. Although heighted visceral hypersensitivity was suggested in the severe pain-predominant group, the differences between this group and the moderate group were not substantial, and regression analysis did not find sensitivity to rectal distention to be a good predictor of pain severity. This study illustrates the crucial role of psychosocial and behavioral disturbance in how pain is perceived and reported in IBS and other painful functional GI disorders. Visceral hypersensitivity has been the focus of intense investigation as a possible mechanism of symptom generation in IBS and the functional GI disorders (2, 7). Although the data of Drossman et al. do not reject a role for visceral hypersensitivity in painful functional bowel syndrome, they suggest that visceral hyperalgesia alone is not sufficient to explain how pain is communicated by patients with functional GI disorders. In particular, somatization disorder has been found to correlate with reduced pain threshold (8) in IBS and is prevalent in functional bowel syndrome sufferers who seek medical care (6). The mechanism by which psychological factors modulate pain reporting and perception is not known. Some attention has been directed to chronic stress as a factor, which is highly prevalent in patients with functional bowel syndrome (9) and is associated with increased intensity of symptoms reported (10, 11). Stress may influence the threshold to painful distention (8). A possible biochemical basis for these effects may involve, at some level, corticotropin-releasing factor, which is an important player in the stress response and which has been demonstrated to influence symptoms in IBS (12). Whitehead and Palsson have proposed a model of pain perception and reporting in IBS that incorporates a dynamic interplay of physiological and psychosocial factors leading to how symptoms ultimately are described by the patient (8). Illness behavior plays a pivotal part in this model and is directly linked to health care use. The results of Drossman et al., appearing in this issue of the Journal, lend support to the "biopsychosocial" model of functional GI disorder. Their findings also emphasize the importance of modification of illness behavior patterns as the most effective means of enacting a favorable outcome for these most challenging patients. How can these findings be applied? There is a need to heighten awareness of the clinician involved in the care of these patients regarding the recognition of important psychosocial factors in functional bowel patients. Symptoms must be interpreted as a complex manifestation of brain-gut interaction and not merely as gut dysfunction. Establishing an effective patient-physician relationship is a crucial step in successfully sorting out such patient issues (1). Once contributing psychological features are identified, effective therapy can be offered, which may include use of psychotropic drugs, cognitive-behavioral therapy, dynamic psychotherapy, hypnotherapy, or other behavioral techniques that have been shown to benefit these patients (1). Thus, we are reminded that effective medical care for these patients requires a thoughtful blend of art and science, based on insightful interview, knowledge of the complexity of factors involved in symptom expression, and the ability to persuade, with sensitivity, patients as to the most helpful intervention. --------------------------------------------------------------------------------aDivision of Gastroenterology and Hepatology, Mayo Clinic Scottsdale, Scottsdale, Arizona http://www-east.elsevier.com/ajg/issues/9504/ajg1973edi.htm
 

· Registered
Joined
·
23,788 Posts
From above"How can these findings be applied? There is a need to heighten awareness of the clinician involved in the care of these patients regarding the recognition of important psychosocial factors in functional bowel patients. Symptoms must be interpreted as a complex manifestation of brain-gut interaction and not merely as gut dysfunction."
 

· Registered
Joined
·
23,788 Posts
Arch Intern Med. 2004 Sep 13;164(16):1773-80. Related Articles, Links Clinical determinants of health-related quality of life in patients with irritable bowel syndrome.Spiegel BM, Gralnek IM, Bolus R, Chang L, Dulai GS, Mayer EA, Naliboff B.Division of Gastroenterology, the VA Greater Los Angeles Healthcare System, the Division of Digestive Diseases.BACKGROUND: Current guidelines recommend routine assessment of health-related quality of life (HRQOL) in patients with irritable bowel syndrome (IBS). However, physicians rarely have the time to measure HRQOL with the appropriate methodological rigor, and data suggest that HRQOL in patients with IBS is often estimated using inaccurate clinical gestalt. The identification of predictive factors could allow physicians to better assess HRQOL without using misleading clinical clues. We, therefore, sought to identify determinants of HRQOL in patients with IBS. METHODS: We examined 770 patients, 18 years or older, with IBS at a university-based referral center. Subjects completed a symptom questionnaire, the Symptoms Checklist-90 items psychometric checklist, and the 36-Item Short-Form Health Survey. The main outcome was HRQOL as measured by the mental and physical component scores of the 36-Item Short-Form Health Survey. We first developed a list of hypothesis-driven HRQOL predictors, and then performed multivariate regression analysis to measure the independent association of each predictor with HRQOL. RESULTS: Seven factors (r(2) = 0.39) independently predicted physical HRQOL: (1) more than 5 physician visits per year, (2) tiring easily, (3) low in energy, (4) severe symptoms, (5) predominantly painful symptoms, (6) the feeling that there is "something seriously wrong with body," and (7) symptom flares for longer than 24 hours. Eight factors (r(2) = 0.36) independently predicted mental HRQOL: (1) feeling tense, (2) feeling nervous, (3) feeling hopeless, (4) difficulty sleeping, (5) tiring easily, (6) low sexual interest, (7) IBS symptom interference with sexual function, and (8) low energy. CONCLUSIONS: Health-related quality of life in patients with IBS is primarily related to extraintestinal symptoms rather than traditionally elicited gastrointestinal symptoms. These findings suggest that rather than focusing on physiological epiphenomena (stool characteristics and subtype of IBS) and potentially misleading clinical factors (age and disease duration), physicians might be better served to gauge global symptom severity, address anxiety, and eliminate factors contributing to chronic stress in patients with IBS. PMID: 15364671Webmedjust fyiMind-Body-Pain Connection: How Does It Work?By Michael Henry JosephWebMD Live Events Transcript Archive Event Date: 05/11/2000.Moderator: Welcome to WebMD Live's World Watch and Health News Auditorium. Today we are discussing "The Mind-Body-Pain Connection: How Does It Work?" with Brenda Bursch, Ph.D., Michael Joseph, M.D., and Lonnie Zeltzer, M.D.Brenda Bursch, Ph.D., is the Associate Director of the Pediatric Pain Program, Co-Director of Pediatric Chronic Pain Clinical Service and Assistant Clinical Professor of Psychiatry & Biobehavioral Sciences at UCLA Department of Pediatrics in the School of Medicine. She has written about asthma, developmental & behavioral pediatrics, emergency medicine, AIDS education and prevention, chronic digestive diseases and pediatric bowel disorders. She has membership in the American Pain Society, American Psychological Association, Munchausen Syndrome by Proxy Network, and the UCLA Center for the Study of Organizational and Group Dynamics. Michael Henry Joseph, MD, is an assistant professor of pediatrics and co-director of Chronic Pain Services at the University of California at Los Angeles Children's Hospital. He is a recipient of the Golden Apple Award for Excellence in Teaching. Lonnie Zeltzer, M.D., is an expert in the field of pediatric pain. She is a former president of the Society for Adolescent Medicine and member of the National Institute of Health?s Human Development Study Section. She is currently a Professor of Pediatrics and Anesthesiology at the UCLA School of Medicine. She is Director of the UCLA Pediatric Pain Program and Associate Director of the Patients & Survivors Section, Cancer Prevention and Control Research Branch of the UCLA Jonsson Comprehensive Cancer Center. She has well over one hundred scientific publications, reviews and chapters in medical journals, and has lectured internationally. Moderator: Doctors, welcome back to WebMD Live.Dr. Bursch: Thank you.Dr. Joseph: Thank you.Dr. Zeltzer: Thank you.Dr. Zeltzer: As you know, the mind-body pain connection is the basis upon which our pediatric pain program at UCLA operates, both in terms of how it conceptually views pain and its approach to treatment. I would like to begin by discussing the physiology that is underlying a lot of our functional definitions of pain and our basic philosophy and our mind-body connection model.Dr. Joseph: I'd like to say the differentiation into components is a fallacy. Your brain and nervous system communicate with the rest of your body just like all other organ systems. All work together. Pain is not a simple entity in which it's like pulling on a string and ringing a little bell in your head. It's more dynamic than that, in which you do have nerve input from fingers and toes and organs that goes to spinal column and then to your brain. You also have nerve pathways that are coming from your brain down your spinal column. There are many factors that change the way we actually perceive pain and can make pain more intense or less intense depending on the situation. This is also true for other symptoms. This connection between your central nervous system and your brain communicates with your peripheral nervous system so nerves coming from organs, arms and legs, and all symptoms that you may be feeling can be altered by your nervous system either increased or decreased. That's true of nausea or difficulty breathing or any symptom you might be feeling. In fact, it's true of all of your senses. Your sense of hearing, smell, taste, vision are also all interpreted perceptions. Different factors that can alter your perception specifically when it comes to pain include how much attention you pay to the symptom, what the meaning of the symptom is. For some people, pain is a good thing such as when you've been working out and you're waiting to feel that burn and the burn has a good context, as opposed to if you pull a muscle, you may have exactly the same amount of tissue damage but the way you perceive the pain is very different. Memory can affect perception of pain. When we are awake, it takes much less stimulus to cause pain than when we are asleep. If we were in a coma, it would take even more, possibly we don't even experience pain.Dr. Bursch: As Dr. Joseph just described, the nature of perception of pain, each individual is different not only in pre-existing neurology but also in their experiences that would contribute to their memories of pain, to their arousal, due to circumstances and their experiences and the meanings they attribute. Also, there are different points at which they would become distressed by the signaling. From a physiologic standpoint, people have different levels at which sensory nerves that carry pain information will send those signals. Some people have the ability to have a lot of stimulation before the signals are sent, and some people are very sensitive and a very little stimulation sends the signal. People with irritable bowel syndrome are known through many studies to have a very low threshold for sensory info sent from their intestine to their brain.Dr. Zeltzer: People can learn different coping skills and ways of blocking out the sensation so they experience them, but it doesn't have to distress them. Since you describe the physiologic basis for how pain becomes pain -- how different tissue injury turns into pain -- maybe you can talk about the body's natural pain control system, from a mind-body perspective?Dr. Joseph: The body has a number of ways of controlling pain throughout different organ systems. The most direct is pathways, nerve pathways, that travel from your brain back down your spinal column and they signal directly to those same nerves that are sending pain signals to your brain. They interrupt those pain signals on their way up. These nerve pathways are activated by a number of factors. The easiest one to recognize is fear. A good example of this is, say you're in a dark parking lot and you accidentally shut your finger in the car door. It hurts a lot. You start hearing footsteps behind you. All of a sudden your finger stops hurting. There's no difference in the amount of tissue damage between when you heard the footsteps and when you didn't, but your brain has sent signals to your body that it is time to run away as opposed to time to feel pain. There are subtle ways that your body controls pain, as well. Your brain makes chemicals called endorphins and enkephalins. These molecules are very similar to drugs such as morphine, which everybody recognizes as a pain fighting drug. Interestingly, not only your brain makes these chemicals but also your immune system. B-lymphocytes actually make these chemicals as well. When you have inflamed or infected areas and sending pain signals, even your immune systems can go to those areas, release pain modulating chemicals into that area and decrease the pain right then, if it's something the person needs to have happen at that time. There are many ways pain can be increased or decreased depending on the needs of the individual at each time.Dr. Bursch: Based on the earlier model that Dr. Joseph presented that delineated the relationship of memory, attention and arousal on the pain system, there are a number of behavioral or cognitive strategies that one can engage in order to impact perception of pain, things as simple as engaging in relaxing activities, using distraction so that you're focusing on something else. It could be using visualization techniques which is similar to distraction technique. You can use your mind and you can use your body in ways that the actual pain perception can be altered if you can alter your arousal or your attention or your memory, or memory you have about the pain. You can change your experience of that symptom.Dr. Zeltzer: It is always amazing to me how powerful the mind is at having actual physical effects on the body, and it always reconfirms my belief (and that of most clinicians and researchers in pain) that the mind and body are tightly linked. It is always amazing that one can have extreme pain and that thinking about something or having a different emotion, like anxiety, joy and happiness, can alter the experience of that pain, and if one were looking through PET (positron emission tomography) scans at brain metabolic activity or if you looked at the signals of the nervous system, one would see actual physical changes going on during these thinkings and emotional events. Maybe you might want to talk a little bit about the role of some of the complementary therapies focusing on the mind-body connection in treating pain?Dr. Joseph: I would love to. We do utilize a number of therapies that work specifically on a mind/body connection, the most obvious of which is biofeedback. Biofeedback is a technique in which sensors are placed on the body to measure either the tension in muscles or they can measure skin temperature or heart rate. These measures are displayed for the patient on a screen with lights, sounds and numbers. The patient is then taught ways and taught skills on how to use their mind to alter different physiologic factors within their bodies such as their muscle tension or their pulse rate. They're taught ways to relax and as they do this, the read out on the computer actually shows them how much success they're having which then reinforces ability of the mind to interact and control what the body is doing. Quite often, a number of pain syndromes are reinforced by ongoing muscle tension. Muscle tension may or may not be cause of pain, but it certainly continues the pain for longer periods of time or makes the pain worse. Learning ways to control how your body reacts to the pain and to stress in general assists the patient in learning control and reducing the overall pain signaling. Other therapies that focus on mind/body reaction include hypnotherapy. It involves state of focused concentration in which patient can use their mind to control a host of physiologic factors including perception of nausea, amount of constriction in their lungs if they have asthma and effectively control perception of pain to the extent where they can turn down pain signaling Additionally, therapies such as movement therapy or integration of the body back to the mind can actually work in the reverse direction, whereby getting your body to move in ways that it is not used to sends signals to the brain that improve pain signaling, or can turn down perception of other symptoms as well. Therapies can be targeted brain to body, or body to brain. Again, operating from the direction of altering perception of symptoms, from the position of arousal and attention, individual psychotherapies, group therapy or family therapy can be helpful. At an individual level, distressing events and increased overall body arousal can contribute to ongoing pain as well as other ongoing symptoms, and addressing those distressing things in one's life can lead to less body arousal and less experience of symptoms.Dr. Bursch: When coping with symptoms and self management of symptoms, this can be addressed through learning of skills focused on relaxation, or how one interprets those signals cognitively, and what they do with the signals once they perceive them. One person might feel body sensations and interpret those as fatal and drive their symptoms higher, or they might understand through education and they might understand the symptoms they're experiencing are really symptoms of panic and they are not going to lead to death. If it is true, rather than having these symptoms lead to catastrophic thinking, it can be a signal for engaging in relaxation techniques. At a family level, parents and siblings can be taught techniques so they don't contribute to arousal or excessive attention to the symptoms. If you are sitting at your computer and very engrossed in a computer game, you might not be paying attention to your abdominal pain. If someone walks into the room and says how is your abdominal pain, your attention will shift from the computer to the abdomen and then you will perceive it and feel pain. Concerned family members often in their attempt to be supportive, contribute to increased perceptions of pain by frequently asking about symptoms. That's an example of how education and changes in behavior can affect pain perception and coping with pain.Dr. Zeltzer: Brenda, you brought up the neural peptides and the role that they play in pain, especially in the development of chronic pain. I assume you mean examples such as serotonin. Would you like to talk more about that?Dr. Bursch: Sure. In my initial discussion of physiology I left out some of the specifics about which neuropeptides and neurotransmitters were involved with chronic pain development. I think that they're interesting for a few reasons, mainly because I think that it's relatively well accepted that neurotransmitters work in your nervous system. Serotonin is involved in pathways that are functional with depression as well as anxiety. There are other neurotransmitters, such as substance P, which is major transmitter of pain, or nociception, which is the nerve signaling portion of pain. I think the truly interesting fact is that many organs other than your nervous system also have receptors for these same neuropeptides, such as substance P not only signals pain but it also causes dilation of blood vessels. That seems somewhat interesting but when you've been injured, not only do you want to tell your brain there's a site of injury but you also want to increase blood flow to that same area because you want the bloods cells that initiate healing to go there. There's the concept that the entire existence of pain evolved to signal the individual that there is some form of tissue injury and you need to stop and begin the healing process. Separate from pain, there are also other neurotransmitters that affect organs. The easiest ones to understand are neurotransmitters such as adrenaline or epinephrine. These signals cause a whole host of both emotional changes as well as physiologic changes. In addition, other neurotransmitters cause various changes in organ function. Quite often when you have different emotional states, that same neuro signaling causes differences in your organ functioning as well. People who are depressed have activated and disregulation in their immune system, as well as alterations in their liver, etc. It's no wonder that quite often chronic physical diseases are also associated with psychological illness, further indications that there is no separation between what we consider the mind and body. Both systems are continually monitoring each other. There is also research that demonstrates that behavioral interventions that increase one's sense of a mastery over a task can improve one's immune functioning. Again, this idea that it works both ways is an important one to remember.Dr. Zeltzer: Given that certain neurotransmitters play a role in both chronic pain and in other emotional states and conditions such as anxiety and depression, maybe you would like to explain why certain antidepressants that are used for treating both anxiety and depression are also useful in treating chronic pain?Dr. Joseph: The medications that we have found useful for treating pain, other than the medications such as opioids that we know have been used to treat pain for eons, have been in the realm of anti-anxiety medications or antidepressants. Ones that are useful are medications such as the tricyclic antidepressants. These medications work through a number of neurotransmitters, specifically norepinephrine and epinephrine. These medications make the specific neurotransmitters available to the nerves for longer periods of time. Not only do they help in depression, but they have been found to be very useful in decreasing pain signaling.Dr. Bursch: Other medications such as Mellaril (thioridazine hydrochloride), which is not an antidepressant but was developed to treat severe anxiety and even psychosis, is active through a different neurotransmitter pathway and is also very effective at decreasing pain signaling, as well as assisting the mind in distracting from the pain and decreasing pain perception. For these reasons, when children come to our pediatric pain clinic with chronic pain, we typically use a variety of treatments that may include medications such as those that Michael described, as well as helping the child and family to change their belief systems about the pain and the controllability of the pain, as well as function, as well as incorporating many alternative and complementary therapies such as biofeedback, acupuncture, massage, and others.Dr. Zeltzer: Certainly, because of the mind-body connection, when pain becomes chronic, it recruits so many different parts of the body -- the mind, the emotions, and the neurochemistry -- that a multi-modal (meaning many different components) approach is needed to treat the pain and help the child be able to go back to school, sleep, and do other activities.Dr. Bursch: I would like to emphasize what Dr. Zeltzer presented and underscore the importance of education.Dr. Zeltzer: Many children coming to us have been placed on drugs, even some of the same drugs we might recommend, but without the other components and because of the mind-body connection, the various components must be addressed, otherwise the drugs alone will not be effective.Dr. Bursch: Many people who have chronic pain spend much time, money, and energy attempting to find that part of their body that is broken, and while it's reasonable to have a thorough evaluation, often one's pain has been going on for a while. It is very difficult or impossible to find the source of that pain. As we've described, the reason for that is because it is a pain signaling issue that can go on, even if the initial reason for the pain has gone away. If you start to treat your pain without an understanding of this, you could spend a lot of time in search for the cause when you will never find one and, of course, be quite distressed in the meantime which can contribute to the pain itself. If you're spending a lot of time in the diagnostic part of this, then you might not be spending time on treatment and getting better. So cognitively understanding how the various systems interact to help pain continue long after the reason for pain has gone away can actually help somebody get better and refrain from causing themselves more distress and more pain.Moderator: Doctors, as we near the end of our time, would you care to offer some closing remarks?Dr. Joseph: I think I would like to reiterate the fact that your mind and your body do communicate with each other on an intimate basis. Your mind is your body and your body is your mind. Those systems are not separate. When we are dealing with chronic illness or chronic pain, what has happened is a discommunication of those normally functioning pathways. Instead of mind and body being one, they become separated and it leads to chronic stress. By learning techniques and reintegrating healthy communication, that communication enables the body and person as a whole to heal and become healthy again.Dr. Zeltzer: Certainly, I would like to provide the phone number for anybody who has a child with a chronic pain problem and would like further information about our pain clinic: It's UCLA, (310) 825 0731.Dr. Zeltzer: Thank you, Brenda and Mike, for participating.Dr. Joseph: Thank you, Dr. Zeltzer, for having us.Dr. Bursch: Thank you. http://my.webmd.com/content/article/1/1700_50465
 

· Registered
Joined
·
23,788 Posts
as I have stated before the HPA axis is part of fighting infection and IS the fight or flight system, the system directly effects gut function in IBS and IBSers are sensitive to stress and the mast cell in the gut is connected to the system. also when the brain is calm it is the result of serotonin. To much causes anxiety and the right amount relaxation.But""Psychophysiological arousal is at the core of treating functional GI disorders. There is so much distress, anxiety, antisipatory anxiety, and negative reaction to symptoms, that calming the Mind and body often makes a significant difference in symptoms."and anology is this article on going to the doctors office and as you can see the fight or flight is triggered by threats either real or perceieved, either conciously or unconciously.Does anyone see a connection?The key to being relatively calm in the dentist�s chair begins wellbefore the actual visit. I say relatively calm because if you�resuffering from dental phobia and have been for a while, it�s unlikelythat you will feel "perfectly" comfortable your first or second visit.Each of us must take an active part in overcoming our fears. Peopledon�t get over their fear of heights for instance, in an flash. It takespractice - practice changing your thoughts. Long before thedreaded event you must take charge of your thinking. If youconsciously make an effort at being more calm, you will be morecalm. Let�s create a mental picture. You�re sitting at your desk and glanceat the calendar. You notice your dental appointment is only twoweeks from today. Immediately your mind kicks into overdrive. "Iknow it�s going to be terrible. What if I get nauseous while I�m in thechair? What if the anesthetic doesn�t take hold quickly enough? Iknow it�s going to hurt. I�m grateful I found a new dentist whoadvertises gentle procedures, but can I trust him to be gentle withmy mouth? Oh I remember that awful antiseptic stench from when Iwas a youngster. I wonder if they�ve found anyway to correct that?"As you think about the upcoming visit, your body begins respondingto your fear thoughts. Physical sensations can range from mild tosevere depending on how vivid a scene you�ve painted in your mind,and how long you engage in the working up process. Yourshoulders and neck may feel tense. Your jaw may start to hurtbecause you�ve got it got your teeth clamped together so tightly.You may find yourself short of breath or a headache may belooming on the horizon. Your stomach may be churning and yourinsides trembling.Actually these body signals can be viewed as good instead of bad.They are a sure sign that you are thinking fear and a signal for youto take action. You see the body doesn�t know the differencebetween an imagined experience and a real one. How can that beyou say! If you doubt my words, think about a frightful dream youexperienced, one where someone or something was chasing you.You awaken from the dream feeling as though your heart ispounding out of your chest, perhaps even perspiring. Your bodywas reacting to an imagined fear, thoughts you were having in adream state. The character in your dream was not reality, yet yourbody responded as if he were genuine.Each and every time you catch yourself anxious about yourupcoming appointment, stop and W.A.I.T. Stop and ask yourself:What Am I Thinking? Rather than letting your thoughts control you,take the time to control your thoughts. Consciously toss out theunhealthy fear thoughts and replace them with healthy secure andrealistic thoughts. Using the picture we created earlier, here are a few ways toreprogram what�s going on in your mind. The original thoughts are initalic, followed by the replacement thought(s).Your dental appointment is only two weeks from today You can view that fact insecurely, the appointment is onlytwo weeks away, or securely - the appointment is still twoweeks away. I know it�s going to be terrible You really don�t know how uncomfortable it�s going to be.The anticipation is always worse than the actual event. What if I get nauseous while I�m in the chair? Feeling nauseous is uncomfortable, but doesn�t necessarilymean that anything worse is going to happen. Feelingnauseous is distressing, but it is not dangerous. Feelingsand sensations will rise, fall and run their course if wedon�t attach danger to them. Take away the fear (danger)and your stomach will quiet down on it�s own accord. What if the anesthetic doesn�t take hold quickly enough? If you feel the first poke of a dental instrument, speak up.Tell the doctor it hurts. If you begin to feel pain while thedrilling�s going on, hold up your hand as a signal to thedoc. You may not be able to speak clearly with theposition you�re mouth is in, but you can make some kind ofsound, Grunt if you need to.- but do show some sign thatyou�re feeling pain. Remember your pain receptors are inyour body. Even though the dentists fingers are in yourmouth, he has no clue of what you�re feeling unless you lethim know. Do not suffer in silence. And if you�re concernedabout sounding a bit odd, don�t. Dentists, assistants andhygienists are used to hearing us "talk with our mouths full."I know it�s going to hurt The replacement thought here is simply: I don�t know if it�sgoing to hurt - because you really don�t know! None of uscan predict the future. I�m grateful I found a new dentist who advertises gentleprocedures, but can I trust him to be gentle with my mouth? Realistically there is no guarantee. But in all probability theman or woman is more compassionate and caring than thedentists of long ago. Oh I remember that awful antiseptic stench from when I was ayoungster. I wonder if they�ve found anyway to correct that? Most probably they have. New technology dentistry nowincludes pleasant flavors for the things they place in ourmouths. If the flavors have improved, so have the scents.Everything on the patient end of dentistry Is moreuser-friendly these days. And all those physical sensations you experience two weeks beforeyour appointment are the direct result of your fear thoughts - theytoo are distressing, but they are not dangerous.Practice in reprogramming thoughts has two beneficial effects. Itcalms down the anticipatory fear you have before your visit, andmakes it easier to calm yourself down at the office. It�s much easierto recall secure and realistic thoughts if you�ve taken the time to usethem before. You can have them at your fingertips or the tip of yourtongue, ready to use while you�re in the chair.Another excellent method for stopping racing thoughts is objectivity- the process of thinking of something measurable and verifiable.This is a great technique to use, when you�re stuck "in the chair."Think about your automobile and picture every detail - interior andexterior colors, number of doors, the shape of the door handles, allthe indicators on the dashboard, the type of fabric on the seats.The list is endless. If you don�t own an automobile, think of aspecific room in your home. Think about the size of the room -length, width, height of the ceiling, how the furniture is placed, thecolors, lamps and all other accessories. It�s a fact that we can onlyhave a single thought in a single instant. Describing in your mind(thinking about) an object or objects that are familiar to you doesn�tgive the mind a chance to harbor racing, upsetting thoughts. Fearthoughts are persistent and they will try to sneak back in. Whenthey do, simply bring your attention (your thoughts) back todescribing your chosen object or place.When you have a fear of dentists you really have the choice of twodiscomforts -the actual discomfort you may feel during theappointment (notice I said "may" have), or you have the discomfortof not going and having the needed work done and beating yourselfup for giving into your fear. The dialogue goes like this: I�m such acoward. But I can�t help it. I�m scared. But I can�t admit it toanyone.Every act of self-control produces a sense of self-respect. Alongwith the relief you feel for having the dental procedure behind youinstead of staring you in the face, I guarantee you that when youface your fear you will gain a realistic sense of self-pride. This nextstep is important whether you do it immediately after you leave theoffice or later on in the day - take time to give yourself a mental paton the back. You deserve it! No one else needs to be aware of it. Itwas your effort that got you through. It�s your victory and you canbe proud of it.Whether your fear is dentists or tax audits, driving or diving, theabove tactics will work at reducing anxiety. If your anxiety hasgrown into a full blown phobia, it�s merely going to take more ofyour effort. The key as with any life skill is do put to use whatyou�ve learned. Changing thoughts is the first step in taking backcontrol of your life.Print this article and carry it with you for easy reference. Memorizeand use the phrase "distressing but not dangerous." Do whatever ittakes to help you be an active participant in reprogramming yourmind.It�s true - Change your thoughts and change your life.1998 Rose VanSickleAuthor - Peace of Body, Peace of Mind
 

· Registered
Joined
·
23,788 Posts
You are just unreal kelSo Kel tell me how you cure all IBSers?Tell me the specific problem and treatment you personally think "cures" ALL IBSer since there is no biological marker in IBS!And Catp CHow many IBSers have bad diets and high stress and anxiety levels and take medications? In the studies posted these causes and effects are not fully addresses in regards to IBS.Then read this.Probiotics:The link between health and diseaseby Lennart Cedg�rd, MD http://www.positivehealth.com/permit/Artic...ent/probiot.htm
 

· Registered
Joined
·
23,788 Posts
Tell me also kel, can they "cure" asthma, arthritis, and diabetes or migraines?
 

· Registered
Joined
·
23,788 Posts
yes, inflammation can contribute to the perception of pain.However why do some people with UC have higher pain thresholds, they have inflammation.and why no matter how many times I post this to you from a world leading expert in IBS and diagnosing IBS, do you ignore it? Do you know more about it then Dr Drossman?" But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it." http://www.romecriteria.org/reading1.html
 

· Registered
Joined
·
23,788 Posts
Kel, I didn't know they could cure all asthma, arthritis, and diabetes or migraines. I wonder why people stil have them.According to this they don't know the exact cause of migranes.A new method for MigranesDiscover MagazineThe Biology of . . . MigrainesGood-bye HeadachesA gun that shoots magnetic pulses puts an end to an age-old scourgeBy Marshall Jon FisherDISCOVER Vol. 25 No. 08 | August 2004 | Mind & BrainPhotograph by Grant DelinScott Fischell, CFO and COO of NeuraLieve, tests a prototype of the company�s portable transcranial magnetic stimulator. The device sends magnetic pulses into the nerves of the head and cerebral cortex, stopping migraines cold.Neil Hughes knows the sensation all too well. Everything goes blurry, and sunlight seems to reach his eyes bent every which way, as though he has suddenly slipped underwater. As the light grows brighter at the periphery of his field of vision, he raises his hands to cover his eyes, like the blinders on a horse. But the gesture is futile: An electrical firestorm, which medical researchers call an aura, is already raging inside his head. Auras are neural disturbances that signal the onset of migraine headaches. They manifest themselves in numerous ways, including multichromatic showers of shooting stars, flashing lights, zigzagging lines, images broken up into herringbone or cubist patterns, loss of vision, weakness, tingling, or confusion. Sometimes the hallucinations mysteriously come and go and are a minor annoyance. More often, what follows is a nightmare: a seemingly interminable bout with throbbing head pain, nausea, and diarrhea. For most of his adult life, Hughes, now 53, got migraines up to six times a month that rendered him violently ill, often with frightening spasms. �I would lose several days of my life lying in bed, not even knowing what time it was,� he says. He tried one remedy after another, to no avail. Doctors, he discovered, barely had a clue about what causes migraines and couldn�t offer him much relief. But now, after taking part in a clinical trial of a new device designed to quell the electrical storms in his brain, Hughes hopes he may never be laid low by a migraine again.For the 40 million or so North Americans who suffer from chronic migraines, the condition has proved maddeningly resistant to treatment�or even explanation. Migraine researchers once focused most of their attention on the constriction and sudden dilation of blood vessels that serve the brain. They knew that stimuli such as bright lights, stress, chocolate, and other foods could trigger changes in cranial circulation. And they found that, in turn, hormonelike substances called prostaglandins were secreted along with other substances that, combined with the dilation of scalp arteries, stimulate the brain�s pain receptors. But that did little to explain what made one person rather than another a migraineur�someone who is prone to migraines. In the early 1960s, researchers found that migraineurs produce low levels of serotonin, which inhibits pain and helps constrict blood vessels. This discovery led to the development of a class of drugs called triptans�most notably sumatriptan�that mimic the effect of serotonin. Triptans are still widely used and relieve active migraines 60 to 70 percent of the time. But they can also have dangerous side effects. When Hughes tried sumatriptan in the early 1990s, the injections set his heart racing and made him feel like his blood was on fire��that�s how you knew it was working,� he says. He was willing to put up with the drug at first because it was so good at stopping migraines. Then he suffered two minor heart attacks. �My cardiologist said the drug could now kill me,� Hughes says. �So there I was, back to square one, living with Anacin.�It wasn�t until the late 1990s that neuroscientists discovered a deeper source of migraines and their auras�and with it the potential for a cure. Migraineurs, they found, have a hypersensitive occipital cortex, which covers the back of the brain. By stimulating the cortical area responsible for vision, some researchers were able to trigger auralike hallucinations much more easily in migraineurs than in other subjects. The same sensitivity may make migraineurs more susceptible to bright lights, noise, and other triggers. Neuroimaging studies showed that such triggers set off an electrical wave of firing neurons that spread over the occipital cortex at a rate of several millimeters per minute. Known as a cortical spreading depression, this phenomenon had been hypothesized as far back as 1941 by the neuropsychologist and migraineur Karl Lashley. The unusual neuronal activity, in turn, seemed to foment the vessel dilation and release of prostaglandins and other substances first noted by migraine researchers.Cortical spreading depression has also been observed in epileptics just prior to seizures, and this insight eventually led to the new migraine treatment Hughes has tested. Adrian Upton, a neurologist at McMaster University Medical Centre in Ontario, first suggested the idea in 2000. Upton had previously worked with the company NeuroPace�founded by the inventor Robert Fischell and his sons David, a physicist, Tim, a cardiologist, and Scott, an M.B.A.�to develop an implantable brain defibrillator for epileptics. By making neurons fire ahead of the cortical spreading depression, as if setting off a prescribed burn in the path of a forest fire, they found they could stop the wave of neurons from spreading, and thereby prevent seizures. �Why wouldn�t the same principle work on migraines?� they wondered.When Upton asked Neil Hughes if he would participate in a clinical trial of the new treatment, Hughes agreed immediately. �Believe me,� he says, �I had nothing to lose.� Soon afterward, Hughes had one of his usual stupefying migraines, and his wife drove him to the McMaster medical center. There, a technician sat him next to a box the size of a desktop computer with a wire leading to what looked like a futuristic flyswatter. The device, known as a transcranial magnetic stimulator, is designed to send a strong electric current through a metal coil, which creates an intense magnetic field for about one millisecond. When held against a person�s head, that magnetic pulse creates an electric current in the nerves of the head and the neurons of the cerebral cortex, forcing them to fire prematurely. The stimulator had previously been used to treat depression, obsessive-compulsive disorder, and schizophrenia, in addition to epilepsy. But it had never been used on a migraine before, and Upton had no idea if it would work.Upton held the magnetic stimulator next to Hughes�s head and pressed a button, sending out two pulses five seconds apart. Hughes says he felt a �surge, like a rush of energy� entering his head. Minutes later, after a second round, the headache was gone. No more pain, no more agonizing sensitivity to light when the blinds were opened. �It was amazing,� Hughes says. �Like a flood of release of the pain and pressure. You�ve no idea unless you�ve had migraines. I even drove home.�In Upton�s clinical trials, three-quarters of all test subjects who arrived at the hospital suffering from a migraine reported feeling much better immediately after treatment. Better yet, every one of Upton�s subjects who has made it to the hospital during the aura phase has found that the magnetic stimulator dispels the aura and prevents the headache from occurring. Migraine drugs all have some side effects, including nausea, chest discomfort, and sometimes rebound headaches. But no side effects have yet been detected as a result of using the stimulator. In fact, Upton says, if the cycle of headaches�or seizures, for epileptics�is broken, then the patient may �forget� the pattern of electrical activity that leads to the symptoms. Since Hughes�s first three treatments, he hasn�t had a migraine in three years.Other new migraine treatments have come along in the meantime. A biotech company called Capnia has developed a nasal spray that shoots concentrated carbon dioxide into the sinuses, where it interrupts cortical spreading depression by irritating nerve endings that lead to the brain. Clinical results have been encouraging. Topamax, an epilepsy drug from Ortho-McNeil Pharmaceutical, has proven extremely effective on migraines in clinical trials: Half of all patients have reported a 50 percent reduction in the frequency of migraines, and more than a quarter have a reported 75 percent reduction.The Roman emperor Justinian sought migraine relief in Istanbul by pressing his head to a �magical� pillar called the column of tears. Later sufferers were purged or bled, or their heads were encircled with a noose. One ninth-century headache tonic contained elderseed, cow�s brain, and goat�s dung in vinegar. But the magnetic stimulator, thanks to its simplicity and lack of side effects, may prove to be the treatment of choice. A spin-off of NeuroPace, called NeuraLieve, is developing a lightweight handheld stimulator that migraineurs can carry around with them like a very large bottle of aspirin. The device, which weighs 2.5 pounds and runs on six AA batteries, will be in clinical trials by year�s end. �It looks a bit like a gun,� Scott Fischell admits with a laugh. �But I don�t think that matters too much. People will do anything to get rid of a migraine.� http://www.discover.com/issues/aug-04/depa...graines/?page=2 Nor is dybosis the cause of inflammtion in IBS, you don't even know what your talking about in your own beliefs, certain overt inflammation causes Dybosis, because the inflammation allows the pathogens in and this can be seen in some UC and IBD patients.But the inflammtion in IBS is not cause by dysbiosis, you just haven't study it throughly enough yet. Its mast cells and they alreay have a good reason for them to be inflammed. The inflammation is those cells and the inflammation is invisable to the nake eye.The truly sad part is the information you two post to this bb and believe in in IBS and then post as what you think are facts""Hey I wonder if we all run around being hypnotized and feeling no pain will we still need doctors??????????????????""I don't and its nice to be 90 percent more pain free with normal bowel movements and less non gi symptoms in my life then I have ever been of living with severe pain for over thrity years.Your last comments are a waste of my time kel, completely.If your doing any treatments right now what so ever this would be false. If you stop the treatments would it come back?You have prove nothing in regards to a cure for all IBS. The reason your so uneducated in IBS is because you don't take the time to do your homework on it and all the information they already have you ignore. You spend more time on proving homeopathy works then researching thouroughly what IBS is an what they know.And again both you and tal, have left out the important of molecular cell changes in the digestive tracts of IBSers! That must not be important to either of you or to IBS? Nor have you spent any time understanding diagnosing IBS and rome, because it shows very clearly that you haven't, yet you run around on the bb posting inaccurate information on IBS!!!!
 

· Registered
Joined
·
23,788 Posts
Kel"quote:-------------------------------------------------------------------------------- Nor is dybosis the cause of inflammtion in IBS --------------------------------------------------------------------------------Its not.Maybe, maybe not. I don't really know."You have that right, but then you go on to say "I suspect that intestinal dysbiosis is a big factor in most of us but "You suspect, its not a matter of a person suspecting, this is the same thing Tal is doing, she suspects with out reading and understanding all the research.For sure the two of you don't even understand the dysbiosis info."Different life situations with stress or disharmony are also very influential in creating a dysbiosis. A great number of medical drugs inhibit the beneficial flora from acting normally. Environmental toxins can also provoke an intestinal dysbiosis. Food supplements taken inadequately will disturb the important balance. It should be noted that the climate supports a variety of different bacterial cultures. This is often experienced when travelling; tourists often suffer from diarrhoea, for instance."Tal, the biggest factors for Dysbiosis, is infection, diet and stress, although medications can also be a factor! Second there can be dysbiosis in people who do NOT have IBS? How do you explain that? Third you don't know a thing about inflammation in IBS.You also cannot compare inflammation in IBD conditions with that of IBS, one is overt the other is not visibale to the naked eye and is specific cells.Probiotics have certainly shown to help IBD, but there is a differebnce between IBD and IBS with the use of probiotics, you just don't understand it yet.You also didn't get inflammation cannot be a marker for IBS. This is a fact, not outdated. It can contribute to the problem however.
 

· Registered
Joined
·
23,788 Posts
Why is there not a higher prevalance of IBS in third world countries and dysbisosis, where there are more enteric infections and again why more women, healcare seeking may be part but not all of the picture?or "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."When I had ameobic dysentarty the start of my IBS, I did not have chronic abdominal pain even though the condition almost killed me, actually I don't remeber any pain from it. And my gut was inflammed for sure and I had severe D and severe projectile nausea.Nor the fact the recent John's hopkins article you cherry picked for intestinal permeability, said IBS is probably a neurologic bowel disorder. regarless IBS is now regonized as brain gut axis disorder anyway you look at it and what ever causes it. Your just not up to date on it yet.Both the brain and gut can cause symptoms.again this is not a competition. That is a fact, both the brain and gut can cause symptoms. You are looking at it withDualism: a theory that proposes a separation between the mind and the body.That it is a only a problem of the gut.as opposed to Holism: a theory built upon the foundation that the mind and body are integrated and utterly inseparable. "IMPLICATIONS FOR FUNCTIONAL GIDISORDERSBased on the concept of dualism, disease was understood in terms of structural abnormalities. Therefore, the validity of a disease rested with the observation of morphological abnormalities. Medical conditions occurring in the absence of such morphological abnormalities and symptoms were not considered legitimate, and were often viewed as psychiatric, consistent with the concept of dualism. The concept of dualism had other effects with regard to treatment. For example, this would include all the functional GI disorders and other somatic syndromes, such as fibromyalgia. Until the latter part of the 20th century, a medical illness was considered amenable to scientific inquiry and treatment. However, patients with psychiatric disorders were interred in insane asylums and considered to no longer be treatable by medical physicians. Unfortunately this concept leads to a clinical dilemma. Specific diseases explain only about 10% of medical illnesses seen by physicians. Furthermore, people with structural (i.e. organic) diagnosis such as inflammatory bowel disease or cancer show considerable variation in their symptom presentation and clinical behavior. Gastroenterologists (as well as other health care practitioners) are all too familiar with the poor correlation between structural findings on endoscopy and their patient's symptoms. "www.med.unc.edu/medicine/fgidc/historyfunctionaldisorders.pdf "Possible causes IBS has no identifiable cause, and endoscopic, radiologic, and laboratory testing is unrevealing. The syndrome has recently been attributed to neurologic or muscular hypersensitivity of the colon. IBS is part of a broader clinical complex known as functional bowel syndrome, which includes nonulcer dyspepsia, an entity with a constellation of upper gastrointestinal tract symptoms such as upper abdominal pain, nausea, and postprandial bloating. People in whom IBS is diagnosed often have symptoms related to nonulcer dyspepsia at various times in their life, and the reverse is true of those in whom nonulcer dyspepsia is diagnosed. This observation suggests that subtypes of functional bowel syndrome--specifically, IBS and nonulcer dyspepsia--do not involve a particular gastrointestinal organ. Thus, IBS is not a disease reflecting intrinsic colonic dysfunction. Instead, the disorder appears to be caused by a central neurologic mechanism that manifests itself as symptoms originating in different organs at various times. "Nor do you understand diagnoses at all in IBS."Diagnostic criteria To characterize IBS and establish criteria for diagnosis, Manning has suggested a constellation of symptoms that differentiate IBS from organic disease (1). These symptoms include lower abdominal pain and irregular bowel evacuation (eg, diarrhea, constipation, straining with bowel movements). Patients often have predominant manifestations of either constipation or diarrhea. Other criteria identified by Manning that are common to IBS include a perception of abdominal distention, the passage of mucus with bowel movements, and a sensation of incomplete evacuation (table 1). Patients often note loose or frequent bowel movements at the onset of abdominal pain, with relief of pain after defecation. Since these complaints also occur with organic disease, each symptom is neither a sensitive nor a specific indicator of IBS. However, with clustering of several symptoms, the likelihood of IBS increases. " "Response to warning indicators Talley and associates (2) also found that people with IBS often have symptoms considered to be warning signs of organic disease. Weight loss, rectal bleeding, recent changes in bowel pattern, and pain or bowel movements that wake a patient are usually attributed to organic disease, especially in older people. Such symptoms always warrant further investigation and are often explainable after evaluation for IBS. In patients with IBS, weight loss may be due to depression, and rectal bleeding is commonly attributed to hemorrhoids or anal fissure caused by straining with a hard bowel movement. However, a thorough evaluation to exclude organic disease is imperative before such symptoms are attributed to IBS. Thus, IBS must be considered a diagnosis of exclusion when these symptoms or other atypical features are present. " http://www.postgradmed.com/issues/2000/03_00/licht.htm This was when they use the manning criteria, they have since use rome l and Rome ll. It is no longer a diagnoses of exclusion either. When the enteric nervous system encounters a pathogen it runs a progam that give a person d and sometimes nausea to dispel the pathogen as quickly as possible. That is not consistent with alternating subtypes in IBS or as mentioned above the cluster of symptoms to diagnose IBS taken together, which using rome ll is a STABLE diagnoses."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 HillAddress correspondence to: Douglas A. Drossman, M.D.Division of Digestive Diseases726 Burnett-Womack Bldg. CB #7080University of North CarolinaChapel Hill, N.C. 27599-7080 The diagnostic evaluation of patients with irritable bowel syndrome (IBS) can be challenging for several reasons. First, there is no biological marker for the disorder. The diagnosis is based primarily on the presence of a clustered set of symptoms relating to abdominal pain or discomfort and altered bowel habit. Second, it follows that a diagnosis based solely on symptoms can be unsettling; clinicians will struggle with the possibility of missing another diagnosis. This level of uncertainty may increase the risk of overdoing diagnostic studies, though many clinicians believe an extensive diagnostic effort justified: it seeks to satisfy the patient's request for a specific diagnosis, as well as the physician's personal interest to "leave no stone unturned". Unfortunately, this approach contributes to the disproportionately high health care costs for IBS relative to other GI disorders as reported in one Health Maintenance Organization study (1). Finally, developing a diagnostic algorithm for IBS can be challenging given the effect of psychosocial co-factors including psychiatric diagnosis, daily and life stress and other psychosocial domains on IBS (2). Currently, the diagnostic evaluation of patients presenting with IBS symptoms has no simple standard; it is based on the art and science of medicine. Several factors can influence the decision making: a) symptom pattern and severity will influence, for example whether mucosal biopsies are taken for diarrhea-predominant symptoms, or ultrasound or CT are done for pain and weight loss(3),
demographic features such as older age on initial presentation or a family history of IBD or colon cancer may lead to a more extensive (e.g., colonoscopic) evaluation, c) a patient's pain communication style or illness-related behaviors must be appraised in the light of objective screening data; this, for example will reduce the tendency merely to order tests based on urgent requests to "do something" ("furor medicus") (4), and finally d), the clinical setting will influence the prior probability of other medical disorders; so primary care physicians more than gastroenterologists will minimize diagnostic studies, treat the symptoms of IBS, and follow the patient expectantly (5), simply because the likelihood of another serious medical disease in a primary care setting is far less than in a referral practice. Efforts to consolidate these many influences on diagnostic decision making have occurred by creating specific published guidelines obtained by consensus (3;6) (7). Most all authors agree that an initial diagnosis of IBS should be fulfilled by: a) meeting symptom-based diagnostic criteria, such as Rome II (6;8), Rome I (9) (10), or occasionally, Manning (11) criteria, obtaining a negative physical examination, and performing a cost-effective, conservative set of screening studies. These usually include a sigmoidoscopy (or colonoscopy for patients older than 50 years), a few laboratory tests (e.g., CBC, stool for occult blood or ova and parasites) and additional studies if certain "alarm" features are found: fever, an abnormal physical examination, blood in the stool, an abnormal CBC or elevated sedimentation rate, significant weight loss, nocturnal symptoms that awaken the patient, or a family history of cancer or inflammatory bowel disease (12;13). Several prospective studies now offer evidence that the proper application of such recommendations rarely leads to a revision in diagnosis, even for patients followed over many years (14;15) (6). In one study, the positive predictive value for the diagnosis of IBS using Rome I criteria and excluding "red flags" over 1-year follow-up was 98% (12). Of course, the gastroenterologist in referral practice may not be content to accept these probabilities without first excluding those rare conditions overlooked by routine evaluations. So how far should the gastroenterologist go in the workup of patients referred to them who typically present with IBS, and have negative screening studies? One gastroenterologist, recently commented to me: "I order breath hydrogen studies and sprue serologies on all my patients referred with IBS". No doubt this comment reflects the concern that as referral gastroenterologists we have an obligation to contribute additional expertise to the diagnostic effort. Recently, the breath H2 test is being requested more actively by physicians and the public alike possibly because of media attention to a study claiming a 73% rate of bacterial overgrowth in patients with IBS referred for breath H2 testing, and a 50% improvement with antibiotic treatment (16). However, the design limitations of this study, including a high ascertainment bias, use of an uncontrolled and unblinded treatment protocol, and only a 30% follow up rate evaluated over a relatively short period of time, makes it unlikely that clinicians in practice will also obtain such dramatic results. So while this study increases awareness of bacterial overgrowth as an entity that can mimic or exacerbate IBS, clinical experience suggests that the diagnostic yield in general GI practice is probably much lower than reported, perhaps 10% or less. What about celiac disease? This disorder should always be considered in evaluating IBS, because the diarrhea and abdominal discomfort due to proximal small intestinal villous atrophy and inflammation will specifically respond to a gluten-free diet. Therefore, making a diagnosis early may be cost-effective. The prevalence of celiac disease in the US is reported to range from 1:250 to 1:1500 (17). However, this is influenced by the method of assessment as well as the prior probability of the disorder being present in the population under study. With regard to the method of assessment, in a study set in Olmstead County (18), the reported prevalence was 1:4,600, and the cases were identified by clinical and pathological criteria. In contrast, when serological methods are used, the prevalence is at 1:250 or even higher (19), and in one recent study the prevalence for women was 1:125 compared to males at 1:250 (20). So, when clinically suspected, primary care physicians and specialists may now obtain anti-gliadin and anti-endomysial IgA antibody serologies. These are reasonably effective screening tests, given that the sensitivities and positive predictive values range from 90% - 100% (17). However, in populations where the prevalence of this disorder is low, many positive serological tests will be false positives. Therefore, because the gold standard of diagnosis requires upper endoscopy with duodenal biopsy, endoscopy is almost always needed for confirmation of the diagnosis. But can we be satisfied that these studies are enough to exclude celiac disease? In this issue of Gastroenterology, Wahnschaffe et al.(21) raise concerns about the possibility of missing a diagnosis of latent or potential celiac disease among persons thought to have IBS. Patients with latent or potential celiac disease have a genetic susceptibility for the disease, but do not have the histopathological findings (i.e., no villous atrophy or notable mucosal inflammation) when exposed to a gluten diet, so a small bowel biopsy will not make this diagnosis. In contrast to potential celiac disease, latent disease is characterized by mucosal changes that occurred at some point in time and recovered on a gluten-free diet. The authors propose that both these groups may still respond clinically to a gluten free diet. This creative study attempted to identify patients with latent or potential celiac disease (i.e., who presumably had negative serological screens for celiac disease) in a sample of 102 IBS patients. They evaluated a variety of serological, intestinal and genetic markers, and compared the findings to control groups with treated and untreated celiac disease, latent celiac disease and normal controls. They found two surrogate markers: a) the expression of HLA-DQ2 alleles DQA1*050/DQB1*0201, a genetic marker for celiac disease, and
an increased intestinal IgA titer against tissue-transglutaminase and/or gliadin were elevated in the small sample of patients with latent celiac disease. Notably, the assessment of intestinal (rather than serological) antibodies is a unique aspect of this study; it is a diagnostic method for celiac sprue that is not commonly done. Then, when evaluating the IBS patients, they found that 35% had expression of the HLA-DQ2 genotype, and this subgroup of IBS patients had significantly increased IgA antibodies against the celiac disease-associated antigens gliadin and/or tissue-transglutaminase in the duodenal aspirate, as well as increased intra-epithielial lymphocytes (also characteristic of celiac disease) when compared to IBS patients without expression of the HLA-DQ2 genotype. Furthermore, 26 IBS patients were put on a gluten-free diet for 6 months. The 13 patients who were positive for the HLA-DQ2 alleles and for the intestinal celiac disease-associated antibodies had a significant reduction in stool frequency and intestinal IgA antibody titers for the celiac disease-associated antigens. This improvement did not occur in the remaining IBS patients on gluten free diet who were negative for HLA-DQ2 gene expression. They conclude that the presence of these two markers in patients with IBS may identify a subgroup with latent or potential celiac disease that may respond to dietary restriction. These findings must be put into a clinical perspective. First, the authors identified the IBS patients as those who had a "�variable combination of abnormal bowel habits in the absence of endoscopic, histopathological, laboratory and microbiological abnormalities." However, these criteria are not sufficient for diagnosing IBS. We do not know how many of these patients actually had abdominal pain, the key symptom criterion for a diagnosis of IBS. Clinically, patients with diarrhea and no pain are considered separate from IBS ("functional diarrhea"), and they define a group where celiac disease is more likely than patients with typical IBS having abdominal pain. In fact, if many of these patients did not have pain, and therefore did not fulfill criteria for IBS, then the findings of the study and its implications for IBS may be quite different. Second, the sample sizes for some of the cells were small. Only 5 patients had latent celiac disease, and the improvement in response to gluten restriction occurred in a sample of 13 patients with IBS who were HLA-DQ2 positive. It will also be valuable to conduct this study in a controlled fashion using a large group of patients with IBS not having celiac disease markers in order to determine the placebo response rate to a gluten free diet. Even the reduction in serologies with a gluten free diet may not provide complete evidence for a clinical response, since dietary restriction of gluten might reduce the antigenic challenge to the immune system, leading to a serological response that is unrelated to the changes in stool frequency. Despite these limitations, this study has raised some important concerns regarding our sense of "security" in accepting normal histopathology to exclude celiac disease in patients having symptoms of IBS, and has opened the door to pursuing these issues in larger clinical trials. Is it possible that some simple and inexpensive tests will emerge to accurately diagnose IBS? I do not think that IBS can by diagnosed by ordering tests, either to make a unitary diagnosis, or by default by excluding other disorders. There is evidence that IBS is a heterogeneous disorder where different physiological subgroups contribute to the clinical expression of the syndrome. For example, there is a subgroup of patients, called "post-infectious IBS" who appear to respond to an enteric infection such as campylobactor jejuni with an increased inflammatory cell response (22). This is associated with activating enterochromaffin cells to produce 5HT, and CD3 cells to produce cytokines, which in turn leads to enhanced motility and lowered visceral sensation thresholds (22;23). But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it. All patients with active celiac disease have microscopic inflammation, but a large proportion do not have abdominal pain, and patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds (24). In individuals with these disorders, there may be central nervous system counter-regulatory measures responding to the peripheral pain/inflammatory processes that increase pain thresholds. With regard to IBS, the gut-related effects of microscopic inflammation may be only one component of a dysfunctional brain-gut system. In addition, and often in response to stress, there may be a failure to activate descending pain inhibitory systems that enable the clinical experience of pain and other symptoms that typify this disorder (25). In one prospective study of post-infectious IBS, it was found that those who retained their symptoms 3-months after an enteric infection had not only increased mucosal cellularity, but also had increased psychosocial distress at the time of the infection. Furthermore, lowered visceral sensation thresholds and increased motility were present after the infection regardless of whether or not the patients retained their symptoms (26). Therefore, the microscopic inflammation and its physiological effects on motility and sensation contribute to, but are not always sufficient for the clinical expression of IBS pain. At least for post-infectious IBS this provides some evidence that psychological distress alters brain pain regulatory pathways to amplify incoming visceral signals leading to the full clinical expression of this syndrome (27;28). Recent studies using brain imaging (29;30)may help us to understand the physiological mechanisms that modulate these CNS responses to pain, and in the process, identify the subgroup with IBS that are more amenable to psychological and psychopharmacological treatments. As we continue to develop the means to assess the pathophysiological determinants of IBS symptoms, we will continue to identify subgroups that will change our diagnostic assessment, and may even redefine what we mean by IBS. Post-infectious IBS, and patients having concurrent psychosocial disturbances (among others to be determined) characterize subgroups that will be more responsive to more specific treatments. For the present, we must still make a diagnosis of IBS based on established guidelines including symptom-based (e.g., Rome) criteria. We must also remain vigilant to identifying other relevant disorders like celiac disease that may mimic or exacerbate IBS, and will use clinical judgment (e.g., ordering anti-endomysial antibodies for patients with predominant diarrhea), rather than routinely ordering tests in all IBS patients just to exclude other disease. With careful appraisal of the historical and laboratory data and good clinical judgment, a positive diagnosis of IBS can be made in a cost-effective manner and with confidence. " http://www.romecriteria.org/reading1.html The above is less then three years old."Gastroenterology Expert ColumnDiagnosing Irritable Bowel Syndrome: What's Too Much, What's Enough?Posted 03/12/2004 Susan Lucak, MD IntroductionIrritable bowel syndrome (IBS) is the most common gastrointestinal disorder diagnosed in clinical practice in the United States. Because there is no biological marker to confirm the diagnosis of IBS, it is a diagnosis that has challenged clinicians for decades. In the past, IBS was a "waste-basket" diagnosis given to patients with unexplained gastrointestinal symptoms. It was considered to be "the diagnosis of exclusion" when extensive work-up for organic disease yielded no diagnosis.In recent decades, it was recognized that patients with IBS experienced a constellation of specific gastrointestinal symptoms. Manning criteria were described in 1978,1 followed by Rome I in 19892 and Rome II criteria in 1999.3 Rome I and Rome II criteria were initially developed by multinational working groups to provide a framework for the selection of patients in diagnostic and therapeutic trials. These criteria are being continuously modified as we gain new knowledge about functional bowel disorders.Recently published diagnostic guidelines4,5 recommend using symptom-based criteria in making the diagnosis of IBS in clinical practice. Using these criteria in conjunction with "alarm features" allows a physician to minimize the extent of diagnostic testing needed to make the diagnosis of IBS. Furthermore, recent systematic review of the literature indicates that performing a number of diagnostic tests did not result in a significant increase in the diagnosis of organic gastrointestinal disease.6EpidemiologyWhen making the diagnosis of IBS, it is helpful to consider it in the context of its epidemiology. IBS is a very common gastrointestinal disorder in the United States, affecting 10% to 20% of the population.7 Female patients outnumber male patients by 1.5-3.0:1.0 in most epidemiologic studies.8 Although it is not well understood why more women present with IBS, differences in healthcare-seeking behavior may partly account for this predominance.Smith and colleagues9 found that psychosocial factors were determinants of healthcare seeking for patients with both organic gastrointestinal disorders and functional gastrointestinal disorders. History of abuse is another important determinant in healthcare seeking.10Symptom-based CriteriaIn a given patient, the diagnosis of IBS is suggested by identification of specific symptoms. The Rome II criteria for diagnosis of IBS include presence of abdominal pain or discomfort for 12 weeks (need not be consecutive) in the preceding 12 months, and at least 2 of the following 3 features regarding symptoms: (1) relieved with defecation, (2) associated with change in frequency of defecation, and /or (3) associated with a change in form or appearance of stool. Patients with IBS may have additional symptoms, including passage of mucus and bloating or abdominal distension (Table 1).3 Although refinement and validation of these criteria are necessary, Rome II criteria are widely accepted as a diagnostic instrument in IBS."Alarm Features"An important aspect of making the diagnosis of IBS is the absence of "red flag" or "alarm features" (Table 2).4,11,12 Unexplained weight loss may reflect disorders such as malignancy, inflammatory bowel disease (IBD), or celiac disease. Persistent diarrhea or severe constipation may be associated with an organic disease.IBS is generally an intermittent and recurrent disorder. Symptoms of IBS tend to disappear at night when the patient is asleep. Thus, nocturnal gastrointestinal symptoms warrant search for a diagnosis other than IBS. The onset of new gastrointestinal symptoms after the age of 50 should prompt the physician to look for organic disease, particularly colorectal cancer. Blood in stool may reflect IBD or an infectious process or colon cancer. Family history of IBD, celiac disease, or gastrointestinal malignancy requires evaluation for these diseases. Fever suggests the possibility of an infectious or inflammatory disorder. Anemia should alert the physician to look for IBD or colorectal cancer. Signs of bowel obstruction, malabsorption, extraintestinal signs of IBD, or thyroid dysfunction should all prompt organic disease work-up. Any laboratory test abnormalities should be pursued appropriately. Absence of these "alarm features" serves to support, not establish, the diagnosis of IBS.Physical ExaminationThe American Gastroenterological Association (AGA) Technical Review on IBS recommends that a physical examination be performed, primarily to rule out organic disease.4 For instance, the presence of abdominal mass, signs of obstruction, or enlarged liver should trigger further investigation. A rectal examination identifying lax sphincter may confirm complaints of fecal incontinence, whereas paradoxical pelvic floor muscle contraction may suggest pelvic floor dyssynergia. In the latter case, anorectal motility study may be appropriate. Digital rectal examination is of further value in the assessment for fecal occult blood. A pelvic examination (performed by a gastroenterologist or a gynecologist) should be performed if symptoms point to the pelvic/lower abdominal area and are associated with menses.Diagnostic TestingReview of the current literature does not support performance of extensive testing in patients who meet symptom-based criteria for IBS and who lack "alarm features."6,13 Cash and colleagues[6] performed a systematic literature review of frequently ordered diagnostic tests as part of IBS work-up (Table 3). After careful assessment of the quality and validity of the selected studies, it was concluded that the pretest probability of organic disorders (such as IBD, colon cancer, thyroid disease, and lactose malabsorption) was not significantly increased in patients suspected of having IBS when compared with the general population. In other words, when patients fulfilled symptom-based criteria for the diagnosis of IBS, performing tests such as flexible sigmoidoscopy, barium enema, colonoscopy, rectal biopsy, complete blood count (CBC), serum chemistries, fecal occult blood test (FOBT), TSH, stool ova and parasites (O&P), hydrogen breath test for lactose malabsorption, or abdominal ultrasound did not result in a significant increase in the diagnosis of organic gastrointestinal disease. Specifically, performing a colonoscopy did not result in identifying gastrointestinal organic disease in more than 1% to 2% of cases.Widespread testing for celiac disease in patients who fulfill symptom-based criteria for IBS is not recommended.4,5 A matched case-control study in the United Kingdom showed 66 of 300 IBS patients had positive celiac disease auto-antibodies and 14 had biopsy-proven celiac disease compared with 2 out of 300 control subjects.14 This demonstrates a 7-fold increase in occurrence of celiac disease in patients suspected of having IBS. This study was, however, conducted in a secondary care setting. Given availability of effective therapy for celiac disease and prevention of long-term morbidity, testing for celiac disease with celiac disease auto-antibodies may not be unreasonable.The most recent AGA Technical Review on IBS4 recommends the performance of screening and other diagnostic tests as listed in Table 4. Colonic visualization with colonoscopy or flexible sigmoidoscopy/barium enema should be performed according to colorectal cancer screening guidelines. A colonoscopy is recommended for patients over the age of 50 years, but in younger patients, performing flexible sigmoidoscopy or colonoscopy needs to be determined by clinical presentation and sound clinical judgment.4,5 In many cases, therapy can be instituted before diagnostic studies are done or completed.The American College of Gastroenterology (ACG) Task Force comments on the value of "reassurance" derived from negative evaluation for organic disease.5 It is pointed out that the value of this "reassurance" is unclear and should be assessed in future clinical trials.The extent to which a diagnostic work-up is performed also depends on the severity of symptoms and where a patient with IBS presents.Primary Care SettingMost patients with IBS (about 70%) present to primary care physicians.4 Patients with IBS in this group have symptoms that tend to be mild in severity. A recently published evidence-based review by the ACG IBS Task Force concluded that routine testing among patients with symptoms "fitting" the Rome II criteria and no "alarm features" is not necessary in the primary care setting.5Secondary Care SettingMore difficult or more severe cases of IBS are generally seen by gastroenterologists referred from primary care physicians. The estimated prevalence of this subgroup is about 25% of all patients with IBS.If screening and other diagnostic tests were done by the primary care physician, they do not need to be repeated. The need for colonic visualization should be determined according to guidelines outlined above. Further evaluation may be warranted if a patient presents with any of the following features: (1) short duration of symptoms or worsening severity of symptoms, (2) onset of symptoms at an older age ( 50 years), (3) family history of colon cancer or IBD, or (4) absence of psychosocial features or absence of healthcare seeking.4During the first visit, it is important to explore with the patient possible contributing factors such as psychosocial issues (stress, anxiety, depression) and history of abuse. Up to 40% of patients may have a history of sexual, physical, or mental abuse.10Clearly, the right balance needs to be struck between making an accurate diagnosis of IBS and, at the same time, not missing other diagnoses that may mimic IBS. It is important to recognize, however, that if a patient diagnosed with IBS does not respond to a therapy, the diagnosis may be reassessed in 3 to 6 weeks and additional evaluation can be performed (see Table 5).4Tertiary Care SettingThe most severe cases of IBS and those most difficult to treat are seen in referral centers. The latter group comprises approximately 5% of all IBS cases. The clinical symptoms for this patient group do not tend to correlate with gut physiology. Rather, these patients tend to have constant symptoms, more psychosocial difficulties, greater healthcare-seeking behavior, more illness behavior (illness behavior is a way in which an individual perceives, interprets, and reacts to physical sensations that can be interpreted as symptoms of disease), and more psychiatric diagnoses.4Generally, most diagnostic studies have been performed by the time a patient with IBS presents to a referral center. Specialized studies such as defecating proctography, rectoanal angle measurement, anorectal motility and balloon expulsion, and investigational testing may be performed depending on clinical presentation and lack of response to previous treatments (see Table 5).4Differential Diagnosis and Durability of DiagnosisDifferential DiagnosisSymptoms of IBS are nonspecific and may mimic a number of disease entities (Table 6).15 It is important to recognize that in a given patient with IBS, these diagnoses need not be "excluded" before a diagnosis of IBS can be established.Durability of DiagnosisA number of studies conducted in community-based and specialty-based clinics over the past 3 decades have demonstrated that once the diagnosis of IBS is made, only a small percentage (0.7% to 6.5%) of patients subsequently receive a diagnosis of organic disease.16-20 These studies provide evidence that once the diagnosis of IBS is established, additional studies are not necessary unless the clinical symptoms change.Legal Risks in Diagnosing IBSSome physicians who see patients with IBS are concerned about the risk of malpractice. Feld21 recently described sources of risk under which physicians may be sued, including negligence, duty to provide care to a patient, and medical practice below standard of care, among others. But the idea that more testing is better in IBS may not always be the case. For example, colonoscopy leads to a change in diagnosis about 1% to 2% of the time and may represent performance of substandard care based on testing guidelines for IBS diagnosis recommended by gastroenterological associations in the United States. Therefore, any complication resulting from "unnecessary" testing may expose a physician to a malpractice suit. Alternatively, if a physician explains to a patient why only limited testing is necessary, this allows a patient to participate in the process and understand inherent uncertainties and thus share in the responsibility when a reasonable decision results in an adverse outcome.21 Feld's risk management recommendations are outlined in Table 7.Summary and ConclusionsWhat's too much when we think about diagnosing IBS is to do exhaustive and duplicate testing. In a retrospective, community-based study in Olmsted County, Minnesota, two thirds of patients who consulted for gastrointestinal symptoms had to wait at least 2 years to have their IBS diagnosed, despite averaging nearly 5 healthcare visits per year.20 Such an approach is not only costly and inefficient, but it delays treatment and fosters frustration on the part of the patient and the physician.What's enough is to use symptom-based criteria, "alarm features," and guidelines proposed by the ACG IBS Task Force and the AGA Technical Review on IBS in making a more timely diagnosis of IBS. Although additional studies are necessary to validate Rome II criteria and to assess diagnostic testing in prospective studies, the expert guidelines allow the diagnosis of IBS to be made with greater efficiency, certainty, and confidence. Furthermore, once a diagnosis of IBS is made, it is retained in more than 93% of cases with a long-term follow-up. Considering legal aspects of IBS diagnosis, symptom-based criteria and guidelines set forth by the ACG and AGA are becoming key elements in establishing standard of care. It has become clear that the diagnosis of IBS can and should be made quickly so that treatment can be initiated as soon as possible. This promotes greater patient confidence in the physician. http://www.medscape.com/viewarticle/465760_9 "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 On the inflammation you still don't get it Tal and nor are they my researchers on IBS they are everyones and one of if not the top center in the US.I have told you this before, you have not put enough time in to be careful of how to interpret a lot of studies you post. You also suffer from extreme tunnel vision that IBS is only dysbiosis and bacteria.Even the people studying it think its a small part of the puzzle"Marshall is the lead author of a new study that may help explain how those symptoms start.The study involved 132 Walkerton residents with IBS and 86 residents without the condition. Average age was 46 years and about 60 per cent were female.Nearly 36 per cent of IBS cases had abnormal intestinal permeability, or "leaky gut syndrome," a condition in which the lining of the intestines allows more bacteria, toxins and food to leak in and potentially irritate the deeper tissue layers. In comparison, less than 19 per cent of non-IBS participants had a leaky gut.Marshall says his findings represent only a small piece of the entire IBS puzzle, but he hopes they will provide the basis for future research in the Walkerton population. "Why did NON IBS patients have "leaky gut"?This was also a virus outbreak.This also does not go into PI IBS infromation.
 

· Registered
Joined
·
23,788 Posts
If your going to tell people what IBS is Tal or even suggest it or how people get it, you better learn more about what they know and how they diagnose it, because you have not even grasped that yet, and while your at it study how digestion works in the first place.
 

· Registered
Joined
·
23,788 Posts
From the the International foundation of functional GI disorders."Characteristicsof IBS How common is IBS?Most people with IBS have mild symptoms. Many people don't recognize IBS symptoms. Yet, IBS is one of the most common disorders seen by physicians. Irritable bowel syndrome is characterized by symptoms of abdominal discomfort or pain, usually in the lower abdomen (although the location and intensity are variable, even at different times within the same person), and altered bowel habit (change in frequency or consistency) -- chronic or recurrent diarrhea, constipation, or both in alternation. Abdominal pain has been reported as primarily crampy or a generalized ache with superimposed periods of abdominal cramps, although sharp, dull, gas-like, or nondescript pains are also common..The abdominal discomfort or pain are usually relieved with a bowel movement. "Irritable Bowel" refers to a disturbance in the regulation of bowel function that results in unusual sensitivity and muscle activity. "Syndrome" refers to a number of symptoms and not one symptom exclusively.Everyone suffers from an occasional bowel disturbance. However, for those with IBS the symptoms are more severe, or occur more often -- either continuously or off and on. IBS affects men and women of all ages. Some or all of IBS symptoms can occur at the same time -- some symptoms may be more pronounced than others. There are no physical findings or diagnostic tests that confirm the diagnosis of IBS. Diagnosis involves identifying certain symptoms consistent with the disorder and excluding other medical conditions that may have a similar clinical presentation. The symptom-based Rome II diagnostic criteria for IBS emphasize a positive diagnosis rather than exhaustive tests to rule out other diseases. These criteria are based on the presentation of a specific set of symptoms. In addition, a detailed history, a physical examination, and limited diagnostic tests help confirm this diagnosis with a high level of confidence. Extensive testing may be reserved for specific situations. The Rome II Diagnostic Criteria (a system for diagnosing functional gastrointestinal disorders based on symptoms) for IBS is as follows:At least 12 weeks or more, which need not be consecutive, in the preceding 12 months of abdominal discomfort or pain that is accompanied by at least two of the following features: 1) It is relieved with defecation, and/or2) Onset is associated with a change in frequency of stool, and/or 3) Onset is associated with a change in form (appearance) of stool. Other symptoms that are not essential but support the diagnosis of IBS: Abnormal stool frequency (greater than 3 bowel movements/day or less than 3 bowel movements/week); Abnormal stool form (lumpy/hard or loose/watery stool); Abnormal stool passage (straining, urgency, or feeling of incomplete evacuation); Passage of mucus; Bloating or feeling of abdominal distension. Upper GI symptoms are commonly reported by IBS patients with 25% to 50% of patients reporting heartburn, early feeling of fullness (satiety), nausea, abdominal fullness, and bloating. Many patients also report intermittent upper abdominal discomfort or pain (dyspepsia). Feelings of urgency, and a feeling of "incomplete" emptying may also be experienced.Many IBS patients also report non-gastrointestinal symptoms such as fatigue, muscle pain, sleep disturbances, and sexual dysfunction. These symptoms may be due to the coexistence or overlap of IBS with another condition such as fibromyalgia, chronic fatigue syndrome, or interstitial cystitis. Symptoms can vary and sometimes seem contradictory, such as alternating diarrhea and constipation. The symptoms of IBS are produced by abnormal functioning of the nerves and muscles of the bowel. In IBS there is no evidence of an organic disease, yet, something -- a "dysregulation" between the brain, the gut, and the central nervous system -- causes the bowel to become "irritated," or overly sensitive to stimuli. Symptoms may occur even in response to normal events. IBS is not caused by stress. It is not a psychological or psychiatric disorder. It is not, "All in the mind." IBS is not caused by stress. It is not a psychological or psychiatric disorder. It is not, "All in the mind." Because of the connection between the brain and the gut, symptoms in some individuals can be exacerbated or triggered by stress. Dietary and hormonal factors can affect symptoms of IBS. IBS is not an indication of another more serious disease, like cancer. Irritable bowel syndrome can, however, seriously compromise a person's quality of life. Chronic and recurrent symptoms can disrupt personal or professional activities, upset emotional well being, and limit individual potential.A significant proportion -- 35% to 40% -- of individuals who report IBS in the community are male. Approximately 60% to 65% of individuals who report IBS in the community are female.IBS is a major women's health issue. Data reveals an increased risk of unnecessary surgery for extra-abdominal and abdominal surgery in IBS patients. For example, hysterectomy or ovarian surgery has been reported in female patients with IBS as high as 47% to 55% and has been performed more often in the IBS patient than in comparison groups.There is a pressing need to support educational programs about IBS to the public and health care providers. Anemia, bleeding, weight loss, or fever are not characteristic of IBS. You should alert your physician immediately if you are experiencing these symptoms. Other factors that may suggest the presence of an organic disease include awakening from sleep at night, family history of colon cancer or inflammatory bowel disease, and onset of symptoms (or change in symptoms) over the age of 50. " http://www.aboutibs.org/characteristics.html
 
1 - 20 of 44 Posts
This is an older thread, you may not receive a response, and could be reviving an old thread. Please consider creating a new thread.
Top