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Discussion Starter · #1 ·
FYIInteresting to note."Is IBS a disease related to inappropriate immune activation of the intestine?""Evidence was reviewed showing that currently availabledata does not support the immune activation hypothesis. Inthe absence of altered perceptual responses to a chronically,mildly inflamed intestine, typical IBS symptoms would be quiteunlikely. Similarly, current evidence does not support that IBSsymptoms only occur in patients with depression or anxiety,and that IBS symptoms in the normal population are generallynot associated with DSM-4 diagnoses. As an alternative, thefollowing hypothesis was proposed:IBS reflects an alteration in the perception of and responseto homeostatic feelings." http://www.ibsgroup.org/ubb/ultimatebb.php...c;f=10;t=001077
 

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Discussion Starter · #2 ·
By the way, in the UNC chat last night, they said there is "definitely" a serotonin problem in the gut in IBS.
 

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Discussion Starter · #3 ·
This is also a new article by Dr Mayer. He is a top neurogastroenterologist at the "UCLA/CURE Neuroenteric Disease Program "This is a new state of the art research center.Both the UNC and UCLA received NIH grant money recently to study IBS and functional disorders."Visceral Sensations and Brain-Gut MechanismsBy: Emeran A. Mayer, M.D., Professor of Medicine, Physiology and Psychiatry; Director, Center for Neurovisceral Sciences & Women's Health, David Geffen School of Medicine at UCLAIntroduction Over the past several years, different mechanisms located within the gut, or gut wall have been implicated as possible pathophysiologic mechanisms underlying the characteristic IBS symptoms of abdominal pain and discomfort. The list ranges from altered transit of intestinal gas, alterations in the 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 ("spastic colitis") and alterations in mucus secretion. While the jury on any of these novel mechanisms 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 conscious perceptions of every alteration in gut homeostasis and internal environment, in particular when these changes are chronic, and when there is no adaptive behavioral response an affected organism could generate. " http://www.aboutibs.org/Publications/VisceralSensations.html
 

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Thanks Eric,I just took another look at the original article that presented the "molecular defect" findings. For new people or anyone who wants to refresh their memory, here it is. http://www.pharma.us.novartis.com/newsroom...=1266&checked=y So my question is, were these conclusions not "definite" at that time? Do you think that what the experts said last night indicated that they are more sure now than they were then? The article also spoke or six or seven other studies that were still being conducted at the time of its publication. I can't wait to see the results.
 

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Discussion Starter · #5 ·
jjohnson , there is a serotonin problem in the gut. IBS for awhile now has been a dysregulation of serotonin between the gut and brain and back.The majority of IBS patients effectively demonstrate this in GI centers.It is just so complex, there is a lot more to figure out.Also, viceral hypersensitivity is being studied more for it cause. Its looking like the problems seen in how the brain processes signals from the gut in IBS is turning out to be more and more important to IBS. so we still havealtered motilityviceral hypersensitivityand brain gut axis dysfunction.The serotonin helps explain the altered motility and to some extent the viceral hypersensitvity and brain gut axis dysfunction.But serotonin might not be the only problem/problems. It is more complex then that I believe. Things can also cause cascading problems where one malfunctions and effects other things and they malfunction. There are also still a lot of chemicals and things to be researched. Brain imaging right now is very important to IBS. As well as how the gut and brain really communicate.Dr Gershon, who you posted there is a world expert on the enteric nervous system, or "gut brain."All of these experts though are making some major headway.They are trying to "The cause of IBS is yet to be determined. However, modern research understands IBS as a disorder of increased reactivity of the bowel, visceral hypersensitivity and dysfunction of the brain-gut axis. There are subgroups being defined as well, including post-infectious IBS which can lead to IBS symptoms. Other work using brain imaging shows that the pain regulation center of the brain (cingulate cortex) can be impaired, as well as good evidence for there being abnormalities in motility which can at least in part explain the diarrhea and constipation. So finding a specific "cause" of IBS has grown out of general interest in place of understanding physiological subgroups that may become amenable to more specific treatments. Hope that helps.Doug " http://www.ibshealth.com/ibs_foods_2.htm
 

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Discussion Starter · #7 ·
jjohnson There are about to have the "6th International Symposium on Functional Gastrointestinal Disorders"If you clink on the "Program & Registration Details Access detailed program information and registration form here.On the right you can see the topics and things of interest. http://www.iffgd.org/symposium2005.html its interesting to check out really.
 

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Discussion Starter · #8 ·
FYI"What Causes Functional Diseases? Physicians are trained to focus on identifying what we call organic diseases -- diseases that are caused by bacteria or other infectious organisms we can isolate, structural changes we can determine with endoscopes or x-rays, inflammation we may see with microscopes, or biochemical abnormalities blood tests may reveal. Whatever does not fall into one of these categories, we tend to label functional. Within the last few decades, we have learned that we need to divide these functional illnesses based on the underlying problem. The normal pattern of contractions may be altered, the balance between secretion and absorption may be offset, or sensory information from the intestine may not be processed properly. My research focuses on the last of the three listed mechanisms: how can nerve function change and lead to an increased sensitivity of inner organs? In the clinic, we call this visceral hyperalgesia, in the laboratory, we prefer the terms sensitization or visceral hypersensitivity. What Causes Visceral Hyperalgesia? In my clinic, I often meet patients who tell me about a bad "stomach flu" that resolved, but left them with pain or other problems that persisted for months or even years. If we do not find an organic disease, many physicians use the label post-infectious irritable bowel syndrome or post-infectious non-ulcer dyspepsia, depending on the type of symptoms present. In the laboratory, I try to identify whether the initial inflammation changed the function of nerves that send information about the stomach or intestines to the spinal cord and brain. Because these nerves have their processes out in the wall of the gastrointestinal tract, we refer to them as peripheral nerves and call alterations in their function peripheral sensitization. To understand mechanisms that lead to peripheral sensitization, we need to focus on the language of the nervous system: the action potential, an electrical signal, travels along the processes of the nerve cell until it comes to a connection with another nerve cell, called a synapse. At this point, the electrical signal is translated into a chemical message, and the release of signaling molecules (i.e., neurotransmitters). The frequency and pattern of these action potentials, also called spikes, is the code of the nervous system. If a nerve cell can generate in response to a weaker stimulus or produces more of these spikes, it is more excitable. We study the electrical currents that underlie the generation of action potentials. The main goal of our work is to determine whether injury and inflammation changes these currents, thereby making nerve cells more excitable. And in fact, when we examined nerve cells that send their processes to the stomach, we were able to see many important changes in the electrical properties of nerve cells that were consistent with the development of peripheral sensitization. Will disease processes stop here? The answer is clearly no. If peripheral nerve cells are sensitized, more information will flow to the spinal cord and brain, structures we collectively refer to as the central nervous system. This ongoing barrage may in turn change the properties of nerve cells in the central nervous system and lead to central sensitization. What Causes Peripheral Sensitization? Considering the potential importance of peripheral sensitization in the development of visceral hyperalgesia, we need to understand more about the signals that trigger changes in nerve function. Staying with the clinical scenario of acute inflammation causing chronic problems, we tried to identify some of the molecules that may affect nerve cells during such acute inflammation. We narrowed in on one potential culprit, nerve growth factor. It increased after injury, thus satisfying one important criterion for a possible mediator of peripheral sensitization. When we examined its effect on nerve cells in the test tube, nerve growth factor changed the properties of these cells in ways that reminded us of findings we had originally obtained when we studied nerve cells after stomach injury. Finally, when we blocked the effects of nerve growth factor, we were able to blunt behavioral changes characterizing visceral hypersensitivity. " http://www.giresearch.org/Bielefeldt.html
 

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Thanks again,I think with both the IFFGD conference in April and Digestive Diseases Week in May, there should be a lot of interesting updates in the next few months. Obviously, from a patient's perspective, these discoveries can't be translated into treatments fast enough. But I think we should be grateful that so much research is now being done.
 

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Discussion Starter · #10 ·
Jjohnson, have you ever been in the UNC Chats?I see alot of peope getting bad information also and treatments that really don't address IBS very well.Curious though if you ever have attended the chats, they are excellent.
 

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I did drop in on the chat about IBS-D last year, although I didn't ask any questions. I had planned on asking about new treatments, but as this is something that is on a lot of people's minds, someone naturally beat me to it.
I was also going to check on this one, but somehow forgot at the last minute. I'm thankful that these experts are willing to put aside their time for these chats and I'll most likely visit them in the future.
 

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Discussion Starter · #12 ·
jjohnson you should watch this, its excellent.Irritable Bowel Syndrome:Evolving Perspectives and Treatment StrategiesA roundtable discussion hosted by Medical Crossfire. Scroll to the bottom of the page to launch the presentation.Irritable Bowel SyndromeEvolving Perspectives and Treatment StrategiesJointly Sponsored by the University of Medicine & Dentistry of New Jersey (UMDNJ)�Robert Wood Johnson Medical School, Department of Medicine; UMDNJ�Center for Continuing and Outreach Education; Medical Crossfire/Liberty Communications Network. MODERATOR Jay L. Goldstein, MDProfessor of MedicineVice Head for Clinical AffairsDepartment of MedicineUniversity of Illinois at ChicagoChicago, Illinois BACK TO TOP PANELISTS Lin Chang, MD Associate Professor of MedicineCo-DirectorCenter for Neurovisceral Sciences & Women�s HealthDivision of Digestive DiseasesDavid Geffen School of Medicine at UCLALos Angeles, CaliforniaWilliam D. Chey, MDAssociate Professor of Internal MedicineDirector, GI Physiology LaboratoryUniversity of Michigan, Ann ArborAnn Arbor, MichiganDouglas A. Drossman, MDProfessor of Medicine and PsychiatryCo-DirectorUNC Center for Functional GI and Motility DisordersDivision of Digestive DiseasesUniversity of North CarolinaChapel Hill, North CarolinaMichael D. Gershon, MDProfessor and ChairmanDepartment of Anatomy and Cell BiologyColumbia University College of Physicians and SurgeonsNew York, New York http://reflectweb.reflectsystems.com/getco...54-5f64d591be04
 
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