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excellent paper. this differential release of mediators is something that is very important and may help explain why HT can at least make some people feel better. also, very possibly have an inhibiting effect on the release. i would be interested to see any results of HT and IgE allergy relief -- i.e., does HT reduce allergy attacks.i don't deny that stress can activate the mast cells -- i know they can. but just so long as you realize that many things are causing this to happen.my big trigger is mold spores and foods. stress gives me more of a cerebral reaction than a gut reaction.we are all different.
 

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Molds are a new one for you yes Kel? I have lost count of how many things you have wrong with you, not related to IBS.At an IBS support group a year ago a clinical hypnotherapist was hypnotizing the group and was telling everyone they were in a garden and to feel smell and breathe the air. Some ladies allergies acted up and she began to sneeze and her nose watered.Kel, its emotions and the fight or flight, and you would not conciously be aware everytime of this happening. SO it can be happening without you knowing it. This is very Important to know in IBS!It has to do with homoestasis!Chronic stressors and negative emotions through worry and emotions like anger for one, activates the HPA axis then the fight or flight responce and this sends signals from the brain to the gut that degranulates the mast cells to release toxins onto the nerve cells of the gut, without a pathogen.Right now there is major research being done on this that may help to explain the pain generation and IBS.Kel, your brain and your gut are majorally connected through the CNS and the ENS and the autonomic nervous system and even though the gut can run on its own for the most part the brain is still in charge of many of its operations, including the immune system."Basic Principles -- Brain-GutModerators: 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 DisordersEpidemiology/Genetic/Behavioral FactorsBrain ImagingEmerging Techniques to Evaluate and Treat Functional GI and Motility DisordersClinical Applications of Diagnosis and TreatmentFunctional GI DisordersGeneral Principles of TreatmentPharmacological TreatmentPsychological TreatmentIFFGD Research AwardsThe brain-gut axis refers to the continuous back and forth interactions of information and feedback that take place between the gastrointestinal tract, and the brain and spinal cord (which together comprise the central nervous system). These interrelated feedback circuits can influence brain processes and bowel functions -- affecting pain perception, thoughts and one's appraisal of symptoms, gut sensitivity, secretions, inflammatory responses, and motility. The brain-gut circuits can be activated by an external or internal factor or stimulus that makes a demand on the system, such as a stressful event, an injury, an emotional thought or feeling, or even the ingestion of food. Symptoms of functional GI disorders may result from a maladaptive response to stimuli at some point within the complex interactions that take place along the brain-gut axis.Basic science is the fundamental approach to understanding how systems work. Basic research takes place in the laboratory and often involves the study of molecules and cells. From this body of knowledge is drawn the means to investigate practical applications and to formulate clinical practices. Translational science converts basic science discoveries into the practical applications that benefit people.One of the more exciting areas of recent research relates to the basic and translational aspects of the effects of stress on inflammation, cytokine and immune modulation, and pain. (Cytokines are a type of protein released by cells of the immune system, which act through specific cell receptors to regulate immune responses.) This series of presentations address three important research areas in the field of functional GI disorders, which have recently attracted considerable attention: the role of immune activation in the gut and the interactions of the gut immune and nervous systems; the role of the central nervous system in the regulation (modulation) of pain perception (nociception); and the emerging field of animal models with relevance for functional GI disorder research. This section demonstrates the rapid progress seen in the last few years in better understanding of basic mechanisms, in particular the neuroimmune interactions underlying symptom generation in patients with "functional" GI disorders.There are immune responses to infections. To defend itself from a foreign substance or invader, such as a bacterium or virus, the body mounts an immune response controlled by the brain. There needs to be a balance between infection and the body's immune response; the immune system needs to turn on and turn off at the right times to destroy the invader but not to the degree that it may harm healthy tissue.Robin Spiller, University Hospital, Nottingham, England began the session by noting the difficulty in separating disorders of structure ("organic") from disorders of function. He noted, "The difference is based on how high the power of your microscope is." This was elaborated upon in his presentation on Post-infectious Functional GI Disorders. It has been observed that IBS-like symptoms, that persist for 6 months to a year or longer, may appear after a bout with an acute infection in the gastrointestinal tract (e.g., food-poisoning). This is termed, "post-infectious IBS." A study by Gwee et al showed that the presence of unusual or amplified life stress at the time of onset of infection increased the chances of developing IBS symptoms. Inflammation persisted in patients with IBS-like symptoms but did not in patients whose symptoms resolved. This suggests that the brain's management of certain stressful stimuli (i.e., psychologic distress) affects the brain-gut system's ability to inhibit inflammation.It has frequently been observed that some individuals with more severe symptoms of IBS have coexisting psychologic distress. Stress has been thought to influence health-care seeking behavior, either by increasing motility, visceral hypersensitivity or inflammation, or by enhancing one's perception of gut symptoms, all of which lead to a greater need to seek care for them. The concept of post-infectious IBS suggests that in some circumstances stress (the biological process by which the body adapts in response to a stimuli) may influence symptoms.An initial response to an infection in the gastrointestinal tract can involve the neurotransmitter, serotonin, which acts as a messenger (mediator) to cells involved with the immune response. Immune cells -- mostly in the blood, but also in the lymphatic system -- enter the infected area and remove the invader. Additionally, the body adaptively removes the infection (e.g., via vomiting or diarrhea -- normal beneficial responses that help the body expel an infecting organism). Persistence of the underlying inflammatory response may lead to post-infectious disorders of function. A variety of neuroimmune responses can lead to intestinal over-responsiveness (sensitization) and other clinical effects.These responses include direct toxicity to nerves that influence intestinal contractions, alteration in gut immune activation, abnormalities of serotonin metabolism, and persisting low-grade inflammation. IBS developing after infective gastroenteritis is associated with subtle increases in enteroendocrine and chronic inflammatory cells in the gut mucosa. The net effect may be to increase serotonin availability in the gut and enhance secretion and propulsive motility patterns. Serotonin antagonists may be beneficial in such patientsNotably, the concept of "post-infectious IBS" has grown to include studies of their application in post-infectious gastroparesis and dyspepsia. 1Major inflammatory responses have not been observed in most IBS patients. However, in some studies subtle changes associated with inflammation have been noticed, such as increased presence of mast cells (a type of immune system cell present in blood and tissue). Jackie Wood, Ohio State University College of Medicine discussed the Effects of Inflammation on the Gut Enteric Nervous System, specifically noting the importance of mast cell degranulation (the release from within the cell of granules, or small sacs, containing chemicals that can digest microorganisms and fight infection).In tissue mast cells accumulate around nerve endings of nerves that contain the neurotransmitter serotonin. The release of substances that can induce activity in excitable tissue (i.e., histamine, Interleukin-1 (IL-1), and bradykinin) by mast cells can affect receptor and neurotransmitter function in the enteric nervous system - the part of the autonomic nervous system that controls function of the gastrointestinal tract. In other words, when mast cells in the intestinal lining empty their contents in response to an infection, they activate nearby nerve endings. In a subgroup of patients, this can have significance in terms of resulting clinical consequences of diarrhea and abdominal discomfort.2Yvette 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.4Jerry 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.5To close the Brain-Gut sessions, Emeran Mayer, University of California Los Angeles discussed Evolving Animal Models of Visceral Hypersensitivity. In contrast to most other disorders of the digestive system, functional disorders of the gut continue to be defined by symptom criteria rather than by biological markers. Realistic animal models of functional gastrointestinal (GI) disorders in which to test hypotheses have not been available until recently. While it is unlikely that there will ever be an animal model to replicate all complexities of the human functional GI disorders, animal research is likely to help us understand some of the key underlying mechanisms responsible for symptom generation. This includes over-responsiveness of central stress circuits to visceral and psychological stimuli, resulting in altered autonomic responses (motility, secretion), increased pain sensitivity (visceral hypersensitivity) and possibly altered immune function of the gut. Future studies with genetically altered (i.e., transgenic) mice that become models for studying specific human diseases and their treatments may further increase our understanding of these mechanisms.6 http://www.iffgd.org/symposium2003brain-gut.html
 

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Also, along with stress............Many Foods Contain Histamine Or Cause The Body To Release HistamineHistamine is a natural substance produced by the body and is also present in many foods. It is released by the body during times of stress and allergy.In an allergic response, an allergen stimulates the release of antibodies, which attach themselves to mast cells. When histamine is released from the mast cells it may cause one or more of the following symptoms:Eyes to itch, burn, or become watery Nose to itch, sneeze, and produce more mucus Skin to itch, develop rashes or hives Sinuses to become congested and cause headaches Lungs to wheeze or have spasms Stomach to experience cramps and diarrheaThis chemical (vasoactive amine) is able to create such havoc with the many body functions because it is contained in almost all body tissues. The main body tissues include the lungs, skin, intestinal mucosa, mast cells, and basophils.The release of histamine can be induced by almost any allergen. Examples include inhalant allergens, drugs, chemicals, insect venoms, and even some foods.Histamine in FoodsThere are many foods that contain histamine or cause the body to release histamine when ingested. Histamine in food may be responsible for some cases of food intolerance.Histamine Rich Foods Include:Anchovies Avocados Beer Canned Foods Cheeses Cidars Eggplant Fermented Beverages Fermented Foods Fish Herring Jams and Preserves Mackerel Meats Processed Meats Salami Sardines Sauerkraut Sausage Some Oriental Foods Sour Cream Spinach Tomatoes Tuna Vegetables Vermouth Vinegars Wines Yeast extract YogurtHistamine Releasing Foods Include:Alcohol Bananas Certain Nuts Chocolate Eggs Fish Milk Papayas Pineapple Shellfish Strawberries TomatoesHistamine PoisoningAt times the ingestion of high concentrations of histamine may lead to histamine poisoning. It is also known as Scombroid Poisoning. High levels of histamine occur in spoilage of foods such as fish products.
 

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quote: i.e., does HT reduce allergy attacks
Just my own experience...I suffer from "severe and extensive" allergies, as my allergist once put it. I did IBS based hypnotherapy, finishing up almost two years ago. I have to say that last spring (spring is when my alllergies are at the worse) I had much fewer problems than usual. I needed my allergy eye drops only twice all spring whereas in the past I needed them almost every day. Could it be coincidence? Sure, it could, but there also could be a connection between the two. I am anxious to see how I react this spring!
 

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donna,thanks for posting that information. a lot of those foods are my biggest triggers.i think it is easy to see that stress and foods can be triggering these chemicals.i am going to look deeper into the various ways that we can try and desensitize these mast cells.
 

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KelHave you read any information about cromolyn sodium. I believe it is a mast cell stabilizer of known effectiveness...I dont know to much about it but I have read something about it here on the board before..
 

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quote: Just my own experience...I suffer from "severe and extensive" allergies, as my allergist once put it. I did IBS based hypnotherapy, finishing up almost two years ago. I have to say that last spring (spring is when my alllergies are at the worse) I had much fewer problems than usual. I needed my allergy eye drops only twice all spring whereas in the past I needed them almost every day. Could it be coincidence? Sure, it could, but there also could be a connection between the two. I am anxious to see how I react this spring!
very interesting. thanks.
 

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i remember MNL talking about it a lot, but he made it sound as though the effects were short lived. that is why i never pursued it, but maybe it has long lasting effects elsewhere in the body.i think i am going to investigate this.
 

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I think his position would be that mast cell changes can be permanent? If we're talking about mast cells we need someone who knows about them. I would suspect this works in much the same way serotonin changes change brain cells reception.tom
 

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From the first paper'Once stimulated, mast cell products may encourage further proliferation, resulting in a self-perpetuating increase in mast cell numbers long after the initiating event has subsided. In IBS, we propose that the mast cell may be an important mediator in a complex interaction between a physiological event (gut insult, inflammation, tissue injury, nerve injury), the nervous system and psychological factors (stressful events, emotions). 'As to how they act - from the first paper-"Potent chemicals derived from mast cells, including histamine, 5-HT, platelet activating factor, prostaglandins, cytokines and leukotrienes, may be implicated in the generation of IBS symptoms via their effects on enteric muscle and nerve function"
 

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i strongly suspect that ibsacol is playing a strong role in stopping some of the inflammatory prostaglandins and leukotrienes from either manufacture or release from mast cells. the best indication is my much lowered asthma response and the fact that i no longer have to take an anti-seizure drug after 3 to 4 weeks on it.i have heard that quercetin can help to control and stabilize the mast cells. i took 1000mg for 6 months but it is hard to tell if it did anything. i have read that 4000 to 6000 mg may be needed.
 

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Interesting, this -------------------"Potent chemicals derived from mast cells, including histamine, 5-HT, platelet activating factor, prostaglandins, cytokines and leukotrienes, may be implicated in the generation of IBS symptoms via their effects on enteric muscle and nerve function"-------------------seems to indicate that mast cells determine serotonin (5HT) but I'm sure it's not that simple.Mike's usually busy when I contact him but maybe I can get him to drop in. Why not send him a PM yourself?tom
 
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