FYII posted this on another thread but figured I would post it here also.""Do people get cured after they have found SIBO? "Sibo is another functional issue, so it might depend on what causes the sibo in the first place
. The speculation that sibo causes IBS is not working out so well. So this is a seperate issue some people have along with IBS. SIBO usally causes d.ON IBSaltered serotonin signaling and ibs compilationhttp://www.ibsgroup....showtopic=80198
There are two cells in IBS that seem to be very important, enterochromaffin (ec) cells and mast cells.There seems to be different cell pathologies for one in different groups of IBSers. For example there are important cellular changes in Post infection IBS after the resolution of the intial infection.Some of these changes are also seen in IBS and some of the problems are also seem connected.The digestive system is extremely complex and the connections to digestion and the brain are extremly complex. This system works or should work in harmony.This is some excellent up to date Post Infectious IBS info.Post-infectious Irritable Bowel SyndromeRobin Spiller; Eugene Campbell"Recent Findings: Recent studies have overthrown the dogma that irritable bowel syndrome is characterized by no abnormality of structure by demonstrating low-grade lymphocytic infiltration in the gut mucosa, increased permeability and increases in other inflammatory components including enterochromaffin and mast cells. Furthermore, increased inflammatory cytokines in both mucosa and blood have been demonstrated in irritable bowel syndrome. While steroid treatment has proved ineffective, preliminary studies with probiotics exerting an anti-inflammatory effect have shown benefit.Summary: The study of post-infectious irritable bowel syndrome has revealed the importance of low-grade inflammation in causing irritable bowel syndrome symptoms. It has suggested novel approaches to irritable bowel syndrome including studies of serotonin and histamine metabolism which may be relevant to other subtypes of of the disease."http://www.medscape....le/518355_print
enterochromaffin or EC cells store the majority of serotonin in the gut. They are pressure sensitive and release serotonin to start gut contractions. Mast cells release histimine.Here is a picture of where those cells are located.
The 5ht3 receptors are involved in D IBS and the 5ht4 receptors C IBS.I will post more on the mast cells because they are also very important.More on the enterochromaffin cells and IBS and serotoninAliment Pharmacol Ther. 2006 Apr 15;23(8):1067-76. LinksReview article: intestinal serotonin signalling in irritable bowel syndrome.Mawe GM, Coates MD, Moses PL.Department of Anatomy and Neurobiology, University of Vermont College of Medicine, Burlington, VT 05405, USA. [email protected]
in motility, secretion and visceral sensation are hallmarks of irritable bowel syndrome. As all of these aspects of gastrointestinal function involve serotonin signalling between enterochromaffin cells and sensory nerve fibres in the mucosal layer of the gut, potential alterations in mucosal serotonin signalling have been explored as a possible mechanism of altered function and sensation in irritable bowel syndrome. Literature related to intestinal serotonin signalling in normal and pathophysiological conditions has been searched and summarized. Elements of serotonin signalling that are altered in irritable bowel syndrome include: enterochromaffin cell numbers, serotonin content, tryptophan hydroxylase message levels, 5-hydroxyindoleacedic acid levels, serum serotonin levels and exp
ression of the serotonin-selective reuptake transporter. Both genetic and epigenetic factors could contribute to decreased serotonin-selective reuptake transporter in irritable bowel syndrome. A serotonin-selective reuptake transporter gene promoter polymorphism may cause a genetic predisposition, and inflammatory mediators can induce serotonin-selective reuptake transporter downregulation. While a psychiatric co-morbidity exists with IBS, changes in mucosal serotonin handling support the concept that there is a gastrointestinal component to the aetiology of irritable bowel syndrome. Additional studies will be required to gain a more complete understanding of changes in serotonin signalling that are occurring, their cause and effect relationship, and which of these changes have pathophysiological consequences.PMID: 16611266Neurogastroenterol Motil. 2007 Aug;19 Suppl 2:25-31. LinksRecent advances in understanding the role of serotonin in gastrointestinal motility in functional bowel disorders: alterations in 5-HT signalling and metabolism in human disease.Spiller R.Professor of Gastroenterology, Wolfson Digestive Diseases Centre, Nottingham, UK. [email protected]
(5-hydroxytryptamine, 5-HT) is present in abundance within the gut, most stored in enterochromaffin cell granules. It is released by a range of stimuli, most potently by mucosal stroking. Released 5-HT stimulates local enteric nervous reflexes to initiate secretion and propulsive motility. It also acts on vagal afferents altering motility and in large amounts induces nausea. Rapid reuptake by a specific transporter (serotonin transporter, SERT) limits its diffusion and actions. Abnormally increased 5-HT is found in a range of gastrointestinal disorders including chemotherapy-induced nausea and vomiting, carcinoid syndrome, coeliac disease, inflammatory bowel disease and irritable bowel syndrome (IBS) with diarrhoea (IBS-D), especially that developing following enteric infection. Impaired SERT has been described in IBS-D and might account for some of the increase in mucosal 5-HT availability. 5-HT(3) receptor antagonists inhibit chemotherapy-induced nausea and diarrhoea associated with both carcinoid syndrome and IBS. While IBS-D is associated with increased 5-HT postprandially, IBS with constipation (IBS-C) is associated with impaired 5-HT response and responds to 5-HT(4) agonists such as Prucalopride and 5-HT(4) partial agonists such as Tegaserod.PMID: 17620085Another very important cell in IBS is the mast cell. You can see where that is located in the picture, they are embedded in the gut wall.Mast cells are involved in fighting infections, allergies and the fight or flight stress responce. They can be activated by the HPA axis or Hypothalamic-pituitary-adrenal axis. The HPA axis has importnt roles in bodily functions, but is also the bodies stress system. The mast cells can degrandulate and release histimine from the mast cells embedded in the gut and this can contribute to pain and D.DR Wood is an expert on food lallergies, but importantly the enteric nervous system and IBS.First from Dr Drossman though.Dr Drossman's comments on foods for IBS Health.Shawn,To say that people with IBS may get symptoms from food intolerances is an acceptable possibility, since the gut will over react to stressors of all types including food (high fat or large volumes of food in particular). Futhermore, there can be specific intolerances. So if you have a lactose intolerance for example, it can exacerbate, or even mimic IBS. Other examples of food substances causing diarrhea would be high consumers of caffeine or alcohol which can stimulate intestinal secretion or with the latter, pull water into the bowel (osmotic diarrhea). The same would be true for overdoing certain poorly absorbed sugars that can cause an osmotic type of diarrhea Sorbitol, found in sugarless gum and sugar substituted foods can also produce such an osmotic diarrhea. Even more naturally, people who consume a large amount of fruits, juices or other processed foods enriched with fructose, can get diarrhea because it is not as easily absorbed by the bowel and goes to the colon where it pulls in water. So if you have IBS, all of these food items would make it worse. However, it is important to separate factors that worsen IBS (e.g., foods as above, stress, hormonal changes, etc.) from the cause or pathophysiology of IBS. Just like stress doesn't cause IBS, (though it can make it worse), foods must be understood as aggravating rather than etiological in nature. 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...ibs_foods_2.htmhttp://www.ibshealth...bsfoodsinfo.htm
Dr Wood's comments for me"Dr. Jack Wood, a renowned physiologist at The Ohio State University calls the ENS the little-brain-in-the-gut."Dear Shawn:Sorry for the delayed reply to your question. I generally agree with Dr. Drosssmans response. A subgroup of individuals when they become sensitized to specific molecules in certain foods respond to ingestion of the molecules with symptoms of cramping abdominal pain, fecal urgency and explosive watery diarrhea. These are also the primary symptoms of diarrhea-predominant IBS. Enteric mast cells, by mechanisms we don't understand, become sensitized to the food molecule and respond to its presence by releasing a signal to the brain-in-the-gut (ENS) which is interpreted as a threat. The ENS responds by running a program which organizes secretion and motility into a behavior pattern of the bowel, which rapidly clears the threat from the lumen. Because to be effective secretion occurs in large volumes and the contractions that accomplish rapid propulsion are strong, running of the program has the side effects of diarrhea and cramping pain. Big brain input to mast cells during stress activates the mast cells to evoke the symptoms resulting from exposure of the mast cells to sensitizing food antigens. Aside from food allergens and mast cells, certain chemicals such as those in hot peppers, stimulate sensory nerves in the ENS and we are beginning to understand how this can also lead to food-related symptoms that might mimic or exacerbate IBS.Hope this helps,Jackie (Jack) D. Wood " FYI"You have two brains: one in your head and another in your gut. Dr. Jackie D. Wood is a renowned physiologist at The Ohio State University. He calls the second brain, "the-little-brain-in-the-gut." This enteric nervous system is part of the autonomic nervous system and contains over one hundred million neurons, which is as many as are in the spinal cord. This complex network of nerves lines the walls of the digestive tract form the esophagus all the way down to the colon. This little brain in the gut is connected to the big brain by the vagus nerves, bundles of nerve fibers running from the GI tract to the head. All neurotransmitters, such as serotonin that are found in the brain are also present in the gut.Dr Wood has discovered that this little-brain-in-the-gut has programs that are designed for our protection and which are very much like computer programs. They respond to perceived threats in the same way that the limbic system or the emotional brain does. So the threat of a gastrointestinal infection can activate the program that increases gut contractions in order to get rid of the infection. The symptoms are abdominal cramping and diarrhea. Dr. Wood has determined that a type of cell found in the body and the gut, called the mast cell, is a key to understanding the connection of the big brain in the head with the little-brain-in-the-gut. Mast cells are involved in defense of the body. In response to certain threats or triggers, such as pollen or infection, mast cells release chemicals, such as histamine, that help to fight off the invader. Histamine is one of the chemicals that causes the symptoms of an allergy or a cold. When an infection of the gut occurs, such as food poisoning or gastroenteritis, the mast cells of the gut release histamine. The little-brain-in-the-gut interprets the mast cell signal of histamine release as a threat and calls up a protective program designed to remove the threat at the expense of symptoms: abdominal pain and diarrhea. The brain to mast cell connection has a direct clinical relevance for irritable bowel syndrome and other functional gastrointestinal syndromes. It implies a mechanism for linking allostasis and the good stress response to irritable states (e.g., abdominal pain and diarrhea) of the gut. Mast cells can be activated to release histamine in response to perceived psychological stress, whether the stressor or trigger is consciously perceived or not. So the end result is the same as if an infection activated the program in the-little-brain-in-the-gut: abdominal pain and diarrhea."http://www.parkviewp...nuggets/n5.html
This is also very important" whether the stressor or trigger is consciously perceived or not"The inflammation seen in some IBSers is MACROSCOPIC and not 'overt inflammation" which is seen in IBD conditions. Normal testing with IBS will not reveal this, until more powerful microscopes are used on specific cells and tissue.Inflammation CONTRIBUTES to the symptoms.There is another issue with inflammation and IBS however. "But microscopic inflammation cannot be a diagnostic marker for IBS because it does nor 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 with patients with IBS seem to have higher pain thresholds."http://www.ibsgroup....showtopic=91184
I am not a doctor. All information I present is for educational purposes only and should not be subsituted for the advise of a qualified health care provider.
Please make sure you have your symptoms diagnosed by a medical practitioner or a doctor.