# Do I have SIBO?



## 22521 (Oct 2, 2006)

Posted this before but didnt get too many answers so thought i would post it again, thanks for your time. Duff.I have been diagnosed with IBS yet have a "slight" reason to believe its SIBO....-it started after a trip around Europe, kicked off in Poland(post infectious IBS, ??)-Its constant and a direct response to ANY food I eat, not trigger foods.-I dont usually have diarhea, its generally 3 toilet visits a day mainly after meals and cramps, yet its the IE thats the worst...thats constant for 2 years (im not kiddin!)Also the symptoms got progressively worse over 2.5 yrs.-My IBS has a somewhat delayed reaction to lager....its the only thing my IBS reacts to, in my diet...it doesnt stop it altogether just slightly calms it.Heres my reasoning, look at the last point, when I drink im usually on a night out enjoying myself. I read a long time ago about the effects of seretonin in the use of illegal drugs, apparently the seretonin is realised on consumption of drugs and large amounts of are realeased, giving the "high" you experience, same with chocolate and I presume alcohol.When the seretonin has been realesed in large amounts, the part of the body that realesed it(cant remember what its called)has been effected so much that it stops releasing it for a while resulting in the "low" you feel or the depression/come down. Also seretonin is realeased and has something to do with the endorphins, am I right? (not too sure on that point?) so when I go out I have alcohol I have a huge realease of seretonin,also i am with friends enjoying myslef so endorphins are released, yet because of the over use of the seretonin i go into a lull afterwards (my hang over etc) this lack of seretonin being released results in the day after drinking i have no effects..ONLY LARGE AMOUNTS OF GAS! Another symptom of bad bacteria, am I right again??? Please correct me if im wrong here!! Then the day after that my IBS goes really bad again..why? Because my seretonin and endorphins are kicking back in! A strange theory like but also.....I have been recieving acupuncture, along with this a was given herbs to take, i have to boil them and drink the fluid...to be honest it just tastes like peppermint to me, but it has again the same effect as the alcohol....its like a strange subdued delay, like the pain threshold has gone up slightly, also when the herbs stop working ( take them twice a day) whats the first symptom I get, GAS!!!! Surely from the food I am still consuming.Another reason is that I dont suffer from stress, dont get me wrong I get pissed off with things but Im more daring than anything, hence the IBS starting while I was travelling around Europe alone.My symptoms are constant and seem to be caused by the act of eating food alone, I have never felt it was IBS and always thought it was a strange allergy of some sort, yet when I read Nanobugs suggestion, DR Pimentals theory on the bacteria, it just sounded like it fits my bill.Oh yeah, I also stopped taking milk and bread, only for my IBS to be reduced then come back again after thinkin for a week i had cracked it, this is also a point made by Pimental.So what do you think, judging on my theory if i just drank everyday i would be fine haha but seriously Im gonna have to ask my doctor about this (AGAIN) and push it this time, do you think i have a case??ANY advice or comments would be grateful. PS does anyone know the link between seretonin and endorphins, i think the case i am referring to was for alzheimers, when a man took ecstacy during an experiment the seretonin/endorphins released enabled him to stop his uncontrolable movements to the point where he was doing flips over a horse in a gym!


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## eric (Jul 8, 1999)

Duff, when they carefully examine people with post infections IBS they have found cell abnormalities in digestive system, specifically a cell called a EC or enterochromaffin cell. These cells are very important, they store the majority of serotonin in the gut and are a major player in intiating gut contractions and signaling to the brain sensations.Another cell they found is called a mast cell. These cells are also important in allergies and the bodies stress system. The bodies stress system also fights infections. So those mast cells can be triggered by both foods and stress.There is strong evidence on serotonin dysregulation in IBS which partially explains the d and c and d/c issues as well as its part in signaling pain to the brain. The brain should then release endorphines back to the gut, but that doesn't seem to happen well in IBS and they are working on it. There is evidence for impairment of an area in the brain called the Anterior Cinculate Cortex. Also a lot of work is being done in that area.There is a lot of information on PI IBS and one of the top doctors in that area of research is Dr Robin Spiller. I will see about posting some info from him here.The majority of serotonin is in the gut. 95%They actally haven't found "bad Bacteria" in IBS, even the SIBO theory isn't really about bad bacteria, but bacteria in the wrong place.A lot of what you are posting is more consistent with IBS really then SIBO, although it looks like some people can have both problems. However at this time they are NOT the same condition.This is also something you can get from the IFFGD on SIBO and IBS and I highly recommend reading it. One the common test lactulose breath testing for it is not that accurate."Gut Bacteria and Irritable Bowel Syndrome By: Eamonn, M. M. Quigley M.D., Alimentary Pharmabiotic Centre, University College Cork, Cork, IrelandBacteria are present in the normal gut (intestines) and in large numbers the lower parts of the intestine. These "normal" bacteria have important functions in life. A variety of factors may disturb the mutually beneficial relationship between the flora and its host, and disease may result. The possibility that gut bacteria could have a role in irritable bowel syndrome (IBS) may surprise some; there is indeed, now quite substantial evidence to support the idea that disturbances in the bacteria that populate the intestine may have a role in at least some patients with IBS. This article presents a discussion of the possible role of bacteria in IBS and various treatment approaches."Do bacteria play a role in IBS?The possibility that gut bacteria could have a role Irritable Bowel Syndrome (IBS) may surprize some; there is indeed, now quite substantial evidence to support the idea that distrubances in the bacteria that populate the intestines may have a role in at least some patients with IBS. What is this evidence? It can be summarized as follows:1. surveys which found that antibiotic use, well known to distrub flora, may predispose individuals to IBS.2. The observation that some individuals may develop IBS suddenly, and for the first time, following an episode of stomach or intestinal infection (gatroenteritis) caused by a bacterial infection.3. recent evidence that a very low level of inflammation may be present in the bowel wall of some IBS patients, a degree of inflammation that could well have resulted from abnormal interactions with bacteria in the gut.4. The Suggestion that IBS maybe Associated with the abnormal presents, , in the small intestines, of types and numbers; a condition termed small bacterial overgrowth (SIBO)>5. Accumaliting evidence to indicate that altering the bacteria in the gut, by antibiotics or probiotics, may improve symptoms in IBS.For some time, various studies have suggested the presence of changes in the kind of colonic flora in IBS patients. The most consistent finding is a relative decrease in the population of one species of 'good' bacteria, bifidobacteria.However, the methods employed in these studies have been subject to question and other studies have not always reproduced these finding. Nevertheless, these changes in the flora, maybe primary or secondary, could lead to the increase of bacterial species that produce more gas and other products of their metabolism. These could CONTRIBUTE to symptoms such as gas, bloating and diarrhea.""We still don't know the exact role bacteria has in IBS. More research is needed."http://www.aboutibs.org/Publications/currentParticipate.htmlI highly encourage others to read the read of this excellent article.also expert info on SIBO and its important to understand some things about SIBO itself. You might want to read this whle thread in context."I wrote to Dr Drossman on this and here is the reply. *Any Idea what those irritating substances are?*sorry its in bold type that is how he worte it into the email so I would see it was his answers."IT IS AN OVERSTATEMENT TO SAY THEY ARE "IRRITATING" SUBSTANCES AT LEAST IN THE SENSE OF BEING SOME TYPE OF TOXIN. THEY ARE NATURAL BYPRODUCTS OF DEGRADATION OF FOOD SUBSTANCES BY BACTERIA WHICH DON'T NORMALLY OCCUR IN THE SMALL BOWEL. SO WITH INCREASED BACTERIA IN THE SMALL BOWEL, THE BACTERIA ARE ABLE TO DIGEST SUGARS FOR EXAMPLE PRODUCING H2 AND CO2 FROM THE SUGARS WHICH ARE GASEOUS BUT WHICH ALSO HAVE OSMOTIC PROPERTIES, I.E. INCREASED PARTICLES THAT CAUSE SECRETION OF FLUID INTO THE BOWEL THUS CAUSING DIARRHEA. IT'S THE SAME PRINCIPLE AS USING NON ABSORBABLE SUGARS LIKE LACTULOSE OR SORBITAL TO TREAT CONSIPATION BY INCREASING FLUID IN THE BOWEL. IT'S JUST THAT WITHOUT BACTERIA IN THE SMALL BOWEL, IT DOESN'T HAPPEN AND THE FOOD SUBSTANCES GET ABSORBED. WITH INCREASED BACTERIA IT COMPETES FOR THE FOOD SUBSTANCES AND PRODUCES THE GAS AND DIARRHEA."*This means these are just in the wrong place and not specific or multiple pathogens?*CORRECT. HOWEVER, THERE IS GROWING INTEREST NOT IN THE AMOUNT OF BACTERIA BUT THE TYPE OF BACTERIA. CERTAIN BACTERIA CAN CAUSE SOME MILD INFLAMMATION OF THE BOWEL AND OTHERS PROTECT THE BOWEL FROM THAT POSSIBILITY. SO THERE IS "GOOD" AND "BAD" BACTERIA. POSSIBLY WHEN PEOPLE ARE TREATING PRESUMED SIBO (WHICH MIGHT NOT ACTUALLY BE HAPPENNING, BECAUSE THE TEST MAY BE INACCURATE) ANTIBIOTICS MAY HELP TO GET RID OF THE BAD BACTERIA AND THAT MAY BE WHY THEY ARE GETTING BETTER. THIS IS WHY SOME PEOPLE GET BETTER AFTER ANTIBIOTIC TREATMENT. BUT IT CAN ALSO GO THE OTHER WAY, I.E., ANTIBIOTICS HAVE BEEN SHOWN TO MAKE IBS WORSE AS WELL. THE OTHER IDEA IS TO USE PROBIOTICS WHICH CONTAIN "GOOD" BACTERIA (E.G., LACTOBACILLUS OR BIFIDOBACTERIA) WHICH REPLACE THE BAD BACTERIA, POSSIBLY REDUCE THE INFLAMMATION AND IMPROVE SYMPTOMS. SO THE ISSUE OF BACTERIA IN THE BOWEL IS MUCH MORE COMPLICATED THAN SIMPLE SIBO, BUT SIBO CAN BE A PART OF THE WHOLE PICTURE (THOUGH NOT THE WHOLE PICTURE FOR IBS).http://ibsgroup.org/groupee/forums/a/tpc/f...322/m/380104372


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## eric (Jul 8, 1999)

FYI for the info"Serotonin Signaling*Of the putative mechanisms underlying the pathophysiology of IBS, the strongest evidence points to the role of serotonin in the GI tract.* The effect of serotonergic mechanisms in the manifestation of IBS symptoms has led to development of a new drug class for the treatment of IBS patients: the GI serotonergic agents.Normal GI function relies on a properly functioning brain-gut axis, which involves the coordinated interplay of the GI musculature, the CNS, the autonomic nervous system, and the enteric nervous system (ENS). The ENS contains millions of neurons embedded in the wall of the digestive tract and functions, at least in part, independently of the CNS. The size, complexity, and independent function of the ENS has resulted in application of the terms "the second brain" and "the mini-brain."[81] Impaired function or coordination of any of these systems, or the communication between these systems and the GI musculature, can lead to symptoms of dysmotility and altered sensory perception, which are characteristic of IBS and select other GI motility disorders.[82]The neurotransmitter serotonin (5-hydroxytryptamine [5-HT]) is a predominant signaling molecule in the ENS. Most (90% to 95%) of the body's serotonin is found in the gut, and smaller amounts are found in the brain (about 3%) and in platelets (about 2%).[83] In the GI tract, serotonin facilitates communication between the ENS and its effector systems (muscles, secretory endothelium, endocrine cells, and vasculature of the GI tract), thus playing a key role in normal GI tract functioning.[84] In addition, serotonin plays a role in the communication between the ENS and the CNS.In the gut, serotonin is synthesized by and stored in the enterochromaffin cells, which are located within the mucosa of the intestinal wall. When material passes through the lumen and the mucosa is stimulated, enterochromaffin cells release serotonin, which then binds to its receptors (primarily 5-HT1P receptors) on intrinsic primary afferent neurons, initiating peristalsis and secretion. Serotonin also binds to 5-HT4 receptors on interneurons, which augments the transmission of signals to motor neurons, resulting in enhanced peristaltic activity. In transgenic mice lacking 5-HT4 receptors, colonic motility is abnormally slow, confirming the role of these receptors in facilitating normal colonic motility.[85] By binding to 5-HT3 receptors on efferent sensory innervations coming from the vagus and the spinal nerves, serotonin mediates signaling between the ENS and the CNS and, thus, modulates pain perception.To regulate the signaling process, excess serotonin must be removed; this is accomplished by the SERT molecule expressed by intestinal epithelial cells.[86] Human studies have shown that defects in serotonin signaling contribute to the pathophysiology of IBS and, potentially, other GI motility disorders. In a recent study by Coates and colleagues,[87] biopsy specimens from patients with IBS showed significantly lower mucosal serotonin concentrations than those from healthy controls, potentially the result of lower mRNA levels for tryptophan hydroxylase (the rate-limiting enzyme in serotonin synthesis), which were also significantly lower in patients with inflammatory bowel disease.[87] There was no significant difference in the number of enterochromaffin cells or in the capacity of these cells to release serotonin under stimulated conditions. In another study, higher serotonin levels were observed in mucosal biopsy samples from patients with IBS with constipation (IBS-C) than in patients with IBS-D or in healthy volunteers.[88]Serotonin levels may also be affected by altering the amount or function of SERT. The study by Coates and colleagues[87] showed a significant decrease in the level of SERT mRNA and SERT protein expressed in the intestinal epithelial cells of IBS patients compared with that of healthy volunteers. In another study,[89] SERT expression and binding capacity in platelets were decreased in women with IBS-D compared with expression and binding capacity in healthy controls. Furthermore, Chen and colleagues[90] showed that mice with a SERT gene deletion had altered colonic motility. It is interesting to note that the mice thrived in laboratory housing conditions, indicating that other transporters could compensate for the lack of SERT. Additional studies have focused on SERT polymorphisms. Yeo and colleagues[91] showed an association between patients with IBS-D and the homozygous short polymorphism of the SERT gene promoter. This mutation results in lower levels of SERT gene transcription and reduced amounts of SERT protein available for reuptake of serotonin. In addition, Camilleri and colleagues[92] showed a possible link between the long promoter polymorphism and patient response to therapy.Thus, a substantially large body of work shows that normal gut physiology is predicated on the interplay between the GI musculature and the ENS, autonomic nervous system, and CNS. One of the central mediators of this complex interplay is the neurotransmitter serotonin. Impairment or imbalance in serotonergic signaling, which can affect GI motility, secretion, and visceral sensitivity, may be affected by defects or deficiencies in serotonin production, specific serotonin receptors, or proteins such as SERT. These changes can manifest in symptoms associated with IBS, including abdominal pain, altered bowel habits (constipation, diarrhea, or alternation between these 2 states), and bloating.http://www.medscape.com/viewarticle/532089_3


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## eric (Jul 8, 1999)

You might also want to read this thread.http://ibsgroup.org/groupee/forums/a/tpc/f...261/m/906107392


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## eric (Jul 8, 1999)

By the way "alcohol which can stimulate intestinal secretion or with the latter, pull water into the bowel (osmotic diarrhea)."http://www.ibshealth.com/ibs_foods_2.htm


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## 17890 (Mar 11, 2007)

eric-thanks for all the info, i enjoy reading it. in your 3nd to last post here, the 1st paragraph mentioned "The effect of serotonergic mechanisms in the manifestation of IBS symptoms has led to development of a new drug class for the treatment of IBS patients: the GI serotonergic agents." I was wondering about the new class for treatment, are there drugs available that we are not already taking? Thanks, Miranda


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## eric (Jul 8, 1999)

Two of them are lotronex and zelnorm of course, there maybe others out now, but I am not positive and there are some still in clinical trials.This is one reason why they maybe using zelnorm for SIBO.


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