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I was looking up the benefits of vitamin B-6. (I take a supplement called ZMA which has zinc magnesium and zinc in it) and it said something about helping with the nervous system. I dug a little more and I found this website http://www.bioterrain.co.uk/IBS.html...It goes on about something called 5-HTP I had a hard time deciphering what it was going on about. I know it said something about vitamin B-6 and magnesium helping with this. I think it has to do with people with IBS taking things so that there vitamins get into there body properly?...Could anyone help me out here?...When you go to that site just hit find on page and type in b6 that should take you to the 5-HTP section. It's all about IBS so yeah! thanks!
 

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FYIThe strongest evidence they have for d, c and d/c in IBS has to do with the role of serotonin-containing EC cells in the gut. Almost all IBSers effectively demonstrate serotonon dysregulation in the enteric nervous system and central nervous system.HarvardThe Trusted Source..Harold J. DeMonaco, M.S.Harold J. DeMonaco, M.S., is senior analyst, Innovative Diagnostics and Therapeutics, and the chair of the Human Research Committee at the Massachusetts General Hospital. He is author of over 20 publications in the pharmacy and medical literature and routinely reviews manuscript submissions for eight medical journals...June 19, 2001.A:Irritable bowel syndrome is now recognized as a disorder of serotonin activity. Serotonin is a neurotransmitter in the brain that regulates sleep, mood (depression, anxiety), aggression, appetite, temperature, sexual behavior and pain sensation. Serotonin also acts as a neurotransmitter in the gastrointestinal tract.Excessive serotonin activity in the gastrointestinal system (enteric nervous system) is thought to cause the diarrhea of irritable-bowel syndrome. The enteric nervous system detects bowel distension (expansion) on the basis of pressure-sensitive cells in the bowel lumen (opening). Once activated, these pressure-sensitive cells promote the release of serotonin, which in turn promotes both secretory function and peristaltic function (the contractions of the intestines that force the contents outward). At least four serotonergic receptors have been identified to be participants in the secretory and peristaltic response.Patients with diarrhea-predominant IBS may have higher levels of serotonin after eating than do people without the disorder. This recognition led to the development of the first drug used specifically to treat diarrheal symptoms of IBS, alosetron (also known as Lotronex). Alosetron blocked the specific serotonin receptors responsible for recognizing bowel distention. In doing so, it blocked the effects of serotonin and reduced both bowel secretions and peristalsis. Constipation was the most common side effect seen. (Note: Alosetron was removed from the market by the manufacturer after repeated reports of a dangerous condition known as ischemic colitis became known.) Tegaserod (Zelmac) is another drug under development and under review by the U.S. Food and Drug Administration for approval. Tegaserod is indicated for the treatment of constipation-predominant IBS and works to increase enteric nervous system serotonin activity.So, increasing serotonin activity in the enteric nervous system produces increased bowel secretions and peristalsis (and potentially diarrhea), whereas depressing serotonin activity produces reduced secretions and reduce peristalsis (and potentially constipation). Increasing serotonin activity in the brain would increase awareness and, in higher doses, produce anxiety, insomnia and restlessness."anda precursor to serotonin is TryptophanMore GI Symptoms, Less Anxiety With Tryptophan Supplementation in IBSNEW YORK (Reuters Health) Dec 21 - Patients with irritable bowel syndrome (IBS) have an increase in gastrointestinal symptoms after ingestion of a large dose of tryptophan, according to a new study. At the same time, they report having fewer symptoms of anxiety and depression.British researchers, led by Dr. Jonathan Shufflebotham of the University of Bristol, studied 18 patients with ROME II-defined IBS and 11 age-matched controls. The subjects were evaluated during a phase of acute tryptophan depletion and a phase of acute tryptophan increase.Participants ate a low-protein diet on the day before each phase of the study and fasted from midnight to 9:00 am on the day of intervention. Baseline levels of tryptophan were measured on that day and patients completed a questionnaire, answering questions about IBS symptoms and symptoms of anxiety and depression.During acute tryptophan increase, subjects drank a concoction containing 2.3 g tryptophan, 150 ml water, 100 ml flavoring of their choice and 2 spoons of sugar. During acute tryptophan depletion, subjects drank the same drink without the addition of tryptophan.Total and free plasma concentrations of tryptophan decreased 73% in both patients and controls during tryptophan depletion and increased approximately 60% on the day of supplementation.IBS patients reported more gastrointestinal symptoms but less anxiety with acute tryptophan increase compared with acute tryptophan depletion. Controls did not have a difference in symptomatology on either day. IBS patients had lower mood scores overall than controls during all phases of the study.In the study published in the November issue of the American Journal of Gastroenterology, Dr. Shufflebotham and colleagues write that the findings "suggest a difference in serotonergic functioning between these two groups and provides evidence to support the hypothesis that 5-HT dysfunction is involved in IBS."IBS symptoms respond to treatment with 5-HT4 agonists and 5-HT3 antagonists in some IBS patients, the researchers note. And, "the differing direction of GI and anxiety symptom responses to 5-HT manipulation is counterintuitive but intriguing.""Further researcher is now needed to clarify which parts of the 5-HT system are dysfunctional in IBS and how this relates to the symptoms experienced by patients with this condition," the team concludes.Am J Gastroenterol 2006;101:2582-2587http://www.medscape.com/viewarticle/549778?src=mpIBS -- Review and What's NewPosted 07/26/2006"Serotonin SignalingOf 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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I was looking up the benefits of vitamin B-6. (I take a supplement called ZMA which has zinc magnesium and zinc in it) and it said something about helping with the nervous system. I dug a little more and I found this website http://www.bioterrain.co.uk/IBS.html...It goes on about something called 5-HTP I had a hard time deciphering what it was going on about. I know it said something about vitamin B-6 and magnesium helping with this. I think it has to do with people with IBS taking things so that there vitamins get into there body properly?...Could anyone help me out here?...When you go to that site just hit find on page and type in b6 that should take you to the 5-HTP section. It's all about IBS so yeah! thanks!
Really happy to know that you found what you were looking for. If you wish to know more about 5 htp please visit 5 htp website.
 

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I have been on the 5-HTP spray for a month now and it has done nothing. Neither have any of the other supplements that the naturopathic dr given me. All I am is broke and still suffering big time.
 

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Unfortunately there is never that much good solid info about any of the dietary supplements.While the nervous system of the gut and brain are involved it isn't as simple as you don't have enough serotonin in your whole body so adding more precursor wil fix it.In theory one could think all these nervous system herbs and vitamins must help, there does not seem to be many that have a lot of people finding success on this board.Possibly because it isn't that there is "not working at all" issues that a supplement might help with assuming it could restore nerve function (which isn't that well established for most things). IBS and some other disorders are more of a "doing the right things at the wrong times" problem and most of the targetted drugs work more at that level than at the boost everything everywhere level.K.
 

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Its not really the amount of serotonin in the body, but the regulation of it and the rlease of it from specific cells in the gut called enterochromaffin cells that store the majoiryt of it in the gut as well as another type of cell called a mast cell.
 

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I have IBS and a condition called hyperhidrosis, which means that I sweat excessively for no reason. I think sweating also has a link to serotonin. Could these two conditions be related? I know that drugs that increase serotonin also have sweating as a side effect. Can anyone shed some light on this? Thanks
Its not really the amount of serotonin in the body, but the regulation of it and the rlease of it from specific cells in the gut called enterochromaffin cells that store the majoiryt of it in the gut as well as another type of cell called a mast cell.
 
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