# My theory of prostaglandin induced ibs-d



## 21207 (Sep 16, 2005)

Hi I have been researching my ibs and have developed a theory that my ibs is not due to any inflamation of my colon (I have had the inspections) but is rather a symptom of excessive prostaglandin E2 in my body. I believe that PGE2 stimulates the excessive secretion of bicarbonate in the colon via stimulation of the EP4 receptors and this results in all the synptoms of IBS. The excessive bicarbonate causes irritation of the colon , burning sensation on defacation and raises the pH level above that at which the normal bacteria function correctly causing gas etc.Now what causes excessive prostaglandin production - well infection for one and it may also be related to the ingestion of carbohydrate. i.e there is a link between carbohydrate and insulin (see the Zone diet). I am still researching...My symptoms are completely relieved by aspirin which acts to stop the formation of prostaglandins in the body and is an easy test.Fish oil also works to prevent the formation of PGE2 via another mechanism and hence also works to a degree but is higher maintenance.I have also noticed, and informed my gastroenterologist, of associated symptoms such as persistent joint pain, ibs-d getting worse a few days before I get sick (like a cold or flu) and a white coating on my tongue. All these are also symptoms of excessive PGE2.So why dont doctors consider this option - I have no idea. There is a lot of research relating to issues with too little bicarbonate secretion but very little on too much. I suppose this is because it is seen as a good thing however too much can also be a problem.I would like to hear from others that share the same symptoms and also benefit from cures that also effect PGE2 formation to see if my theory has merit.cheerskevin


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## Kathleen M. (Nov 16, 1999)

One question on your theory about one point.Normal bacteria are what cause the gas as they digest carbohydrates that you do not.If they are not functioning they are not producing gas. It is not abnormal bacteria produce gas and normal ones do not. Most normal bacteria in the colon produce gas, one subset of them, the probiotic bacteria, do not. I don't think there is a pH difference at which they live and the other normal gas producing bacteria do not


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## 21207 (Sep 16, 2005)

Hi Kathleen M.the research I have performed seems to indicate that good bacteria enjoy a pH of around 7 and do not function as efficiently above this as some bad bacteria.The pH / Bacteria is only a side statement though as my main concern is the feeling that my stool contains an irritant - something the gastroenterologist did not seem to entertain except for the possibility of bile salt - d but I think this may on the wrong track.cheerskevin


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## Kathleen M. (Nov 16, 1999)

Bile salts is a common irritant in stool and causes the burning diarrhea thing.Lots of people who use things like calcium carbonate, psyllium and other soluble fibers or Questran all of which should bind bile find they help.K.


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## Kathleen M. (Nov 16, 1999)

PS Good and bad do not always translate to produce gas and do not produce gas. Some good bacteria that are OK in there produce gas.K.


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## Talissa (Apr 10, 2004)

Also to add further to K's excellent info--good bacteria produce fermentation which produces gas.Gas is normal.It's fermentation that also produce butyrates, which keeps colonic inflammation down & protects us from colon cancer. Fiber is good for us because bacteria use it and this creates fermentation.Taking aspirin which can increase small intestinal bacterial overgrowth over time is not good advice~~ "Nonsteroidal anti-inflammatory drugs (NSAIDs), used extensively in clinical medicine, tend to cause adverse effects in the gastrointestinal tract. ...Changes in gut flora in response to the drug were also studied, as it has been shown that luminal bacteria play a role in the pathogenesis of NSAID-induced intestinal damage. There was a significant increase in the number of bacteria in the luminal contents of the small intestine and caecum in these animals, as compared with controls. The number of bacteria adherent to the intestinal mucosa was also significantly higher in the drug-treated group....These changes may contribute to the enteropathy observed as a result of NSAID treatment."Int J Biochem Cell Biol. 2005 NovYou really aren't helping people Kevine w/ this info & your theories & unsubstantiated "research". IMO, its quite the opposite.


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## flux (Dec 13, 1998)

> quote:I have been researching my ibs and have developed a theory that my ibs is not due to any inflamation of my colon (I have had the inspections) but is rather a symptom of excessive prostaglandin E2 in my body. I believe that PGE2 stimulates the excessive secretion of bicarbonate in the colon via stimulation of the EP4 receptors and this results in all the synptoms of IBS.


Actually, part of your theory sounds like the theory for the mechanism of collagenous colitis.But that is *not* IBS. IBS is not a secretory process. I would think that if you had this going on, you'd have very severe diarrhea and the disease process would be seen on colonoscopy.I'm not sure where bicarbonate/pH fits into this at least from the mechanism you describe. If you dump Cl- into the colon, you're going to have secretory diarrhea, so the excess HCO3 (which doesn't necessarily involve PGE), is irrelevant.


> quote:raises the pH level above that at which the normal bacteria function correctly causing gas etc.


Also, as K noted above, gas is the normal function of the bacteria and you want the pH to be raised to allow for the reactions to continue.


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## Talissa (Apr 10, 2004)

I thought collagenous colitis, under the umbrella of "microscopic colitis" which also includes lymphocytic colitis, is only detected by microscopic examination of intestinal biopsy? Plus there needs to be several tissue samples from diff parts of the colon taken because its very easily missed with just one sample?Also from the microscopic colitis bb, there are some patients, not many, who don't have diarrhea as a symptom(just like some, not many, w/ UC). Some only have pain as a symptom.


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## Talissa (Apr 10, 2004)

Pls just ignore this--strange bb blip I had to edit out. (if curious, it repost part of my first post on this page--no idea why)


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## 21207 (Sep 16, 2005)

Hi fluxIBS is a name for a cluster of symptoms that a doctor can find no obvious cause for. Having excluded known diseases, the medical profession settles on a term IBS. IBS as you well know stands for irritable bowel syndrome. Well I believe that an excess of bicarbonate can make my bowel irritable.Bicarbonate is caustic and although may irritate at high level, is the substance that actually protects our colon. This may be why IBS never progresses into something more serious - ie people have IBS their whole lives yet never develope inflamation.This is just a theory and I am hopefull that input from folk on this board will assist in providing more evidence one way or another.I am also not saying this is a diffinative cause of IBS rather there could be a sub type of IBS experienced by some people.In this case , I think, IBS may be a symptom not the disease which is why doctors can find no cause.


> quote:Originally posted by flux:Actually, part of your theory sounds like the theory for the mechanism of collagenous colitis.But that is *not* IBS. IBS is not a secretory process. I would think that if you had this going on, you'd have very severe diarrhea and the disease process would be seen on colonoscopy.I'm not sure where bicarbonate/pH fits into this at least from the mechanism you describe. If you dump Cl- into the colon, you're going to have secretory diarrhea, so the excess HCO3 (which doesn't necessarily involve PGE), is irrelevant.
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> > quote:raises the pH level above that at which the normal bacteria function correctly causing gas etc.
> ...


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## flux (Dec 13, 1998)

> quote:IBS is a name for a cluster of symptoms that a doctor can find no obvious cause for. Having excluded known diseases,


Note the last part of what you wrote. Isn't collagenous colitis is one of them? Besides, collagenous colitis generally appears in middle-aged woman and it's probably unlikley to be confused with Rome criteria for IBS. IBS is not secretory diarrhea and couldn't have volume seen in a secretory process.


> quote:Well I believe that an excess of bicarbonate can make my bowel irritable


The mechanism you describe is *not* how it works in the colon, so this part of your theory is DOA. Also, where is bicarbonate? Do you even have proof of an alkaline stool?


> quote:Bicarbonate is caustic and although may irritate at high level, is the substance that actually protects our colon.


Huh?


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## 21207 (Sep 16, 2005)

Hi flux Have you really researched how the colon works? Bicarbonate is released into the duodenum due to a number of triggers. Increase in acid in the stomach, extention of the stomach - ie food ingestion and via PGE2 stimulation of the EP4 receptors. It is interesting to note that the EP4 receptor / prostaglandin stimulation is much greater than that caused by food or acid. Also, yes I have tested my stool over a number of months using universal indicator paper and consistently have a pH of 9-10. This is 100x more alkaline than the normal colon pH of around 7.Also, it is interesting to note that of the 6 drugs/ aids that assisted ibs-d - 5 of them had side effects of decreasing bicarbonate production. The actual mechanism of most drugs is unknown.Also, perform some research into what fish oil and apsirin have in common. Both of these help my condition.


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## flux (Dec 13, 1998)

> quote:Bicarbonate is released into the duodenum due to a number of triggers.


What's the duodenum have to do with the colon?


> quote:Also, yes I have tested my stool over a number of months using universal indicator paper and consistently have a pH of 9-10. This is 100x more alkaline than the normal colon pH of around 7.


How many stools from other people have you also tested? Would it surprise you if they *all* tested at 9-10?


> quote:Also, it is interesting to note that of the 6 drugs/ aids that assisted ibs-d - 5 of them had side effects of decreasing bicarbonate production..


Huh?


> quote: fish oil and apsirin have in common. Both of these help my condition.


What if someone switched the aspirin with a sugar pill? Would it surprise you if it had the same effect?


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## 21207 (Sep 16, 2005)

fluxYou shoudl actually attempt to be more constructive and research before you provide flippant remarks. It may amaze you to find out the duodenum empties into the colon - i.e everything in the duodenum ends up in the colon.I havent tested othe rpeople but research on the internet shows that a normal colon runs at aprox neutral i.e 7.The aspirin / sugar comment doesnt even warrant a reply as the plkcebo effect is short lived and I notices the effect of aspirin after I took it not that I took it for my disorder.Also, do some research on how Aspirin works.


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## flux (Dec 13, 1998)

> quote:It may amaze you to find out the duodenum empties into the colon - i.e everything in the duodenum ends up in the colon.


If that were true, we would barely be alive for a week. The duodenum empties into jejunum where the nutrients are absorbed. Bile acids and some water are absorbed in the ileum. The remainder (mostly undigested food and water) is what ends up in the colon.


> quote:I havent tested othe rpeople but research on the internet shows that a normal colon runs at aprox neutral i.e 7.


There is no one colonic pH. The luminal pH varies along the length of the colon. And that is separate from the fecal pH, which you would probably find to be 9-10 in everyone else too if you had tested them with your "universal indicator" paper.


> quote:The aspirin / sugar comment doesnt even warrant a reply as the plkcebo effect is short lived


The placebo effect may not only be long-lived, but even permanent.


> quote:I notices the effect of aspirin after I took it not that I took it for my disorder.


Coincidence?


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## 21207 (Sep 16, 2005)

Flux I am really not going to wast more time arguing with you having reviewed some of your other posts. On the 21st May you stated in another message that it is normal for stool to be acidic and yet you argue with me that it may be normal to be alkaline.It seems as though you go opposite to whatever the view is. Go take some more sugar pills.I would like to get this messaqge thread back on track in terms of finding out from other people whether they experienced the same cluster of symptoms as I identified earlier in the thread.


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## flux (Dec 13, 1998)

> quote:May you stated in another message that it is normal for stool to be acidic and yet you argue with me that it may be normal to be alkaline.


No, I don't think your stool is alkaline. I wouldn't be surprised it were acidic. I think the problem is not with your stool; it is with your measurements!


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## eric (Jul 8, 1999)

Kevinhttp://ibsgroup.org/eve/forums/a/tpc/f/71210261/m/397106832


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## 21207 (Sep 16, 2005)

FluxUniversal indicator paper is relatively easy to use - just match the colour to a chart. Anyway, to get back on track - Prostaglandin induced diarrhea is well documented on the internet and I have all the symtoms including treatment that works. My theory as to the bicarbonate effect is where I make a leap but that is based on research available on the inernet showing prostaglandin (pge2) activation of EP4 cells so nothing I have stated is out of the realm of possibility.If you research prostaglandin induced diarrhea and you also research EP4 receptors / pge2 activation you will see why I made the connection.What my concern is , is why my prostaglandin level is high and has been for so many years.Ther are numerous causes including food sensitivity, insulin disorders, infection etc but I cannot understand if PGE2 induced diarrhea is so well documented why my doctors/ gastro failed to highlight the possibility.


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## flux (Dec 13, 1998)

> quote: Universal indicator paper is relatively easy to use - just match the colour to a chart.


So why can't you get it to work?


> quote:Anyway, to get back on track - Prostaglandin induced diarrhea is well documented on the internet and I have all the symtoms including treatment that works.


Things don't get documented on the Internet. They get documented in research papers.


> quote:My theory as to the bicarbonate effect is where I make a leap


You have no evidence that you have a secretory process going on yet, let alone alkaline stools.


> quote:What my concern is , is why my prostaglandin level is high and has been for so many years.


How do you know it's high?


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## 16593 (Jun 22, 2005)

Ok, I have to jump in here. I first began experiencing IBS symptoms the day after I gave birth. My symptoms were horrible cramping and diarrhea. My OB/GYN recommended a gastro by the name of Dr. John Mathias who works at the Texas Women's Hospital. This particular doctor diagnosed me with IBS after conducting all of the usual tests to rule out anything else (blood and stool samples, colonoscopy etc...). He then began to tell me his theory of why he thought I had IBS. He said that after I gave birth, my prostaglandins(PGE2 series) were elevated, which is normal during labor but subside after the delivery. For whatever reason, mine did not, They remained elevated, causing my cramping and diarrhea, as PGE2s increase inflammation in the body. After doing a TON of research on prostaglandins, especially the 2 series, it made perfect sense to me. This may be a bit personal as I am a female and I am pretty sure you are male, but when a woman menstruates, her PGE2 levels spike, along with other hormones, that cause uterune cramping, along with intestinal cramping. This is why many women with or without IBS complain of diarrhea and cramping during mestruation. Anyway, male or female, hormones are hormones. Both sexes have the same ones, just at different levels. He put me on a low glycemic diet (basically following the same principles as The Zone Diet which you mentioned earlier) to help control my insulin levels as high insulin levels increase PGE2s. You want to decrease pro-inflammatory prostaglandins and increase the anti-inflammatory ones. A low glycemic diet, omega 3 fish oils will help to block the pro-inflammatory pathways and increawe the anti-inflammatory ones. I know this sounds simplistic and I could probably go into a LOT more detail if it were not so late, and I could dig in my box of doctor's notes to better expalin. Frankly, sfter I began feeling better, I kind of put the "why I have IBS" thory out of my mind until I read your e-mail. I honestly had not heard of anyone else, besides my doc, who felt that elevated PGE2 levels may account for some cases of IBS. Anyway, I can't tell you how much that diet helped me out. I went from a pain level of 9 and having diarrhea every day to a pain level of 2 to 3 and attacks of diarrhea very rarely. This all happened gradually, but I did notice that I got better and better with each passing week and month. He also had me taking Omega 3s 2 - 3 times a day to help lower my PGE2s as well. It has been 2 years since I have been on the diet and I feel that, although not perfect, I am better than I have ever been. I have had to go off the diet due to the fact that I have a hard time keeping weight on. I am naturally very thin, even underweight, and this diet was not helping me in that department. I have had to add more carbs to my diet to add some weight back on, but since I have stabalized my PGE2 levels, I am able to do this. I still have problems around that time of the month. During that time, I try to only eat low-glycemic foods. I also take Ibuprofin during that time to block the PGE2s as well. I know that these drugs are a double edged sword because they also block the cox 1's, but I only take them sparingly. Now, I am not saying that this is why people have IBS. As we all know, IBS can be caused by a number of diferent factors. I believe this is why I personally got IBS. I am not cured by any means. I will have IBS forever I ma pretty sure, but I am now beter able to control it now that I have been able to reduce my PGE2 levels.By the way, what are you doing to control your PGE2s?? Hope this was helpful.


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## 21207 (Sep 16, 2005)

Hi Dana Thank you very much for jumping in with your story. I had a consultation with a respected practioner today who , after a lengthy consultation, agrees that Prostaglandin induced diarrhea is a distinct possibility based on the cluster of symptoms and she has arranged a series of tests to try to support or disprove the possibility.As you say, some women experience diarrhea monthly during menstruation and this is typically treated with something like mefenanic acid - to lower the pge2 levels. Considering these women are normal for the remainder of the month and have no obvious colonic disorder it is reasonable to conclude that should the levels of PGE2 remain high based on hormonal issues that the diarrhea would persist on a daily basis. This is therefore evidence that PGE2 levels in the body , not necessarily related to the colon, can cause the symptoms of d. Hence my belief that my d could be based on a systemic disorder with d as a symptom - not the disease.It also explains why Aspirin works in my case and interestingly enough there is now support growing for the use of Aspirin in HIV related D and cancer treatment d.I have also left the Aspirin and embarked on a daily fish oil suplement and am finding a steady improvement in the cluster of symptoms although the d is only about 40% improved - however it is early days.There is also growing evidence that PGE2 related to gum disease causes heart problems and premature birth so it seems again feasable that system PGE2 levels can have all sorts of impact.There may just be a sub class of IBS-d people who have PGE2 issue so time will tell.I am happy that you have managed to control your symptoms so well but cant help wondering what the trigger is that causes such a change. (child birth aside







)cheerskevin


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## Talissa (Apr 10, 2004)

Kevine,I'm so glad you're no longer taking aspirin! & are having good luck w/ the omega 3s.









> quote:There may just be a sub class of IBS-d people who have PGE2 issue so time will tell.


You're right. It's well-known now that many peeps w/ IBS, esp all those w/ post-infectious IBS, have low-grade intestinal inflammation. So of course along with other proinflammatory cytokines, PgE2 is involved.I just don't think the bicarbonate is involved, & really, as long as you're having success lowering the inflammatin in a healthy way--who cares?That's how I've gotten better, by focusing on lowering inflammation(btw, ever since taking antibiotics for 365 days in a row as a teen, I've had gum disease...)Do you mind sharing what brand of fish oil you're taking, & how much? Might be helpful for others.







Glad you're getting a handle on things, & doing so well. It's a great feeling, isn't it? T-


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## 21207 (Sep 16, 2005)

Hi TalissaI am happy not to be taking Aspirin but will also not feel too concerned about taking it as required as a low dose is required to achieve good results.The fish oil I am using is Blackmores 1000mg gelatine capsules. I am taking the dose that is advised on the label for treatment of inflamation. Not sure if this is an international brand but it is here in Australia. I would guess that fish oil would be much the same in quality if purchased from any reputable brand. I chose not to use something like cod liver oil as you have to be careful about ingesting too much vitamin A.It is good to see results but I alway try to understand the root cause of something so if it turns out to be a PGE2 issue , I still want to understand the cause of that.cheerskevin


> quote:Originally posted by Talissa:Kevine,I'm so glad you're no longer taking aspirin! & are having good luck w/ the omega 3s.
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## 16608 (Mar 30, 2006)

Kevin,Back when I had regular, intense menstrual periods my OBGYN said it was high prostaglandins that caused it. I often also had diarrhea the first few days. Interesting connection, because HE only connected the prostaglandins to the bad cramping, and prescribed NSAIDs (such as Anaprox, Naproxin) for it. I generally take either borage, primrose or Omega oils daily, have for years, and rarely get diarrhea when I do happen to get a period. Hope you continue to see improvement, visit the forums, and I see you've already learned how nonproductive arguing with Flux can be! He DOES seem to know a lot...he just doesn't know how to be very constructive.


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## 21207 (Sep 16, 2005)

Thanks ArtgirlI am seeing an improvement which I hope continues. My doctor immediataly connected my prostaglandin (pge2) concern with the known menstruation info and acknowledged that if exogenous pge2 can cause d then pge2 levels in the body, unrelated to any intestinal issue, could have exactly the same effect. The investigation will now try to prove that my IBS-d is a symptom of a systemic problem. Interestingly, I have long said the doctors that the white coating on my tongue seems to fluctuate with symptoms - being thicker when I am bad and lighter when I am better.Considering the mucous lining on the tongue as similar receptors to the colon, it is evident that the tongue may visually display what the colon is mirroring.As for Flux, yes I wish there was a mute button. When I identified that he was arguing two opposing views with two different people, he turned it into a personal attack on my competency without any proof of what or how I had completed my tests.I think he is some self styled IBS-truth evangelist who has little better to do than patrol the board responding with arogant one liners of little constructive value. Thank goodness he is not my doctor. cheerskevin


> quote:Originally posted by artgirl2:Kevin,Back when I had regular, intense menstrual periods my OBGYN said it was high prostaglandins that caused it. I often also had diarrhea the first few days. Interesting connection, because HE only connected the prostaglandins to the bad cramping, and prescribed NSAIDs (such as Anaprox, Naproxin) for it. I generally take either borage, primrose or Omega oils daily, have for years, and rarely get diarrhea when I do happen to get a period. Hope you continue to see improvement, visit the forums, and I see you've already learned how nonproductive arguing with Flux can be! He DOES seem to know a lot...he just doesn't know how to be very constructive.


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## eric (Jul 8, 1999)

Just fyi"Hypersensitivity to normal amounts of intraluminal distention exists, as does a heightened perception of pain in the presence of normal quantity and quality of intestinal gas. The pain of IBS seems to be caused by abnormally strong contraction of the intestinal smooth muscle or by increased sensitivity of the intestine to distention. Hypersensitivity to the hormones gastrin and cholecystokinin may also be present. However, hormonal fluctuations do not correlate with clinical symptoms. The caloric density of food intake may increase the magnitude and frequency of myoelectrical activity and gastric motility. Fat ingestion may cause a delayed peak of motor activity, which can be exaggerated in IBS. The first few days of menstruation can lead to transiently elevated prostaglandin E2, resulting in increased pain and diarrhea. This is not caused by estrogen or progesterone but by the release of prostaglandins."http://www.merck.com/mrkshared/mmanual/sec...apter32/32a.jsp


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## 21207 (Sep 16, 2005)

Hi EricI agree with the hypersensitivity. If you research PGE2 , you will find that it causes a change in the cell electrical potential that makes it fire at a lower threshold - hence an increase in sensitivity. It also causes mucous production - so that ties the sensitivity to the increased mucous.On the subject of PGE2 induced d, I also wondered why my symptoms were not that bad during the night i.e. myself and many other IBS sufferers - although suffering from d, still seem to sleep through the night.I went looking for an association between PGE2 and sleep and found an interesting article that stated PGE2 decreased by aprox 40% during the sleep cycle. I think this gives further support to the Prostaglandin - d theory as it helps explain the sleep issue.


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## Talissa (Apr 10, 2004)

> quote:I think this gives further support to the Prostaglandin - d theory as it helps explain the sleep issue.


K, PgE2 is a well-known component of the low-grade inflammation of PI-IBS. The inflammatory cytokines seem to trigger the inflammatory prostaglandins. This inflammation is also seen in some w/ IBS and no known connection to an infection...Ie,MEDSCAPE~~"...*The second study using the T. spiralis model showed that exposure of muscle cells to interleukin-4 or interleukin-13 increased transforming growth factor (TGF)-1Î², cyclooxygenase 2 (COX2) protein and prostaglandin E2. * COX2 inhibitors attenuated this hypercontractility and the authors conclude that maintenance of hypercontractility in the long term depends on increased expression of TGF-Î²1 and upregulation of COX2 and prostaglandin E2.[28*] *The final common pathway appears to be prostaglandin E2, which increases the contractile response of muscle cells to carbachol. * *The same group from McMaster also showed that Lactobacillus paracasei was able to specifically reduce TGF-Î² production and the associated COX2 and prostaglandin E2 levels in muscles.*This effect was seen during treatment with both the probiotic culture and spent culture medium, which contained only soluble mediators.[29*] These animal data give support to the idea that probiotics might be effective in PI-IBS."http://www.medscape.com/viewarticle/518355_8Here's a study that similarly implicates inflammatory transforming growth factor beta1 (TGF-beta1)in IBS & its resulting upregulation of PgD2, among other inflammatory cells~~"Furthermore, TGF-beta1 dramatically changed the profile of mediators released by MC following IgE receptor crosslinking. Release of histamine, cysteinyl-leukotrienes, and tumour necrosis factor alpha was strongly reduced whereas prostaglandin D2 generation and cyclooxygenase 1 and 2 expression were upregulated by TGF-beta1. CONCLUSIONS: Our data indicate that TGF-beta1 acts as a novel potent inhibitor and modulator of human intestinal MC effector functions. The change in MC mediator release profile and protease expression induced by TGF-beta1 might be of relevance for the control of MC associated disorders of the intestine such as allergic reactions, Crohn's disease, irritable bowel syndrome, and parasitic infection."Gut. 2005 Jul;54(7):928-34IMO, many of us w/ this low-grade inflammation(I've been tested & I definitely have it) may have the problem they're finding in crohn's disease, just to a lesser degree--an abnormal inflammatory reaction to normal enteric bacteria. This abnormal reaction is triggered IMO by the loss of beneficial bacteria which would normally keep the reactions in check. That's my theory...(btw, L paracasei is now just called "L Casei" in case anyone's interested in trying this probiotic out. I take it in the probiotic mix iFlora)


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## Kathleen M. (Nov 16, 1999)

Kevin, the colon is much less active in everyone at night.You don't have to invoke some special mechanism for it. it is the normal circadian rhythm of the colon that it "sleeps" when you do.When you have something that disrupts that rhythm then you look for abnormalities. You don't need something abnormal to enforce a normal part of how the body works.


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## 21207 (Sep 16, 2005)

Hi Kathleen Ever tried sleeping with food poisoning or another form of a stomach virus causing sectretory d







cheerskevin


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## Kathleen M. (Nov 16, 1999)

Yep, and that is why diarrhea at night when you should be asleep is usually one of those red flags that what is going on is *NOT* IBS.Yes, I've had food poisoning for days on end and know about dozing all night in the bathroom.I've gotten a few people here to get tested for microscopic colitis that turned out to be why they had diarrhea at night. It is common for that, rare for IBS because IBS follows, generally, the very normal pattern of colon active vs colon at rest. All the times IBSers normally have symptoms tend to be the exact same times that a totally completely normal colon is most active. When a totally completely normal colon is normally at rest, IBSers generally do not have symptoms.Some things over-ride the normal rhythm of the colon. But you don't need to come up with something abnormal to explain why IBSers do not normally have diarrhea at night, and that was what it sounded like you were doing.It seemed like you thought that if the colon calmed down at night you used that to support your theory of something being wrong. It has nothing to do with any abnormality of any kind. Less active at night is the normal state abnormal things throw that off, not reinforce it.


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