Irritable Bowel Syndrome caused by MCAS? New report.
- Thread starter MCASMike
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Thanks for sharing. This study made headlines a week or two ago.
A couple comments:
A couple comments:
- We have to be careful not to confuse IBD (Inflammatory Bowel Disease) with IBS (Irritable Bowel Syndrome).
- This study claimed to study IBS, but it didn't. It studied acquired food intolerance, which is not at all the same as IBS.
- All this study showed was that when people with a food intolerance were fed that food, the mast cells in their intestines became activated.
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I believe this is the nature article referred to:
Local immune response to food antigens drives meal-induced abdominal pain
https://www.nature.com/articles/s41586-020-03118-2
Local immune response to food antigens drives meal-induced abdominal pain
https://www.nature.com/articles/s41586-020-03118-2
That study says "Moreover, injection of food antigens (gluten, wheat, soy and milk) into the rectosigmoid mucosa of patients with irritable bowel syndrome induced local oedema and mast cell activation."
I reckon if people are shoving food up their bum, they're feeding into the wrong orifice!
I reckon if people are shoving food up their bum, they're feeding into the wrong orifice!
Dr Pimentel is the foremost researcher into IBS and he has recently published studies showing that in the vast majority of cases IBS is in fact either SIBO (small intestinal overgrowth) or IMO (Intestinal Methanogen Overgrowth).
A proportion of patients will experience SIBO after a severe bout of food poisoning either from Campylbacteor, E Coli, Shingella or Salmonella. These bacteria create a bacterial toxin called Cytolethal Distending Toxin (CdtB) with can lead to autoimmunity with anti-vincolin antibodies developing. You can get rid of the CdtB if after a period of time you don't have anymore food poisoning issues but in some people these antibodies stay high and you also develop the anti-vincolin antibodies which cause a loss of function of the Migrating Motor Complex and also nerve damage which will result in bacterial overgrowth and IBS which is really SIBO and can make some sufferer's health really deteriorate.
In one of his latest published studies Dr Pimentel's team injected rats or mice with these antibodies and they developed IBS. He also knows which bacteria overgrow in the small intestines because of the loss of function of the MMC but he hasn't published this information yet.
The treatment is the antibiotic Rifaximin if its just hydrogen producing bacterial that are overgrown in the small intestines but if there is an overgrowth of methanogens then other antibiotics have to be taken alongside the Rimfaximin. They use Neomycin or Metronizadone. Alternatively herbal type antibiotics can be used but a course of these is around 6 weeks as against 2 weeks for Rimfaximin. It is common for difficult cases to have a combination of excess methanogens and hydrogen and a breath test should confirm if this is the case.
The team at Mount Sinai have also been developing a breath test to see if hydrogen sulphide is causing the SiBO and the new test is called Trio Smart and they think this will pick up the 25% of patients who have a flat line response to the breath test but who still have bad symptoms.
There is also a blood test called the Smart Test to find out if one has the antibodies as mentioned above and I would love to get this done but only know of one clinic in the UK who offer it but I am not well enough to travel to this clinic. They will send a phlebotomist to your home for a blood draw but it adds £80 to the price whereas my local surgery would do this for nothing. Unfortunately the clinic only offer the two choices of one attending the clinic or the phlebotomist coming to your home.
This is a huge topic but I don't think there is any doubt now that for the majority of people, I think it was around 80% in their studies, IBS is in fact SIBO or IMO.
I completely relate to the whole scenario that has been set out as I had severe Camplybacter poisoning for 2 weeks in 1998 and was extremely unwell virtually passing out with a very high temperature. It was confirmed to be this by my local hospital when I wasn't improving. I developed severe IBS a while after this and have never had normal bowel function since with a mixed picture of one day being constipated and then reverting to very loose bowels on the following days.
Though my health wasn't good after this poisoning it's interesting that full blown ME developed by 2000 and I could no longer teach or have any sort of normal life.
There are many excellent You Tube videos of Dr Pimentel explaining his work, the latest one only a month or so ago.
Pam
A proportion of patients will experience SIBO after a severe bout of food poisoning either from Campylbacteor, E Coli, Shingella or Salmonella. These bacteria create a bacterial toxin called Cytolethal Distending Toxin (CdtB) with can lead to autoimmunity with anti-vincolin antibodies developing. You can get rid of the CdtB if after a period of time you don't have anymore food poisoning issues but in some people these antibodies stay high and you also develop the anti-vincolin antibodies which cause a loss of function of the Migrating Motor Complex and also nerve damage which will result in bacterial overgrowth and IBS which is really SIBO and can make some sufferer's health really deteriorate.
In one of his latest published studies Dr Pimentel's team injected rats or mice with these antibodies and they developed IBS. He also knows which bacteria overgrow in the small intestines because of the loss of function of the MMC but he hasn't published this information yet.
The treatment is the antibiotic Rifaximin if its just hydrogen producing bacterial that are overgrown in the small intestines but if there is an overgrowth of methanogens then other antibiotics have to be taken alongside the Rimfaximin. They use Neomycin or Metronizadone. Alternatively herbal type antibiotics can be used but a course of these is around 6 weeks as against 2 weeks for Rimfaximin. It is common for difficult cases to have a combination of excess methanogens and hydrogen and a breath test should confirm if this is the case.
The team at Mount Sinai have also been developing a breath test to see if hydrogen sulphide is causing the SiBO and the new test is called Trio Smart and they think this will pick up the 25% of patients who have a flat line response to the breath test but who still have bad symptoms.
There is also a blood test called the Smart Test to find out if one has the antibodies as mentioned above and I would love to get this done but only know of one clinic in the UK who offer it but I am not well enough to travel to this clinic. They will send a phlebotomist to your home for a blood draw but it adds £80 to the price whereas my local surgery would do this for nothing. Unfortunately the clinic only offer the two choices of one attending the clinic or the phlebotomist coming to your home.
This is a huge topic but I don't think there is any doubt now that for the majority of people, I think it was around 80% in their studies, IBS is in fact SIBO or IMO.
I completely relate to the whole scenario that has been set out as I had severe Camplybacter poisoning for 2 weeks in 1998 and was extremely unwell virtually passing out with a very high temperature. It was confirmed to be this by my local hospital when I wasn't improving. I developed severe IBS a while after this and have never had normal bowel function since with a mixed picture of one day being constipated and then reverting to very loose bowels on the following days.
Though my health wasn't good after this poisoning it's interesting that full blown ME developed by 2000 and I could no longer teach or have any sort of normal life.
There are many excellent You Tube videos of Dr Pimentel explaining his work, the latest one only a month or so ago.
Pam
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Did you mean Rifaximin, sold under the brand name Xifaxan, to treat SIBO?
I hear that sometimes longer courses or repeat courses of Rifaximin are needed. Crazy to think there are tests nowadays for SIBO when blank stares used to be the norm for IBS!!!
I also had to address MCAS with Cromolyn Sodium to control 20+ years of IBS. @bertiedog have you tried to access both treatments to see if that helps your long standing IBS?
I hear that sometimes longer courses or repeat courses of Rifaximin are needed. Crazy to think there are tests nowadays for SIBO when blank stares used to be the norm for IBS!!!
I also had to address MCAS with Cromolyn Sodium to control 20+ years of IBS. @bertiedog have you tried to access both treatments to see if that helps your long standing IBS?
That's a very interesting theory about the development of SIBO. Basically, what Dr. Pimentel is saying, is that food poisoning damages the nerves that control intestinal movement, and the slow intestinal movement results in the overgrowth in SIBO?
This sounds similar to the theory proposed in this thread:
https://forums.phoenixrising.me/thr...dysautonomic-gastrointestinal-motility.81362/
This is where you lose me.
IBS-C (constipation-predominant IBS) is related to unusually slow contraction of the intestinal muscles. IBS-D (diarrhea-predominant IBS) is related to unusually quick contraction of the intestinal muscles, often with painful cramping of these muscles.
Since the intestinal muscles are controlled by autonomic nerves, this would make IBS a form of dysautonomia.
Now, in IBS-C, the slow intestinal movement can lead to bacterial/archaeal/fungal overgrowth in the small intestine, which is SIBO.
So I see how IBS-C can cause SIBO, but what does IBS-D have to do with SIBO?
This sounds similar to the theory proposed in this thread:
https://forums.phoenixrising.me/thr...dysautonomic-gastrointestinal-motility.81362/
This is where you lose me.
IBS-C (constipation-predominant IBS) is related to unusually slow contraction of the intestinal muscles. IBS-D (diarrhea-predominant IBS) is related to unusually quick contraction of the intestinal muscles, often with painful cramping of these muscles.
Since the intestinal muscles are controlled by autonomic nerves, this would make IBS a form of dysautonomia.
Now, in IBS-C, the slow intestinal movement can lead to bacterial/archaeal/fungal overgrowth in the small intestine, which is SIBO.
So I see how IBS-C can cause SIBO, but what does IBS-D have to do with SIBO?
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And if it is dysautonomia, isn't that possibly caused by mast cell degranulation? I've had several issues that from what I can tell are dysautonomia-related (laryngospasm, proctalgia fugax, swallowing difficulty, breathlessness and significant rise in heart rate upon very minor exertion, lightheadedness upon standing, waking up gasping for breath, "exploding head syndrome" right before or as I'm falling asleep, etc.), but now these are all rare or gone, and if they are still present and rare, they are not as pronounced, that is, after taking meds and supplements designed to deal with MCAS.
I'll also mention my GI med history: "colitis" as infant (1960s), "pre-colitis" as teenager (I had a little pill box with a couple of Lomotil pills in it that I always carried around). In college, age 19, I developed food poisoning type symptoms when I ate fried food (I didn't make the connection at the time), so I tried a vegetarian diet, then quickly switched to vegan, but still had that problem if I ate something like fried falafel. In late 1999, I developed a wasting disorder, characterized by significant weight loss in a short period of time after one of these food poisoning type incidents, usually after eating at a restaurant (no fried food and vegan). During this time I alo had bloating. I eventually thought it might be low stomach acid, because I had never experienced acid reflux (it was just like water when I had reflux), so I took Betaine HCl and in less than a year this was resolved. Since then, no major GI problems. I have noticed that whenever I eat something new, even if I ate it several days earlier (apple sauce is one "benign" example), I will often have to urinate in the middle of the night, whereas if I eat the same items as I did the previous day, I can easily get through the night without urinating (10 hours or more); I wrote up a thread about that a couple months ago, for those interested.
I'll also mention my GI med history: "colitis" as infant (1960s), "pre-colitis" as teenager (I had a little pill box with a couple of Lomotil pills in it that I always carried around). In college, age 19, I developed food poisoning type symptoms when I ate fried food (I didn't make the connection at the time), so I tried a vegetarian diet, then quickly switched to vegan, but still had that problem if I ate something like fried falafel. In late 1999, I developed a wasting disorder, characterized by significant weight loss in a short period of time after one of these food poisoning type incidents, usually after eating at a restaurant (no fried food and vegan). During this time I alo had bloating. I eventually thought it might be low stomach acid, because I had never experienced acid reflux (it was just like water when I had reflux), so I took Betaine HCl and in less than a year this was resolved. Since then, no major GI problems. I have noticed that whenever I eat something new, even if I ate it several days earlier (apple sauce is one "benign" example), I will often have to urinate in the middle of the night, whereas if I eat the same items as I did the previous day, I can easily get through the night without urinating (10 hours or more); I wrote up a thread about that a couple months ago, for those interested.
Actually it isn't a theory anymore because his team's many studies have proved it to be true with the rats for instance and they see thousands of patients with IBS and have been studying it for 20 years I think he said. All their papers have been accepted in traditional gastro type journals and they are expecting it to be accepted now that IBS is SIBO or IMO for the vast majority of people. He is based at Mount Sinia Hospital btw.
My understanding is that the antibodies created from the food poisoning bugs damage the nerves in the small bowel and this is what happens with the rats when they give them one of the bugs that cause food poisoning, E Coli or Campylabactor for instance. They will develop the 2 different sort of antibodies first and over a period of time then go on to develop the symptoms of IBS.
They looked at whether stress could cause the same symptoms and so they did a study looking at soldiers who had been in the front line during one of the Gulf War some of whom went on to develop IBS. It turned out that only the ones who had food poisoning developed IBS, none of the other soldiers who were on the front line experiencing massive stress developed it so the theory again was proved.
Because the MMC is damaged after the food poisoning because of the toxin contained in the bugs it becomes less efficient so the cleaning wave doesn't happen as it should after eating and fermentation takes place in the small intestines and gases are produced from the bugs which are eating your food. The gases are hydrogen, methane and hydrogen sulphide.
Each one of these gases produce different symptoms namely with hydrogen its diarrhoea, with methane its constipation and with hydrogen sulphide its predominantly diarrhoea but you can also have methane too and then you will have a mixed picture like I have. I think he said that generally his patients who have hydrogen sulphide are the sickest.
So its the gases from the bacteria that are then causing problems every time you eat any carbohydrate and symptoms develop on a daily basis.
The second most common reason for developing problems with SIBO are adhesions from any abdominal surgery because again this can damage the nerves in the small intestines but with this problem you wouldn't have any antibodies, these only occur from the bugs that caused the initial severe food poisoning.
Pam
My understanding is that the antibodies created from the food poisoning bugs damage the nerves in the small bowel and this is what happens with the rats when they give them one of the bugs that cause food poisoning, E Coli or Campylabactor for instance. They will develop the 2 different sort of antibodies first and over a period of time then go on to develop the symptoms of IBS.
They looked at whether stress could cause the same symptoms and so they did a study looking at soldiers who had been in the front line during one of the Gulf War some of whom went on to develop IBS. It turned out that only the ones who had food poisoning developed IBS, none of the other soldiers who were on the front line experiencing massive stress developed it so the theory again was proved.
Because the MMC is damaged after the food poisoning because of the toxin contained in the bugs it becomes less efficient so the cleaning wave doesn't happen as it should after eating and fermentation takes place in the small intestines and gases are produced from the bugs which are eating your food. The gases are hydrogen, methane and hydrogen sulphide.
Each one of these gases produce different symptoms namely with hydrogen its diarrhoea, with methane its constipation and with hydrogen sulphide its predominantly diarrhoea but you can also have methane too and then you will have a mixed picture like I have. I think he said that generally his patients who have hydrogen sulphide are the sickest.
So its the gases from the bacteria that are then causing problems every time you eat any carbohydrate and symptoms develop on a daily basis.
The second most common reason for developing problems with SIBO are adhesions from any abdominal surgery because again this can damage the nerves in the small intestines but with this problem you wouldn't have any antibodies, these only occur from the bugs that caused the initial severe food poisoning.
Pam
Pam, nothing is proven in science (that is for logic/math), but instead a theory is created. The theory is always open to refutation/invalidation/falsification. There are also precise observations, which one might argue are facts, and of course some research scientists will do that as well. One major problem in science today is that funding is almost always crucial yet it's not easy or it may be impossible to obtain if you want to try and refute a theory that is regarded highly.
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Excellent question. We may have a chicken-or-the-egg scenario here.
Generally speaking, mast cells can be degranulated by either biological threats OR by the autonomic nervous system. The autonomic nervous system can also increase the sensitivity of mast cells, without degranulation.
The classic example of mast cell degranulation due to dysautonomia is urticaria, commonly known as hives. In this case, dysfunction of the autonomic nervous system leads to degranulation of mast cells throughout the skin, despite the absence of a biological threat in the skin. (although there may be a biological threat elsewhere in the body)
But degranulation of mast cells can also affect nearby nerves, and if those are autonomic nerves, the mast cells could conceivably induce dysautonomia.
If you're interested in reading more about this, here are two good papers:
The parasympathetic nervous system as a regulator of mast cell function
https://pubmed.ncbi.nlm.nih.gov/25388249/
Mast cell–nerve axis with a focus on the human gut
https://www.sciencedirect.com/science/article/pii/S092544391100130X
That makes perfect sense. If the dysautonomia is causing mast cells to degranulate, but you are taking mast cell stabilizing medication, the dysautonomia will fail to degranulate the mast cells, and the mast cells will not affect any nearby nerves. The end result: fewer symptoms.
Generally speaking, mast cells can be degranulated by either biological threats OR by the autonomic nervous system. The autonomic nervous system can also increase the sensitivity of mast cells, without degranulation.
The classic example of mast cell degranulation due to dysautonomia is urticaria, commonly known as hives. In this case, dysfunction of the autonomic nervous system leads to degranulation of mast cells throughout the skin, despite the absence of a biological threat in the skin. (although there may be a biological threat elsewhere in the body)
But degranulation of mast cells can also affect nearby nerves, and if those are autonomic nerves, the mast cells could conceivably induce dysautonomia.
If you're interested in reading more about this, here are two good papers:
The parasympathetic nervous system as a regulator of mast cell function
https://pubmed.ncbi.nlm.nih.gov/25388249/
Mast cell–nerve axis with a focus on the human gut
https://www.sciencedirect.com/science/article/pii/S092544391100130X
That makes perfect sense. If the dysautonomia is causing mast cells to degranulate, but you are taking mast cell stabilizing medication, the dysautonomia will fail to degranulate the mast cells, and the mast cells will not affect any nearby nerves. The end result: fewer symptoms.
Statins are shaping up to be the most effective med for methane SIBO or IBS-C (methanogens are archea species, not bacteria).
http://agaperspectives.gastro.org/sibo-make-sense-diagnoses-treatment-strategies/
https://siboguru.com/new-treatment-for-methane-sibo-ibs-c-in-phase-2-clinical-trials/
Interestingly, the alterations in gut microbiota by statins may be one of therapeutic targets for the treatment of hyperglycemia.
https://www.frontiersin.org/articles/10.3389/fmicb.2019.01947/full
Conclusion;
[Statin therapy with atorvastatin and rosuvastatin significantly altered the gut microbiota during high fat diet in an aged obese mice model. The abundance of the genera Bacteroides, Butyricimonas, and Mucispirillum was significantly increased by statins, and this was related to hyperglycemia and hyperlipidemia. In particular, Butyricimonas may be related to the anti-hyperglycemic effect of statins. Furthermore, the downregulation of IL-1β and the upregulation of TGFβ1 by statins were significantly correlated with the abundance of those bacteria. These results suggest that the alterations in gut microbiota by statins may be one of therapeutic targets for the treatment of hyperglycemia.]
http://agaperspectives.gastro.org/sibo-make-sense-diagnoses-treatment-strategies/
https://siboguru.com/new-treatment-for-methane-sibo-ibs-c-in-phase-2-clinical-trials/
Interestingly, the alterations in gut microbiota by statins may be one of therapeutic targets for the treatment of hyperglycemia.
https://www.frontiersin.org/articles/10.3389/fmicb.2019.01947/full
Conclusion;
[Statin therapy with atorvastatin and rosuvastatin significantly altered the gut microbiota during high fat diet in an aged obese mice model. The abundance of the genera Bacteroides, Butyricimonas, and Mucispirillum was significantly increased by statins, and this was related to hyperglycemia and hyperlipidemia. In particular, Butyricimonas may be related to the anti-hyperglycemic effect of statins. Furthermore, the downregulation of IL-1β and the upregulation of TGFβ1 by statins were significantly correlated with the abundance of those bacteria. These results suggest that the alterations in gut microbiota by statins may be one of therapeutic targets for the treatment of hyperglycemia.]
The team at Mount Sinai have done a trial on a statin on IMO but they were disappointed with the results but they haven't given up yet they are going to try a different approach I think Dr Pimentel said.
Pam
Pam
Yes sorry I didn't check my spelling but have now corrected it. I ordered mine from an online pharmacy.
"I also had to address MCAS with Cromolyn Sodium to control 20+ years of IBS. @bertiedog have you tried to access both treatments to see if that helps your long standing IBS?[/QUOTE]
I have taken Rifaximin previously but didn't combine it with anything else so though I had a slight improvement which didn't last long which is to be expected as I obviously have a difficult case., I am now on day 4 of 400 mg x 3 Rifaximin with 100 mg oregano oil x 3 and a pro kinetic which is essential with a damaged MMC. The pro kinetic that I am using is the only one I can buy online (or could find at the time) and its Erythromycin around 100 mg taken last thing at night. The recommended dose for Erythromycin is around 50-60 mg but I could only buy 400 mg tablets so cut them into 4.
There is already a big change in bowel movements on this combination. When I didn't add in the Oregano oil my stools were very loose with a lot of bloating and pain but yesterday was the first day of adding it in and this stopped that from happening. Also today is the first day after adding in the pro kinetic with everything else so will see how it goes. I am aiming for at least a 2 week course but might have to go to 3 weeks and then carry on with the Prokinetic and lower fibre diet than I would normally have for a further period of time before gradually increasing this if tolerated.
I had come to the conclusion that my problem was SIBO with the added problem of the methanogens which showed up in last year's G I Effects Stool Test. Other than that the test showed mild dysbiosis with an excess of proteobacteria which is consistent with Dr Pimentel's findings. Last month I also did a Biomesight stool test and their analysis was that it looked like my microbiome was something like 90% healthy! Obviously this isn't the case and interestingly the methanogens didn't show up at all in this test. Having checked this they only showed up when the bacteria were cultured using PCR which isn't the technique used by the companies like Biomesight, Thrive, etc for their stool tests.
Pam
"I also had to address MCAS with Cromolyn Sodium to control 20+ years of IBS. @bertiedog have you tried to access both treatments to see if that helps your long standing IBS?[/QUOTE]
I have taken Rifaximin previously but didn't combine it with anything else so though I had a slight improvement which didn't last long which is to be expected as I obviously have a difficult case., I am now on day 4 of 400 mg x 3 Rifaximin with 100 mg oregano oil x 3 and a pro kinetic which is essential with a damaged MMC. The pro kinetic that I am using is the only one I can buy online (or could find at the time) and its Erythromycin around 100 mg taken last thing at night. The recommended dose for Erythromycin is around 50-60 mg but I could only buy 400 mg tablets so cut them into 4.
There is already a big change in bowel movements on this combination. When I didn't add in the Oregano oil my stools were very loose with a lot of bloating and pain but yesterday was the first day of adding it in and this stopped that from happening. Also today is the first day after adding in the pro kinetic with everything else so will see how it goes. I am aiming for at least a 2 week course but might have to go to 3 weeks and then carry on with the Prokinetic and lower fibre diet than I would normally have for a further period of time before gradually increasing this if tolerated.
I had come to the conclusion that my problem was SIBO with the added problem of the methanogens which showed up in last year's G I Effects Stool Test. Other than that the test showed mild dysbiosis with an excess of proteobacteria which is consistent with Dr Pimentel's findings. Last month I also did a Biomesight stool test and their analysis was that it looked like my microbiome was something like 90% healthy! Obviously this isn't the case and interestingly the methanogens didn't show up at all in this test. Having checked this they only showed up when the bacteria were cultured using PCR which isn't the technique used by the companies like Biomesight, Thrive, etc for their stool tests.
Pam
Hi Pam-
It sound like you are on the right track. I hope you beat your SIBO and can tell us it's history, once and for all!
You might want to think about adding in biofilm disruptors to increase the likelihood of getting rid of your SIBO and keeping it from returning. I still haven't gotten rid of my SIBO, even though I've been treating it daily for 4 years.
Last week I added in enteric coated pancreatic enzymes, which breakup gut biofilms. I've seen and felt a big improvement already in my energy and clarity of mind.
I think the 2 biggest reasons I haven't been able to get the best of my SIBO is because I haven't used prokenetics for my MMC AND what I think might be even more important, I haven't been using things to breakup the biofilms that make killing the bacteria within them extremely difficult.
I've read that around 80% of all very difficult to treat bacterial infections or overgrowths, live within biofilms.
It sound like you are on the right track. I hope you beat your SIBO and can tell us it's history, once and for all!
You might want to think about adding in biofilm disruptors to increase the likelihood of getting rid of your SIBO and keeping it from returning. I still haven't gotten rid of my SIBO, even though I've been treating it daily for 4 years.
Last week I added in enteric coated pancreatic enzymes, which breakup gut biofilms. I've seen and felt a big improvement already in my energy and clarity of mind.
I think the 2 biggest reasons I haven't been able to get the best of my SIBO is because I haven't used prokenetics for my MMC AND what I think might be even more important, I haven't been using things to breakup the biofilms that make killing the bacteria within them extremely difficult.
I've read that around 80% of all very difficult to treat bacterial infections or overgrowths, live within biofilms.
Hi Jim
Yes I had read about these and would be happy to add them in once I see how its going. Today has been the best so far, bowel movement much more normal and less fermentation until I just ate rather a lot of peanuts and cashews! I haven't taken any probiotics the last few days either and that seems to help but might well need to restart when this current treatment is over.
The pro kinetic is absolutely key if there is damage to the nerves of the gut and it has been mentioned that some people need to take this for evermore or they relapse. The Vinculin antibodies never go away apparently with severe sufferers.
Hope you too get everything under control so we can get out of this perpetual, daily problem.
Pam
Yes I had read about these and would be happy to add them in once I see how its going. Today has been the best so far, bowel movement much more normal and less fermentation until I just ate rather a lot of peanuts and cashews! I haven't taken any probiotics the last few days either and that seems to help but might well need to restart when this current treatment is over.
The pro kinetic is absolutely key if there is damage to the nerves of the gut and it has been mentioned that some people need to take this for evermore or they relapse. The Vinculin antibodies never go away apparently with severe sufferers.
Hope you too get everything under control so we can get out of this perpetual, daily problem.
Pam
Thanks Pam.
I really need to add in at least one prokinetic, maybe more. I realize now that I have been too focused on diet and herbal antibiotics and not focused on prokinetics and breaking up biofilms.
At this point I know I need to do everything I can. Prokinetics, diet, herbal antibiotics, biofilm disruptors, everything!
I'm excited about your approach to treating your SIBO! I really hope it goes well.
I really need to add in at least one prokinetic, maybe more. I realize now that I have been too focused on diet and herbal antibiotics and not focused on prokinetics and breaking up biofilms.
At this point I know I need to do everything I can. Prokinetics, diet, herbal antibiotics, biofilm disruptors, everything!
I'm excited about your approach to treating your SIBO! I really hope it goes well.
This is very interesting, it seems that research is moving fast in the world of IBS and SIBO.
Not so long ago, IBS and SIBO were considered different diseases (even though SIBO could manifest as IBS, and get misdiagnosed as IBS).
But from what you are saying, and from the work of Dr Mark Pimentel, most people with IBS in fact have SIBO.
In fact, here it says that "glucose breath test (hydrogen breath test) is the current gold standard for diagnosis of irritable bowel syndrome".
That's news to me, as previously there were no tests for IBS, it was just diagnosed by symptoms (eg Rome criteria), much like ME/CFS.
But now it seems they are saying that IBS is diagnosed by the breath test, which was previously the standard way of diagnosing SIBO. So this seems to show that IBS is increasingly being seen as SIBO (or IMO, the new name for methane-predominant SIBO).
Though if there is a small subset of IBS patients who do not have SIBO, I guess this suggests there is still an separate disease of IBS which is different to SIBO, which we might call "true IBS". I wonder if Dr Pimentel provides any insight on what this true IBS is, in terms of its causes and pathophysiology?
Apparently these anti-CdtB and anti-vinculin autoantibodies are at high levels in patients with IBS-D and IBS-M, but not in IBS-C.
So this suggests IBS-C may be a different condition to IBS-D and IBS-M.
Is IBS-C perhaps the "true IBS", would you know?
Just came across a new IBS test called IBS Smart developed by Dr Pimentel that detects anti-CdtB and anti-vinculin antibodies.
According to Chris Kresser, this IBS Smart test basically tells you if you would benefit from prokinetic drugs:
Not so long ago, IBS and SIBO were considered different diseases (even though SIBO could manifest as IBS, and get misdiagnosed as IBS).
But from what you are saying, and from the work of Dr Mark Pimentel, most people with IBS in fact have SIBO.
In fact, here it says that "glucose breath test (hydrogen breath test) is the current gold standard for diagnosis of irritable bowel syndrome".
That's news to me, as previously there were no tests for IBS, it was just diagnosed by symptoms (eg Rome criteria), much like ME/CFS.
But now it seems they are saying that IBS is diagnosed by the breath test, which was previously the standard way of diagnosing SIBO. So this seems to show that IBS is increasingly being seen as SIBO (or IMO, the new name for methane-predominant SIBO).
Though if there is a small subset of IBS patients who do not have SIBO, I guess this suggests there is still an separate disease of IBS which is different to SIBO, which we might call "true IBS". I wonder if Dr Pimentel provides any insight on what this true IBS is, in terms of its causes and pathophysiology?
Apparently these anti-CdtB and anti-vinculin autoantibodies are at high levels in patients with IBS-D and IBS-M, but not in IBS-C.
So this suggests IBS-C may be a different condition to IBS-D and IBS-M.
Is IBS-C perhaps the "true IBS", would you know?
Just came across a new IBS test called IBS Smart developed by Dr Pimentel that detects anti-CdtB and anti-vinculin antibodies.
According to Chris Kresser, this IBS Smart test basically tells you if you would benefit from prokinetic drugs: