Ok, I'm going to make a wild guess here, and guess that those who have bile acid malabsorption have type A, B, or AB blood.
And my second guess it that my first guess is wrong (but if if the first one happens to be correct, that opens the door to an interesting possibility).
Tex
More on Bile Acids (an important piece of the MC puzzle?)
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
Polly,
I have type O blood, also. I was pretty sure this wouldn't pan out, but there are a few old research articles that suggest that bile might be capable of supporting the production of antibodies (especially IgA antibodies) independently of other medium (such as blood). IOW, this raises the possibility that bile might be dumping antibodies into the intestines, or it might even be propagating antibodies after delivery into the small intestine.
Another article shows that bile duct antibodies may be specific to the blood types I mentioned, (but that issue might be irrelevant to MC anyway). I can't find any more recent research where this has been explored further during the past 25 years, though. I don't understand why no one considers the possibility that bile might be capable of producing antibodies to be interesting enough to do additional research on the topic. 
Bile duct antibodies crossreacting with blood group antigens in primary sclerosing cholangitis.
Love,
Tex
I have type O blood, also. I was pretty sure this wouldn't pan out, but there are a few old research articles that suggest that bile might be capable of supporting the production of antibodies (especially IgA antibodies) independently of other medium (such as blood). IOW, this raises the possibility that bile might be dumping antibodies into the intestines, or it might even be propagating antibodies after delivery into the small intestine.
Another article shows that bile duct antibodies may be specific to the blood types I mentioned, (but that issue might be irrelevant to MC anyway). I can't find any more recent research where this has been explored further during the past 25 years, though. I don't understand why no one considers the possibility that bile might be capable of producing antibodies to be interesting enough to do additional research on the topic. Appearance of IgG and IgA antibodies in human bile after tetanus toxoid immunization.Peak responses in bile, while generally of smaller size, exceeded those of paired sera when expressed as antibody/mg of IgG or IgA present. This calculation showed that during the peak response bile was up to nineteen-fold more abundant in IgG antibody than was serum taken at the same time, and up to forty-five-fold more for IgA. Enrichment of antibody in bile is not consistent with the Ig of bile being solely conferred by plasma, and may mean the involvement of local synthesis too.
Serum was collected from: 29 patients with primary sclerosing cholangitis, 18 patients with ulcerative colitis alone, 19 patients with extrahepatic biliary obstruction of other causes, and 42 healthy control subjects. Bile duct antibodies reacted with an antigen localised to the small and large intrahepatic bile ducts. When blood group A human liver was used they were detected in 34% of patients with primary sclerosing cholangitis. They were not detected when blood group O human liver was used.
And if you read the "Results" section of the article, you will see that bile duct antibodies were detected in a similar proportion of the UC subjects (who did not have primary schlorosing cholangitis), and in normal subjects.We conclude that bile duct antibodies are disease, species, and tissue non-specific and react with blood group A/B antigens present in human and rabbit bile ducts and rabbit colon.
Bile duct antibodies crossreacting with blood group antigens in primary sclerosing cholangitis.
Love,
Tex
Hiya Tex,
I have similar thoughts to you on all of this. There is just so much we don't know!
I agree that it is not always good to lower cholesterol for the average person. However, there are many instances where it is necessary. For example, people with preexisting heart disease in some cases and those with familial hypercholesterolemia. About 1 in 500 has a heterozygous mutation that causes markedly elevated cholesterol (especially LDL) and can result in heart disease as early as ages 20-30. Statins and sequestrants are important for treating this problem.
Interesting point about the extra stress on the liver to produce more cholesterol. Let me think out loud (or on paper) here....... In the case of BAD, the liver is already working much harder because of the defective feedback mechanism, so I guess the cholestyramine may not be contributing to a huge amount of additional stress (by causing the liver to increase cholesterol production). Would it be possible that the cholestyramine does little to address the feedback defect? - is it simply removing the excess bile acids before they can move on to inflame the colon. It appears that the amount of bile acid produced by people with BAD varies - some people need only very small amounts of cholestyramine, while others need a great deal. If this theory is correct, then shouldn't people with BAD naturally have lower cholesterol? I wonder if anyone has looked at that? In the case of people without BAD (who have an intact feedback system) who are taking it to lower cholesterol, then I think it would make the liver work significantly harder. Am I thinking this out properly? What am I missing here?
From my research online, it appears the cholestyramine does not really cure the problem. The people with chronic D after gall bladder or terminal ileum removal have taken it for years - often 20 or more and have reported no long term adverse effects (that I could find). So, what is happening that makes the ileum unable to work properly and absorb bile acids? That's the million dollar question, no?
So, yeah, the big question is what has changed/damaged the terminal ileum? We know that people who have had a large amount of ileum removed, as well as those who have documented damage to the ileum (like Crohn's) are at risk for BAD. Is it continued exposure to food antigens as you suggest? Or, I would think that it could be AI....that antibodies are perhaps now being produced against FGF 19 or other important parts of the ileum. We know that AI diseases go hand in hand with MC and often pop up later in the course of the disease. Or hey, what about this?.....an ongoing, low-grade infectious process has damaged the ileum. I am thinking of weird bugs like M.paratuberculosis........weird because it can totally escape detection and treatment - remember, it can change its cell membrane into a cell wall to become resistant to antibiotics. You and I have always believed that the jury is still out with regard to infectious agents and MC. Here's another reason the think infection......cholestyramine is excellent at removing bacterial toxins from the body. It is often used as part of the treatment for C. difficile (along with vancomycin) because it is so good at removing the C. diff toxins.
Whew....my brain hurts! As usual, it's always fun tossing around ideas with you!
Love,
Polly
P.S. Back again! I just found this article from 2104: http://www.futuremedicine.com/doi/pdf/10.2217/fmb.14.52
Don't worry - the "global warming" in the title is not political! LOL!
I have similar thoughts to you on all of this. There is just so much we don't know!
I agree that it is not always good to lower cholesterol for the average person. However, there are many instances where it is necessary. For example, people with preexisting heart disease in some cases and those with familial hypercholesterolemia. About 1 in 500 has a heterozygous mutation that causes markedly elevated cholesterol (especially LDL) and can result in heart disease as early as ages 20-30. Statins and sequestrants are important for treating this problem.
Interesting point about the extra stress on the liver to produce more cholesterol. Let me think out loud (or on paper) here....... In the case of BAD, the liver is already working much harder because of the defective feedback mechanism, so I guess the cholestyramine may not be contributing to a huge amount of additional stress (by causing the liver to increase cholesterol production). Would it be possible that the cholestyramine does little to address the feedback defect? - is it simply removing the excess bile acids before they can move on to inflame the colon. It appears that the amount of bile acid produced by people with BAD varies - some people need only very small amounts of cholestyramine, while others need a great deal. If this theory is correct, then shouldn't people with BAD naturally have lower cholesterol? I wonder if anyone has looked at that? In the case of people without BAD (who have an intact feedback system) who are taking it to lower cholesterol, then I think it would make the liver work significantly harder. Am I thinking this out properly? What am I missing here?
From my research online, it appears the cholestyramine does not really cure the problem. The people with chronic D after gall bladder or terminal ileum removal have taken it for years - often 20 or more and have reported no long term adverse effects (that I could find). So, what is happening that makes the ileum unable to work properly and absorb bile acids? That's the million dollar question, no?
So, yeah, the big question is what has changed/damaged the terminal ileum? We know that people who have had a large amount of ileum removed, as well as those who have documented damage to the ileum (like Crohn's) are at risk for BAD. Is it continued exposure to food antigens as you suggest? Or, I would think that it could be AI....that antibodies are perhaps now being produced against FGF 19 or other important parts of the ileum. We know that AI diseases go hand in hand with MC and often pop up later in the course of the disease. Or hey, what about this?.....an ongoing, low-grade infectious process has damaged the ileum. I am thinking of weird bugs like M.paratuberculosis........weird because it can totally escape detection and treatment - remember, it can change its cell membrane into a cell wall to become resistant to antibiotics. You and I have always believed that the jury is still out with regard to infectious agents and MC. Here's another reason the think infection......cholestyramine is excellent at removing bacterial toxins from the body. It is often used as part of the treatment for C. difficile (along with vancomycin) because it is so good at removing the C. diff toxins.
Whew....my brain hurts! As usual, it's always fun tossing around ideas with you!
Love,
Polly
P.S. Back again! I just found this article from 2104: http://www.futuremedicine.com/doi/pdf/10.2217/fmb.14.52
Don't worry - the "global warming" in the title is not political! LOL!
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
I am adding my personal info because choestyramine has helped me and I am not sure why it has been so effective. Prior to taking it my entire small intestine seemed sensitive, I would get gurgling just from taking supplements, which I can take now and my gut stays quiet.
I had a Genova stool analysis done 12/11/14 and the results showed that I had normal absorption of LCFA, Cholesterol, TG, Total Fecal fat and Phospholipids.
My Short Chain Fatty Acids (SCFA) were low, and they indicated these come from the fermentation of dietary fiber and help regulate fluid balance in the colon. My diet was very low in fiber at the time of the test.
My Eosinophil Protein X was elevated and this can be associated with CC. I also had an elevated level of Klebsiella oxytoca, which can contribute to diarrhea.
The only dietary change I made after the test results was to lower my carbohydrate as Klebsiella thrives on carbs, therefore, the fat in my diet increased and I did notice more fat in my stools.
I had a Genova stool analysis done 12/11/14 and the results showed that I had normal absorption of LCFA, Cholesterol, TG, Total Fecal fat and Phospholipids.
My Short Chain Fatty Acids (SCFA) were low, and they indicated these come from the fermentation of dietary fiber and help regulate fluid balance in the colon. My diet was very low in fiber at the time of the test.
My Eosinophil Protein X was elevated and this can be associated with CC. I also had an elevated level of Klebsiella oxytoca, which can contribute to diarrhea.
The only dietary change I made after the test results was to lower my carbohydrate as Klebsiella thrives on carbs, therefore, the fat in my diet increased and I did notice more fat in my stools.
Donna
Diagnosed with CC August 2011
Diagnosed with CC August 2011
Morning Polly,
I apologize for dropping the ball on this topic. I've been spending too much time on other projects, and the days just don't seem to be long enough. Thank you for inspiring me to check out that connection, because I found it to be very enlightening.
Perhaps this will make up for my shirking, on this topic: I wasn't aware that Johne's disease originates in the terminal ileum, nor was I aware that it involved the formation of giant cells. But what's left of my memory reminds me that there is a form of MC known as (logically enough) "Microscopic colitis with giant cells". How about that? It's barely mentioned in passing in my book, because not much seems to be known about it, but obviously this could be a missing link.
The red emphasis is mine of course. How about that? Even a blind hog finds an acorn now and then.
Here's a link to another abstract.
Microscopic colitis with giant cells: a clinico-pathological review of 11 cases and comparison with microscopic colitis without giant cells.
Love,
Tex
I apologize for dropping the ball on this topic. I've been spending too much time on other projects, and the days just don't seem to be long enough. Thank you for inspiring me to check out that connection, because I found it to be very enlightening.
Perhaps this will make up for my shirking, on this topic: I wasn't aware that Johne's disease originates in the terminal ileum, nor was I aware that it involved the formation of giant cells. But what's left of my memory reminds me that there is a form of MC known as (logically enough) "Microscopic colitis with giant cells". How about that? It's barely mentioned in passing in my book, because not much seems to be known about it, but obviously this could be a missing link.
Microscopic colitis with giant cells: a rare new histopathologic subtype?Abstract
Collagenous and lymphocytic colitis might be part of the same disease spectrum. In this report, we present a histopathologic subtype of microscopic colitis characterized by the presence of subepithelial multinucleated giant cells. This reaction is very unusual and not explicable by any underlying disease process or previous treatment. Among 490 cases of microscopic colitis (MC) diagnosed between 1992 and 2002, we found 2 cases with macrophages and giant cells (0.4%). One case of lymphocytic colitis (LC) and 1 case of collagenous colitis (CC) presented aggregates of macrophages and giant cells located in the superficial part of the lamina propria. Infectious or non-infectious colonic granulomatous diseases were excluded on histologic, clinical, and biological grounds. The recognition of this feature in an MC is important to avoid the diagnosis of granulomatous infectious or idiopathic colitis such as Crohn's disease. Even if very unusual, this subtype of MC evolves favorably since the 2 patients responded well to corticosteroid treatment.
The red emphasis is mine of course. How about that? Even a blind hog finds an acorn now and then.
Here's a link to another abstract.Microscopic colitis with giant cells: a clinico-pathological review of 11 cases and comparison with microscopic colitis without giant cells.
Love,
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Hi Polly,
You should find this to be very interesting, also:
As you are probably aware, calves are infected by MAP when they are young, but the disease doesn't cause any clinical symptoms until they are adults
From the article at the following link:
http://www.johnes.org/handouts/files/Co ... urnal2.pdf
But anyway, looking back at this information, there seem to be some interesting correlations. Of course as we all know, these might simply be coincidences, rather than correlations. But they are interesting, nonetheless.
Love,
Tex
You should find this to be very interesting, also:
As you are probably aware, calves are infected by MAP when they are young, but the disease doesn't cause any clinical symptoms until they are adults
From the article at the following link:
http://www.johnes.org/handouts/files/Co ... urnal2.pdf
When I originally attempted to get a diagnosis in the year 2000, I asked the person doing the CT scan if there was anything remarkable about the scan. I was told that the walls of my intestine appeared thick and my gut seemed flattened.Infiltration of infected tissues with millions of lymphocytes and macrophages progresses over years leading to visible thickening of the intestine.
A report from a CT scan of my abdomen in November, 2005, prior to my first surgery for a stenosis in the sigmoid colon, showed the remark:A particular finding in some cattle with Johne's disease is calcified plaques in the wall of the aorta.
From the article cited above (referring to progression of the infection in calves):Atherosclerotic calcifications are demonstrated.
You probably remember that during my February, 2010 surgery, the surgeon noted on the operative report:The ileum is no longer thin and pliable and can not be easily stretched.
Altogether, it was a long, tedious procedure, and they had to rerun the small intestine 5 or 6 times to make sure that they hadn't missed any tears of other issues. Plus, my heart was showing signs of distress (presumably due to massive loss of blood prior to the surgery) so I was lucky that they didn't eventually just give up and throw my ass in the nearest dumpster.The bowel was quite friable, and simple traction on the intestine resulted in a full thickness tear of an isolated segment of the ileum which was repaired transversely using an inner row of continous 3-0 chromic catgut and an outer row of interrupted Lembert stitches of 3-0 silk. Some 2-1/2 to 3 hours was then consumed carefully mobilizing the entire length of small intestine from the ligament of Treitz down to the ileocecal valve. Several small, superficial, serosal tears were made with traction on this patient's friable intestines, and these were repaired using interrupted sutures of 3-0 silk.
But anyway, looking back at this information, there seem to be some interesting correlations. Of course as we all know, these might simply be coincidences, rather than correlations. But they are interesting, nonetheless.
Love,
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
I am taking 1/2 packet of questran daily, tonight was my 3rd dose. Yay for 1 BM today and it wasn't water. But is anyone having constipation with it? I feel like I may be going in that direction, just curious. This is exciting though! Thanks
Martha E.
Philippians 4:13
Jul 2008 took Clindamycin for a Sinus infection that forever changed my life
Dec 2014 MC Dx
Jul 15, 2015 Elimination Diet
Aug 17, 2015 Enterolab Test
Dec 2015 Reflux
Sept 2016 IC
Philippians 4:13
Jul 2008 took Clindamycin for a Sinus infection that forever changed my life
Dec 2014 MC Dx
Jul 15, 2015 Elimination Diet
Aug 17, 2015 Enterolab Test
Dec 2015 Reflux
Sept 2016 IC
I've never had constipation with it, and I've used it for 18 months in much larger doses than you. On some occasions the BM's have been on the hard side of normal, though. I'm so glad that this seems to work for you as well! The low dose should minimize the risk of malabsorption of micronutrients.
Life's hard and then you die
Tor,
Did you ever experience nausea while taking it? I have had nausea while taking it, but can't figure out if it's the questran. I am going to increase it to 1 packet tonight to see what happens. I always experienced nausea while on Imodium when my BMs start to form. Praying this will go away. Taking meclizine to control the nausea. Thank you for your info!
Did you ever experience nausea while taking it? I have had nausea while taking it, but can't figure out if it's the questran. I am going to increase it to 1 packet tonight to see what happens. I always experienced nausea while on Imodium when my BMs start to form. Praying this will go away. Taking meclizine to control the nausea. Thank you for your info!
Martha E.
Philippians 4:13
Jul 2008 took Clindamycin for a Sinus infection that forever changed my life
Dec 2014 MC Dx
Jul 15, 2015 Elimination Diet
Aug 17, 2015 Enterolab Test
Dec 2015 Reflux
Sept 2016 IC
Philippians 4:13
Jul 2008 took Clindamycin for a Sinus infection that forever changed my life
Dec 2014 MC Dx
Jul 15, 2015 Elimination Diet
Aug 17, 2015 Enterolab Test
Dec 2015 Reflux
Sept 2016 IC
I have never experienced nausea, or any other bad side effects that I know of. I have worried a bit about malabsorption of micronutrients and calcium, and I take supplements. A new DEXA scan last week showed improved bone health while on Questran and calcium.crervin wrote:Tor,
Did you ever experience nausea while taking it? I have had nausea while taking it, but can't figure out if it's the questran. I am going to increase it to 1 packet tonight to see what happens. I always experienced nausea while on Imodium when my BMs start to form. Praying this will go away. Taking meclizine to control the nausea. Thank you for your info!
I have noticed increased insulin sensitivity. I have Diabetes 1, and I consider that a positive side effect. I can't rule out that this side effect can cause low blood sugar which in turn can cause nausea.
-- Tor
Life's hard and then you die