not autoimmune?
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not autoimmune?
My Gasto. Doc says that MC is not autoimmune. Is he correct?
Only if my claim that AI diseases do not actually exist (because they are all caused by either a vitamin D deficiency or a food intolerance) is correct. MC meets the current official medical definition of an AI disease just as well as celiac disease or any other disease meets it.
Tex
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.
That's what I thought. This is what I have to deal with. I've been trying to see if ANY of my doctors ( Gastro., Endo, immunologist….) would be willing to try LDN with me because since taking the Tamoxifen, my gut is inflamed and hurts to the touch ( no D). I'm scared to give up the Tamoxifen because it does cut my risk of cancer recurrence by nearly 50%. After reading Moniques's post, I'm thinking I'd try it, but none of them have heard of using it in this way ( eye roll). So frustrating. I may just order it on line and do it myself.
Thanks
Leah
Thanks
Leah
I had thought about just buying the LDN online. It would be better to get a script and have my insurance pay for it and my GI monitor it.
I have been having D since I stopped the Zyrtec about a week ago. I mostly just thought I was having rebound effects, haven't had much sinus problems and ragweed season is over. The D has gradually gotten worse with more urgency.
Yesterday I had more pain than I have ever had along with WD. I tried again to call my GI and just got a busy signal or his answering service. I left a message "I have UC and I am in a flare! He instructed me to call him if this happened! Please have him or the nurse return my call."
Still nothing. I went ahead and started back on the Uceris. I have an appointment Dec 9th and if I don't get an apology and a reason why his office has been out of touch I will find another GI. I plan to just take the Uceris until then even though it has side effects.
I have been having D since I stopped the Zyrtec about a week ago. I mostly just thought I was having rebound effects, haven't had much sinus problems and ragweed season is over. The D has gradually gotten worse with more urgency.
Yesterday I had more pain than I have ever had along with WD. I tried again to call my GI and just got a busy signal or his answering service. I left a message "I have UC and I am in a flare! He instructed me to call him if this happened! Please have him or the nurse return my call."
Still nothing. I went ahead and started back on the Uceris. I have an appointment Dec 9th and if I don't get an apology and a reason why his office has been out of touch I will find another GI. I plan to just take the Uceris until then even though it has side effects.
Theresa
MC and UC 2014
in remission since June 1, 2014
We must all suffer one of two things: the pain of discipline or the pain of regret. ~Jim Rohn
MC and UC 2014
in remission since June 1, 2014
We must all suffer one of two things: the pain of discipline or the pain of regret. ~Jim Rohn
Hi Leah and all,
Strictly speaking, autoimmune means that the body attacks itself by forming antibodies to one of its own products or tissues. So it is obvious that certain diseases are AI - like Crohn's, Hashimoto's thyroiditis, diabetes type I. In each case, the body is making antibodies to its own tissue/hormones, etc. MC is AI because the basic mechanism is that the body begins forming antibodies to its own (innate) "good" bacteria, thus allowing the "bad" bacteria to overgrow and lead to colitis.
In the case of food food sensitivities, however, things are not as clear cut . If the body is forming antibodies to foods, this is not the same thing as forming antibodies to its own tissues - it is attacking a foreign substance (the food). This would be akin to the way the immune system fights off infection - it attacks a "foreign" invader. So food sensitivities are not necessarily AI by definition.
So your doc may not be totally off-base.
Polly
P.S. I hope you can minimize the effects of the med.
Strictly speaking, autoimmune means that the body attacks itself by forming antibodies to one of its own products or tissues. So it is obvious that certain diseases are AI - like Crohn's, Hashimoto's thyroiditis, diabetes type I. In each case, the body is making antibodies to its own tissue/hormones, etc. MC is AI because the basic mechanism is that the body begins forming antibodies to its own (innate) "good" bacteria, thus allowing the "bad" bacteria to overgrow and lead to colitis.
In the case of food food sensitivities, however, things are not as clear cut . If the body is forming antibodies to foods, this is not the same thing as forming antibodies to its own tissues - it is attacking a foreign substance (the food). This would be akin to the way the immune system fights off infection - it attacks a "foreign" invader. So food sensitivities are not necessarily AI by definition.
So your doc may not be totally off-base.
Polly
P.S. I hope you can minimize the effects of the med.
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
Hi Polly,
Good points. To expand on what you said a bit, IMO here is the main reason why the official medical position to oppose the classification of MC as an AI disease is based on bad science:
Consider celiac disease for example. The primary reaction experienced by celiacs is obviously directed against certain peptides in the gluten molecule that cannot be further broken down during the digestive process (for example, the alpha gliadin peptide, known as the 33-amino-acid [33-mer] peptide). But if gluten remains in the diet, and damage continues to accrue to the small intestine, eventually a point will be reached at which this chronic reaction will promote an autoimmune response against self , and antibodies will be produced against tissue transglutaminase enzyme (which is an enzyme native to the body). This phenomenon whereby anti-tissue transglutaminase antibodies are produced begins approximately when the level of damage in the small intestine reaches the Marsh 3 level (at that point, research shows that approximately 70 % of celiacs will produce an anti-tTG antibody level sufficient to trigger a positive test result).
Obviously, prior to a Marsh 3 level of damage, celiacs are bound to be producing some level of anti-tTG antibodies (but the test is not sufficiently discriminating to be capable of triggering a positive test result because of low test sensitivity). And note that even though a Marsh 3 level of damage is a relatively serious level of damage (marked by extensive villus flattening), approximately 30 % of celiacs still fail to show a positive test result, even at that level of extensive small intestinal damage. That's a very insensitive test.
At a Marsh level of only 1 or 2, the likelihood of a celiac producing anti-tTg antibodies is very low to negligible. Because of this and related testing issues, it's thought that roughly 95 % of celiacs remain undiagnosed. So it's no wonder that current medical testing methods are incapable of determining AI status for MC.
So here is the problem (as I see it) with MC. As usual, it is flummoxed by arbitrary diagnostic criteria based on low-sensitivity testing methods, which are not capable of the level of sensitivity necessary to detect anti-tTG antibodies below a Marsh 3 level of small intestinal damage. With MC, damage to the small intestine at a Marsh 1 level is very common, and occasionally a Marsh 2 level may be reached, but unless a patient presents with a Marsh 3 level of damage (which, of course would be diagnostic of celiac disease), anti-tTG antibodies will never reach a blood level capable of producing a positive test result (at least not when conventional testing methods are used).
Therefore, IMO, MC has been excluded from AI classification status by the arbitrary criteria used by the medical community for determining ant-tTG antibody levels. They need to get their ducks in a row and develop a test that is actually sensitivity enough to diagnose not only the other 95 % of celiacs who are missed by the current testing methods, but also AI status for MC patients.
So yes, any doctor can officially claim that MC is not an AI disease. But that determination is not based on science — it's based on poor testing methods, which means that it's based on poor science. This is just one of many examples of why MC continues to be so poorly understood by the medical community.
Love,
Tex
Good points. To expand on what you said a bit, IMO here is the main reason why the official medical position to oppose the classification of MC as an AI disease is based on bad science:
Consider celiac disease for example. The primary reaction experienced by celiacs is obviously directed against certain peptides in the gluten molecule that cannot be further broken down during the digestive process (for example, the alpha gliadin peptide, known as the 33-amino-acid [33-mer] peptide). But if gluten remains in the diet, and damage continues to accrue to the small intestine, eventually a point will be reached at which this chronic reaction will promote an autoimmune response against self , and antibodies will be produced against tissue transglutaminase enzyme (which is an enzyme native to the body). This phenomenon whereby anti-tissue transglutaminase antibodies are produced begins approximately when the level of damage in the small intestine reaches the Marsh 3 level (at that point, research shows that approximately 70 % of celiacs will produce an anti-tTG antibody level sufficient to trigger a positive test result).
Obviously, prior to a Marsh 3 level of damage, celiacs are bound to be producing some level of anti-tTG antibodies (but the test is not sufficiently discriminating to be capable of triggering a positive test result because of low test sensitivity). And note that even though a Marsh 3 level of damage is a relatively serious level of damage (marked by extensive villus flattening), approximately 30 % of celiacs still fail to show a positive test result, even at that level of extensive small intestinal damage. That's a very insensitive test.
At a Marsh level of only 1 or 2, the likelihood of a celiac producing anti-tTg antibodies is very low to negligible. Because of this and related testing issues, it's thought that roughly 95 % of celiacs remain undiagnosed. So it's no wonder that current medical testing methods are incapable of determining AI status for MC.
So here is the problem (as I see it) with MC. As usual, it is flummoxed by arbitrary diagnostic criteria based on low-sensitivity testing methods, which are not capable of the level of sensitivity necessary to detect anti-tTG antibodies below a Marsh 3 level of small intestinal damage. With MC, damage to the small intestine at a Marsh 1 level is very common, and occasionally a Marsh 2 level may be reached, but unless a patient presents with a Marsh 3 level of damage (which, of course would be diagnostic of celiac disease), anti-tTG antibodies will never reach a blood level capable of producing a positive test result (at least not when conventional testing methods are used).
Therefore, IMO, MC has been excluded from AI classification status by the arbitrary criteria used by the medical community for determining ant-tTG antibody levels. They need to get their ducks in a row and develop a test that is actually sensitivity enough to diagnose not only the other 95 % of celiacs who are missed by the current testing methods, but also AI status for MC patients.
So yes, any doctor can officially claim that MC is not an AI disease. But that determination is not based on science — it's based on poor testing methods, which means that it's based on poor science. This is just one of many examples of why MC continues to be so poorly understood by the medical community.
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.
'Polly wrote:Hi Leah and all,
MC is AI because the basic mechanism is that the body begins forming antibodies to its own (innate) "good" bacteria, thus allowing the "bad" bacteria to overgrow and lead to colitis.
Polly
Hi Polly,
If this is correct, how can we upper the "good" bacteria? So that we always are on step ahead of the "bad" ones?
I have just finished Diclocil medications I had to take because of S. aureus, and I have been taking probiotics all the way. I will also follow Tex' advice as to continue taking probiotics approx 14 days after.
The Diclocil did not give me D, but that is probably because I'm on Entocort.
However, would it be a good idea to take probiotics on a daily basis for a good amount of time, also after I have tapered off Entocort?
I appreciate all thoughts on the subject.
Lilja
Collagenous Colitis diagnosis in 2010
Psoriasis in 1973, symptom free in 2014
GF, CF and SF free since April, 2013
Psoriasis in 1973, symptom free in 2014
GF, CF and SF free since April, 2013