Do irritating foods delay the "healing" process?

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Sue777
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Do irritating foods delay the "healing" process?

Post by Sue777 »

I wasn't sure how to word the subject line to most accurately summarize my question so I apologize if it's misleading.

I am in my 5th week of re-starting Asacol and although I do see some improvement it's not nearly as good as I had hoped. (I think, but I'm not certain, that it worked much faster and better the first time - 8 years ago).

I try very hard to only eat things that are least-problematic but I'm having a hard time with that. I have spent the past several years eating tons of fruits, veggies, high-fiber foods, and avoiding carbs like white rice, white bread, white potatoes, etc. Now, it seems that's about all I can eat and I hate it!

So my question is: am I delaying my "remission" or healing (do we ever truly heal?) by occasionally eating foods that bother me, or is this flare up going to get better in it's own due time regardless of what I'm eating right now? If I knew that living on white carbs for a few weeks would get me back to "normal" sooner I could probably do it, but if it really doesn't matter then I may as well just eat healthy, keep the imodium handy, and wait until the Asacol "kicks in".

Your thoughts?
Sue
Sue
Diagnosed November 2004, Used Asacol and Lialda, sometimes worked, sometimes made it worse. Entocort always works but hate it. Remission only lasts 3-6 months and then back on Entocort. Enterolab test July 2017, now gluten free. Time will tell!
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tex
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Post by tex »

If you happen to be one of the very few who are lucky enough to experience spontaneous remissions, then eating irritating (or even inflammatory) foods may or may not delay remission.

If you are like most of us, though, then it may be impossible to achieve remission while eating foods that irritate the gut UNLESS the drugs that you are taking have above average efficacy for you. IOW, for most of us, drugs are not enough, and we have to carefully watch our diet as well, because once the gut is inflamed, it doesn't take much to keep it inflamed, unfortunately. Some people are lucky enough that drugs are much more effective for them, and they're able to achieve remission with minimal or even no diet changes. Few of those individuals are members of this board, however, so we don't know how common that status might actually be. In general, experience shows that it's not nearly as common as the medical experts would have us believe, because a huge majority of patients never completely eliminate all their symptoms by drug treatment alone. In fact, most are unable to achieve remission unless they also change their diet significantly.

Those who experience spontaneous remission are exceptions to all this, though, and all bets are off for them. So the answer to your question is, "Sure, for most of us, eating irritating foods will definitely delay (or completely prevent) remission, but it's impossible to say that this will apply to everyone, and you might be one of those rare exceptions". :shrug: Also, patients who are willing to take a drug for the rest of their life, and/or tolerate certain lingering symptoms, can get away with with fewer diet restrictions.

Tex
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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.
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Post by Sue777 »

Hey Tex,
I think you answered this thread's question perfectly when you commented on my other thread. :)

You said:

Controlling MC is not a short-term project (we can't measure progress in terms of days) -- we have to measure progress over months. If you're going to eat inflammatory foods every other day or so, you might as well eat them every day, because it takes many months to heal the damage caused by gluten, if you happen to be sensitive to it, for example. The damage caused by other food sensitivities heals faster, but still requires weeks to months. The amount of healing that can be accrued in one day is negligible. That's why you can't see any difference.

Tex


So yes, I guess there is "healing" that needs to take place. I never really understood the dynamics of this disease (doesn't the colon look fine during a colonoscopy, meaning there is no apparent inflammation or ulcerations?) So I wondered if there were anything that needed to actually "heal". I guess it would probably be beneficial for me to learn how Asacol works - maybe that would help me understand this disease a little better.

Sue
Sue
Diagnosed November 2004, Used Asacol and Lialda, sometimes worked, sometimes made it worse. Entocort always works but hate it. Remission only lasts 3-6 months and then back on Entocort. Enterolab test July 2017, now gluten free. Time will tell!
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Post by Christine. »

Sue
I remember Tex commenting on the diagnostic criteria for cc and lc on another thread but I can't seem to find it. Suffice it to say that there are changes to the lining of the colon visible under a microscope. If Asacol works for you, you are lucky. Diet change was the key for me.

After 6 months of good progress I plan to add 1 questionable food at a time to see what I can now tolerate. Tomorrow is egg yolk day.....yippee! :lol:

But even if I react I'm pleased to eat my safe foods awhile longer in exchange for living life again.
Best of luck.
Chris
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Post by tex »

Sue wrote:I never really understood the dynamics of this disease (doesn't the colon look fine during a colonoscopy, meaning there is no apparent inflammation or ulcerations?) So I wondered if there were anything that needed to actually "heal".
Yes, the inflammation can only be seen under a microscopic (thus the name), but that doesn't mean that the damage is not just as significant as damage that's visible to the unaided eye. With LC, the damage is in the form of "killer" T cells that infiltrate the mucosa of the intestines, both at the epithelial surface and in the layer of connective tissue underlying the epithelium known as the lamina propria. These T cells keep the tissue inflamed, and in order for healing to take place, the T cell numbers have to return to normal levels (less than 20 lymphocytes per 100 enterocytes). The vertically-elongated cells that make up the single cell layer at the surface of the mucosa are known as enterocytes.

Interestingly, inflammation is necessary for healing, and it is always the first stage of the healing process (marked by redness, swelling and fluid retention). Unfortunately, with MC, the healing process gets stuck at the initial stage (inflammation), and cannot progress past that stage, because the T cells continue to be replaced, thereby maintaining the inflammation. The source of the T cells, of course, is immune system reactions to various food or drug sensitivities within the digestive system. IOW, the food and/or drug sensitivities have to be removed from the diet (to interrupt the inflammatory process), in order for healing to progress.

With CC, the damage is in the form of thickened collagen bands in the lamina propria. For healing to take place, the bands have to return to normal thickness (less than 10 microns). However, with CC, T cells are almost always also present, and those numbers have to be reduced, also.
Sue wrote:I guess it would probably be beneficial for me to learn how Asacol works - maybe that would help me understand this disease a little better.
That would also help doctors to understand the disease better, because currently, no one in the medical profession understands the actual mechanism by which the mesalamine-based drugs such as mesalamine work to suppress inflammation. For that matter, they also don't have the foggiest idea how budesonide or any of the other corticosteroids suppresses inflammation -- they just know that they somehow help to suppress the inflammation.

Tex
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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.
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Post by Sue777 »

tex wrote:
Yes, the inflammation can only be seen under a microscopic (thus the name), but that doesn't mean that the damage is not just as significant as damage that's visible to the unaided eye. With LC, the damage is in the form of "killer" T cells that infiltrate the mucosa of the intestines, both at the epithelial surface and in the layer of connective tissue underlying the epithelium known as the lamina propria. These T cells keep the tissue inflamed, and in order for healing to take place, the T cell numbers have to return to normal levels (less than 20 lymphocytes per 100 enterocytes). The vertically-elongated cells that make up the single cell layer at the surface of the mucosa are known as enterocytes.

Interestingly, inflammation is necessary for healing, and it is always the first stage of the healing process (marked by redness, swelling and fluid retention). Unfortunately, with MC, the healing process gets stuck at the initial stage (inflammation), and cannot progress past that stage, because the T cells continue to be replaced, thereby maintaining the inflammation. The source of the T cells, of course, is immune system reactions to various food or drug sensitivities within the digestive system. IOW, the food and/or drug sensitivities have to be removed from the diet (to interrupt the inflammatory process), in order for healing to progress.

With CC, the damage is in the form of thickened collagen bands in the lamina propria. For healing to take place, the bands have to return to normal thickness (less than 10 microns). However, with CC, T cells are almost always also present, and those numbers have to be reduced, also.

Wow, that was amazing information, much better than anything I've ever been able to find in my research, and explained in a way that I almost understood it all. :) think I'm pretty clear on LC, but I'm still confused about CC: what causes the bands of collagen to thicken, and why would thickened bands of collagen cause all this unpleasantness?

That would also help doctors to understand the disease better, because currently, no one in the medical profession understands the actual mechanism by which the mesalamine-based drugs such as mesalamine work to suppress inflammation. For that matter, they also don't have the foggiest idea how budesonide or any of the other corticosteroids suppresses inflammation -- they just know that they somehow help to suppress the inflammation.

I guess that's why I've never been able to find any info on how and why Asacol works.

You did say you're writing a book, right? I certainly hope so! :)
Sue

Tex
Sue
Diagnosed November 2004, Used Asacol and Lialda, sometimes worked, sometimes made it worse. Entocort always works but hate it. Remission only lasts 3-6 months and then back on Entocort. Enterolab test July 2017, now gluten free. Time will tell!
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Post by tex »

Sue wrote:think I'm pretty clear on LC, but I'm still confused about CC: what causes the bands of collagen to thicken, and why would thickened bands of collagen cause all this unpleasantness?
Well, unfortunately, there's no official medical explanation for any of that, either. So here are my thoughts on it:

My guess is that the thickened collagen bands tend to stiffen the gut wall, which very likely interferes with peristalsis and therefore has an adverse effect on normal digestive processes. When food can't be digested properly, the result is D. When I had my first CT scan, the technician pointed out that the walls of my colon appeared to be unusually thick, and my colon seemed to be sort of stiff and flattened. Of course, that didn't mean anything to my GI doc. :roll:

Those collagen bands are located in the lamina propria layer. The lamina propria is where all the mast cells are located. This is strictly a guess, but it seems logical that one or more of the inflammatory mediators that are released by the mast cells promotes inflammation in those collagen bands, causing them to thicken. I have no idea which mediator (or which mediators) might be responsible, but it seems rather likely that this is basically what happens. IOW, this implies that in order to allow the collagen bands to return to their normal state (to heal), the mast cell degranulation must be controlled (diminished).

Incidentally, collagen is connective tissue, so that means that CC is a connective tissue disease. While that has implications for other purposes, it's probably irrelevant to this particular discussion.

Yes, the book is almost finished, but the board is so busy these days that along with my other duties, I'm having a tough time finding the time to wrap up the final details. I have to work on it whenever I have a few spare minutes.

Tex
:cowboy:

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.
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