newbie questions!

[mydizzylife]

hello, all--i'm a newbie. glad to have found you.

had gallbladder surgery in november, 2016; diarrhea started then and except for a 2 month bout of constipation, pretty much hasn't stopped. finally got the LC diagnosis in june. i'm starting the entocort weaning process now (i'm on week 6). entocort isn't helping much, it's just cut down the frequency. still having puff poop. some days the pain is so great, it breaks through imodium AND bentyl combined. any suggestions? i'm now fasting and working reduced hours due to the pain and diarrhea.

also, has anyone here also been diagnosed with vestibular neuritis or other vestibular disruptions? wondering if the two conditions are possibly related, and have only been able to find research linking it to UC. i have not been tested for celiac at this time, but have ruled out all autoimmune diseases that an ANA panel covers. MS has also been ruled out.

thanks for the great info on this site.

[tex]

Hi,

Welcome to the forum. We're glad you joined us, but sorry that you needed to. I did a quick search of the archives using only the word "vestibular", and I got 10 hits for old threads. But we have accumulated many members in 12 years. It's probably not associated. A celiac screening test would be pointless because the treatment is covered by the dietary requirements for MC. Here's why the celiac tests are pointless for an MC patient:

FWIW, most newly-diagnosed MC patients would swear under oath that they are not gluten-sensitive, because gluten is a very insidious and deceptive allergen, and for many of us, relatively brief GF diet trials provide misleading evidence. It took me roughly 6 months on a GF diet before I could tell when I was reacting to any particular food. Before that I seemed to react to anything and everything at random. I seemed to react to everything except gluten, and gluten was the main problem. Part of the problem is the fact that gluten (anti-gliadin) IgA antibodies have a 120-day half-life, and this tends to dominate our immune system's attention. IgA antibodies to most other foods have only about a 6-day half-life.

MC is usually not caused by food sensitivities, but food sensitivities tend to develop after the disease begins. Research shows that when the genes that predispose to microscopic colitis are triggered, the genes that predispose to gluten sensitivity are also triggered. Gluten sensitivity causes increased intestinal permeability (also known as "leaky gut") and this allows partially-digested peptides from certain foods to enter the bloodstream, which provokes an immune system response (because those peptides are obviously not supposed to be in the blood). The immune system then begins to react to certain proteins in those foods every time they are eaten. This is why some of the foods that we have been eating for most of our life can suddenly begin to cause chronic inflammation by provoking our immune system to produce antibodies against them.

Many, many doctors have mistakenly informed many, many MC patients that they are not sensitive to gluten based on a negative celiac test result. That simply is not true, because doctors have no way to officially diagnose non-celiac gluten sensitivity. A positive celiac test result can confirm gluten sensitivity, but a negative celiac test result cannot rule out gluten sensitivity. Many doctors mistakenly believe that a negative celic blood test result rules out gluten sensitivity, but there is absolutely no medical justification for making that assumption, it's simply incorrect.

The bottom line is everyone who is diagnosed with MC is sensitive to gluten.

One question . . . "Have you given cholestyramine a fair shot by trying several different doses for a month or so at each dose?" You might have bile acid malabsorption.

Again, welcome aboard, and please feel to ask anything.

Tex

[mydizzylife]

thanks, Tex. cholestramine was my GI's first thought until the biopsy came back for LC, then she abandoned the idea and went with entocort, bentyl and imodium. they don't want to test me for celiac now because i have been consuming gluten inconsistently and the GI is afraid i will suffer a setback if i go back to eating gluten in order to test. i guess i should just give it up and see what happens?

[Gabes-Apg]

HI there

re the celiac blood test
this article also explains why it is not 100% accurate.

From the article

But we now know that people can and do react to several other components of wheat and gluten. The diagram (in the article below shows how wheat and gluten are broken down in the body:

Current laboratory testing for gluten intolerance only tests for alpha-gliadin and transglutaminase, the two components of gluten implicated in celiac disease (highlighted in red in the diagram). But as you can see, wheat contains several other components including lectins like wheat germ agglutinin (WGA), other epitopes of the gliadin protein like beta-gliadin, gamma-gliadin and omega-gliadin, another protein called glutenin, an opioid peptide called gluteomorphin, and a compound called daminated gliadin produced by the industrial processing or digestion of gluten.

So here’s the thing. Studies now clearly show that people can react negatively to all of these components of wheat – not just the alpha-gliadin and transglutaminase that celiacs react to. And the worst part of this is that up until about 2 weeks ago, no commercial labs were testing for sensitivity to these other subfractions of wheat.

https://chriskresser.com/beyond-paleo-2/

long story short - gluten is highly inflammatory to ALL people and with conditions like MC, we are best to avoid inflammatory foods/drinks etc


Cholestryamine
your GI is a bit out of date with the approaches to helping MC. Cholestryamine is one of the treatment protocols recommended by the USA GI specialists association. here is a link to that discussion and the article if you want to share it with your Specialist as a means of using cholestryamine.

there are a few members that have had good results with cholestraymine.
http://www.perskyfarms.com/phpBB2/viewt ... +guideline

hope this helps

[mydizzylife]

thanks, gabes. the only dietary restriction my GI gave was to eat a low fat diet until i mentioned that gluten seemed to make my pain worsen. it sounds like i should just cut gluten no matter what until this goes into remission (if it ever will).

[Jess02]

Hello everyone.

I'm also new here, and I got my biopsy results 2 weeks ago, which it confirmed lymphocytic colitis.
I noticed, after reading a lot of comments here in the forum, that a lot of people are sensitive to gluten, but I'm totally fine with it, at least for now. Since the day of my colonoscopy, which was 1 month and half ago that my symptoms started disappearing as I changed my diet (low fat, no dairy, no coffee, no raw fruit and no raw veges), so I presume that I'm in remission now, since I have a normal bowel movement every day, and I dont get very bloated anymore.
During this past month and half, I've been eating french toasts with ham and cheese for breakfast, and toast with butter during the afternoon, which means that I've being eating gluten every day. I also like sweet foods a lot, so I couldnt handle not eating cake or cookies for a long time, so one day I went back eating 1 or 2 chocolate cookies since my symptoms were better, and also, a few days ago was my birthday and I ate some cake and desserts, and also drank a glass of champagne... And nothing happened... I was still having a normal bowel movement every day (thankfully!) And almost every day I eat 1 or 2 chocolate cookies. I also can eat cucumbers with no problem now. I just haven't tried fruit yet, except for banana, because they gave me a really hard time before, especially apples, so I'm kinda afraid to try, even though I love fruit so much.

Someone above said that everyone with MC is eventually sensitive to gluten, and that kinda worries me because if gluten starts becoming a trigger, I actually dont know what to eat for breakfast or during the afternoon besides things like french toast, bread, etc. Also I cant eat dairy, I dont think fruit is going to do me that well too and I dont really like veges. And I really can afford to lose weight, because I was really on the edge of being underweight since my body didnt accepted any food before, and now I finally got my weight back...

In my biopsy results that said that I had slight active colitis at the time of my colonoscopy, and I entered remission right after. Since it's not severe, and it's only slight active, maybe it is because of that, that I'm not reacting that bad to gluten, sugar and others?

Does being in remission means that the inflammation is not active for now? Because I'm kinda afraid that even though my body is not reacting bad to gluten or sugar now, that the inflammation may be increasing or something like that...

I still havent gone to my doctor yet as I just got my biopsy results 2 weeks ago, but I already have an appointment for this friday, 18th.
I'm also not taking any medications. I only take probiotics everyday, the moment I wake up.

Thanks :)

[tex]

mydizzylife,

Here's a quote taken from the manuscript of the new book I'm working on that you might find interesting. It
explains some of my thoughts about the use of bile acid sequestrants for treating MC.

Bile acid malabsorption (BAM) is a very common cause of chronic diarrhea.

When microscopic colitis fails to respond to treatments that are normally effective, consider treatment for bile acid malabsorption as a possible option. Bile acid malabsorption has been shown to be present in 60 % of LC cases and 44 % of CC cases (Ung et al, 2000, Fernandez-Banares et al., 2001).2, 3 That doesn't mean that the treatment will bring remission in 60 % of LC cases and 44 % of CC cases, but in a few cases that have been unresponsive to other treatments, the diarrhea may stop if a bile acid sequestrant is added to the treatment program. Based on actual results among members of a microscopic colitis discussion and support forum who tried the treatment, using regular cholestyramine (not the lite version) seems to provide the best results. Be aware that cholestyramine will significantly affect the absorption of nutrients in food and supplements and many medications unless the timing of the dosage is carefully controlled. As a general rule, it should be taken at least two hours after or four hours before eating or taking other medications or vitamin or mineral supplements.

Results suggest that cholestyramine should be considered later in MC treatment programs, rather than as an initial treatment.
Informally comparing the results of those who tried cholestyramine early in their treatment program with the results of those who tried it later in their treatment, it appears that in most cases, success rates have been significantly higher for those patients who have used cholestyramine after they have been treating the disease for more than a year, but have been unsuccessful in completely stopping the diarrhea.

Gastroenterologists seem to prefer trying a chlestyramine treatment early on simply because of the prevalence of BAM relative to MC. But the reason why this is usually unsuccessful is because the intestines of microscopic colitis patients are highly inflamed and cholestyramine doesn't really address this inflammation. Although it is capable of sequestering inflammatory agents in the fecal stream, it is not capable of reducing inflammation within the tissue of the intestinal mucosa. This inflammation usually must be controlled first.

So while cholestyeramine is effective for treating bile acid malabsorption, it's not so good for treating microscopic colitis. Therefore, after a restricted diet and other methods known to normally bring remission in similar cases have been used to stop or significantly limit intestinal inflammation, but diarrhea still remains, there is a good chance that it may be due to BAM. If so, cholestyramine may be used to successfully remove the bile acids from the intestine. The key may lie in finding the optimum dose. But early on, treating BAM tends to be relatively ineffective in most cases, because BAM is not the primary cause of diarrhea in the early stages of MC. The diarrhea is primarily due to the intestinal inflammation. BAM may be present early on, but that may merely be a coincidence and it's relative influence is overshadowed by the secretory diarrhea associated with MC. After the lymphocyte levels have been suppressed by diet changes, then if remission is still elusive, it might be time to consider BAM as the possible cause of the remaining diarrhea.

Recycling of bile acids appears to be controlled by cortisol.
Experimenting with specially-altered mice (mice that had no glucocorticoid receptors in their livers), Rose et al. (2011) found that compared with normal mice, they lost weight on the same diet because their ability to digest fat was compromised.3 They weren't able to normally recycle bile acids and they developed gallstones.

An adequate supply of bile is stored in the gallbladder. When the body becomes hungry, it releases cortisol (which is a glucocorticoid). Cortisol is a hormone and it attaches to the glucocorticoid receptors in the liver and the liver responds by producing bile and storing it in the gallbladder, in anticipation of the next meal. When the meal is actually eaten, bile is released through the common bile duct into the small intestine to emulsify the fat in the food. Additionally, lipase from the pancreas is added to the bile in the common bile duct to further digest the fat in the small intestine.

Normally, the body recycles about 95 % of the bile that's released into the small intestine. It's reabsorbed in the terminal ilium (the last section of the small intestine). If it's not reabsorbed, it stays in the intestine, where it may cause diarrhea. But in addition, if bile acids are not adequately reabsorbed, the liver may soon be unable to maintain a normal level of bile in the gallbladder because without the recycling, it simply cannot produce enough bile. And the body's ability to digest fat will be limited, leading to weight loss. Thus the researchers were able to prove that cortisol controls the recycling of bile acids.

Rose et al. (2011) also discovered that this effect apparently also applies to humans. Cortisol is normally produced by the adrenal glands. When people have a rare disorder called Addison's disease, their immune system attacks their adrenal glands and their ability to produce normal amounts of cortisol is disrupted. The researchers found that when they examined blood samples of Addison's disease patients taken before and after eating, bile acid recycling was also compromised, similar to the mice that had no glucocorticoid receptors in their livers. So apparently cortisol also controls bile acid recycling in humans.

This appears to have interesting implications for MC patients.
This might suggest that MC patients who tend to lose weight during a flare may be short of cortisol. It also might suggest that these individuals may not be able to properly recycle bile acids and may therefore possibly be more likely to respond to cholestyramine treatment than those who do not usually lose weight during an MC flare. There is no published research on which to base such a determination, therefore, this is strictly a speculative observation. It may have merit, or it may not.

At any rate though, the discovery that cortisol controls bile acid recycling would surely have implications for patients taking a corticosteroid to treat MC. Products such as budesonide (Entocort or Uceris) obviously must be capable of boosting bile acid absorption, since budesonide is an anti-inflammatory corticosteroid with potent glucocorticoid activity. So perhaps it is this capability of improving bile acid absorption that allows budesonide to be so useful for controlling diarrhea for many MC patients. Perhaps this explains why patients who take budesonide are more likely to gain weight as a side effect of the drug.

Here's why bile acid sequestrants may be a poor choice for treating MC.
Bile acid sequestrants were developed to lower cholesterol, not to treat MC. When cholestyramine or a similar product is taken, bile acids are tied up by the drug and purged (because they will remain in the stool and end up in the toilet). They cannot be recycled, so bile acid absorption will decrease dramatically. By contrast, if budesonide is taken to treat MC, the cortisol boost means that bile acid absorption will increase, which is the opposite effect of a bile acid sequestrant. This results in improved fat absorption, allowing patients to gain weight, rather than lose weight.

The bottom line is that bile acid sequestrants such as cholestyramine may seem like a good idea, but the fact that their use results in the wholesale loss of bile acids and the fat that they were put there to digest in the first place, means that their actual usefulness is severely limited. Using bile acid sequestrants tends to waste nutrients, and many MC patients can ill afford to lose any more nutrients.

Correcting the problem of fat and bile acids malabsorpion is definitely a useful goal for treating MC. But trying to correct the problem by flushing bile acids and fat down the toilet is a rather poor solution. Patients need those bile acids and fat for their health. Therefore, if you're going to use a drug to treat the disease, budesonide at least appears to be a much more practical choice than cholestyramine.

But all medications have undesirable side effects. Budesonide is far less likely to suppress the functioning of the adrenals than the other corticosteroids, but eventually, if used long enough, it may tend to suppress adrenal function. And of course that will eventually promote reduced bile acid recycling and reduced fat absorption. Perhaps this is why many patients find that budesonide is less effective as time passes, and it may eventually stop working for them.

Here are the references from that quote:

1. Ung, K., Gillberg, R., Kilander, A., & Abrahamsson, H. (2000). Role of bile acids and bile acid binding agents in patients with collagenous colitis. Gut, 46(2), 170–175. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1727822/

2. Fernandez-Bañares, F., Esteve, M., Salas, A., Forné, T. M., Espinos, J. C., Martín-Comin, J., & Viver, J. M. (2001). Bile acid malabsorption in microscopic colitis and in previously unexplained functional chronic diarrhea. Digestive Diseases and Sciences, 46(10), 2231–2238.

3. Rose, A. J., Berriel Díaz, M., Reimann, A., Klement, J., Walcher, T., Krones-Herzig, A., . . . Herzig, S. (2011). Molecular control of systemic bile acid homeostasis by the liver glucocorticoid receptor. Cell Metabolism, 14(1), 123–130. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/21723510

Tex

[tex]

Hello Jess,

Welcome to the forum. To answer your question, yes, if you are experiencing no clinical symptoms you probably have minimal inflammation. And you are correct in thinking that the inflammation is probably rebuilding. It's not uncommon for MC patients to go into remission after a colonoscopy because of the caustic effect of the cleanout solution on the intestines. And it's not uncommon for inflammation due to gluten consumption to take a relatively long time to reach a point at which reactions resume. If they do not resume, consider yourself extremely lucky, because the odds of that happening are rather slim, unfortunately. But it does happen, occasionally.

In the meantime, enjoy your remission and hope it lasts. If it doesn't, you will need to reconsider the gluten. Again, welcome aboard, and please feel free to ask anything.

Tex