Here's Why I Believe That Celiac Disease Is An IBD :shock:

[tex]

Hi All,

A study of celiac patients shows the following result:

Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.

http://www.dldjournalonline.com/article ... 1/abstract

This study is almost 3 years old, but this is the first time that I've seen this information. In essence, what this study shows, is that the degree of villus atrophy appears to have no significance with regard to the severity of celiac clinical symptoms. That's a pretty profound observation, with far-reaching implications.

Okay, if the amount of damage is irrelevant to the clinical symptoms, then the question arises, "is any degree of apparent villus damage even necessary, in order to verify celiac disease. Obviously, the logical answer to that question is not "no", but "hell no!" To the best of my knowledge, the "experts" have been blaming the symptoms of celiac disease, (primarily D, and it's side effects), on villus atrophy. Without the presence of villus atrophy, many/most celiac docs will not even diagnose celiac disease, regardless of clinical symptoms.

If the conclusion of the researchers in this study is correct, then what could be causing the D? Why, by default, it will have to be those pesky little lymphocytes that always infiltrate the mucosa in the small intestine, that have always been noted by pathologists, but pretty much ignored, otherwise, and considered to be simply a coincidence. Those lymphocytes are doing the same thing in the small intestine, that they do in the colon, with MC - they are causing inflammation, and the inflammation causes the D. So what does that imply? It suggests that celiac disease is an inflammatory bowel disease, in medical terminology.

Of course, actually, I'm not claiming that "celiac disease" is a disease at all, let alone an IBD, (though it certainly meets the medical description of an IBD). I'm saying that celiac disease is a symptom of gluten-sensitivity that presents in the small intestine, just as MC is, (for most of us), a symptom of gluten-sensitivity, (among other sensitivities), that presents in the colon. Neither "disease" is actually a disease - they are symptoms, (of food or drug sensitivities).

Polly, I may be wrong, but I'm guessing that you will agree with me on this, at least on the celiac part of it. We've discussed this in the past, and since MC has many causes, that seems to make it more difficult to pin down, but IMO, that makes it more likely to be a symptom, rather than a disease, so maybe you will agree with me on this theory about MC, also.

Am I all wet?

Tex

[mbeezie]

Tex,

If a celiac's villous atrophy heals and they accidentally get glutened, they still get a response, indicating there is more to it than atrophy. When there is evidence of healing do those biopsies still show lymphocytes? Polly had no evidence MC and didn't get glutened, but still got sick shortly after her A+ colonoscopy report. Her doctor proclaimed no evidence of MC, just a doctor would proclaim villous healing, but she still got sick and without gluten involvement. There still seems to be some missing piece IMHO.

Mary Beth

[tex]

Mary Beth,

Good point, but I have a hunch that the lymphocytes will be there, any time that persistent clinical symptoms develop. The immune system tends to respond rather quickly, as we are all aware. I didn't mention chemical triggers - I should have said "food and chemical sensitivities", rather than "food and drug sensitivities", because drugs are actually a source of chemical agents, and that would cover the effects of stress, also, since stress causes the release of adrenaline, which leads to all sorts of adverse chemical and hormonal reactions in chronic stress situations.

Adrenaline alone is enough to trigger D, without any inflammation, but if it becomes a chronic condition, then the immune system is going to step in and try to fight the "toxic agent" that is causing the problem. At least, that's the way that I see it.

Tex

[Polly]

Interesting discussion, you two!

Tex, that finding is indeed thought-provoking. It just proves what we have believed all along - that there is much more unknown than known about MC/gluten sensitivity I agree totally with you that we need a whole new way of looking at our MC/gluten sensitivity/celiac issues, a new paradigm, so to speak.

Of course, lymphocytes are non-specific and will appear anywhere in the body with any kind of chronic inflammation, regardless of the cause. What actually CAUSES these lymphocytes to appear is the real crux of the problem, IMHO. Is it genetic, chemical, bacterial/viral, mechanical irritation/trauma, mind/body (stress) or some or all of these together? Or additional factors we do not yet understand? What makes our immune systems go haywire and begin recognizing our own gut bacteria and certain foods as the enemy? The million dollar question!!! Maybe it is even related to something that happened when we were fetuses (fetusi? LOL) Researchers are finding that the 1st 9 mo. of life have a huge impact on later health problems. Even things like heart disease, which supposedly is mainly life-style-related.

These discussions are so important. Perhaps one of these days we will be able to come up with some answers - if not us (the REAL MC experts), then WHO?

Love,

Polly

[Zizzle]

I agree. We are looking for a new paradigm here. I believe whatever is spurring the tremendous rise in autoimmune diseases, autism, celiac, etc. is responsible for our MC (non drug-induced MC). I think some of our answers probably lie in autism research. Is it inability to clear mercury and other heavy metals from our bodies? Are certain infections and/or vaccines to blame? Is autism an early, exagerated response to our polluted environment and polluted womb? Is microchimerism involved (fetal/maternal cells being transfered from baby to mom and vice versa)? When we develop celiac and/or MC later in life, is it a response to years of bioaccumulation of PCBs, fire retardants, vinyl chloride, BPA, mercury, gluten, etc. deranging our immune systems -- our bodies finally reach a toxic breaking point?

What I do understand is that once that autoimmune mechanism is triggered, there is no going back. Our immune system "memory" is permanently changed in favor of attacking something that is "self." Celiac may be triggered and fed by gluten, but once it begins, tolerance to self is lost, and the "associated autommine diseases" can eventually develop. If the rates of undiagnosed celiac are true, then only a fraction of celiac cases also have diarrhea. Those that do may have progressed to an "associated autoimmune disease," namely MC.

It the study mentioned above, they did not factor in the presence of other autoimmune diseases. They only looked at degree of villous atrophy and it's relationship to disease presentation. I would bet money that if they tested for other autoantibodies and/or accounted for other autoimmune conditions, they would find that the cases with other autoimmune markers or diseases present with diarrhea in much greater numbers, regardless of villous atrophy. Lupus patients often have diarrhea - I bet there is lymphocitic infiltration of the colon involved there.

I think Dr. Fasano's Celiac Center in Baltimore is on the right track - they view celiac as the tip of the autoimmune iceberg. It is a condition with a known trigger that can help researchers understand all those diseases that lack a known trigger.

I predict we will soon refer to a celiac "spectrum" much like the autism spectrum.

P.S. Here's an article about microchimerism in autoimmune thyroid disease. My autoimmune issues began 3 months after the birth of my first child, a son. I've often wondered if his cells circulating in my body are creating all this mayhem. I don't have Hashimoto's, but my two friends with Hashimoto's also have sons.
http://jcem.endojournals.org/cgi/content/full/86/6/2494

[tex]

Hmmmmmmm. Interesting article. It raises the question of the possibility of the involvement of a "leaky placenta", (though that wasn't implicated in the "conclusions"). That makes me wonder if the tight junctions in the placenta are modulated by the same mechanisms involved with the leaky gut syndrome. I would guess that there is a very good chance that they are. That opens the door for all sorts of chemical "shenanigans" for mothers with autoimmune issues.

For example, it might be somehow connected with the relatively high female to male ratio of patients with CC. IOW, I wonder if most or all female patients with CC have given birth to a son, before their CC symptoms presented.

Tex

[Zizzle]

I see the need for a ladies-only poll!

[ant]

Wow......what a thread........ what a debate.....Bingo! I think this is right on the money......

And talking of money...could this thinking be packaged up and presented to the Gates Foundation for some well funded research to change the paradigm?........or is that Fundation also in cahoots with big pharma?

I hope Bill is beyond that.

Best, ant

[tex]

Tex

[Zizzle]

I'm headed in a different direction now. Back to my theory of post-infectious IBS leading to my LC. The antibiotic Rifaxan is back in the news as a possible cure for IBS - of course you need retreatment every 2-3 months...hardly a cure.

http://www.cbsnews.com/stories/2006/10/ ... 6522.shtml

I tested borderline/negative for SIBO. Anyone know how accurate the test is? False negative rate?


This abstract about post-infectious IBS and the inflammatory changes it causes in the colon makes me think it is the precursor to LC, at least in my case. I think it also explains late-onset food intolerances (mucosal permeability)--


Irritable bowel syndrome (IBS) is a gastrointestinal disorder characterized by abdominal pain and changes in bowel habits, not sustained by structural changes. There is now consistent evidence indicating that IBS may be the adverse outcome of an acute episode of infectious gastroenteritis, the so-called postinfectious (PI) IBS. The infectious agents involved in the development of PI-IBS include pathogenic bacteria, parasites, and viruses. Abdominal pain and diarrhea are the most common symptoms of PI-IBS. Several studies identified a number of risk factors increasing the susceptibility for PI-IBS development. These include the virulence of the pathogen, the severity, and duration of the acute enteritis, younger age, female sex, and psychological disturbances. Several mucosal abnormalities in the colon or ileum of patients who develop PI-IBS have been described. These changes include increased mucosal permeability, an increased amount of intraepithelial lymphocytes, lamina propria T cells, and mast cells, as well as serotonin-containing enteroendocrine cells. The mediators released by these activated cells may evoke enteric nervous system responses, excite sensory afferent pathways, and induce visceral hyperalgesia. Little is known about the prognosis of PI-IBS, although it is likely better than that of nonspecific IBS. There is little evidence about a specific treatment for PI-IBS. Although probiotics and antibiotics may be promising in the prevention of PI-IBS, the efficacy of these treatments should be assessed in an ad hoc designed study.

http://www.ncbi.nlm.nih.gov/pubmed/19300138

Anyone know what serotonin-containing enteroendocrine cells do??

Several articles link Shigella infection and chronic Giardiasis to these conditions. Anyone here been diagnosed with either of these? My gastroenteritis episodes overseas never got a diagnosis - just "leukocytes in the stool". I would give anything to go back and find out what bugs I had.

My daughter had shiga-toxin positive E.Coli this year from our trip to Guatemala, which I realize now could have been Shigella (same toxin). I'm going to call the health department and demand answers (they were supposed to call once the state lab identified the strain).

[tex]

FWIW, Ciprofloxacin will also "cure" MC with about 99.9% efficacy, as will most of the antibiotics in the fluoroquinolone family. Unfortunately, though, a few days after the treatment ends, the patient will virtually always relapse.

These changes include increased mucosal permeability, an increased amount of intraepithelial lymphocytes, lamina propria T cells,

Call me slow, but that meets the pathological definition for a diagnosis of MC, (LC). So why are they calling it IBS?

Enteroendocrine cells are simply specialized endocrine, (hormone-producing), cells, located in the gastrointestinal tract. Most enteroendocrine cells are found in the islets of Langerhans, (the areas of the pancreas that contain its hormone-producing cells - of course the endocrine cells in the pancreas are mostly known for the production of insulin), but they're also found in other locations. They produce many different hormones such as serotonin, somatostatin, motilin, cholecystokinin, gastric inhibitory peptide, neurotensin, vasoactive intestinal peptide, and enteroglucagon. An example of enteroendocrine cells in other locations, is the cells which secrete gastrin, (located in the stomach), which stimulates the production of gastric acid by the parietal cells of the stomach, and aids in gastric motility. The dueoenum also contains a lot of enteroendocrine cells.

Tex

[Zizzle]

These changes include increased mucosal permeability, an increased amount of intraepithelial lymphocytes, lamina propria T cells,

Call me slow, but that meets the pathological definition for a diagnosis of MC, (LC). So why are they calling it IBS?

Tex

EXACTLY!! Why are people referring to MC as a rare condition, and failing to name it in extremely common conditions like IBS?!?!?

Regarding those Enteroendocrine cells, is there a connection or 2 to be made here? We know celiac increases the risk of diabetes. Perhaps these cells on the pancreas are affected by the same pathologic process? If post-infectious IBS (a.k.a MC) affects serotonin-producing endocrine cells, does this have anything to do with serotonin in the brain and the liklihood that women affected often have mood/anxiety issues? Is this why some people get relief from low dose naltrexone??

[tex]

Regarding those Enteroendocrine cells, is there a connection or 2 to be made here?

Probably, but the relationships are probably too complex to recognize. We know that MC affects hormone production, and we know that hormones affect MC, but the possibilities are so numerous that it's somewhat mind-boggling.

We know celiac increases the risk of diabetes. Perhaps these cells on the pancreas are affected by the same pathologic process?

We know that MC leads to pancreatitis and other pancreas issues, but as far as I'm aware, there doesn't seem to be a link with diabetes. I've often wondered why, but, of course, one should never look a gift horse in the mouth.

If post-infectious IBS (a.k.a MC) affects serotonin-producing endocrine cells, does this have anything to do with serotonin in the brain and the liklihood that women affected often have mood/anxiety issues? Is this why some people get relief from low dose naltrexone??

There is more serotonin in the gut, than in the central nervous system, (CNS), (roughly 80 % of the body's total amount). In the gut, it regulates intestinal movements. In the CNS, of course, it regulates mood, appetite, and sleep, as well as muscle contraction, (plus playing a part in memory and learning).

The serotonin secreted in the gut, eventually finds its way into the blood, where it's taken up and stored in platelets. When the platelets bind to a clot, they release serotonin, where it serves as a vasoconstrictor and helps to stop the bleeding. In view of the fact that serotonin originating in the gut is eventually stored in the blood, (and can function as a vasoconstrictor), that suggests to me that even though serotonin originating in the gut may never be released into the CNS, it still might serve to affect mood/anxiety issues.

Ever notice how pale our skin becomes when we are sick? That's due to vasoconstriction, since there is less warm blood available to the skin, the color fades, and we feel colder. Blood pressure also rises. This effect is most likely due to the release of epinephrine into the blood, however, since this is a dominant event, (relative to a serotonin-based event). The epinephrine, (adrenaline), release is the result of stress, of course. Typically, the purpose of the effect is to retain more body heat, in order to preserve the core temperature. Of course, vasoconstriction is also one of the mechanisms by which the body regulates and maintains blood pressure. Anyway, the point is, even though vasoconstriction is usually regulated by norepinephrine, it's certainly conceivable that the serotonin that originates in the gut, might also have an effect under certain circumstances, and vasoconstriction in general, can certainly affect mood/anxiety issues.

I'm not sure about LDN. It affects opioid receptors. Does it affect serotonin receptors?

Tex

[grannyh]

I think the easy answer is one my favorite family doctor gave me years ago... IBS=I don't know... Doctors hate to say I don't know why you are filling your pants 20 times a day.. so they give you an all inclusive diagnosis of IBS...:)
grannyh