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Guest Doll

Celiac And Other Autoimmune Diseases

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Please check out what Peter Duesberg has to say about AIDS: http://www.duesberg.com/about/index.html

That was pretty interesting. I only read a few articles, but what I noticed was that they're pretty old. Any newer news on this topic, seems like science might have done more research to possibly back him up in the last 13 or so years since those articles have been writen.

The answer is yes, it's possible, but not likely. But these differences did come about by mutation. It just takes time (and maybe plagues of any sort) to weed out the ones that don't work.

The reason we can't fight it is because it infects our lymphocytes and destroys the cells that we use to fight with.

Thanks Fiddle-Faddle, I had been wanting to look that up

Thanks!

So is there another example of a pathogen that invades a cell yet doesn't destroy the immune system cells? Or can the body even protect against this?

Hm, my previous post seems to have been deleted so I'll reply to this. The trigger for celiac disease is thought to be infection with the adeno virus. It is found in the intestines of many people and its protein coat is simillar to gliadin.

Here's an excerpt from a study:

>A 12 amino acid sequence from the adenovirus 12 E1B protein is homologous at the protein level with a >similar 12-mer derived from the wheat protein A-gliadin. It has been suggested that exposure to Ad 12 >could sensitise individuals to gliadins with resultant gluten sensitive enteropathy

So the way this happens, is that there's cross reaction between the antibodies produced against the adenovirus and gluten, so now the body views gluten as an infectious agent.

Indeed. Supposedly Candida albicans also has a similar protein coat compared to gliadin and is a substrate for tissue transglutaminase. And given that the following are also substrates: HIV envelope glycoproteins gp120 and gp41, HIV aspartyl proteinase, Hepatitis C virus core protein; it makes me wonder if these last for viral proteins also have a similar protein coat. Did these also start the body off as thinking gluten is an infectious agent?

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From the same paper:

The results do not, however, support the hypothesis that prior exposure to Ad 12 is implicated in the pathogenesis of coeliac disease.

Then the question is perhaps the one I posed earlier.

Can damage to the intestine and inflammation perhaps allow a foot hold for a pathogen which would not normally be able to live in the intestine?

I remember reading was that Sickle Cell was protective against a disease (malaria?) and that how perhaps Celiac was protective against something as well.

Erm... hence why I used sickle cell anaeamia as a analogue.

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Could this be only one of many possible triggers? For one example, many women find that they become full blown celiacs after the birth of a child. Does that mean that they all had the adeno virus at the time of pregnacy? My first symptoms developed after I was impaled and had to rescue myself when I was about 5. Where does the virus fit in here? I do believe that a stress on the body contributes to excaberation of the process and that the adeno virus would fit into that but there are so many instances when people can link symptoms to specific events and illnesses other than adeno. Or perhaps this is a virus that can lie dorment in the body until something triggers an 'attack', like we see with the herpes virus?

This is what I think, that it is one of many triggers. Considering the viral and bacterial proteins with similar protein coats. Perhaps you could have had this virus, or candida, or hepatitis, or some other unknown pathogen with a simalar coat. Or even some other mechanism. Yes, indeed other illnesses than edeno, and I've given quite a few of them. :) Yes, I think Mono is another one of those dormant pathogens.

Then the question is perhaps the one I posed earlier.

Can damage to the intestine and inflammation perhaps allow a foot hold for a pathogen which would not normally be able to live in the intestine?

Erm... hence why I used sickle cell anaeamia as a analogue.

I've got a response to Jegstar and perhaps your comment as well. :)

Yes, I saw that after I responded to the orginal message. Still trying to catch up, sorry. :)

From the same paper:

The results do not, however, support the hypothesis that prior exposure to Ad 12 is implicated in the pathogenesis of coeliac disease.

Yes, and this is where I think they made their biggest mistake. I read almost every study, well at least the abstracts. And this is where I think they made a mistake. They assumed that Ad12 was the only virus that could do this, with this assumption and their finding that antibodies weren't found to the virus, and thus not everyone with celiac had Ad12, then clearly their assumption lead them to believe that Ad 12 isn't the cause of pathogenesis. In fact this is the same mistake I saw in studies of Candida, they didn't find it in everyone so they (making the assumption that Candida was the only cause) said it couldn't be candida.

Here's what they were missing, they didn't study any other virus or pathogen in relationship to this disease. If they took into account that all of these similar protein structure pathogens could be a cause would they find that indeed all folks with celiac had these disease before they got celiac? My guess would be yes, though perhaps there are other pahtogens out there yet to be discovered that look like gliadin.

So with their assumption their conclusion isn't correct. They didn't test for the right thing(s).

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This is what I think, that it is one of many triggers.

Oh Yeah! This was the other thing I was going to rant about!

Since polymorphisms tend to travel in groups, but without a perfect association, I think it's entirely possible that the DQ2/8 marker is just that, a marker. (Still an active part of the disease, but not the cause.)

What if the actual cause of the disease is a different gene that has not yet been studied. This would suggest that there may not be a trigger; that you have the disease or you don't. This doesn't mean that you'd necessarily show symptoms. Asymptomatic (pre-symptomatic?) Celiac is documented.

Maybe it's just possible that you get sick/injured/whatever and deplete your resources to a point that your body can no longer compensate for the lack of nutrition. And then you startr feeling like crap.

Thoughts?

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My question is -- if you're non-celiac gluten intolerant, don't have the celiac genes, can your intolerance go away if you get your body back to functioning well?

I thought that the answer was no, but my doctor seems to think it can happen and I've read that on the internet as well. As you can see below, I do have the autoimmune reaction, not just the gluten reaction.

From skimming over the past couple pages of this thread, it seems the answer would be that it would not be possible to rid the body of an autoimmune reaction once it's triggered.

What do you think?

This is a very good question. And I really don't want folks to experiment or try this on their own. But I think that this very well could be a possibility. From my understanding, someone will correct me I'm sure, is that one's body could lose memory of this pathogen. The only way this would be possible though is to be 100% gluten free for a long time. How long I'm not sure. How long does it take for a cell that has a memory for this pathogen to die. It's longer than red blood cells for sure, but there is a limited time I would think. I think memory for the pathogen only exists if the pathogen is present and their are cells alive that still have memory for this pathogen.

One problem is that what ever triggered it before could trigger it again. So we're right back to square one if we do get triggered again. Perhaps someday down the road, there could be a test for this if indeed this is all correct.

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How long I'm not sure. How long does it take for a cell that has a memory for this pathogen to die. It's longer than red blood cells for sure, but there is a limited time I would think. I think memory for the pathogen only exists if the pathogen is present and their are cells alive that still have memory for this pathogen.

I was wondering about this time line too. I haven't looked up anything, but two examples come to mind.

You need a tetanus shot every 7-10 years to maintain immunity.

It is said (but I don't know if proven) that everyone over 35-40 is no longer immune to small pox because none of us that got the shot were ever exposed to small box to get "boosted".

Seems like a big time spread and I don't know how you'd define the gliadin time point.

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That was pretty interesting. I only read a few articles, but what I noticed was that they're pretty old. Any newer news on this topic, seems like science might have done more research to possibly back him up in the last 13 or so years since those articles have been writen.

Anyone who tries to support his theories is immediately blacklisted by the scientific community, just as he has been. I did notice some papers he had written on this from 2003. I also read that the government had tried to pay him to shut up. Not surprising.

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Oh Yeah! This was the other thing I was going to rant about!

Since polymorphisms tend to travel in groups, but without a perfect association, I think it's entirely possible that the DQ2/8 marker is just that, a marker. (Still an active part of the disease, but not the cause.)

What if the actual cause of the disease is a different gene that has not yet been studied. This would suggest that there may not be a trigger; that you have the disease or you don't. This doesn't mean that you'd necessarily show symptoms. Asymptomatic (pre-symptomatic?) Celiac is documented.

Maybe it's just possible that you get sick/injured/whatever and deplete your resources to a point that your body can no longer compensate for the lack of nutrition. And then you startr feeling like crap.

Thoughts?

Excellent idea. DQ2/8 alone doesn't do the trick, but some other marker does, but DQ2/8 are still involved.

Yep, and what I found quite interesting recently is that along my path of learning about Tissue Transglutaminase I discovered an amino acid called Coenzyme Q10. In folks who would have malabsorption Q10 is produced in lower amounts. Why might that be, because there are quite a few vitamins required for the body to make Q10 and also because the Q10 found in foods wouldn't be absorbed as well. Q10 is an antioxident for the body, and from what I've read a pretty powerful one at that. And without this antioxident (or others for that matter) the oxidation damages the cells of the body, including those of the digestive system. Is this part of the whole mechanism of bowel and other diseases as well? Q10 has been shown to help with Colitis as well as hypertension (I think that was the other disease).

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I was wondering about this time line too. I haven't looked up anything, but two examples come to mind.

You need a tetanus shot every 7-10 years to maintain immunity.

It is said (but I don't know if proven) that everyone over 35-40 is no longer immune to small pox because none of us that got the shot were ever exposed to small box to get "boosted".

Seems like a big time spread and I don't know how you'd define the gliadin time point.

In a similar vein (pardon the pun) what about my natural TB immunity?

I was completely asymptomatic to the test but they gave me the BCG anyway and I'm the only person I know my age without a TB scar.

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Ya know, I don't know.

I guess my question would be is there really a non-celiac gluten intolerance? or is it really not-yet-celiac gluten intolerance?

And given what I've learned about the immune system and ttg I'm wondering if the tests are really even the best they could be. The antibodies for everything they test could be explained by some other possible mechanism. Antibodies to gliadin could be explained by the idea of leaky gut, I have a bad enough leaky gut, injest enough gluten the body is bound to produce antibodies, but do I really have the gene for gluten sensitivity or celiac. Perhaps not. Antibodies to ttg could be explained by another virus that ttg uses as a substrate. Antibodies to other body tissues further explained by the antibodies to ttg. All of which may or may not point to one getting or having celiac. A very good posibility in the positive, but meaningless in the negative. Even the "gold standard" of biopsy is full of holes, they could have missed where the damage is, there could be very little damage, or there could be no damage... yet!

Or how do we know that this damage doesn't occur elsewhere in the body? Like say the colon/lower GI, like say in a person who has the gene for celiac and gluten sensitivity (um like me) who has inflamation (lymphocytes in the tissue of the gi - Lymphocytic Colitis) (um like me) and indeed reacts to gluten. Heck perhaps this other gene that might signal Celiac might have a version that signals for Lymphocytic Colitis or some other intestinal diseases.

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From my understanding, someone will correct me I'm sure, is that one's body could lose memory of this pathogen. The only way this would be possible though is to be 100% gluten free for a long time. How long I'm not sure. How long does it take for a cell that has a memory for this pathogen to die. It's longer than red blood cells for sure, but there is a limited time I would think. I think memory for the pathogen only exists if the pathogen is present and their are cells alive that still have memory for this pathogen.

The memory B cells and memory T cells live for 30-40 years sometimes even life , so once you're exposed to something it's very hard to lose the immune response to it. The problem with tetanus is that the vaccine is an immunoglobulin which binds with the tetanus toxin, and inactivates it and these immunoglobulins decay over time. It's a form of "passive" immunization not active. Active immunity is very hard to lose.

As for the other trigers of celiac, you'd also have to take into consideration the trigers for autoimmunity in general. One of the most important is hormones, especially estrogens (unfortunately). Infections can also cause autoimmunity through many mechanism other than cross reacting antibodies. For example damage to an organ may result in autoimmunity because damaged proteins on the surface of cells can be intertpreted by the immune system as foreign. But stress, as far as I know, is not a trigger for autoimmunity because stress tends to decrease the immune system.

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Please check out what Peter Duesberg has to say about AIDS: http://www.duesberg.com/about/index.html

Ok, I've only made it through the first six references of "the chemical bases of the various AIDS epidemics..." and none of these are available on line because of their age, but the couple with available abstracts do not suggest that the authors have drawn the conclusion that duesberg has from their data and in fact in the last one, Beral et al, 1990, in the abstracts the authors make a statement that is contrary to what Duesberg is citing it for.

Addressing specific questions in the abstract:

"The virus-AIDS hypothesis was instantly accepted, but it is burdened

with numerous paradoxes, none of which could be resolved by 2003: Why is there no HIV in most AIDS

patients, only antibodies against it?"

Not true. In fact presence of virus is the method used to determine the extent of the illness.

"Why would HIV take 10 years from infection to AIDS?"

Why does Celiac take so long to show up? Shingles?

"Why is AIDS not self-limiting via antiviral immunity?"

Someone has to survive and overcome the virus. No one ever has. Aids is 100% fatal (without treatment). Like tetanus.

"Why is there no vaccine against AIDS?"

I think lots of answers to this. virus mutates frequently, vaccine uses the lymphocytes - AIDS attacks the lymphocytes. A vaccine tells the body what to destroy and would attack it's own lymphocytes.

"Why is AIDS in the US and Europe not random like other viral epidemics?"

Not sure what he means by this.

"Why did AIDS not rise and then decline exponentially owing to antiviral immunity like all other viral epidemics?"

Again, someone has to survive. Why isn't there immunity to Ebola?

"Why is AIDS not contagious?"

It is?!

"Why would only HIV carriers get AIDS who use either recreational or anti-HIV drugs or are subject to malnutrition?"

What about well-fed Africans? What about hemophiliacs infected by transfusion? What about malnourished people in isolated countries with no HIV?

"Why is the mortality of HIV-antibody-positives treated with anti-HIV drugs 7–9%, but that of all (mostly untreated) HIV-positives globally is only 1×4%?"

I have no idea where he got this statistic, but people in 3rd world countries usually die of TB or malaria or some other infection that is made worse by their compromised immune system. In other countries, like Russia, the government didn't admit to AIDS being present in their country and so listed other causes of death.

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Yes, for celiacs there has been research. What my doctor was saying is that it can go away for non-celiac gluten intolerants. Or is anyone with the autoimmune reaction actually a celiac, even without the genes for celiac and without the intestinal damage (my tests can't count as I had an inadequate gluten challenge)?

It's a problem of semantics. The issue is that all people with intestinal damage, most of them pretty sick, are considered to be "celiac", while all people who are gluten-intolerant, from those who are clinically asymptomatic to those who are near death, are lumped in one category as though this is a meaningful characterization for making generalizations.

I just think we need some more descriptive terms to describe the different stages of the illness.

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Oh Yeah! This was the other thing I was going to rant about!

Since polymorphisms tend to travel in groups, but without a perfect association, I think it's entirely possible that the DQ2/8 marker is just that, a marker. (Still an active part of the disease, but not the cause.)

What if the actual cause of the disease is a different gene that has not yet been studied. This would suggest that there may not be a trigger; that you have the disease or you don't. This doesn't mean that you'd necessarily show symptoms. Asymptomatic (pre-symptomatic?) Celiac is documented.

Thoughts?

I think this is quite possible. I also question that some are asymptomatic. I think there are so many other body systems that are effected, some long before GI symtpms develop, and so many things that we accept as normal that many don't realize are symptoms. Take for example my rumbing tummy, from childhood my tummy was so loud that you could hear it across the room. It usually occured after I ate, not becasue I was hungrey. This was always passed over as normal when it turns out it is one of the first things to occur if I've been glutened. Many folks think the occasional 'tummy virus' or heartburn are normal. Many think joint pain and fatigue are a normal part of ageing. I think many people who think they are asymptomatic in reality are not.

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It's a problem of semantics. The issue is that all people with intestinal damage, most of them pretty sick, are considered to be "celiac", while all people who are gluten-intolerant, from those who are clinically asymptomatic to those who are near death, are lumped in one category as though this is a meaningful characterization for making generalizations.

I just think we need some more descriptive terms to describe the different stages of the illness.

I agree with you. I was as sick as a celiac, but didnt' test out as one. My genes are for gluten intolerance.

There is obviously much need for more research.

That's very interesting about the memory of the cells to be 30-40 years. Makes perfect sense ... like really getting the chicken pox rather than getting the vaccine and losing your immunity later.

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I agree with you. I was as sick as a celiac, but didnt' test out as one. My genes are for gluten intolerance.

There is obviously much need for more research.

You and I are both in the same category, and I have never had any digestive problems, only swelling and pain in the feet and swelling of the hands.

Maybe they would make more progress on the research if some of it was done by a linguist. :P

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You and I are both in the same category, and I have never had any digestive problems, only swelling and pain in the feet and swelling of the hands.

Maybe they would make more progress on the research if some of it was done by a linguist. :P

Linguist :lol:

I did have the classic celiac symptoms. When I went to the GI, celiac was the first thing he said. Of course, when my tests came back negative, he was on to my gall bladder (I left ...). I said I felt better off gluten, he kept insisting, through his office staff as he was too important to talk to me himself, that I needed my gallbladder tested anyway.

Fortunately, now I have found a doctor who is educated on alternative medicine and understands the meaning of feeling bad because of sub-clinical problems.

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:unsure: I'm kind of confused. It seems like a lot of people on this board seem to think that other autoimmune diseases can be prevented by going gluten-free. Where is the scientific evidence for this? Where did this idea come from?

So, you can see, I am quite confused. Why does everyone here think this? Does anyone have a legit scientific link (NOT a personal webpage, alternative medicine page etc.) that can set this straight?

Please help!

Hi Doll,

I tried posting a response the other night, but this forum went down for a bit (or at least I couldn't get access back)...and I lost the post. Haven't had the time to redo until now. I don't have time to read the other five pages of responses here, so I apologize if I offer repeat information, but I have a few things to offer.

First off, an excerpt from Emerging Concepts in Celiac Disease by William Treem,

The association of celiac disease with autoimmune diseases, particularly

Type 1 diabetes and autoimmune thyroid disease,

has been widely reported with some investigators

finding a ten-fold increase in patients with celiac disease compared

with the general population [68,69].Less clear is the link

between celiac disease and Sjögren syndrome, primary biliary cirrhosis,

Addison disease, autoimmune chronic active

hepatitis, cardiomyopathy, and peripheral neuropathy

(not due to B-12 or vitamin E deficiency) [70–73•,74•].

When both celiac disease and autoimmune disease occur in a patient,

celiac disease is most often silent.The autoimmune disease

is diagnosed first with the diagnosis of celiac disease the result of

serologic screening in this high-risk population.

The question whether the early diagnosis and treatment

of celiac disease reduces the risk of developing other autoimmune

diseases is still open to debate.There are several lines of

evidence that support the notion that celiac disease is a causative

factor in the development of other autoimmune diseases.

A recent study suggests that the prevalence of autoimmune

diseases is closely related to the duration of gluten

exposure and the age of initiation of a GFD with children

diagnosed and treated before 2 years of age having

little subsequent increased risk [75].Older children diagnosed

with celiac disease have a higher than expected frequency

of organ-specific autoantibodies that tend to disappear

after starting a GFD.Anecdotal reports suggest that socalled

"celiac neuropathy", IgA nephropathy, juvenile

rheumatoid arthritis, and autoimmune myocarditis will

all improve when patients who have underlying celiac disease are

maintained on a strict GFD [73•,74•,76,77].

Other than that, I have a personal website to offer, BUT it does have many references to medical journal abstracts and articles.

Check out the links on autoimmune thyroid disease and diabetes, and the page on OTHER autoimmune disease. Although there are not reports of diabetes reversing on a gluten free diet, there are reports of thyroid antibodies disappearing if a gluten free diet is begun early enough.

Both casein and gluten sensitivity are being looked at with diabetes...they have had clinical trials removing casien from the diets of children with a high risk for developing diabetes. Check out the info on zonulin, too.

Also check out the page psoriasis (found at the bottom of the right bar)..lots of research going on there in regard to gluten sensitivity/ improved psoriasis. There are reports of many various autoimmune and other conditions improving on a gluten free diet, usually in the context of co-existing celiac disease, but sometimes just gluten sensitivity. It is one thing when gluten sensitivity/celiac disease is associated with other disease (association does not prove cause), but when those associated conditions improve after a gluten free diet has begun... that's a whole 'nother thing, IMO. The research is early and ongoing.

I've met several people who had MS diagnoses who have reversed their symptoms by dietary changes outlined in the MS-Direct site (gluten free, casein free, legume free, more). I personally know somebody whose Sjogren's symptoms and associated antibodies reversed on a gluten, casein, soy, and corn free diet. Personally, I think some of the reports on heart disease, liver disease, and kidney disease remitting on a gluten free diet are most remarkable...so don't miss those pages either.

In any case, it isn't just lay people who are thinking this. Researchers are actively looking at these things, and the spectrum of gluten sensitivity does seem to be widening.

Hope this helps~ The Gluten File

Cara

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What I was confused about was that gluten DOES NOT appear to be the inital trigger. For example, only 80% of twins both develop Celiac despite having the same genetics. In 20% of cases, 1 twin will react to gluten, the other will not.

Do you mean identical twins? Non identical do not have the same DNA.

I do agree that the immune system is "revved" up when gluten is ingested, but I always thought that the additional autoimmune disease problem lays with related genetics for other autoimmunities/leaky gut, poor regulator T-cell production, and other triggers for each individual disease.

I am confused because people who develop other autoimmune diseases PRIOR to Celiac DO NOT react to gluten, and it does not trigger their immune system.

Well probably but I wouldn't want to be certain that anyone has ever routinely tested. It also depends if you mean celiac disease = total villous atrophy or raised IgA, IgG.

So THAT was why I wondered where I could find info saying that the gluten-free diet prevented other autoimmunities! I had heard this from people on this board, but didn't know where this info came from! Hopefully now you guys can see why am I confused!

I think that is a seperate question.

If you have celiac disease and continue eating gluten or not.

Neither does it need to be 100% ... just like celiac disease it might not develop but the question is do people who continue to eat gluten have an increased risk of developing other autoimmune diseases have an increased chance of developing these diseases over people who do not.

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:unsure: I'm kind of confused. It seems like a lot of people on this board seem to think that other autoimmune diseases can be prevented by going gluten-free. Where is the scientific evidence for this? Where did this idea come from?

While it's true that Celiac is related to other autoimmune diseases, isn't it thought to be because of the shared common genetics and "leaky gut" letting in triggers?

Why is it that many people still continue to develop other autoimmunites despite going gluten-free, even if they start early on in life (I.e. infancy or early childhood).

Why is it that autoimmune diseases don't (generally) go into "remission" once gluten-free, since the body has been shown to repair itself if the autoimmunity can be removed? This is shown by the autoimmunity block research, and subsequent beta cell regeneration work of Dr. Denise Faustman.

How is it that 80% of kids with Type 1 diabetes (an autoimmune disease) and Celiac develop Type 1 FIRST, but do not express Celiac. They have the genes for it of course, but have not had them "triggered", like in all autoimmune diseases. Most people with Celiac, Type 1 diabetes genes, etc. do NOT develop the disease. You do not have the disease without the trigger. Celiac is NOT 100% genetics only. I don't mean gluten as the trigger, since these people tolerate gluten normally until the Celiac is set off by an initial "event".

I am excluding cases in which Celiac was previously present but not diagnosed, of course.

Also, why do most people with other autoimmune diseases NOT have Celiac?

So, you can see, I am quite confused. Why does everyone here think this? Does anyone have a legit scientific link (NOT a personal webpage, alternative medicine page etc.) that can set this straight?

Please help

From personal experience my thyroid returned to optimal fx after my nutritionist kinesiologist treated me with a 3 month course of organically bound minerals, by standard process. he works alot with this auto immune disorder and feels thats the key to resolving thyroid. I was also doing other supplements as well Like thytrophin- which is designed for the thyroid. This makes me feel it is related to the malabsorption of nutrients that other organs become deficient. But like you said where's the proof rather than ancedote. Hope you find your path through this part of your journey.

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Guest Doll
I personally don't think there's sufficent evidence for the leaky gut hypothesis causing other autoimmune diseases for 2 reasons.

First if you have foreign proteins entering the body than they would first go by the portal vein to the liver. The portal vein is the only vein that drains the intestines. The function of the liver is to detoxify any foreign materials absorbed through the intestines. If you had foreing particles in the liver it would start and inflamatory reaction and autoimmune hepatitis and cause cirrhosis pretty fast.

I think I read somehwere that celiac causes elevations of AST/ALT but not anywhere near the levels that would be found if there were foreing proteins deposited on daily basis there. So I think it's pretty safe to say that there's some leakage of proteins, but not enough to cause problems because there are only MILD elevations of AST/ALT ( marker of liver inflamation).

Second if you had cirulating foreign proteins in the blood there would be antibodies formed against them and they would produce so called "circulating antigen-antibody complexes" like in lupus. They would also be deposited in the kidney (the organ that detoxifies the blood) and cause renal failure.

As far as I undertsand it, the common factor behind celiac and other autoimmune diseases that come with it is mutation of HLA genes which causes T cell to recognize self tissues as foreign and attack them.

That last part is right, but a trigger plus other genetics are required. I do know that specific subtypes of HLA types are needed for development of autoimmune diseases. I have posted enough on that already! ;p

I also know there is a defective mechanism between autoreactive T-cells and regulator T-cells. I assume the issue starts in the Thymus, which allows out defective autoreactive T-cells in the first place. There then is a lack of regulator cells, allowing the autoreactive T-cells to flourish if you will.

I am curious about the triggers. Some say gluten alone is the trigger for all autoimmunities and I wanted to know how this could be the case. I have heard conflicting evidence, so I thought it would be a valid thread with valid questions. I was not sure where that info had come from.

As for the leaky gut issue, there has been evidence to suggest the leaky gut plays a role in Type 1 diabetes and Celiac. As you know, in science we cannot fully prove anything 100%, but there is enough evidence to suggest the leaky gut hypothesis is right. Alba Therapeutics has had so much success with it's Zonulin inhibitor that it may be fast tracked.

I do agree that in some cases, genetics may override, and the immune system may be so defective that it will cause autoimmunity with ANY kind of trigger.

I personally, however, feel that the leaky gut hypothesis makes sense. I am not sure that the liver damage in Celiacs is caused by gluten ingestion or the "leaky gut" supposedly letting in large amounts of environmental toxins.

If Casein for example was the trigger for Type 1, yes, a whole foreign casein protein let in by a leaky gut would trigger an immune response, but would it casue liver damage????

Do you mean identical twins? Non identical do not have the same DNA.

Well probably but I wouldn't want to be certain that anyone has ever routinely tested. It also depends if you mean celiac disease = total villous atrophy or raised IgA, IgG.

I think that is a seperate question.

If you have celiac disease and continue eating gluten or not.

Neither does it need to be 100% ... just like celiac disease it might not develop but the question is do people who continue to eat gluten have an increased risk of developing other autoimmune diseases have an increased chance of developing these diseases over people who do not.

LOL! Of course I mean identical twins!!! Otherwise my point would be kind of mute!

Sorry! I mean for you to have raised antibody levels, a marker for Celiac. One twin will have them (or a positive biopsy), and yet the other will not.

I would think that if you do not actually have Celiac (an autoimmune disease with specific autoimmunity prone genetics) and without any indication your body reacts immune mediated to gluten (positive antibodies, biopsy, etc.) then I don't understand how you could develop autoimmunities from gluten exposure.

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Guest Doll
You say, "Also, why do most people with other autoimmune diseases NOT have Celiac?"

Actually, there is a significant statistical correlation between celiac disease and many other autoimmune diseases. Study after study is now rolling out that demonstrate when people with other autoimmune diseases are tested for celiac disease they often have it too. For instance, I read one the other day from Ireland where they tested 40 some people with Adison's disease (an autoimmune disease of the adrenal gland) and found that about 12% of those people were also Celiacs.

Steve

Thank you for that Steve. I did not mean to imply that Celiac is not related to to other autoimmune diseases (the genetics or defective immune mechanism seem to overlap) but rather most of them do not present with Celiac (negative bloodwork).

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