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Celiac And Other Autoimmune Diseases

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I tried to put it in very simple terms. It's obviously a lot more complicated than a simple mutation, because autoimmune diseases are caused by multiple factors, but the presence of abnormal HLA genes is the most important.

Well explain it and Jestgar can translate....for the rest of us.

(please Jegstar)

I'm still interested in mutation of the HLA and non celiac autism spectrum as well btw.

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Well explain it and Jestgar can translate....for the rest of us.

(please Jegstar)

I'm still interested in mutation of the HLA and non celiac autism spectrum as well btw.

My guess is that the terminology he used is incorrect. He said mutation, wheras he probably meant to say that the HLA gene makes one susceptible to autoimmune diseases. Though the term abnormal is a bit off as well now due to data to be published soon by Dr Fine, as indicated in the article I posted a link to found here on this site "Understanding the Genetics of Gluten Sensitivity by Dr. Scot Lewey". Seems that the gene's that potentially can cause autoimmune diseases related to gluten sensitivity would be found in even a greater number of folks. Though the level of said diseases would range from the minor symptoms to major autoimmune diseases.

One thing to remember is that autoimmunity is actually going on all the time as a normal process of the human body. Which is why I find the term autoimmune to be a bit strange. The body has to target self at times to keep the body healthy. Without this cells damaged by outside mechanisms could never be removed by the body and disease would run rampant. Think about what has to happen in the case of a virus getting into a cell as part of body tissue, how would the body rid itself of this cell if it could not target self?

Mike

Hey Mike,

here's a kink: http://www.landesbioscience.com/journals/e...act.php?id=1938, although it uses many technical terms.

Thanks for the link, though only reading through the abstract, I don't see anything about mutations or abnormal genes. Though I don't have access to the whole article.

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Perhaps this might clear up one point I'm trying to make about how this process isn't a mutation or abnormal. Take for example the symptom/disease of a stroke. What happened is that this enzyme Factor XIII (fibrin-stabilizing factor) [transglutaminase of a different type than Tissue transglutaminase] caused a clot to form, it just so happens that this clot broke free and lodged itself in the wrong place, thus causing blood not to get to an important organ of the body, in most cases the brain. So one might argue that this fibrin is a mutation or abnormal since it (in simple terms) attacked the brain. But without this enzyme you'd bleed to death.

Same with the HLA genes, in some instances the food we eat (all of which are recent addtions to our human diet) cause autoimmune reactions. But without this HLA gene perhaps we won't or wouldn't have survived some "real" pathogen/virus. If we had never had access to gluten containing grains or never thought to eat it or domesticate/farm it we wouldn't even have this forum to talk about this. Perhaps we'd be on a forum talking about how well all survived some virus that infected the world whereas those without it didn't survive, how we morn those without our perhaps protective genes.

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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.

The first point you make is what contributed or directly caused the death of my twin brother. He died a long time ago and all the doctors could tell us was that his liver had been destroyed, most likely since birth. He was still a teen when he died of cirrosis. Not all celiacs have only a mild elevation.

The second statement about these circulating antigen-antibody complexes they did cause symtoms much like lupus and MS for me. I also have impaired kidney function. I also have some joints that were effected by the same autoimmune problems. These antibodies would not have been triggered without the celiac disease. Without gluten the processes have stopped completely.

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I don't think the gluten sensitivity/autoimmune issue is completely understood. There's lots of theories but that's about it.

I did just get this from Clan Thompson today that relates:

Dr., A friend of mine who's son has Type I Diabetes (age 8) has been advised by her physician to test for Celiac Disease every 6 months. She has been doing this and so far has been negative for Celiac Disease.(She was never advised to do genetic testing for Celiac Disease, which I recommended to her). She was told by her physician that the reason for testing a diabetic for Celiac Disease is that Diabetes causes Celiac Disease. I was under the impression that Celiac Disease leads to other autoimmune diseases, Diabetes being one of them. Could you clarify; does Diabetes lead to Celiac Disease or does Celiac Disease lead to Diabetes? Thank you, Amy

Dear Amy: The close association between celiac disease and many autoimmune conditions, and especially type 1 diabetes, is well known. While they may simply coexists due to the fact that all autoimmune disorders tend to have a similar genetic basis, it is likely that indeed one (celiac disease) triggers the others. You are right: the current thinking is that indeed celiac disease pre-exists (often without symptoms) and may "open the way" to the development of diabetes, not vice versa. That said, you do need to test repeatedly for celiac disease patients with diabetes, as research has shown that individuals with diabetes may turn positive for celiac disease later in time. The frequency of this re-testing however doesn't need to be as often as every 6 months: we recommend every 2-3 years. Sincerely, Stefano Guandalini, M.D.

Dr. Fine says that 30% of the people with autoimmune thyroiditis who go gluten-free have a remission.

From his essay on enterolab.com:

For many years there has also been proof that the intestine is not the only tissue targeted by the immune reaction to gluten. The prime example of this a disease called dermatitis herpetiformis where the gluten sensitivity manifests primarily in skin, with only mild or no intestinal involvement. Now from more recent research it seems that the almost endless number of autoimmune diseases of various tissues of the body also may have the immune response to dietary gluten and its consequent autoimmune reaction to tissue transglutaminase as the main immunologic cause. A study from Italy showed that the longer gluten sensitive people eat gluten, the more likely they are to develop autoimmune diseases. They found that in childhood celiacs, the prevalence of autoimmune disease rose from a baseline of 5% at age 2 to almost 35% by age 20. This is a big deal if you think how much more complicated one’s life is being gluten sensitive AND having an autoimmune disease.

So preventing autoimmune disease is one very important reason why early diagnosis and treatment of gluten sensitivity is important. Early diagnosis before celiac disease develops also holds the potential of preventing other clinical problems such as malnutrition, osteoporosis, infertility, neurologic and psychiatric disorders, neurotube defects (like spina bifida) in your children, and various forms of gastrointestinal cancer. Another reason for early diagnosis and treatment is very straightforward and that is because many gluten sensitive individuals, even if they have not yet developed celiac disease (villous atrophy), have symptoms that abate when gluten is removed from their diet. Furthermore, from a study done in Finland, a gluten sensitive individual who reports no symptoms at the time of diagnosis can improve both psychological and physical well-being after treatment for one year with a gluten-free diet.

There's too much there to quote it all: http://enterolab.com/StaticPages/EarlyDiagnosis.htm

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I have only a vague understanding of the HLA system and I'm finding even the terminology hard to hang on to since everyone seems to be using a variation and I haven't spent enough time looking things up.

What I do study is the innate immune system which has some overlap in proteins and results, but I study the genetics of it in blood which is not nearly as complex as the gut.

This is what I think IMR was trying to say:

There are polymorphisms (small changes) in everyone's genes. I believe this is nature trying out new things to see if they work better.

One of the common ones in the HLA gene system is what most people here refer to as DQ2. This particular polymorphism can (somehow) learn to grab the gliadin molecule and present it as something that needs to be destroyed.

In a process that I haven't quite put together, when this molecule is presented in the gut, it can induce the T-cells to emit toxins that start killing the gut cells. (There are a couple painfully scientific articles about this that I'll try to post references for.) also see the fabulous review put up by 2kids4me.

I think Mike said it more clearly:

"Same with the HLA genes, in some instances the food we eat (all of which are recent addtions to our human diet) cause autoimmune reactions. But without this HLA gene perhaps we won't or wouldn't have survived some "real" pathogen/virus. If we had never had access to gluten containing grains or never thought to eat it or domesticate/farm it we wouldn't even have this forum to talk about this. Perhaps we'd be on a forum talking about how well all survived some virus that infected the world whereas those without it didn't survive, how we morn those without our perhaps protective genes."

although I disagree with his statement that autoimmunity is going on all the time. In the case of viruses, for example, the antigen presenting cells chew up a virus and "present" it for the bodies other immune cells to look at. When B-cell that happens to recognize this foreign protein "sees" it, that B-cell

1) calls in reinforcements, and

2) starts making antibodies. (OK it's not just one cell, but the ideas the same).

In the ensuing carnage, some normal cells get damaged, but mostly the attacks are directed against cells that have the foreign protein.

I really just study the genetics of this so if my explanation is wrong, someone please correct me. In the meantime I'll try to review this. I should probably know more about the basic biology of it anyway...

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I don't think the gluten sensitivity/autoimmune issue is completely understood. There's lots of theories but that's about it.

I did just get this from Clan Thompson today that relates:

Dr. Fine says that 30% of the people with autoimmune thyroiditis who go gluten-free have a remission.

From his essay on enterolab.com:

There's too much there to quote it all: http://enterolab.com/StaticPages/EarlyDiagnosis.htm

Nancy, thanks for the info, it reminded me of something I just read today. That is that we know that HLA-DQ2 is the more common gene found in Celiacs as compared to DQ8. Guess what, the article I read also pointed out that DQ8 is found often in Type I diabetics and DQ2 less frequently. At least that's what I got out of the article.

I have only a vague understanding of the HLA system and I'm finding even the terminology hard to hang on to since everyone seems to be using a variation and I haven't spent enough time looking things up.

What I do study is the innate immune system which has some overlap in proteins and results, but I study the genetics of it in blood which is not nearly as complex as the gut.

This is what I think IMR was trying to say:

There are polymorphisms (small changes) in everyone's genes. I believe this is nature trying out new things to see if they work better.

One of the common ones in the HLA gene system is what most people here refer to as DQ2. This particular polymorphism can (somehow) learn to grab the gliadin molecule and present it as something that needs to be destroyed.

In a process that I haven't quite put together, when this molecule is presented in the gut, it can induce the T-cells to emit toxins that start killing the gut cells. (There are a couple painfully scientific articles about this that I'll try to post references for.) also see the fabulous review put up by 2kids4me.

I think Mike said it more clearly:

"Same with the HLA genes, in some instances the food we eat (all of which are recent addtions to our human diet) cause autoimmune reactions. But without this HLA gene perhaps we won't or wouldn't have survived some "real" pathogen/virus. If we had never had access to gluten containing grains or never thought to eat it or domesticate/farm it we wouldn't even have this forum to talk about this. Perhaps we'd be on a forum talking about how well all survived some virus that infected the world whereas those without it didn't survive, how we morn those without our perhaps protective genes."

although I disagree with his statement that autoimmunity is going on all the time. In the case of viruses, for example, the antigen presenting cells chew up a virus and "present" it for the bodies other immune cells to look at. When B-cell that happens to recognize this foreign protein "sees" it, that B-cell

1) calls in reinforcements, and

2) starts making antibodies. (OK it's not just one cell, but the ideas the same).

In the ensuing carnage, some normal cells get damaged, but mostly the attacks are directed against cells that have the foreign protein.

I really just study the genetics of this so if my explanation is wrong, someone please correct me. In the meantime I'll try to review this. I should probably know more about the basic biology of it anyway...

I'm confused by one part that I didn't know. You're saying that the genes can change? Wouldn't that mean that if I got a genetic test and found that I have HLA-DQ2 and HLA-DQ8 that these genes could change to HLA-DQ4 and HLA-DQ7? That doesn't sound right. So I must be misinterpreting something. Any recommended reading on what you mean by this?

Ah, you caught me, I didn't mean all the time, I guess I meant more often than what we see with what are classified as autoimmune diseases.

I've got a question about virus and blood. How does the body get rid of a virus that invades a blood cell? Or is there even such a thing?

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GFP,

well if you're interested, it's been a while since I've taken immunology but this is the way I remeber: HLA genes, especially Dp/Dq/Dr code for molecules called "MHC class II molecules" which is the protein on the cells called "antigen presenting cells" that present foreign antigens to Th lymphocyte.

For example let's say you have a bacteria in the body. An antigen presenting cell takes up pieces of that bacteria and uses the MHC class II molecule to say to the Th cell that "look here's a foreign antigen, there must an infecion somewhere in the body." This MHC molecule causes activation of the Th cell which causes activation of the immune system to fight off the infection. Th cells than activate Tc cells which are the cells which that come in and release toxins to kill the virus infected cell. This is why there are Th/Tc cells in the intestine of some people with celiac.

Idealy only foreign antigens are recognized but an abnormal HLA gene whcih occur through genetic polymorphism causes abnormal functioning of the MHC class II molecule causing it to present more self antigens rather than foreign antigens. This pattern of autoimmunity is called cell mediated/organ specific, the second type is "systemic autoimmunity", like in lupus, where there's a dysfunction of B cells rather than T.

These abnormal HLA genes, and MHC molecules are present in all T cells in the body, and in say the pacnreas, or the thyroid .... and this causes the T cells in these organs to recognize the organs as foreign.

This is just one the factors involved in producing autoimmunity, although the most important one. Although a precentage of the population also has these genes they never develop autoimmunity because of other factors like hormones, infection with a virus, etc.

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I'm confused by one part that I didn't know. You're saying that the genes can change? Wouldn't that mean that if I got a genetic test and found that I have HLA-DQ2 and HLA-DQ8 that these genes could change to HLA-DQ4 and HLA-DQ7? That doesn't sound right. So I must be misinterpreting something. Any recommended reading on what you mean by this?

Sorry, I didn't say that very clearly. You probably have a combination of your parents genes. So your haplotype or genetic complement is different from either of your parents. There are, however, certain spots that are more likely to undergo a single base-pair change when the egg or sperm are made. So you don't change over your lifetime, but you might produce a child with a change. Keep in mind that any change that makes a big difference is unlikely to be compatible with life, but subtle changes do make a difference in, for example, how your body responds to bacteria.

There's a great paper on TLR5 and legionaire's disease if you want to read up on it. Pretty jargony though. If I find a review I'll pm you.

I've got a question about virus and blood. How does the body get rid of a virus that invades a blood cell? Or is there even such a thing?

Umm, like HIV/AIDS?.......

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So general question to the experts (applying the 20% rule on experts)

It seems the HLA haplotype is one of the more studied sequences and better understood sequences in humans.

I think mike's hypothesis about this being a genetic mutation giving an advantage in respect to certain illnesses is certainly mertiable and worth persuing.

The most common analogy from the top of my head would be perhaps sickle cell anaemea?

(Reasoning, its genetically disadvantageous over non mutation unless a specific disease is prevalent)

What is the incidence of this in mixed race African-American's (including those who appear externally and beleive themselves to be to be 100% caucasian) over genetically purer populations in Africa and perhaps genetically more mixed populatins in say Cuba? How does this correlate with a far more commonly known and published genetic marker like blood type? (i.e. the incidence of Rh +ve in African-American's (about 7%) is far higher than African's in Africa which is i beleive about 7/10,000 .. especially if it is assumed as a working hypothesis the majority of population they mixed with were caucasian with around 16% Rh -ve to start off with. This hypothesis is easily tested since the amero-indian and Asian mutation is different.

Secondly I have seen research comparing the prolamine carbohydrate exterior with the waste product of certain viri.

I am wondering if the specific auto immune system triggers are due to cross reactive epitopes.

well if you're interested, it's been a while since I've taken immunology

Yes but probably not so long as the last time I studied biology... (21 years ago and much has changed since then) and even back then I wasn't really very interested in it it was just an easy exam to pass .. actually come to think of it I dropped the subject 23 years ago at 13-14 (UK edication system)... and just took the exams at 16 largely because it required too much drawing and I'm terrible at drawing ...

I was forced to catch up a little in my PhD which was in organic geochemistry but i'm still working with an almost empty toolkit!

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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

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:unsure:

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".

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.

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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.

Secondly I have seen research comparing the prolamine carbohydrate exterior with the waste product of certain viri.

That would be the research I remembered.

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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.

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?

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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.

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.

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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?

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

I think the answer to this might be... they're not celiacs but they're gluten sensitive and have been for many years. If, as Dr. Fine posits, that you're having non-celiac (no villious atrophy yet) antigenic reactions in the bowel to gluten (or other foods) it is setting you up for additional autoimmune diseases. He had a slide on how many years of gluten exposure and what your likelyhood of acquiring an autoimmune disease is.

Now, is there something else underlying this entire thing? Probably. What is that first step that makes us have an autoimmune reaction to food? The virus thing sounds plausible.

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?

Doubt it. The autoimmune system doesn't seem to forget what it has been edumacated to attack. Although... some autoimmune diseases do go into remission. I wonder why?

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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.

What do you think?

I just read a paper that addresses one aspect of this.

From Gianfrani et al. JI 2006, 177:4178-4186

p 4184

"Our results are consistent with the hypothesis that gliadin specific Tr1 cells (a type of T cell) are recruited to/differentiated in the inflammed intestinal mucosa during the acute disease..."

"...they must remain in the treated mucosa as long-lived memory T cells"

Essentially, they took biopsies from treated celiac disease(on gluten-free diet), untreated celiac disease, and normal people and exposed the cells to gliadin. They found that the treated celiac disease peoples' response went back to the level of the untreated celiac disease, so no, you don't regain tolerance.

Although,

I read a different paper in which a single person who had been strictly gluten-free for more than 10 years was experimentaly reintroduced to gluten at low levels and was tolerant of it.

I think the caveat to the second experiment is the strictly gluten-free part. Your memory T cells die off over time, but it takes years. Every time you get glutened you re-activate them.

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p 4184

"Our results are consistent with the hypothesis that gliadin specific Tr1 cells (a type of T cell) are recruited to/differentiated in the inflammed intestinal mucosa during the acute disease..."

"...they must remain in the treated mucosa as long-lived memory T cells"

Essentially, they took biopsies from treated celiac disease(on gluten-free diet), untreated celiac disease, and normal people and exposed the cells to gliadin. They found that the treated celiac disease peoples' response went back to the level of the untreated celiac disease, so no, you don't regain tolerance.

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)?

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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?

Since this really isn't an experiment you could do, I'm not sure there will ever be a real answer.

You can always test it yourself. Try gluten after a few years and see if you have the same reactions.

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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?

Since this really isn't an experiment you could do, I'm not sure there will ever be a real answer.

You can always test it yourself. Try gluten after a few years and see if you have the same reactions.

Yea, no way! I'm not going to be the guinea pig!!!! :)

I was just wondering what all of you thought, I thought doc was wrong!

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Sorry, I didn't say that very clearly. You probably have a combination of your parents genes. So your haplotype or genetic complement is different from either of your parents. There are, however, certain spots that are more likely to undergo a single base-pair change when the egg or sperm are made. So you don't change over your lifetime, but you might produce a child with a change. Keep in mind that any change that makes a big difference is unlikely to be compatible with life, but subtle changes do make a difference in, for example, how your body responds to bacteria.

There's a great paper on TLR5 and legionaire's disease if you want to read up on it. Pretty jargony though. If I find a review I'll pm you.

Umm, like HIV/AIDS?.......

Damn, so much good stuff in this thread. Well for me the nerd boy. ;)

I'm still not sure I have it clear, but I'm guessing if I read more I'll understand. Let me pose this particular question. Let's say that my dad has gene X1 and X3, and perhaps my mom has X2 and X4, and let's say that there are 5 different versions of this gene. Are you saying that it's possible for me to get something like say X1 from my dad, but then to have X5 (this polymorphed gene) from my mom? Again, I'll read more for sure as this is rather interesting. It does make some sense, but given that some gene that has survived for thousands of years then at some point gets changed to some random gene seems odd. But it does make sense in that if this never happens and with the HLA genes some disease comes along that wipes out all these folks that this mechanism might just protect some folks and thus keep some humans around to keep populating the earth.

Well, I guess HIV/AIDS isn't the best example (in that our bodies don't seem to do so well at fighting it), but it is an interesting one especially since guess what... that glue in our bodies tissue transglutaminase is a substrate for it. What that means I don't know, but it is rather interesting. :) Also rather intresting is that this disease started in Africa (well according to what I've read) and given that S Africans HLA-DQ genes are not the same as folks who get celiac. Is another interesting coincidence don't ya think? Oh and finally, I read (I really need to figure out where) a rather interesting thing where they were talking either about celiac and/or gluten in the context of Sickle-cell disease. Are all of these things somehow related?

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Well, I guess HIV/AIDS isn't the best example (in that our bodies don't seem to do so well at fighting it), but it is an interesting one especially since guess what... that glue in our bodies tissue transglutaminase is a substrate for it. What that means I don't know, but it is rather interesting. :) Also rather intresting is that this disease started in Africa (well according to what I've read) and given that S Africans HLA-DQ genes are not the same as folks who get celiac. Is another interesting coincidence don't ya think? Oh and finally, I read (I really need to figure out where) a rather interesting thing where they were talking either about celiac and/or gluten in the context of Sickle-cell disease. Are all of these things somehow related?

UGG!!! I think I may very well be mistaken about reading about celiac and Sickle cell disease. I think that what I remember is thinking about Sickle Cell disease in the context of Celiac. Probably where I got this virus idea. What I think (I'm probably going to have to correct myself again :lol: ) I remember reading was that Sickle Cell was protective against a disease (malaria?) and that how perhaps Celiac was protective against something as well.

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I'm still not sure I have it clear, but I'm guessing if I read more I'll understand. Let me pose this particular question. Let's say that my dad has gene X1 and X3, and perhaps my mom has X2 and X4, and let's say that there are 5 different versions of this gene. Are you saying that it's possible for me to get something like say X1 from my dad, but then to have X5 (this polymorphed gene) from my mom?

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.

Well, I guess HIV/AIDS isn't the best example (in that our bodies don't seem to do so well at fighting it)

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

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

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

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