6 replies to this topic

[Seeking2012]

Celiac Disease (as I currently understand it) means that there is villous atrophy that is being caused by the body’s immune reaction against gliadin proteins. According to literature I’ve read by Dr. Alessio Fasano, an individual can develop Celiac Disease at any time during their lifetime.

Here are the tests that are currently used in the medical community to diagnose Celiac Disease:

• Tissue Transglutaminase Antibodies (tTG-IgA, tTG-IgG)
• Anti-Gliadin Antibodies (AGA-IgA, AGA-IgG)
• Anti-Endomysial Antibodies (EMA-IgA, EMA-IgG)
• Deamidated Gliadin Peptide Antibodies (DGP-IgA, DGP-IgA)
• Total IgA count

Here are the reference ranges for the above-mentioned tests:

Deamidated Gliadin Peptide Antibody IgA:
0-19 is defined as normal

Deamidated Gliadin Peptide Antibody IgG:
0-19 is defined as normal

Tissue Transglutaminase Antibody IgA:
0-3 is defined as normal

Tissue Transglutaminase Antibody IgG:
0-5 is defined as normal

Total IgA Antibody count:
70-400 is defined as normal

Let’s try and define “normal.” What does “normal” mean? Does this mean that people who are perfectly healthy, who are having no reaction to gluten at all, have those numbers? Or does it just mean that people who may be having a reaction to gluten, but not enough to cause villous atrophy, may have those numbers?

I especially find “weak positive” vs “positive” to be hilarious. What does “weak positive” mean? I mean, come on! Does “weak positive” mean they THINK it might cause villous atrophy?

I suppose that scientists and/or doctors have arrived at these numbers as their definition of what (they think) is (maybe) going to cause villous atrophy. However, there are many questions and doubts I have about this, as follows:

1. How do they know that these numbers will or will not cause villous atrophy? What if a DGP IgA value of 15 causes villous atrophy in some people whereas a number of 21 does not cause villous atrophy in others?

2. What if the guy with the 21 number does not have villous atrophy yet because his body only started reacting to gliadin proteins a few months ago and not enough time has passed to develop villous atrophy?

3. Is villous atrophy all we care about? What other forms of damage can a DGP-IgA value of 20+ be doing? What about a value of 15? 10? 5? 1 even?

4. If you have a number greater than 0 of any of these SELF antibodies, doesn’t that mean you have a form of autoimmune disorder? If not, then does the body just make these antibodies just because it feels like it? Is the human body programmed by evolution to make at least a certain amount of these self antibodies (I seriously doubt it), or does it make them in response to stimuli?

5. If the latter, can the stimuli be anything besides gliadin and glutenin proteins? If so, what?

My theory: if your body is making ANY antibodies against SELF tissues, you have an autoimmune disorder, but I don't know what is causing it, nor can I tell you what type of damage it is doing to your body. I know, that's very helpful, isn't it?

What do you guys think?

[Kamma]

Hi Seeking.

Very thought provoking post and you ask some of the same questions that I have been asking myself as well. I too would like to know how they come up with establishing the ranges of normalcy. As of yet, I haven't found out the answers despite looking. I do know that my neurologist, when telling me my test results (which were 'inconclusive'), looked up at me and said, "Don't worry about that because who knows how many people in the test range were actually unconfirmed celiacs and skewed the ranges".

In one of Dr. Mario Hadjivassiliou's (UK researcher in gluten ataxia) interviews that I read on the celiac about.com page with Jane Anderson, he stated that anyone with elevated IGA should try a gluten free diet.

I have been trying to understand the ttg Iga response as well but am having a hard time wrapping my head around some of it. There are different kinds of ttg: tttg 2 (intestinal celiac), ttg3 (DH) and ttg6 (gluten ataxia - which is currently being developed for testing of gluten ataxia). So, what exactly is ttg (an enzyme, I believe) and is IgA specifically linked to ttg or is it linked other kinds of enzymes in the body but they only test for the ttg IgA?

Sorry that I can only offer more questions here and not answers but I would like to add in my voice and ask if anyone else has any answers for your questions.

[tarnalberry]

I don't have a lot of time, but I wanted to make a note, which I think is important:

You seem to be assuming that test results are ACTUALLY WHAT EXISTS. Tests are, by their nature, imprecise things. You get a reading of "3" on something, and there's a margin of error. Maybe what's really in your body is a 1 or a 6 (or something else - error varies by test, test type, and many, many factors). So, there needs to be some accounting for the fact that there is error in a test.

Additionally, "normal" ranges are generally set by running the test on a "large" group of "healthy" control subjects to find out what the normal range of results is. Various statistics are run, and you get what normal ranges are. Is this prone to mistake? Yes. Is this a less than perfect answer? Yes. Is it the best method we've got at the moment? Yes.

Finally, with celiac in particular, when people come up with a new blood test, you have to have something to compare it to, and that has been the classic standard of an endoscopy, which is looking for villous atrophy. So, yes, there is a bias that way. Because there is no other well established standard to compare it to.

Is testing flawed? Yes. It's getting better, but it's hardly likely to ever be perfect. Measuring these sorts of things in the human body is extraordinarily difficult, both from a "how the heck do we do a useful measurement accurately" and from the "what is it that we're measuring for".

But, you know, there is a LOT in the world that is flawed. We work with what we've got.

[psawyer]

Thank you, Tiffany. Well said.

[Kamma]

Hi Seeking,

I'd like to say thanks for posting those questions since it motivated me to search a little harder for a few things. I found a laboratory medicine wiki for the second year university students at the University of California. This link outlines how labs establish the reference ranges for testing:

http://ucsdlabmed.wi...t.com/chapter-1

Also, in answer to your third question about villous atrophy being the sole concern of damage from antibodies, in gluten ataxia research, the atrophy or shrinkage of the cerebellum as a result of the ttg 6 IgA antibodies attacking the Pukinje cells contained within it is also used as a marker.

In answer to your fifth question, a very recent study came out in which they drew the conclusion that continued unresponsivity to a gluten free diet could be due to antibody cross reacitivity to non-gliadin foods. You can download the PDF of the study here:

www.scirp.org/journal/PaperInformation.aspx?PaperID=26626

[dilettantesteph]

I don't think that it is flawed so much as there isn't enough known yet. They are researching and trying to figure it out as fast as they can with all the difficulties involved. Here is an article about the difficulties with funding with medical research: http://www.forbes.co...dical-research/

[dilettantesteph]

In answer to your fifth question, a very recent study came out in which they drew the conclusion that continued unresponsivity to a gluten free diet could be due to antibody cross reacitivity to non-gliadin foods. You can download the PDF of the study here:

www.scirp.org/journal/PaperInformation.aspx?PaperID=26626

This source says "We also observed significant cross-reactivity between a-gliadin 33-mer and various food antigens, but some of these reactions were associated with the contamination of non-gluten foods with traces of gluten."

It could be from cross reactivity or contamination.

In my experience, I don't react to things when I grow them myself, even if I do when I get the item elsewhere. There is also the problem of botanically unrelated items having very similar reactivity. I believe it is more likely to be contamination than cross reactivity.