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Dear listmembers,

I've been reading time and time again confusion about what exactly is
happening in our poor Celiac bodies.  We see the declining health, feel
the effects of gluten, and hear innumerable confusions about what
exactly is GF, and so forth.

Well, last year my boyfriend--a med student--and I--a
microbiology/immunology student--put our scientific minds together to
wade through some recent journal articles.  You'd be surprised to learn
that it's only in the last few years that scientists have even scratched
the surface of the physiology of CD.  We read approximately a dozen
journal articles from reputable sources, and put together a ten-page
paper on the results.  I presented this paper to all of my science
classes in which there were pre-med/pharmacy/physician's assistant
folks.  It was my small attempt at increasing education about CD to the
medical communnity.

In any case, I wanted to give "ya'all" (as we say in Indiana) a brief,
"easy read" summary on what the paper covered.  I think that this may
help expand your vocabulary on our condition, as well as provide some
insight into your condition.

Gluten, as we know, is a protein coating on certain grains.  It contains
something called "gliadin"--a protein component, shall we say.  For all
intents and purposes, proteins are big molecules that our bodies have to
process (break down) before they can really use them.  They are,
however, very essential to how our cells and overall metabolism (energy-
yielding processes) function.

Breakdown of gluten actually begins (on a chemical level) in your
stomach.  There are enzymes there that assist in that process.
Eventually this gliadin ends up in your small intestine, where most of
your digestion takes place.  If there is some kind of damage to your
small intestine--or genetic "predisposition" that has yet to be fully
researched--something called tissue transglutaminase can get into your
small intestine.  This stands for tissue transglutamase.  tissue
transglutaminase is an enzyme, and enzymes look for something called a
substrate that they can fit together with.  This is called an
enzyme-substrate complex, but you can think of it as a "lock and key."
When the key goes into the lock, something happens.

tissue transglutaminase and gliadin should never meet.  Gliadin is not
its normal substrate in the body.  The tissue transglutaminase recognizes
the gliadin as a prime substrate, the two hook up, and your immune system
goes berzerk.  Your body sees this complex as a foreign presence, and the
resulting immune reaction causes the symptoms of CD that we know and
"love."  This is harmful and abnormal--hence, the title "autoimmune
disease."

Now, scientists are still uncertain as to whether the genetic component
relates to tissue transglutaminase getting into areas that it doesn't
normal enter, or whether the body's tendency to attack that complex is
based on genetics.  They generally think that it is the latter, and
something like a virus, trauma, or such causes a lysis (tear) in the
small intestine that lets the tissue transglutaminase into a party where
it just doesn't belong.

Now, my best guess as to the functioning of a CD-prevention pill would be
to give that tissue transglutaminase an alternate substrate so that it
wouldn't hook up with the gliadin.  Whether or not the pill could provide
enough substrate so that there was no reaction or damage, I don't know.
I do know that, in answer to a much earlier question, the more substrate
you provide the more complexes you will get and the larger the immune
response.

Finally, one quick last note about a lot of postings that I see.  "Ig"
stands for immunoglobulin.  That is the same thing as antibody.  There
are five basic classes of antibodies, two of which are "IgG" and "IgA."
The G and A stand for Gamma and Alpha, but that gets into how the
antibody was formed and it's not really something to worry about.  Just
know that they do different things.  In fact, they do many things in
many parts of our body (particularly IgG, which is the most common
antibody), and are not just found in Celiacs.

I hope that this didn't confuse you.  Please do not give me the "third
degree" about any of this.  I am sharing what I remember from a paper
that I wrote a year ago, and from the knowledge that I have as an
undergraduate "budding" immunologist.  The research changes so fast, and
ideas are constantly being revised or thrown out entirely.  I hope to go
onto grad school to study autoimmune disorders, so maybe someday I will
be able to tell you more.

Happy eating.

Jessica