Hi Philip, 
Thank you for the very interesting post. 


> I would appreciate people's input on this.

>HYPOTHESIS: gluten and other modern food proteins can trigger the human
immune system to attack hair-like epithelial cells, smooth muscle cells(SMA)
and mitochondria in the body that are similar in structure to the protein
cells of bacteria and viruses, and therefore mistaken as invaders through a
process known as molecular mimicry. (I will focus on >hair-like cells and
gluten.)

Martin Kagnoff was publishing work that explored viral infections among
celiac patiente from the 1980's. His work showed an increase of adenovirus
12 antibodies among those who had developed celiac disease. The
investigative focus has now shifted, as you mention, to looking for signs of
prior rotavirus infection. Researchers have long known that there is some
other factor that  contributes to the development of celiac disease. The
increase in anti-viral antibodies does, as you point out, suggest that viral
infections may be a factor that differentiates those with celiac disease
from those without celiac disease but who do have the same genetic
propensity. 

The more interesting part of your hypothesis, from my perspective, is the
identification of constituent proteins of fibrous or hair-like cells, which
may have similar sequences of amino acids to those found in gluten. Do you
know if these protein structures have been characterized? The gluten
proteins certainly have been. It might be worthwhile to compare each of
these protein structures to see if there are regions of similar or identical
amino acid sequences. Such evidence would certainly support your hypothesis
and open an important area of investigation. 

My own bias is that gluten-induced illness is affecting a much broader
segment of the population than the ~1% with celiac disease. Frankly, I think
that it was an unfortunate miscue when medical researchers became
preoccupied with gluten-induced intestinal damage in the mid-1950s. The
evidence clearly shows that there are many people who suffer from a variety,
and wide range of severity, of gluten induced illnesses without any
identifiable damage to the villous architecture. The artificial restriction
of the therapeutic use of this diet to celiac patients is, in my opinion,
highly questionable. 

Dr. Dicke's discovery of the efficacy of the gluten-free diet (circa 1934)
was made long before intestinal biopsies could be undertaken. (Dr. Dicke's
thesis is available on my website in pdf format at:
http://members.shaw.ca/dicke/)  When his patients demonstrated symptoms of
celiac disease, he treated them with the diet and those symptoms went away.
Today, many symptomatic individuals are never offered a gluten-free diet
when they do not show the antibodies or damaged intestinal villi that have
been associated with celiac disease. 

Yet these many of these individuals do demonstrate IgG antibodies against
gliadin and they do have a significantly increased risk of neurological
diseases, autoimmunity, as well as learning disabilities and behavioural
disorders. Thus, I suspect that much of the research that is restricted to
celiac disease alone is missing the larger picture. 

Your hypothesis, assuming that sequence homology can be demonstrated between
one or more of gliadin sequences and the constituent proteins of hair-like
or fibrous cells that you have identified, may well provide an important
insight into this process and a bridge that connects gluten sensitivity in
all its forms, including celiac disease. 

I believe that Fasano et. al. have shown that zonulin is a major player in
allowing foreign peptides and proteins to be leaked into the circulation,
which leads to activating molecular mimicry. Some investigations of the
protein structures of islet cells are currently under way. I do not know if
this work has yet identified any homologous sequences. But one case was
reported in the peer-reviewed literature in which type 1 diabetes was
reversed through a gluten-free diet alone. I consider that to be smoking gun
evidence of molecular mimicry. I would sure like to see your hypothesis
investigated as it could provide another important dimension of
understanding of this complex and widespread problem.

I am posting this to the list as I noticed that another list member was
interested in my response. 

Best Wishes, 
Ron