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question

> 2)  How much gluten can be tolerated with de minimus damage?  It is said that
> the intestines can be damaged even when the patient feels fine after eating a
> small amount of gluten.  The mechanics of damage to the villi seem to imply
> that very small amounts of gluten are sufficient to bind to ALL the villi
> cells, so that once this initial quanta of gluten has been ingested, all the
> damage is already done, and additional amounts of gluten do no further
> damage.....unlike a dieter cheating on his diet for a CD patient the damage
> is not proportional to the amount of cheating.  Is this true?

Although there are many speculations, I would say that there is no clear
understanding of how certain peptides, derived by digestion of gluten
proteins, trigger responses in the body that ultimately lead to destruction
of intestinal epithelial tissues, including the absorptive cells or
enterocytes.  This makes it difficult to speculate then on whether minimal
amounts of these peptides can be tolerated or not.  For the sake of
discussion, however, I put forward the following considerations:  It is my
impression (based on the work of C. E. Rubin) that it is not unusual for a
celiac with full blown disease and severe damage to the parts of the
intestine nearest to stomach to have NO damage to the distal small bowel
(farthest downstream part of small intestine, or ileum). Yet the ileum is
capable of being damaged when gluten proteins are instilled directly into
it.   J. R. Hobbs and others have suggested that this is a pretty good
indication that the intestine is capable of digesting the harmful peptide or
peptides.  The access of the peptides to the intestinal surface in the
upstream part of the intestine is sufficient to trigger the mechanisms that
lead to damage, but even large amounts of gluten proteins and peptides
eventually are digested as they move along the considerable length of the
small intestine--thus the lack of damage to the ileum.

Accordingly, it is possible that very small amounts of these peptides might
be digested before they cause significant harm.  This is speculation that
cannot be evaluated right now without detailed understanding of mechanisms.

Consider an alternative.  It is possible that binding to a key (but as yet
unknown) receptor site is stronger than binding to the enzymes capable of
digesting the peptide and takes precedence for first exposure, even for very
small amounts of protein.  Eventually, however, the weaker binding to the
proteolytic enzymes could still result in complete digestion before the
peptides reach the far end of the small intestine.

Donald D. Kasarda