I enjoyed reading Ron Hoggan's recap of the celiac disease/gluten
connection. However, there are several points I am unclear on due to
undefined terminology. Ron, would you be so kind as to fill in the blanks
for those of us without the extensive background you have in the field?
Specifically here are the words and concepts I am unclear on:

>Neurological and auto-immune diseases, as well as malignancies, are
>over-represented among celiacs (5), suggesting that glutens/gliadins may be
>a major environmental contributor to such diseases.

The word gliadins here seems to slip in without any definition--only some
sort of unclear similarity (in my mind) to glutens due to the context. What
exactly are gliadins and why are they distinguished here from glutens
rather than simply lumped in together under the catchall term "gluten" that
you are using as a catchall for many other proteins also found in cereal
grains?

>There is abundant evidence connecting the advent of agriculture with
>retardation of long bone growth, dental enamel hypoplasia, iron deficiency
>anemia (indicated by porotic hyperostosis), juvenile osteoporosis, and joint
>disease (18). Do these conditions sound familiar?

All but two. I would like to know in plain terms what "dental enamel
hypoplasia" is, as well as "porotic hyperostosis." I know from past study
in the research that the latter is some kind of bone disease, but I can't
remember exactly what kind. Please fill me in.

>We know, from palenotologists' study of human remains from the ancient past,
>that when a culture begins to cultivate cereal grains they experience
>substantial reductions in height, which is variously reported as 5" and
>6"(2,4). Clearly, the reduction is substantial and significant. We know,
>too, that these remains demonstrate weaker bone structure (through
>reductions in peak bone-mass) and evidence of articular damage(3).

I am not sure I know what "articular damage" refers to. Could you please
explain? (Maybe just a technical term of good ole "arthritis"? :-\ )

>W.J.Lutz (4) has offered an alternative perspective on the "French Paradox."
>(The "French Paradox" is the unusually low rate of death by myocardial
>infarction among the French despite quite high per-capita rates of fat
>consumption.)

I know this may be being a bit picky about the language here, but is there
any reason "myocardial infarct" could not more simply be rendered as "heart
attack" so it would be more clear to more people, or is there some reason
"heart attack" is just not considered an accurate-enough term, and
therefore it is mandatory to use "myocardial infarct" instead?

Further on...

>This work is confirmed by Simmoon's observation that there is a negative
>correlation between the frequency of antigen HLA-B8 and the length of time
>wheat farming has been practised in various parts of Europe (19).

What is "antigen HLA-B8," is this negative correlation good or bad, and
what does it do in the body? It doesn't tell me a whole lot that there is a
negative correlation when I don't even know what HLA-B8 is in the first
place. I thought an antigen was a foreign protein the body reacted to by
producing antibodies. The above statement--in my mind--seems to suggest
that somehow a substance the body does not produce somehow varies with the
consumption of wheat. That doesn't seem to make sense to me. Either that,
or I am just not getting something here. Please explain.

>Another interesting study done in China produced what the investigators
>found to be rather surprising results(8). In this investigation, the
>researchers plotted the diets of more than 3500 rural Chinese women, and
>measured their levels of SHBG (sex-hormone binding globulins). They were
>very surprised to find that wheat consumption, and perhaps reduced fish
>consumption, were the strongest predictors of levels of SHBG, which would
>indicate an increased risk of cardiovascular disease.

I cannot figure out from the above whether the levels of SHBG went up or
down in relation to wheat and fish consumption, only that there is some
sort of correlation. Does SHBG go up when wheat and fish consumption go up,
or is it the reverse? Furthermore, it is not clear to me from the above
whether *higher* or *lower* levels of SHBG result in an increased or
decreased risk of cardiovascular disease. It only seems to say that there
is some sort of correlation, but what that correlation is is unclear to me
here. Beyond this, what the heck do sex-hormone binding globulins (SHBG) do
in the body in the first place, and why would it be good or bad if their
levels went up or down?

>Another study has connected gluten with neurological illness (9). This group
>of researchers tested 53 patients with neurological illness of unknown
>origin for antibodies against gliadin. More than half of them (30 people)
>demonstrated these antibodies. Nine of those folks proved to have celiac
>disease, but the other 21 only demonstrated an immune response to gluten, of
>a type that is often dismissed as meaningless. This study has some
>far-reaching implications for neurological research.

This seems clear enough--that an immune response to gluten might still be
problematic even if the person does not have classic hereditary markers for
celiac disease.

>Yet another indication that celiacs are not the only segment of the
>population to suffer from the adverse effects of gluten is a study that was
>carried out on a very small group of siblings of celiacs(10). When subjected
>to rectal gluten challenge, half of the siblings showed an immune response
>to gluten, but these results did not correlate with the hereditary
>predictors of celiac disease.

I am not sure I understand the underlying assumptions here you are basing
your statements on. Are you saying that certain immune responses somehow
are used as "markers" for certain hereditary characteristics (which perhaps
cannot be directly determined except through these markers) that may
predict for celiac disease? And that there are additional immune responses
that you are postulating may also predict for it, but conventional
scientific wisdom does not yet acknowledge them?

>As for the connection between autoimmunity and cereal grains, it is clear
>and compelling. The theoretical perspective of molecular mimicry suggests
>that gliadin-derived peptides may activate the immune system against
>collagenous tissues, and since intestinal permeability (not celiac disease)
>is all that is required to allow the passage of these peptides into the
>bloodstream, a significant number of many types of autoimmune diseases seem
>likely to benefit from a gluten-free diet (11 ).

This seems clear enough except for the part about collagen. According to my
dictionary, collagen is a "fibrous protein constituent of bone, cartilage,
tendon, and other connective tissue." So what? What is the point about
collagen here? I would guess there is perhaps sp,e postulation being made
here that the immune system's action against collagen could be the
mechanism behind bone deterioration seen in Neolithic farming communities,
but this is a leap I am simply guessing at. Is this is fact what is being
suggested, or am I completely off base? I am unclear.

>In total, then, there are several studies which demonstrate (often
>coincidentally) that a much larger group than those with celiac disease are
>mounting an immune response against gluten, and that this response is
>causing or contributing to serious illness. Phytic acid in whole cereal
>grains binds to minerals, including calcium. This chemical bond is not
>broken in the GI tract. The net result is the binding and wasting of
>much-needed dietary  calcium, even among those whose immune systems can
>tolerate gluten, and these grains may be implicated in osteoporosis (12).

Okay, clear enough.

>I would now like to draw your attention back to the issue of malignancy.
>_Medical Hypotheses_ will soon publish a paper I have written which
>suggests (among other things) that gluten may be implicated in a great many
>cases of lymphoma (14). Gluten has been demonstrated to interfere with the
>celiac patient's ability to mount an immune response to malignancies
>(15,16,17). In my paper, I have postulated a dynamic whereby gluten may have
>a similar effect in others who are simply sensitive to gluten, or who have a
>sub-clinical form of this disease.

This is clear language--thanks.

>I would like to suggest that the evidence from antiquity, the pattern of the
>spread of agriculture in Europe coinciding with the patterns of civilizatory
>illnesses, the levels of SBHG associated with wheat consumption, the high
>incidence of gliadin antibodies among those with neurological illnesses of
>unknown origin, the sensitivity to gluten among siblings of celiacs in spite
>of the absence of genetic indicators associated with celiac disease, and my
>own investigation of the literature regarding lymphoma, all point to the
>strong possibility that gluten is a dangerous substance to many more people
>than just celiacs.

Several questions here. Again, please explain what gliadin is and why
antibodies against it would be something that might lead to neurological
illness. What are the possible mechanisms you would postulate? And again,
what do SBHGs do in the body, and are their correlated levels with
increased wheat consumption ones of increase or decrease, and is more or
less SBHG good or bad? I don't have the background in physiology or
pathology to have a clue about any of this.

Thanks, Ron. I know it may seem tedious to you to explain these things, but
remember, not all of us have the background you do. I take Discover
magazine, Science News, and read several issues of Scientific American a
year, and I like to think I am science-literate for a lay person, but I am
really struggling here with some of this.

--Ward Nicholson <[log in to unmask]> Wichita, KS