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Janet,
I've been thinking about what the possible immunological effect could be of
absorbing opiates into the blood stream formed from gluten and gliadin
fractions in wheat. There was an article from Scientific American that
appeared on American OnLine that talked about the effect of opiates on the
immune system. These investigations came under the umbrella of
psychoneuroimmunology. The author was PAUL H. BLACK, Professor of
Microbiology and Medicine at Boston University Medical School.
His article said that the effect of opiates on immune function in various
studies seems to have been mixed, but usually the opiates seem to be
immunosuppressive. But if your immune system is less active after quitting
gluten then if gluten was previously a source of opiates for you then you've
experienced an opposite effect, wouldn't you say? (That's a big if, I'd say!)
My daughter, Grace (who doesn't have celiac but is intolerant of gluten),
has recently had an incredibly overactive immune system. She has been
gluten free and casein free for several months, but two things happened
about a month ago. First, she started a glutathione loading program that
was initiated to try to correct some amino acid abnormalities she had. Then
also, she had chicken pox. We're not sure what caused what!
Dr. Black's article did mention something about a defect being possible in
autoimmune disease where the body does not appropriately turn off the immune
system. Since celiac is an autoimmune disease, this information is probably
relevant. Here are a few excerpts:
[HPA axis is the hypothalamic-pituitary-adrenal axis. CRF is corticotropin
releasing factor.]
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(from Scientific American)
Thus, most aspects of the response to the different stressors (environmental,
physiological, psychological, or cytokine-induced) are similar. The net
effect of cytokines on the brain is to turn off or down regulate the immune
response. This is likely to occur in most immune reactions and indicates that
the brain, via the HPA axis, is an important controlling factor.
HPA Axis Disorders May Cause Disease
If CRF is an important regulator of the HPA axis, it is possible that
dysfunction or dysregulation of this axis may be associated with disease. The
animal model is the Lewis rat, which is susceptible to a wide variety of
inflammatory and autoimmune diseases. In response to inflammatory cytokines,
most notably IL-1, the Lewis rat produces markedly diminished corticotropin
and corticosteroids. When the rat is challenged with CRF, the response is
also subnormal. There is apparently a hypothalamic defect in the synthesis or
secretion of CRF, which may be due to inappropriate regulation of the CRF
gene. The immune system is apparently turned on or, more appropriately, is
not turned off, due to this defect in the hypothalamic feedback loop.
It is of interest that Lewis rats subjected to various physical stressors
(cold, restraint, ether, or open field), in addition to low corticotropin and
corticosteroid responses, did not develop any of the behavioral
characteristics (behavioral adaptation) of stress that other rats, not
susceptible to these diseases, displayed.
In several studies of "chronic fatigue syndrome" patients, low CRF levels and
hypofunctioning of the HPA axis were found. Future studies will determine
whether failure of central nervous system regulation of the immune response
is a factor in the etiology of certain autoimmune diseases.
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What do you think, listmates? Does this sound relevant?
Susan Owens
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(Walter & Susan Owens)
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Dallas, Texas USA
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