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dvjorge
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flailingWcandi wrote:

There is an strong link between CRC and autoimmune diseases. Candida Albicans can suppress cell-mediated immunity and down regulate the suppressor cells. The suppressor cells are those that regulate an immune response against our own tissues and organs.
Jorge.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC358175/

Wouldn’t this tie into adrenal fatigue/hypothyroid since the endocrine systems play an important role in regulating the immune system through hormones?

From my understanding it’s almost impossible to NOT have a compromised immune system by the time CRC happens, since a faltering immune system is what allows it to get out of control. To me this suggests adrenal/thyroids are a component to solving this puzzle – tail chasing: what came first scenarios. I’m leaning towards the endocrine systems being the first to crash in the chain reaction but, that just this week. ha!

As always, Jorge thank you for sharing your generous and informative insight.

Natacha – you are correct in how leaky gut is part of this syndrome from my understanding but, I wouldn’t say foreign particles since they are mostly large molecule food particles the body doesn’t recognize as food and mounts an immune response to what it thinks are invaders. Think leaky gut causes much of the histamine reactions typical of CRC sufferers.

Blessings

Here you can learn still more:

People can become
unresponsive to an antigen by exposing them more or
less continually to this antigen. This may be carried
out with very high doses of antigen—called “highzone
tolerance”—or with very low doses, “lowzone
tolerance.” High-zone tolerance tends to
render unresponsive both T- and B-cells, whereas
low-zone tolerance weakens or blocks the T-cell
response only. Thus the cellular immune response
(T-cell) is more easily blocked, and such blockage
is easier to sustain than is the humoral (B-cell)
response. Furthermore, unresponsiveness (or
“tolerance”) is easier to induce with soluble than
with aggregated antigens.
Thus immunologic tolerance is most readily
achieved by more or less continual exposure to a
soluble antigen, with T-cell paralysis being much
easier to achieve and sustain.
When mucous membranes are chronically infected
by yeast, cells of the immune system are exposed
continually to Candida antigens, thus satisfying the
conditions for tolerance induction. This weakened
immunologic response allows the yeast to thrive in
the tissues, and a vicious cycle is established. An
analagous situation has been reported in
lepromatous leprosy. In this, the widely
disseminated form of leprosy, impairment of the
immune response has been demonstrated in vivo by
reversion to negative of the lepromin skin test, and
in vitro both by impairment of the lymphocyte
transformation test on exposure to the leprosy
bacillus or phytohemagglu-tinin, and release of the
migration inhibitory factor on exposure to the
bacillus. In the tuberculoid form of leprosy,
however, this does not occur. This is the localized
form of the disease, which carries a good
prognosis. Thus widespread involvement is
associated with impairment of the immune
response.
With Candida infection, as with leprosy, there
may be for each individual a critical point beyond
which the total area of involvement is such that the
antigenic stimulus paralyzes rather than stimulates
the immune system, particularly the T-cell compartment.
Until this state of immunologic
unresponsiveness is broken, drug therapy of the
yeast infection will be less than fully effective.