Re: Chronic Illness progression & Th1/Th2 issues?

[Guest guest]

Duramater, I don't think your questions are rudimentary, when

compared to the state of the science.

What's his face has misled many people about that by making

unqualified, declarative statements and implying they are scientific

in nature. So even people who don't buy what he's saying often get

mistaken impressions of how much is currently known.

I think your question about total T cell populations vs the ratio of

Type 1 to Type 2 cells is very appropriate, I've read a squillion

abstracts relating to this and I don't see much of a consensus.

For a long time I avoided that whole discussion, because it seemed

like such a murk. But then I kept coming across Lyme research that

made it seem potentially very signficiant. Because the outer surface

proteins on Bb spirochetes 'force' naive T-cells into the Th1

phenotype. This is not a universal behavior for bacterial pathogens.

It seems that Type 2 cells are needed to form effective antibodies.

To me, and to some researchers, this suggests that forcing Type 1

cells to develop would protect spirochetes.

Yet Bb also locates intracellularly. An inflammatory response is

presumably needed to force antibodies or antibiotic medications deep

into the tissue.

So whadda we do?

Bear in mind, I don't even 'know' that I'm stating a real dilemma.

There are researchers who describe it in these terms, but's that's

about all I'm sure of.

>

> [in part]:

> " IMO, here is the progression:

>

> Acute infection--> chronic/occult infection -> chronic

inflammation -->

> symptoms present as specific disorders depending on tissue type

> (genetics, host-pathogen relationship) ---> secondary symptoms

emerge

> over time- allergies, GI problems, chemical and food sensitivities

etc. "

>

> I absolutely concur about your hypothesized progression, albeit

not

> from a scientific place but rather an experiential position.

>

> What I'm particularly curious about is the Th1/Th2 relationship

with

> such a progression. I feel pretty confident in saying that in the

> latest stage you hypothesize (allergies, chem & food

sensitivities)

> there is an over-regulation of Th2. But do we think there is a

> concommitent up-regulation in Th1 (as hypothesized by whats his

face)?

> Or what is going on with Th1 if anything? From whence does the

> inflammation arise?

>

> And being new to the literature on Th1/Th2, please SOMEONE correct

my

> rudimentary knowledge if its wrong... My understanding is that as

one

> tries to, say, downregulate Th1, T cells are shifted to Th2. So

(A)

> can one have too much Th1 AND Th2? (seems like you can if just too

much

> T cells are being generated in general) and ( lets say both are

being

> over-done. If one tries to tamp down Th1 (in the context of too

high

> Th1 & Th2), will that shift it over to EVEN MORE Th2????

>

> Lastly, what happens to folks taking benicar/mino if it really

does

> tamp down Th1 cytokines but they already have too much Th2? Do

Th2-

> related symptoms get even worse?

>

> Again, apologies for the rudimentary nature of these questions,

but I'm

> just starting to work on my understanding of these areas involving

> Th1/Th2 & cytokines.