Guest guest Posted March 28, 2005 Report Share Posted March 28, 2005 [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. Quote Link to comment Share on other sites More sharing options...
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