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About testosterone I'm wondering why the patches were working for you Demo, and not the T shots. I heard that Andriol (oral T pills) is safe for the liver (bypass the liver) and is absorbed through the lymphatic system. Is it possible that the same is happening with patches ? (less strong on liver)) An other possibility is that T is absorbed very slowly in a more regular manner with patches so the androgen receptors are not downregulated by sudden high doses of T (hypothesis).
Now, how to boost androgen receptors: someone here a long time ago told us to try carnitine for that..
My theory is that MORE testosterone can help a number of POIS sufferers.
you were saying "only the first [testosterone] shot was effective, subsequent were placebo." and I gave up.One thing is sure I'm reticent to take T for the next 50 years.
I did not see any improvement with high doses of injectable T, 2x a week.
Before doing T shots, I did 3 forms of topical testosterone.I did Androgel patches, which did nothing but burn my skin severely.I did a compounded cream, with no results.I did Testim, which did nothing but made me very nauseous.None of the topicals raised my T level of any significance.The T shots, 2x a week have been the most helpful by far, raising my T level from 105 to 896, and increased my libido. It has done nothing for the POIS however.
I'm now trying Tribulus Terrestris - its basically like swallowing testosterone. TT, short for Tribulus Terrestris, stimulates LH that stimulates testosterone.
http://www3.interscience.wiley.com/cgi-bin/fulltext/120778223/HTMLSTARThttp://scholar.google.com/scholar?hl=en&q=author:%22Elenkov%22+intitle:%22Stress+hormones,+proinflammatory+and+antiinflammatory+...%22+&um=1&ie=UTF-8&oi=scholarrhttp://www.google.com/search?hl=en&q=catecholamines+and+inflammation&aq=f&oq=&aqi=I gave google search for one of articles,html link and abstract the articles are to long. ABSTRACTAbstract: Recent evidence indicates that glucocorticoids and catecholamines, the major stress hormones, inhibit the production of proinflammatory cytokines, such as interleukin (IL)-12, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ, whereas they stimulate the production of antiinflammatory cytokines, such as IL-10, IL-4, and transforming growth factor (TGF)-β. Thus, systemically, an excessive immune response, through activation of the stress system, stimulates an important negative feedback mechanism, which protects the organism from an "overshoot" of proinflammatory cytokines and other products of activated macrophages with tissue-damaging potential. Conversely, in certain local responses and under certain conditions, stress hormones actually may boost regional immune responses, through induction of TNF-α, IL-1, and IL-8, and by inhibiting TGF-β production. Therefore, conditions that are associated with significant changes in stress system activity, such as acute or chronic stress, cessation of chronic stress, severe exercise, and pregnancy and the postpartum period, through modulation of the systemic or local pro/antiinflammatory cytokine balance, may suppress or potentiate autoimmune diseases activity and/or progression.--------------------------------------------------------------------------------
this post [below] is to the response that my links do not work, i hope this ones works. And instead of posting the main article i posted the abstract.
http://www3.interscience.wiley.com/cgi-bin/fulltext/120778223/HTMLSTARThttp://scholar.google.com/scholar?hl=en&q=author:%22Elenkov%22+intitle:%22Stress+hormones,+proinflammatory+and+antiinflammatory+...%22+&um=1&ie=UTF-8&oi=scholarrhttp://www.google.com/search?hl=en&q=catecholamines+and+inflammation&aq=f&oq=&aqi=I gave google search for one of articles,html link and abstract the articles are to long. ABSTRACTAbstract: Recent evidence indicates that glucocorticoids and catecholamines, the major stress hormones, inhibit the production of proinflammatory cytokines, such as interleukin (IL)-12, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ, whereas they stimulate the production of antiinflammatory cytokines, such as IL-10, IL-4, and transforming growth factor (TGF)-β. Thus, systemically, an excessive immune response, through activation of the stress system, stimulates an important negative feedback mechanism, which protects the organism from an "overshoot" of proinflammatory cytokines and other products of activated macrophages with tissue-damaging potential. Conversely, in certain local responses and under certain conditions, stress hormones actually may boost regional immune responses, through induction of TNF-α, IL-1, and IL-8, and by inhibiting TGF-β production. Therefore, conditions that are associated with significant changes in stress system activity, such as acute or chronic stress, cessation of chronic stress, severe exercise, and pregnancy and the postpartum period, through modulation of the systemic or local pro/antiinflammatory cytokine balance, may suppress or potentiate autoimmune diseases activity and/or progression.
An other possibility is that T is absorbed very slowly in a more regular manner with patches so the androgen receptors are not downregulated by sudden high doses of T (hypothesis).