I had read in a post of KSman’s that, FT has a short half life. I have been trying to find information about the life of endogenous testosterone, but haven’t come across anything. Assuming that the production of endogenous testosterone is around 10ng/day at best, 40-50ng/wk, we are not going to produce nearly enough to maintain a 600-800ng TT value if the half life is short.
What I am asking is: If FT has a short half life, and can only be reproduced in small amounts that would make it difficult if not impossible to add up to 600-800TT(assuming that the T would die before enough was produced to add up to TT numbers), does the half life of Testosterone bound by albumin or SHBG get greatly extended to allow for more stable levels of TT?
In other words, roughly 98% of our TT is bound, right? By being bound, does it make the half life or life a lot longer/more stable, allowing levels to remain high in comparison to the general production of endogenous T?
Lastly, what is the rough half life of endogenous FT? Similar to that of enanthate?
Hopefully this makes sense the way I posed the question. Thank you.
Damn! i meant ng, but what I meant is wrong. It is mg , and with that, it throws my whole presumption out the window. I guess just disregard it. 5-7mg daily converts to a whole lot of ng daily, so I suppose it is normal to expect daily or weekly production to maitain levels wether bound or unbound.
100 mg test ester [cyp/eth] yields around 70mg T. So 100mg/week is around 10mg/day and guys get to TT=800-900 with that. 10mg/day is often reported to be a good reference point for production in young healthy males; but note that there is a lot of variability.
FT has a short half life and is released in pulses in normal guys. The peaks decline quite fast, however, T receptors are been activated.
When on TRT, especially frequent injections, FT levels are quite steady. So FT lab results have significant value. FT labs for natural guys is a snap shot of a moving target and the numbers are thus not so useful.
While FT can be around 2% more or less, depending on SHBG levels, a lot of T is weakly bound to albumin and perhaps some other proteins and this weakly bound T can be released in tissues to activate T receptors.
T is never released from SHBG - NEVER. SHBG-T is simply rubbish waiting for cleanup by the liver. SHBG-T is not a transport mechanism for delivering T to receptors. Estrogens bind less tightly to SHBG and SHBG-E can deliver estrogens to tissues. Because of this, many have stated that SHBG can transport T to receptors, but that is simply wrong and once stated on the WWW it never will go away.
SHBG-T is functionally inert from an androgen point of view.
Such things are not timed. I have read that weakly bound T, such as albumin-T releases T in tissues when local enzymes do this. There may be other release mechanisms. As this is local, the hypothalamus is not on the playing field at all.
When guys use transdermal T products, T levels can spike and drop fast after that. Some FT directly acts on receptors. Albumin-T carries a significant amount of T that will continue to activate receptors. The receptors once activated have an effect that is long duration. So one should not have the impression that the effects of FT are short lived even when the half life appears to be short.
Transdermal T can build T levels in the skin layers that act as a limited time release reservoir. Note that SHBG exists in the blood stream, not in tissues and organs. So T there is not subject to the same half life dynamics as SHBG-T binding cannot occur there. As T is hydrophobic and likes fats, T may also be buffered in fat under the skin.