Interesting...
I believe i made myself unclear, i was talking about without any supplementation, the HPTA axis will undergo negative feedback.
Without any supplementation the HPTA is at semi-steady state conditions: there is no positive or negative feedback. If you didn't take anything, and experienced negative feedback, you would up and stop producing testosterone.
The Hypothalamus will release GnRH to the Anterior Pituatary which releases LH to the gonads and test is made within the sertolli cells. When a certain amount of test is circulating the hypothalamus will cease release of GnRH halting the axis(this occurs naturally without the use of any supplementation).
Now for the part i am still slightly confused...you say an AI will plug into the estrogen receptors in the hypothalamus(or reduce the receptor activity...by what means i am unsure). Two questions:
1) Not only was i unaware of these estrogen receptors found within the hypothalamus but i believe only testosterone receptors effect the HPTA output. To my knowledge testosterone can be converted to estrogen within the hypothalamus but this does not in any way suppress or modulate the HPTA axis ( study done by R. J. Santen J Clin Invest. 1975 December; 56(6): 1555–1563 to state a primary reference). So my question...how does the binding to estrogen receptors or downregulation of said receptors upregulate LH and testosterone within the hypothalamus?
An AI is an acronym for aromatase inhibitor. This is an enzyme which converts an androgen into an estrogen. It does not bind to the estrogen receptors.
You've taken this study out of context. It compares aromatizable testosterone to DHT on HPTA response. Re-read the second-to-last paragraph of the abstract, where it states estrogen is responsible for diminishing LH-RH responsiveness from the pituitary gland. Also see references 1 thru 9, which suggest what I spoke of earlier.
All in all, this is still somewhat arbitrary to the central argument of our little debate. You've concluded that a natural testosterone booster won't cause a false positive because of negative feedback. I will agree that a control system is in progress, but when you take a compound which modulates the characteristics of said control system, it is quite difficult to make the assumption that we have the same cut-off limits. You seem to still be thinking that the increased testosterone production is occuring independent of the HPTA, and this is not the case.
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2) I was under the impression AI prevent the conversion to estrogen allowing a higher ratio of T to E, which increases the bioavailability of T when mixed with a SHBG(i believe) to free bound T...is this not the case?
The ratio modulation is one piece of the pie, but it's certainly been shown that they also upregulate HPTA through the mechanism I've explained.
SHBG binds to T, not free it. I think you might be referring to a product like MassFX? This product contains constituents, which bind to this protein, allowing for an increase in free testosterone.
Now what i am now finding fascinating is that ones body can continue to over produce T naturally without triggering the receptor found within the hypothalamus...this is still puzzling me. Im sorry if im missing something ridiculously obvious. Post finals and my brains be fried.
I guess I wasn't clear in my last post.
The test booster upregulates test production UNTIL it triggers the receptors needed to cause this negative feedback. In order to get to that point, with a test booster, your testosterone levels need to be higher.