Forget DHT now, levels of DHT will follow T levels and this can be explored later when your TRT is right.
Your day of testing was totally wrong. If you start anastrozole with weekly injections I think that you would do very poorly. If you inject, you need to inject often to get steady T levels, then do E2 labs and see what you get.
I think that you should not be injecting and need let things recover and then use anastrozole to manage E2 levels. With E2 in the lower 20’s, see where TT and FT go. You can try 0.5mg/week anastrozole in divided doses. read up and understand issues re anastrozole over-responders.
I have a lot to think about. I just received my new Test and Anastrozole in the mail today. My plan was to inject every 3.5 days to keep my levels more steady, and follow it up with a once weekly Anastrozole of 1mg.
If I stop injecting all together, will I start to produce Test again on my own or do I need to get on HCG. And if this is the route I choose, how long should it take for my levels to return to pre-injection levels. My level was actually above the normal range for my age, at least for my TT, not my free T. How long should I wait to get myself retested?
I only have 4 tabs of Anastrozole, a months supply. Is this enough time to really have a significant effect on E2 levels? If and when I stop, should I get myself retested before I start taking the Anastrozole.
-Time on=Time off (per an Endo at another site) for levels to return to pre-TRT.
-You will start producing again, but you will go back to where you were before TRT.
-HCG will start your balls up again but remember that it is also suppressive of the HPTA since it mimics LH.
I don’t think that LH is directly HPTA repressive, only the increased T and E2 that hCG can lead to. And E2 is very much more repressive than E2. Remember that males are a deviation of the female blueprint. The HPTA is very much working the same as the HPOvarianA which is dominated by E2 as the feedback signal.
[Prolactin is also very HPTA repressive. Prolactin is a peptide, while T and E2 are steroid hormones. You can read more about prolactin here: Prolactin - Wikipedia
It is really an odd-ball hormone. It may be that the conditions that lead to increased prolactin levels are HPTA repressive, not the prolactin itself. But I really do not know and am not inclined to read deeper.]
My main theory for why HcG may be somewhat repressive is that it is exogenous and its tendency to convert to estrogen and E2 is what signals the hypothalamus to stop producing LH. It is excellent at restarting the testicles, just not at restarting the pituitary.
From EndoText on HcG and excessive estrogen:
“The mechanism underlying the development of gynecomastia in this setting appears to be excessive secretion of estrogen in response to hCG stimulation of the Leydig cells.(116, 124)”
[quote]JLWilson wrote:
My main theory for why HcG may be somewhat repressive is that it is exogenous and its tendency to convert to estrogen and E2 is what signals the hypothalamus to stop producing LH. It is excellent at restarting the testicles, just not at restarting the pituitary.
From EndoText on HcG and excessive estrogen:
“The mechanism underlying the development of gynecomastia in this setting appears to be excessive secretion of estrogen in response to hCG stimulation of the Leydig cells.(116, 124)”[/quote]
I think this is very accurate. Although I use more than TRT doses of AAS I also have used hcg. I never had more gyno reaction than when I was on hcg.
That should read: The mechanism underlying the development of gynecomastia in this setting appears to be secretion of estrogen in response to excessive hCG stimulation of the Leydig cells.(116, 124)
Technically, hCG [or any peptide] cannot be converted to any steroid. [yes, I am an engineer] Do not confuse conversion with promoter. T is converted to E2 by the aromatase enzyme.
hCG is not repressive, levels of E2 induced by hCG are repressive. Lets try to differentiate between direct and indirect effects. If hCG or LH is directly HPTA repressive, I have not seen this described and that effect, if it exists, may be minor. Note that in cases of castration, steroid levels are very low, only what the adrenals make. The HPTA does not see any negative feedback signals and basically goes “open loop”. I this situation, LH levels can be very high. Also, when LH levels are high, this is diagnostic for primary hypogonadism aka testicular failure. Now if LH were directly HPTA repressive, LH levels for a castrated man would be limited and there does not seem to be any evidence for that at all. If that was true for LH, there is no reason to not expect the same from hCG. If one took a castrated man with high LH and injected that man with hCG, if that caused LH levels to decline, that would be evidence for hCG having some degree of direct HPTA repression. One never knows all of the minor roles of hormones in the body.
Regardless, it is an exogenous substance that produces testosterone and estrogen. Each time you inject, you are closing the feedback loop as the body detects testosterone and estrogen and the hypothalamus decides not to produce any GnRH.
No, LH itself is not repressive, but the introduction of any exogenous substance that closes the feedback loop as HcG does IS repressive.
Look at bodybuilders and steroid use. If HcG were not somewhat suppressive, then why do most bodybuilders avoid using it post-cycle? Most use it while ON-cycle so their testicles are ready for PCT when they will re-activate the HPTA loop using a SERM. I know, bad example since it lacks any medical research, but I stand by the argument that anything that introduces an exogenous precedent or antecedent of testosterone, whether it be LH, GnRH, DHT, DHEA or anything, will be suppressive on the HPTA.
I don’t think it’s nearly as suppressive as TRT since it doesn’t shut down the testicles. I think that that the higher you go on that chart in terms of treatment, the less suppressive it is on the HPTA since it takes less and less out of equation. Example: TRT is more suppressive than HcG since it shuts down the testicles AND the HP while HcG only shuts down the HP. GnRH shuts down the H while not suppressing the P or the T.
I respect your opinion, however. Sorry if this was rushed, my dog is whining to go pee and I know when I leave it’ll be blank! I will edit it later if I see any mistakes.
I agree, I mean the facts are the facts. The only way to determine whether or not it is suppressive is to have someone on HcG monotherapy do a blood test 3 days after their shot.