Someone posted their HRT protocol here a few days ago as the following: 100mg test-e/wk, 250iu hcg eod, 25mg aromasin ED.
It’s my understanding that the HCG is to prevent HPTA shutdown and keep all of the hormone pathways open, and it does so by acting like LH in the body.
I know that the rise in T-levels from letrozole and anastrozole is mediated through an increase in LH levels caused by those compounds, which also significantly raises T levels.
Most HRT doses of an AI are way to small to induce the kind of LH increase necessary to prevent shutdown, but wouldn’t a dose of 25mg day of aromasin be enough to prevent shutdown, making the use of hcg unnecessary?
Just testing my understanding of the subject… any ideas appreciated. Thanks![/quote]
Ya, that was me.
On HRT, HCG prevents/reverses testicular shrinkage, and increases adrenal function through the conversion of cholesterol to pregnenolone via the P450 SCC liver enzyme.
HCG increases endogenous testosterone production resulting in a larger overall total testosterone level.
HCG also increases well-being through a differant mechanism than increased testosterone. It may be from increased adrenal function, or it’s LH agonist properties, or some other unknown function.
Aromasin works similarly to Arimidex and Letrozole, by decreasing estradiol levels which then increase LH.
When on TRT taking an AI or SERM will not prevent shutdown due to supraphysiological levels of T. If you go off TRT an AI or SERM will increase T due to T levels being low at this time.
Both testosterone and estrogen increase the feedback loop that lowers endogenous production of T.
The reason I chose Aromasin wasn’t for any special reason. It seemed to have a more favourable side effect profile (lipids, cholesterol, libido), but it ended up not being strong enough, therefore I am going to switch to Arimidex to see if it will do a better job lowering my E2 levels.