HCG worth it?

But also practically, you do need higher doses of AI to reduce intratesticular E2 concentrations. It is more difficult to suppress them, this is partly a function of how inhibiting enzymes works (need higher doses to get lower levels lower; and intra-testicular aromatase at endogenous/natural T levels accounts for only ~20% of circulating E2 meaning that supraphysiological T reduces that relative contribution even more so) but also because that intra-testicular aromatase has a rapid action.
Would small amount of Anastrozole be recommended to reduce higher E2 concentrations rather than AI?
 
Research whats means AI and you will find your answer
Thx for the response but I already know that an AI is an aromatase inhibitor. Maybe I should have rephrased my question better? (Background: I use anastrozole. I use hcg. I haven't used any AI's while using HCG as part of my TRT protocol.) What I am surmising based on the specific verbiage in Type-IIx's response stating "reduction of intratesticular E2 concentrations" is that an AI, shows a greater affinity for binding at the E2 Receptors inside the Testicles, thus making HCG more effective on the Leydig cells than simply lowering estrogen in the body overall?

Perhaps a better question is: Why not keep estrogen levels in check via anastrozole in the first place rather than using an AI? -or- Does using an AI in conjuction provide added leydig cell support while on HCG, even with normal range Estradiol while on T & HCG?
 
Perhaps a better question is: Why not keep estrogen levels in check via anastrozole in the first place rather than using an AI? -or- Does using an AI in conjuction provide added leydig cell support while on HCG, even with normal range Estradiol while on T & HCG?

He probably said that because anastrozole IS an AI too.
 
Thx for the response but I already know that an AI is an aromatase inhibitor. Maybe I should have rephrased my question better? (Background: I use anastrozole. I use hcg. I haven't used any AI's while using HCG as part of my TRT protocol.) What I am surmising based on the specific verbiage in Type-IIx's response stating "reduction of intratesticular E2 concentrations" is that an AI, shows a greater affinity for binding at the E2 Receptors inside the Testicles, thus making HCG more effective on the Leydig cells than simply lowering estrogen in the body overall?

Perhaps a better question is: Why not keep estrogen levels in check via anastrozole in the first place rather than using an AI? -or- Does using an AI in conjuction provide added leydig cell support while on HCG, even with normal range Estradiol while on T & HCG?
First of all an ai doesn’t target e2 receptors. It inactivates enzymes by entering their active which is completely different than a receptor. Ai are not signaling hormones.

Arimidex is an ai. I think you are confusing serms with ai. There is no mechanism known that an ai can support leydig cells. They are not signalling hormones
 
He probably said that because anastrozole IS an AI too.
First of all an ai doesn’t target e2 receptors. It inactivates enzymes by entering their active which is completely different than a receptor. Ai are not signaling hormones.

Arimidex is an ai. I think you are confusing serms with ai. There is no mechanism known that an ai can support leydig cells. They are not signalling hormones

Thx Guys; You are absolutley correct. I appreciate you both taking the time to respond. My reference terminology (due to brain rust) is incorrect but my point (question) is valid between SERM and AI. My apologies for the confusion. I meant to say that Clomid would target receptor sites specific to the Testes/Leydig cells and if so, provide added benefit, vs using Adex alone (Is this correct?) So, has there been added benefit in using a SERM like Clomid and HCG simultaneously while on TRT - due to the specific action of ""reduction of intratesticular E2 concentrations?"

Basically, does the SERM potentiate the effects of HCG within the leydig cells due to the "reduction of intratesticular E2 concentrations?" - I've looked for scientific articles specifically mentioning this, but didn't find any via query in the Science Direct database.
 
Thx Guys; You are absolutley correct. I appreciate you both taking the time to respond. My reference terminology (due to brain rust) is incorrect but my point (question) is valid between SERM and AI. My apologies for the confusion. I meant to say that Clomid would target receptor sites specific to the Testes/Leydig cells and if so, provide added benefit, vs using Adex alone (Is this correct?) So, has there been added benefit in using a SERM like Clomid and HCG simultaneously while on TRT - due to the specific action of ""reduction of intratesticular E2 concentrations?"

Basically, does the SERM potentiate the effects of HCG within the leydig cells due to the "reduction of intratesticular E2 concentrations?" - I've looked for scientific articles specifically mentioning this, but didn't find any via query in the Science Direct database.
Clomid does not target leydig cells! That what HCG is doing. Clomid is designed to target e2 receptors in breast tissue and in the brain. It stimulates LH and FSH output which then target cells in the testes.
I would argue that while on trt and hcg, there is no point in running clomid because you are already suppressing LH and FSH.
And again, clomid, as a serm, does nothing with the amount of circulating e2. It only blocks it at certain e2 receptors.
 
Clomid does not target leydig cells! That what HCG is doing. Clomid is designed to target e2 receptors in breast tissue and in the brain. It stimulates LH and FSH output which then target cells in the testes.
I would argue that while on trt and hcg, there is no point in running clomid because you are already suppressing LH and FSH.
And again, clomid, as a serm, does nothing with the amount of circulating e2. It only blocks it at certain e2 receptors.
 
As it seems that high E2 can have a negative impact on T levels as the body can think to much T is being produced. And lower T production. So leydig call activity can be decreased that way. So indirectly AI could have a positive impact on leydig activity and T production.
 
Thank you. You confirmed everything I already knew. I was fixated on this term "intratesticular" thinking there was some newly discovered mechanism that I was unaware of with E2 inside the testes and some new relationship with different ancillaries. I appreciate the clarification.
 
by 'blocking' receptors this means estrogen cant work, so effectively lowering estrogen effects and for all intents "lowers" estrogen impact on all tissues... @mochul remember if took just clomid, your T would go up, and with elevated T so would estrogen, HOWEVER impact of estrogen is less as cannot work ie estrogens effects less potent.
 
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