Hyperresponder and/or overdid hCG

[Jin23]

A "known forum anecdote," how authoritative, heh.

Haha yes indeed, but!, I did not use that reference in order to validate any claims I was making. Take a bit more time to read posts : )

I've found you to sometimes be in the dark about forum anecdotes, so this is the reason for me describing the above mentioned discourse. Especially now as your answers on the matter were vague and undefined ... Anyway, ... I gather you don't believe in the fact that hcg elevates e2 more then an equal dose of exogenous testosterone would? And if that is so, how do you explain the low elevation of TT compared to the high elevation of e2, that you get from hcg? Genuinely interested, I have no afferent predisposition to any claims on the matter. The forum anecdotes are just that; anecdotes, again, not using them to validate anything.

 

[Type-IIx]

Haha yes indeed, but!, I did not use that reference in order to validate any claims I was making. Take a bit more time to read posts : )

I've found you to sometimes be in the dark about forum anecdotes, so this is the reason for me describing the above mentioned discourse. Especially now as your answers on the matter were vague and undefined ... Anyway, ...

I try to do my best to filter out the anecdotes as potentially relevant that have at least face validity (measurements at a glance are of what they are supposed to measure) and reliability (repeatability), (but I am not perfect at this, of course). But if a claim/anecdote is not simultaneously valid on its face and repeated under the same conditions yielding the same result (stated another way, if a claim/anecdote doesn't actually measure what it's supposed to or is not repeated under the same conditions yielding the same result), it's not worth any attention.

If the anecdote is valid and repeatable, then it's a hypothesis worth investigating (so long as it's at least minimally intriguing). It (the claim/anecdote) can then be used as a hypotheses (by stating as the null hypothesis), that, if something of any clinical relevance, is likely to be addressed by authoritative sources, and in the literature.

This is my basic process. I don't just say, "hey, this gentleman truly believes this, and he's confident, so it's likely valid and reliable." I instead think, "humans are inherently poor at disentangling cause from effect and make mistakes of attribution as a matter of course;" and, often mutter, "God, these private bloodwork resources have caused so much more harm than good, because well-meaning folks pore over them, making these mistakes of cause/effect/attribution and they promote illusory feelings of control (or its counterpart, loss of control). I sure wish that people would only rely on professional interpretations of bloodwork to treat actual symptoms instead of playing whack-a-mole with arbitrary bloodwork values, striving to find their inner peace."

I gather you don't believe in the fact that hcg elevates e2 more then an equal dose of exogenous testosterone would?

Is this what you mean, mg per mg? As in, you gather I do not believe that 3500 IU hCG elevates E2 > 350 mg of exogenous testosterone?

I've never even considered a per-mg comparison. But in this example, I do not believe that a single bolus of 3500 IU hCG yields a greater AUC of E2 than a single bolus of 350 mg testosterone suspension, no.

I believe that there is an upper limit to testis aromatase activity (accounting for its minimal 15-20% of total circulating E2 versus the remainder in extratesticular tissues; where Test stimulates both).

And if that is so, how do you explain the low elevation of TT compared to the high elevation of e2, that you get from hcg? Genuinely interested, I have no afferent predisposition to any claims on the matter. The forum anecdotes are just that; anecdotes, again, not using them to validate anything.

Because there is rapid acute testis aromatase activity (T=(Aromatase)=>E2) stimulated in the Leydig cells by hCG.

I don't see this as inconsistent with anything you've said, aside from the claimed (nonauthoritative) evidence that AIs cannot help reduce E2 stimulated by hCG.

Certainly, completely abolishing the ~15-20% of circulating E2 that is derived from testis aromatase activity is not something AIs are great at. Yet, it does not follow that AIs cannot reduce actual elevations in E2 induced by hCG.

 

[Jin23]

Is this what you mean, mg per mg? As in, you gather I do not believe that 3500 IU hCG elevates E2 > 350 mg of exogenous testosterone?

Oh no no, god no. I meant the resulting change in serum total testosterone and comparing that to the same serum testosterone change from exogenous T. For instance; if 250 IU's eod gives a resulting 200 ngdl raise in serum TT and a +20 pgdl raise in serum E2, how would that compare to a theoretical 20 mg's of test (presuming one would see a Cmax of the same 200 ngdl) and it's resulting aromatase activity. Hcg seem to raise serum E2 much higher then exogenous testosterone, when equating for serum TT change. I apologies, but I'm half a sleep and can't word this better atm my head just isn't working.

Just to be on the safe side:
Assuming one has TT at 1000 ngdl and E2 at 30 pgdl. This person now injects an additional 20 mg's of test e, which results in TT of 1200 ngdl and E2 of 35 pgdl.
Now, the same person injects 250 iu's of hcg, his TT goes to 1200 ngdl, but his E2 goes up to 45.

Certainly, completely abolishing the ~15-20% of circulating E2 that is derived from testis aromatase activity is not something AIs are great at. Yet, it does not follow that AIs cannot reduce actual elevations in E2 induced by hCG.

Yeah, this exactly. I didn't say, or think, that you can't do anything about the E2 from hcg, rather, that it's hard to control. It seems like it though, that it's more then 15 to 20%. Much more then that in fact. At least from my personal experience. And the anecdotal reports claiming E2 is hard to control, would seem to indicate the same. I understand your thought process, but this is an internet drug abusing forum, full of juiced up monkeys, trying to spell out supraphysiological ....so ... getting used to the word anecdote would give you much needed peace haha.

 

[Type-IIx]

Oh no no, god no. I meant the resulting change in serum total testosterone and comparing that to the same serum testosterone change from exogenous T. For instance; if 250 IU's eod gives a resulting 200 ngdl raise in serum TT and a +20 pgdl raise in serum E2, how would that compare to a theoretical 20 mg's of test (presuming one would see a Cmax of the same 200 ngdl) and it's resulting aromatase activity. Hcg seem to raise serum E2 much higher then exogenous testosterone, when equating for serum TT change. I apologies, but I'm half a sleep and can't word this better atm my head just isn't working.

Just to be on the safe side:
Assuming one has TT at 1000 ngdl and E2 at 30 pgdl. This person now injects an additional 20 mg's of test e, which results in TT of 1200 ngdl and E2 of 35 pgdl.
Now, the same person injects 250 iu's of hcg, his TT goes to 1200 ngdl, but his E2 goes up to 45.

Do you see the problem with this entire set of assumptions and arbitrary values?

Speculating about these (you must admit that they are arbitrary?) values, dynamics, etc. are neither valid (measuring what they are purported to) nor reliable (repeatable).

This entire thought exercise is irrelevant man.

Comparing per-mg test suspension to hCG at doses that are used in practice (say 750 IU vs. 75 mg test suspension), in a model relevant to supraphysiological AAS use and maintaining or restimulating fertility/HPG axis functioning at least permits valid and repeatable results that we could test and retest, without this seemingly schizophrenic "add 20 mgs of test E resulting in TT of 1200 ng/dL and E2 of 35 pg/dL..." are these values based on, like, one of your bloodwork results where you think you're able to tease out cause/effect?

Yeah, this exactly. I didn't say, or think, that you can't do anything about the E2 from hcg, rather, that it's hard to control. It seems like it though, that it's more then 15 to 20%. Much more then that in fact.

Evidence?

At least from my personal experience. And the anecdotal reports claiming E2 is hard to control, would seem to indicate the same. I understand your thought process, but this is an internet drug abusing forum, full of juiced up monkeys, trying to spell out supraphysiological ....so ... getting used to the word anecdote would give you much needed peace haha.

I'm fine with anecdotes when they're given their due (very low) weight as evidence.