High Dose HCG, Low Dose Testosterone

[DixieWrecked]

For you secondary guys, has anyone tried this approach? I am theorizing that adding HCG once someone has their Testosterone dosage dialed in results in being overmedicated. Could this be the reason why we see elevated E2 once adding in HCG.

Does anyone do 1000-2000iu of HCG along with a test dosage of 80mg or lower weekly?

 

[Vince Carter]

Plausible idea but so few are secondary

 

[Cataceous]

On the contrary, most cases of hypogonadism seem to be secondary. I can count on two hands the number of primary cases I've read about, but there are hundreds of clearly secondary cases, with low-to-medium LH and low testosterone.

Higher doses of hCG are less likely to be a viable long-term treatment because of the aromatization problem. By the time you take enough hCG to get decent endogenous testosterone production you're stimulating excessive amounts of intratesticular estradiol creation, which is resistant to aromatase inhibitors.
Acute stimulation of aromatization in Leydig cells by human chorionic gonadotropin in vitro.

 

[captain]

You see guys saying they have elevated E2 without labs. Then you see them saying they crashed their E2 without labs. You can't really tell much when every problem a guy has is E2 related. I am using HCG 1050iu a week with E2 always in a range of 15-25. I don't use AI and never needed to.

 

[Cataceous]

You see guys saying they have elevated E2 without labs. Then you see them saying they crashed their E2 without labs. You can't really tell much when every problem a guy has is E2 related. I am using HCG 1050iu a week with E2 always in a range of 15-25. I don't use AI and never needed to.

My results show a strong aromatization effect from hCG. Here are the labs, no AIs, same EOD protocol, very constant hormones:

Without hCG:
Total testosterone per week—67 mg
Estradiol: 57 pg/mL

With 1,050 IU hCG per week:
Total testosterone per week—43 mg
Estradiol: 57 pg/mL

That's right, for me 1,050 IU per week of hCG creates as much additional estradiol as a 56% increase in the dose of testosterone.

Edit: For me the hCG dose generates negligible endogenous testosterone. Total testosterone for the above results are 1,240 ng/dL and 750, respectively.

 

[Vince Carter]

The without labs is the problem it's really only a very experienced guy that can even start to operate on symptoms alone as the high/low do mirror each other and there's only a few that are clear and distinct. Like low E and painful joints...that's solely on low E.

 

[DixieWrecked]

My results show a strong aromatization effect from hCG. Here are the labs, no AIs, same EOD protocol, very constant hormones:

Without hCG:
Total testosterone per week—67 mg
Estradiol: 57 pg/mL

With 1,050 IU hCG per week:
Total testosterone per week—43 mg
Estradiol: 57 pg/mL

That's right, for me 1,050 IU per week of hCG creates as much additional estradiol as a 56% increase in the dose of testosterone.

Edit: For me the hCG dose generates negligible endogenous testosterone. Total testosterone for the above results are 1,240 ng/dL and 750, respectively.

What were your testosterone levels on each of those tests? Not looking to debate usefulness of T/E ratio but still curious of the objective effects of the two different protocols.

 

[DixieWrecked]

On the contrary, most case of hypogonadism seem to be secondary. I can count on two hands the number of primary cases I've read about, but there are hundreds of clearly secondary cases, with low-to-medium LH and low testosterone.

Higher doses of hCG are less likely to be a viable long-term treatment because of the aromatization problem. By the time you take enough hCG to get decent endogenous testosterone production you're stimulating excessive amounts of intratesticular estradiol creation, which is resistant to aromatase inhibitors.
Acute stimulation of aromatization in Leydig cells by human chorionic gonadotropin in vitro.

I wonder why hCG stimulates E production more than endogenous LH and FSH.

 

[Cataceous]

What were your testosterone levels on each of those tests? Not looking to debate usefulness of T/E ratio but still curious of the objective effects of the two different protocols.

I'd added the numbers to the post (1240 and 750), close to the ratio of the testosterone doses and supporting the conclusion that hCG at his level is stimulating minimal endogenous testosterone creation.

I wonder why hCG stimulates E production more than endogenous LH and FSH.

Another question I've pondered. In part it's because the half-life of hCG at ~36+ hours is much longer than that of LH, ~40 minutes. In addition, LH is delivered in short pulses, meaning you get these short peaks, whereas hCG stays up for a long time. See what LH looks like:

 

[captain]

The daily low dose HCG that may not stimulate for 24hrs is probably the idea of using it that way. It gives some time for things to clear. The 500iu dose goes for 3 days. The best dose that was in the study on here would depend on what you wanted to happen.

 

[xqfq]

Another possibility RE: E2, which I’ve maybe commented on here, is that HCG produces DHEA, which can turn into Androstenediol. This isn’t “E2” so it won’t show up on a blood test, but may create E2-like symptoms:

“Androstenediol possesses potent estrogenicactivity, similarly to DHEA and 3β-androstanediol.[SUP][2][/SUP]It has approximately 6% and 17% of the affinity of estradiol at the ERα and ERβ, respectively.[SUP][3][/SUP]Although androstenediol has far lower affinity for the ERs compared to the major estrogen estradiol, it circulates at approximately 100-fold higher concentrations, and so is thought may play a significant role as an estrogen in the body.[SUP][4]”[/SUP]

This is just a random guess though. No evidence as far as I can tell in terms of labs, data, etc. But if someone wants to dig in more it might be a good starting place.

For me, higher dose HCG hasn’t worked great because HCG is so..tricky. It varies so much in potency between vials and the phase of the mood that I never felt consistent when I was getting a lot of testosterone production from HCG.

It’s also almost impossible to travel with which is a big deal for me. Doesn’t matter much if you’re not getting a lot of your hormones from HCG, but if you are then it might suck.

 

[Cataceous]

Another possibility RE: E2, which I’ve maybe commented on here, is that HCG produces DHEA, which can turn into Androstenediol. This isn’t “E2” so it won’t show up on a blood test, but may create E2-like symptoms:
...

Maybe we should be monitoring androstenediol too?

Possibly of lesser concern with increased DHEA is the path to estrone, E1. Certainly DHEA supplementation can make E1 almost arbitrarily high, which could start to make a difference even if E1 has a tenth the potency of E2.

That said, at least for me, hCG at low doses does not seem to affect DHEA-S levels significantly.