HCG Efficacy: Should We Measure 17-OH-progesterone to Titrate HCG Dose?

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Nelson Vergel

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Fertil Steril. 2008 Feb; 89(2): 380–386.


Serum 17-hydroxyprogesterone strongly correlates with intratesticular testosterone in gonadotropin-suppressed normal men receiving various dosages of human chorionic gonadotropin


Setting:

Healthy volunteers in an academic research environment.

Patients:

Twenty-nine normal men.

Intervention:

We determined ITT concentration by testicular aspiration before and after treatment in men receiving exogenous testosterone to block endogenous gonadotropin production and randomly assigned to one of four doses of human chorionic gonadotropin (hCG) (0, 125 IU, 250 IU, 500 IU every other day) for 3 weeks.

Outcome measures:

The association between serum 17-hydroxyprogesterone, androstenedione and dihydroepiandrosterone (DHEA) and ITT.

Results:

With testosterone administration alone, serum 17-hydroxyprogesterone decreased significantly and increased significantly when 500 IU hCG was administered. End-of-treatment ITT strongly correlated with serum 17-hydroxyprogesterone. Moreover, serum 17-hydroxyprogesterone, but not androstenedione or DHEA, was independently associated with end-of-treatment ITT by multivariate linear regression.

Conclusion:

Serum 17-hydroxyprogesterone is highly correlated with ITT in gonadotropin suppressed normal men receiving testosterone and stimulated with hCG. Serum 17-hydroxyprogesterone is a surrogate biomarker of ITT and may be useful in research and in men receiving gonadotropin therapy for infertility.

Keywords: intratesticular testosterone, 17-hydroxyprogesterone, male infertility, male contraception

Full Paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674872/
 
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Defy Medical TRT clinic doctor
Is there a laymans explanation, I'm not exactly catching the meaning.

Like I explained in this video, HCG increases upstream hormones shut down by TRT.

https://www.excelmale.com/content.p...t-for-Men-on-Testosterone-Replacement-Therapy

17-OH-progesterone is one of those upstream hormones. Higher levels have been linked to improved efficacy of HCG on testicular function. The old studies used to aspirate testicular tissue to determine intratesticular T as a way to measure HCG efficacy. Of course, that is risky and uncomfortable. Testing for 17-OH-progesterone blood levels may be as effective and easier in determining HCG's efficacy. The study also enforces my view that HCG doses of 350-500 IU are needed for proper testicular function. I do not believe in daily low dose HCG as recommended by Dr Crisler and others.
 
After watching Nelson's shoulders injecting video, where he uses 500iu of HCG. I also decided to use that amount. I believe it helps keeps my libido strong.��
 
So does this drive to the place where some of us guys state that we get no feeling from use of HCG, obvious the testes are being prevented from dormancy but there's no other "feeling", like well-being, or libido, like Vince says. Ive tried all manner of HCG dosing and frequency but never so much as 500iu E3.5D. I've done 400 iu EOD as the high ceiling and then 100iu daily and everything in between. Ive sometimes been concerned about E conversion in the testes at higher doses, reason I've cut to 200iu E3.5D. But through a process of elimination (or reduction) with HCG, removing DHEA/Pregnenolone supplementation, and then the Test cream I was using for DHT purposes, my E has stayed high. For no known reason, very high, 88 at last test.
 
I may be wrong about this. I believe a man's estrogen problem is belly fat and low DHT. I don't think HCG will raise E2 much.
 
Hcg doesn't raise everyone's e2, mine included. I am now using a higher does per the doc to see if I get better volume and libidio.
 
I've tried everything under 500. Been off hcg for about 2 months. Getting bloodwork next week and then I'll try 500 iu twice a week.
 
17-OH-progesterone is one of those upstream hormones. Higher levels have been linked to improved efficacy of HCG on testicular function... Testing for 17-OH-progesterone blood levels may be as effective and easier in determining HCG's efficacy.
So, the StAR expression is stimulated by LH (hCG mimics), which starts the p450scc enzyme to produce Pregnenolone from cholesterol. Then Pregnenolone converts to Progesterone (3B-HSD via StAR) or to 17OH-Pregnenolone (17,20 lyase via StAR). These two can convert to 17OH-Progesterone (by same enzyme conversions) - which you are now going to start measuring.
Does anyone know the rates of these enzyme conversions? Is one weaker or stronger than the other?
Would supplementing with a small amount of Pregnenolone while on TRT + hCG enhance the conversion process? My thinking here is: if less hCG is needed for the P450scc to convert to Pregnenolone, there would be more hCG available for the other downstream conversions?
 
Beyond Testosterone Book by Nelson Vergel
My thinking here is: if less hCG is needed for the P450scc to convert to Pregnenolone, there would be more hCG available for the other downstream conversions?

Not sure that it works that way. My take is that if your HCG protocol is adequate, then no "backfilling" of some of these upstream hormones (pregnenolone, DHEA) would even be necessary. But it's not clear to me why one would choose 17-OH-progesterone over other upstream hormones like pregnenolone or progesterone to titrate HCG. Supplementing pregnenolone would of course muddy the picture.
 
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