Latest posts

Forum Statistics

Threads
24,540
Posts
482,148
Members
27,480
Latest Member
Beth Anney
What's New?

Using Aromasin during PCT

dr jim

dr jim

MuscleHead
Apr 7, 2014
785
168
#13
Have you read the study? The men were healthy and normogonadal and had testosterone induced hypogonadism (for the purpose of evaluating the effect of hCG on testosterone production),exactly as is the case with juicers. hCG injection at 250 IU EOD seemed to approach physiological levels of testosterone production based on intratesticular testosterone measurements.
The purpose of the study was to determine the EFFECT OF HCG on SPERMATOGENESIS while the GONADOTROPINS LH and FSH were being SUPPRESSED WITH EXOGENOUS TT!

Yes I'm familiar w the study but are you comparing INTRATESTICULAR TT levels with that of SERUM? I hope not because that particular study reinforces what Iv'e been saying, that HCG increases INTRTATESTICULAR TT needed for spermatogenesis. So what else is new. It's amazing the study was even published IMO

The reason AI don't effect GONADAL TT production secondary to HCG use? They do NOT cross the blood/gonadal barrier in either males or females, and is A PRIMARY REASON AI's are not "as efficacious" in females with BREAST CA whom have not reached menopause.

AI's also do not effect ADRENAL E-2 production. Their PRIMARY benefit is the reduction in PERIPHERAL AROMATIZATION of TT into E-2, a process which is responsible for roughly 80% of MALE E-2 production yet only 30% in MENSTRUATING females.

I will try to post the entire study.

Regards
Jim
 
Last edited:
dr jim

dr jim

MuscleHead
Apr 7, 2014
785
168
#14
The purpose of the study was to determine the EFFECT OF HCG on SPERMATOGENESIS while the GONADOTROPINS LH and FSH were being SUPPRESSED WITH EXOGENOUS TT!

Yes I'm familiar w the study but are you comparing INTRATESTICULAR TT levels with that of SERUM? I hope not because that particular study reinforces what Iv'e been saying, that HCG increases INTRTATESTICULAR TT needed for spermatogenesis. So what else is new. It's amazing the study was even published IMO

The reason AI don't effect GONADAL TT production secondary to HCG use? They do NOT cross the blood/gonadal barrier in either males or females, and is A PRIMARY REASON AI's are not "as efficacious" in females with BREAST CA whom have not reached menopause.

AI's also do not effect ADRENAL E-2 production. Their PRIMARY benefit is the reduction in PERIPHERAL AROMATIZATION of TT into E-2, a process which is responsible for roughly 80% of MALE E-2 production yet only 30% in MENSTRUATING females.

I will try to post the entire study.

Regards
Jim
i can't cite the complete study until my "posting quota" of 2.7 kb is increased. Hopefully admin will get that done today,
jim
 
dr jim

dr jim

MuscleHead
Apr 7, 2014
785
168
#15
i can't cite the complete study until my "posting quota" of 2.7 kb is increased. Hopefully admin will get that done today,
jim
Hey GS this is a study abstract where hypogonadism was induced using Te at 250 mg per week. And of course SPERMATOGENESIS ceased shortly thereafter.

However while receiving T-e at a dose of 250mg/wk study subjects were further "challenged" with FIVE THOUSAND IU OF HCG THREE TIMES A WEEK and the TT level INCREASED FROM 1200ng/dl to ONLY 1800 ng/dl, which was NOT statistically significant and is at the upper physiologic limit.

Obviously although the quantity of HCG used in this study was at least 20 TIMES what many have suggested as a "gonadal maintenance dose". the change in TT which occurred, did NOT result in a significant elevation of TT!

We all have observed the difference HCG can make in the post cycle BB, but it's capabilities are limited to a physiologic norm. Whether the failure of HCG (5000 IU 3 x PER WK) to raise TT during a cycle, is the consequence of "negative feedback", fixed ligand binding or equilibrium based is purely speculative, but it's use is best reserved for the POST-CYCLE phase of AAS.


View attachment Stimulation of sperm production by human ch... [J Androl. 1985 May-Jun] - PubMed - NCBI.pdf
 
dr jim

dr jim

MuscleHead
Apr 7, 2014
785
168
#16
I'll post the complete studies of both citations once my limit is raised
jim
 
dr jim

dr jim

MuscleHead
Apr 7, 2014
785
168
#17
Hey GS this is a study abstract where hypogonadism was induced using Te at 250 mg per week. And of course SPERMATOGENESIS ceased shortly thereafter.

However while receiving T-e at a dose of 250mg/wk study subjects were further "challenged" with FIVE THOUSAND IU OF HCG THREE TIMES A WEEK and the TT level INCREASED FROM 1200ng/dl to ONLY 1800 ng/dl, which was NOT statistically significant and is at the upper physiologic limit.

Obviously although the quantity of HCG used in this study was at least 20 TIMES what many have suggested as a "gonadal maintenance dose". the change in TT which occurred, did NOT result in a significant elevation of TT!

We all have observed the difference HCG can make in the post cycle BB, but it's capabilities are limited to a physiologic norm. Whether the failure of HCG (5000 IU 3 x PER WK) to raise TT during a cycle, is the consequence of "negative feedback", fixed ligand binding or equilibrium based is purely speculative, but it's use is best reserved for the POST-CYCLE phase of AAS.


View attachment 5964

Here's the complete ABSTRACT I hope!
 

Attachments

GetXXL

GetXXL

Member
Oct 3, 2012
27
1
#18
The purpose of the study was to determine the EFFECT OF HCG on SPERMATOGENESIS while the GONADOTROPINS LH and FSH were being SUPPRESSED WITH EXOGENOUS TT!

Yes I'm familiar w the study but are you comparing INTRATESTICULAR TT levels with that of SERUM? I hope not because that particular study reinforces what Iv'e been saying, that HCG increases INTRTATESTICULAR TT needed for spermatogenesis. So what else is new. It's amazing the study was even published IMO

The reason AI don't effect GONADAL TT production secondary to HCG use? They do NOT cross the blood/gonadal barrier in either males or females, and is A PRIMARY REASON AI's are not "as efficacious" in females with BREAST CA whom have not reached menopause.

AI's also do not effect ADRENAL E-2 production. Their PRIMARY benefit is the reduction in PERIPHERAL AROMATIZATION of TT into E-2, a process which is responsible for roughly 80% of MALE E-2 production yet only 30% in MENSTRUATING females.

I will try to post the entire study.

Regards
Jim
AIs, such as exemestane, diffuse past plasma membranes due to their polarity and size as far as I know. I do have my doubts about the non-steroidal ones tho.

And I'm not comparing ITT to serum testosterone, I really don't care about its effect on serum testosterone. Adequate [ITT] not only maintains spermatogenesis, it also maintains the size of the testes and subsequently its responsiveness to LH (and hCG as they share the same receptor).
 
dr jim

dr jim

MuscleHead
Apr 7, 2014
785
168
#19
AIs, such as exemestane, diffuse past plasma membranes due to their polarity and size as far as I know. I do have my doubts about the non-steroidal ones tho.

And I'm not comparing ITT to serum testosterone, I really don't care about its effect on serum testosterone. Adequate [ITT] not only maintains spermatogenesis, it also maintains the size of the testes and subsequently its responsiveness to LH (and hCG as they share the same receptor).


Sorry it took so long for my reply but, better late than never:)

That's a huge leap for several reasons
1) Intra-testicular TT levels are 100 fold higher than serum in NORMAL MALES
2) It's been well established the best means off assaying LH function is the measurement of serum TT levels
3) Based on infertility studies, the serum TT level needed for adequate spermatogenesis is around 200ng/dl AND an ITT of only about 1000ng/dl
4) Because the Seritoli/Leydig cell concentration approximates ONE HUNDRED to ONE, testicular size bears a strong association to spermatogenesis, yet it's correlation with (LH mediated) TT production is VERY POOR

Consequently the an HCG mediated rise of intra-testicular testosterone while useful for INFERTILITY purposes (which is why this study AND many others like it were conducted) is a POOR PREDICTOR of functional LH recovery, as a consequence of AAS use. The primary reason is relatively straight forward, the amount of gonadotropin (HCG or LH) necessary to support the LOCAL physiologic demands (spermatogenesis) of a organ weighing only a few OUNCES, pales in comparison to that which is required for the SYSTEMIC androgenic/anabolic needs of a 70 KG male.

In summary whether intra-cycle HCG is of benefit depends upon first the TESTOSTERONE LEVEL itself, because the higher the TT level the more HCG will be required. For this reason UNLESS your financial resources are endless, the benefit of HCG is best realized POST-CYCLE

Finally as I mentioned earlier, the precise mechanism which renders AI's ineffective in reducing either GONADAL or OVARIAN E-2 synthesis is UNKNOWN. However their efficacy is known to be the result of reduced PERIPHERAL aromatization of TT.

JIM
 
Last edited:
GetXXL

GetXXL

Member
Oct 3, 2012
27
1
#20
1) Intra-testicular TT levels are 100 fold higher than serum in NORMAL MALES
Yes, and 250 IU hCG EOD is proven to maintain that level. I'm in the dark how this is an argument for making it a huge leap?

2) It's been well established the best means off assaying LH function is the measurement of serum TT levels
INSL3 is a better predictor, and why would serum TT be a better measurement? It highly influenced by serum binding protein concentrations and consequently metabolism of the AAS. Serum TT levels can be normal with extremely high levels of SHBG, prolonging half-life of T, which thus in some cases might mask primary hypogonadism.

Based on infertility studies, the serum TT level needed for adequate spermatogenesis is around 200ng/dl AND an ITT of only about 1000ng/dl
Yes, the treshold for spermatogenesis is relatively low. I'm missing the point though?

Because the Seritoli/Leydig cell concentration approximates ONE HUNDRED to ONE, testicular size bears a strong association to spermatogenesis, yet it's correlation with (LH mediated) TT production is VERY POOR
Is it? Oligospermia without hypogonadism can have perfectly normal testes volume. Besides that, I'm only guessing its the ITT which maintains the size of the testes (regardless of spermatogenesis) based on some in vitro material (atleast for me ITT was the most likely candidate downstream of LHR activation, feel free to suggest others). The reason I'm writing this is to explain what I'm observing: people who recover within a few weeks, regardless of how long they have been anabolic steroids. I didn't came up with it for the sole purpose of coming up with something new. Bodybuilders I've worked with who used anabolic steroids for prolonged periods of time in conjunction with hCG simply don't have any problems with recovering from hypogonadism

In summary whether intra-cycle HCG is of benefit depends upon first the TESTOSTERONE LEVEL itself, because the higher the TT level the more HCG will be required. For this reason UNLESS your financial resources are endless, the benefit of HCG is best realized POST-CYCLE
Why would your balls care about the amount of testosterone in circulation? 0 LH & FSH is all they care about. Regardless whether it is due to 1 gram of testosterone or 10 grams of testosterone every week.
 
dr jim

dr jim

MuscleHead
Apr 7, 2014
785
168
#21
Yes, and 250 IU hCG EOD is proven to maintain that level. I'm in the dark how this is an argument for making it a huge leap?


INSL3 is a better predictor, and why would serum TT be a better measurement? It highly influenced by serum binding protein concentrations and consequently metabolism of the AAS. Serum TT levels can be normal with extremely high levels of SHBG, prolonging half-life of T, which thus in some cases might mask primary hypogonadism.


Yes, the treshold for spermatogenesis is relatively low. I'm missing the point though?


Is it? Oligospermia without hypogonadism can have perfectly normal testes volume. Besides that, I'm only guessing its the ITT which maintains the size of the testes (regardless of spermatogenesis) based on some in vitro material (atleast for me ITT was the most likely candidate downstream of LHR activation, feel free to suggest others). The reason I'm writing this is to explain what I'm observing: people who recover within a few weeks, regardless of how long they have been anabolic steroids. I didn't came up with it for the sole purpose of coming up with something new. Bodybuilders I've worked with who used anabolic steroids for prolonged periods of time in conjunction with hCG simply don't have any problems with recovering from hypogonadism

Why would your balls care about the amount of testosterone in circulation? 0 LH & FSH is all they care about. Regardless whether it is due to 1 gram of testosterone or 10 grams of testosterone every week.
---------------------------------------------------------------------------------------------------------
Hey if you want to believe ITT is a more accurate means to assay LH recovery from HCG when the concentration required is 100 fold less than serum so be it. However there is no EVIDENCE to support this opinion because the primary utility of ITT is it's effect on spermatogenesis, which is WHY it's used in fertility trials LIKE YOURS.

Why is serum TT a better predictor. Because the SERUM LEVEL is what systemic cells are exposed to (or close to it) and in spite of the factors you mentioned such as albumin and SHBG.

The ITT level required to maintain spermatogenesis is indeed very low, which is ANOTHER reason ITT levels do not correlate with serum. This is particularly relevant because MANY AAS users use gonadal size as a measure of LH recovery. However an increase in testicular size bears little to no correlation to SYSTEMIC TT levels, LH recovery or the benefits of HCG exclusive of spermatogenesis.

Oligospermia with normal testicular size, oh I know that would be rare. Why else is gonadal palpation and sonography used in the initial evaluation of infertility.

Gonadotropins are REQUIRED for spermatogenesis and absence their stimulation TESTICULAR ATROPHY follows. There are a few rare exceptions such as; disease onset, genetic or metabolic defects, BUT those are rare EXCEPTIONS and certainly not the norm in AAS users.

Well "your balls better care" about the amount of TT within the systemic circulation because the TT level influences
(in addition to E-2) HTPA LH secretion.

Regarding the HTPA recovery of BB many have difficulties with recovery. The reasons are legion and range from mis-information, cycle selection, duration and potency. Most whom do have problems and there are SEVERAL ON TID, cycled for prolonged periods and "cruised" in between their "high end cycles".

Now for those who choose the correct methods and enable an adequate HTPA recovery interval most will do just fine.

The same can be said for "Pro" BB (those whom are fully sponsored and view BB as a career and or full time occupation) nope those guys have literally everything at their disposal and recover fine, providing they are not cruisers also.

Thx for corresponding GS
JIM
 
Last edited:
Top