HCG timing and dosing for shut down recovery....logic behind it all ??

[DLMCBBB]

Administrator,

Is that Scully article published in a peer reviewed journal?

Dustin

 

[Matt Muscle]

Shooting 2500 EOD for 8 shots total, that will be 15 days long.
Clomid 50 mg twice a day 12 apart 100mg total for 30 days.
20 mg nolvadex for 45 days.

I am day 8 right now and feel awesome.

Hackskii, are you taking the clomid and Nolva alongside the hCG or do you start the SERMS when you have nearly finished the hCG therapy?

 

[Zaven]

Shooting 2500 EOD for 8 shots total, that will be 15 days long.
Clomid 50 mg twice a day 12 apart 100mg total for 30 days.
20 mg nolvadex for 45 days.

I am day 8 right now and feel awesome.

I think I'm gonna have to give this pct a try....It sounds good to me

I don't think me running clomid alone is doing enough or anything for that matter...

How long after the last hcg injection do you start running the clomid..?

 

[1cc]

Mike,

Wouldn't HCG shots of 2500iu have a danger of causing leydig desensitization? At what point does this become a concern?

bump for Dr. Mike

 

[DLMCBBB]

Im awaiting for Dr. Mike to respond.

Maybe he can adress some of the questions we posed about his protocl.

Dustin

 

[DLMCBBB]

Good question. Also, are higher dosages for a short period of time safer and/or more effective that lower dosages for an extended period of time? I know this issue has been debated with regard to other protocols as well.

My point exactly bro! And in the grand scheme of things, does it even really matter?

Nobody has commented on this study yet:

J Clin Endocrinol Metab. 2005 May;90(5):2595-602. Epub 2005 Feb 15. Related Articles, Links


Low-dose human chorionic gonadotropin maintains intratesticular testosterone in normal men with testosterone-induced gonadotropin suppression.

Coviello AD, Matsumoto AM, Bremner WJ, Herbst KL, Amory JK, Anawalt BD, Sutton PR, Wright WW, Brown TR, Yan X, Zirkin BR, Jarow JP.

Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA. a-coviello@northwestern.edu

In previous studies of testicular biopsy tissue from healthy men, intratesticular testosterone (ITT) has been shown to be much higher than serum testosterone (T), suggesting that high ITT is needed relative to serum T for normal spermatogenesis in men. However, the quantitative relationship between ITT and spermatogenesis is not known. To begin to address this issue experimentally, we determined the dose-response relationship between human chorionic gonadotropin (hCG) and ITT to ascertain the minimum dose needed to maintain ITT in the normal range. Twenty-nine men with normal reproductive physiology were randomized to receive 200 mg T enanthate weekly in combination with either saline placebo or 125, 250, or 500 IU hCG every other day for 3 wk. ITT was assessed in testicular fluid obtained by percutaneous fine needle aspiration at baseline and at the end of treatment. Baseline serum T (14.1 nmol/liter) was 1.2% of ITT (1174 nmol/liter). LH and FSH were profoundly suppressed to 5% and 3% of baseline, respectively, and ITT was suppressed by 94% (1234 to 72 nmol/liter) in the T enanthate/placebo group. ITT increased linearly with increasing hCG dose (P < 0.001). Posttreatment ITT was 25% less than baseline in the 125 IU hCG group, 7% less than baseline in the 250 IU hCG group, and 26% greater than baseline in the 500 IU hCG group. These results demonstrate that relatively low dose hCG maintains ITT within the normal range in healthy men with gonadotropin suppression. Extensions of this study will allow determination of the ITT concentration threshold required to maintain spermatogenesis in man.

 

[painman]

So is this saying that those of us that maintain testosterone with low dose hcg will have a harder time coming off hcg? Is that correct that when using higher doses 500 i.u. that test increased 26 percent over baseline? If I am reading this correct the study suggests that higher doses leaves the patient with an improved endogenous testosterone post hcg therapy?

Is that right?

ITT increased linearly with increasing hCG dose (P < 0.001). Posttreatment ITT was 25% less than baseline in the 125 IU hCG group, 7% less than baseline in the 250 IU hCG group, and 26% greater than baseline in the 500 IU hCG group. These results demonstrate that relatively low dose hCG maintains ITT within the normal range in healthy men with gonadotropin suppression. Extensions of this study will allow determination of the ITT concentration threshold required to maintain spermatogenesis in man.

 

[DLMCBBB]

So is this saying that those of us that maintain testosterone with low dose hcg will have a harder time coming off hcg? Is that correct that when using higher doses 500 i.u. that test increased 26 percent over baseline? If I am reading this correct the study suggests that higher doses leaves the patient with an improved endogenous testosterone post hcg therapy?

Is that right?

Gonadotropin levels returned to normal basline levels in all participants at the end of the recovery phase.

What this study show's is that gonadotropin supression without hCG administration caused a dramatic reduction in ITT in 94% from baseline in the TE and placebo hCG group. So take your hCG

And the dose of hCG required to maintain basline ITT concentrations in men with maximal gonadotropin supression is significantly lower than that historically utilized in the treatment of infertility due to HH ( hypogonadotropic hypogonadism).

Low dose hCG shown here may or may not normalize ITT in hypogonadotropic infertile men. Lower doses than traditionally used may be sufficient to restore spermatogenesis.

Dustin

 

[DLMCBBB]

So is this saying that those of us that maintain testosterone with low dose hcg will have a harder time coming off hcg? Is that correct that when using higher doses 500 i.u. that test increased 26 percent over baseline? If I am reading this correct the study suggests that higher doses leaves the patient with an improved endogenous testosterone post hcg therapy?

Is that right?

Yes ITT increased 26 % in the TE/500 IU hCG group, but post treatment was not statistically different from baseline. In this group, there were 7 individuals, ITT increased from baseline in 5, and decreased in 2.

Dustin

 

[1cc]

And the dose of hCG required to maintain basline ITT concentrations in men with maximal gonadotropin supression is significantly lower than that historically utilized in the treatment of infertility due to HH ( hypogonadotropic hypogonadism).

Also, something to bear in mind is that the HCG doses quoted in the study are even higher than what a regular guy on TRT would require to maintain ITT. This is because in the study they were aiming to completely suppress endogenous T production by injecting 200mg TE per week. A regular guy on TRT would take much smaller doses of TE which would not lead to complete suppression, and therefore would require even smaller doses of HCG than quoted in the study to maintain ITT. Thats why SWALE recommended much smaller doses of HCG. Taking more HCG than is required to maintain ITT will most likely result in greater estrogen and progesterone conversion. There is also the question of desensitization of the leydig cells to HCG or LH, but I'm not sure at what dosage or frequency that would occur.

 

[DLMCBBB]

Also, something to bear in mind is that the HCG doses quoted in the study are even higher than what a regular guy on TRT would require to maintain ITT. This is because in the study they were aiming to completely suppress endogenous T production by injecting 200mg TE per week. A regular guy on TRT would take much smaller doses of TE which would not lead to complete suppression, and therefore would require even smaller doses of HCG than quoted in the study to maintain ITT. Thats why SWALE recommended much smaller doses of HCG. Taking more HCG than is required to maintain ITT will most likely result in greater estrogen and progesterone conversion. There is also the question of desensitization of the leydig cells to HCG or LH, but I'm not sure at what dosage or frequency that would occur.

I agree, but exogenous T has been shown to dramatically suppress gonadotropin release when administred at supra-physiologic as well as physiologic doses. Some men completely go over the top at 75mg.

Anderson RA, Wallace AM, Wu FC 1996 Comparison between testosterone
enanthate-induced azoospermia and oligozoospermia in a male contraceptive
study. III. Higher 5 alpha-reductase activity in oligozoospermic men administered supraphysiological doses of testosterone. J Clin Endocrinol Metab 81:902-8

Matsumoto AM 1990 Effects of chronic testosterone administration in normal
men: safety and efficacy of high dosage testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production. J Clin Endocrinol Metab 70:282-7

1cc, nice name BTW LOL

Have you ever seen any studies with low dose hCG where the reacher's noticed the T it induced to have a bi-phasic responce?

Dustin

 

[DLMCBBB]

Also, something to bear in mind is that the HCG doses quoted in the study are even higher than what a regular guy on TRT would require to maintain ITT. This is because in the study they were aiming to completely suppress endogenous T production by injecting 200mg TE per week. A regular guy on TRT would take much smaller doses of TE which would not lead to complete suppression, and therefore would require even smaller doses of HCG than quoted in the study to maintain ITT. Thats why SWALE recommended much smaller doses of HCG. Taking more HCG than is required to maintain ITT will most likely result in greater estrogen and progesterone conversion. There is also the question of desensitization of the leydig cells to HCG or LH, but I'm not sure at what dosage or frequency that would occur.

1CC,

For some odd reason, the post I wrote you last night, does not show up. It only show's up when I look at all the "posts" that I wrote under profile.

I'll try again.

Exogenous T has been shown to dramatically supress gonadotropin release when administered at supra-physiologic as well as physiologic doses. I think I even remember SWALE saying, he has some guys go over the top under 100mg of cyp.

Anderson RA, Wallace AM, Wu FC 1996 Comparison between testosterone
enanthate-induced azoospermia and oligozoospermia in a male contraceptive
study. III. Higher 5 alpha-reductase activity in oligozoospermic men administered supraphysiological doses of testosterone. J Clin Endocrinol Metab 81:902-8

Matsumoto AM 1990 Effects of chronic testosterone administration in normal
men: safety and efficacy of high dosage testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production. J Clin Endocrinol Metab 70:282-7

And as soon as I posted this, now I see my post from last night. Computer's I tell you :/



Dustin

 

[pmgamer18]

So what are you saying maybe I am having a senior moment never though I would get old enough to say that. But are you saying one should not do more T then it takes to keep LH and FSH going. Some can do this on 2.5g's of Androgel and shut this down. I feel this is going to happen on TRT no matter what dose you do that gets your levels up.

 

[DLMCBBB]

So what are you saying maybe I am having a senior moment never though I would get old enough to say that. But are you saying one should not do more T then it takes to keep LH and FSH going. Some can do this on 2.5g's of Androgel and shut this down. I feel this is going to happen on TRT no matter what dose you do that gets your levels up.

No im not, and your correct, this supression will eventually happen on TRT no matter what dose you use. Hence why one cannot use Androgel even at 2.5mg for a bridge between AAS cycles.

It's funny my little girl was talking to me the other day, and I totally spaced out. She said, hey dad, are you having your "senior" moment! LOL
Dustin

 

[1cc]

I agree, but exogenous T has been shown to dramatically suppress gonadotropin release when administred at supra-physiologic as well as physiologic doses. Some men completely go over the top at 75mg.

The idea is to try to ensure that one's T level does not go over the normal range whether using shots or transdermals. The higher the T level above the normal range, the greater the HPTA supression. When I was doing shots my weekly dosage was 50mg T Cyp (21mg done E3D) and 100iu HCG every day.

At appropriate TRT doses, I do not believe HCG is necessary to maintain adequate fertility.

From this link:
https://thinksteroids.com/community/threads/134236574

1cc, nice name BTW LOL

Thanks, I couldn't think of anything else at the time.

Have you ever seen any studies with low dose hCG where the reacher's noticed the T it induced to have a bi-phasic responce?

No I haven't. Here are some threads on the subject. I believe the studies posted are for HCG at very high dosages.

https://thinksteroids.com/community/threads/134238958

https://thinksteroids.com/community/threads/134234726

 

[DLMCBBB]

The idea is to try to ensure that one's T level does not go over the normal range whether using shots or transdermals. The higher the T level above the normal range, the greater the HPTA supression. When I was doing shots my weekly dosage was 50mg T Cyp (21mg done E3D) and 100iu HCG every day.

1CC,

In the study I posted above showed that T enanthate (300 mg/week), was no more effective than 100 mg/week in suppressing LH, FSH, and sperm production. And that T enanthate (50 mg/week) suppressed LH and FSH levels and sperm counts to 50% of those in placebo-treated men.

You got to remember that the hCG that restores spermatogenesis in patients is not doing anything to restore function of their HPTA; it is merely promoting spermatogenesis. Once these patients start producing viable sperm and conception occurs, the hCG is withdrawn and the patients once again become infertile.

Dustin

 

[1cc]

You got to remember that the hCG that restores spermatogenesis in patients is not doing anything to restore function of their HPTA; it is merely promoting spermatogenesis.

Correct.

Once these patients start producing viable sperm and conception occurs, the hCG is withdrawn and the patients once again become infertile.

Swale has said many times, "Appropriate TRT will not make a fertile man infertile". If one replaces T that is deficient, then this should not greatly affect the endogenous production. If one takes a dosage beyond that, then it will affect endogenous production.

 

[DLMCBBB]

Swale has said many times, "Appropriate TRT will not make a fertile man infertile". If one replaces T that is deficient, then this should not greatly affect the endogenous production. If one takes a dosage beyond that, then it will affect endogenous production.

Appropriate TRT from SWALE includes intermittently administered hCG along with T. Deficient T, can be the result of low LH/FSH, so how could adding any amount of exo T have a positive effect on LH/FSH. And if your LH/FSH are ok, again how could any amount of exo T have a positive effect on LH/FSH? You cannot hide androgens from the HP, there is just no way getting around it.

I have heard at a few lectures that exogenously administered androgens might act directly on the seminiferous epithelium to support spermatogenesis in a gonodotropin depleted environment, and this effect might explain the variability of fertility in TRT patients. Then there issues with ITT, and 5-AR activity.

Dustin

 

[1cc]

Appropriate TRT from SWALE includes intermittently administered hCG along with T.

At appropriate TRT doses, I do not believe HCG is necessary to maintain adequate fertility.

Deficient T, can be the result of low LH/FSH, so how could adding any amount of exo T have a positive effect on LH/FSH.

It wouldn't. Someone with low LH/FSH who is still fertile, would most likely be able to maintain that level of fertility with appropriate TRT.

And if your LH/FSH are ok, again how could any amount of exo T have a positive effect on LH/FSH?

A person whose LH/FSH are okay, would not require TRT.

You cannot hide androgens from the HP, there is just no way getting around it.

More so, excessive androgens, above what the body requires.

Then there issues with ITT, and 5-AR activity.

The greater the conversion to DHT, the greater the effect on the HPTA.

 

[DLMCBBB]

It wouldn't. Someone with low LH/FSH who is still fertile, would most likely be able to maintain that level of fertility with appropriate TRT.

Suppression of gonadotropins, just less than 5 percent of baseline results in uniform suppression of sperm concentration to below .1 million/ml. Is that to you a fertile man?

A person whose LH/FSH are okay, would not require TRT.

Wong, the treatment would still be the same. A patient can have normal levels of LH/FSH, yet have low T. Normogonadotropic hypogonadism refers to the combination of normal gonadotropin (LH & FSH) levels and low testosterone. Normally one would expect low testosterone to exert a feed forward drive on the hypothalamus and pituitary to increase LH production. In this kind of hypogonadism that feed forward is nonexistent

More so, excessive androgens, above what the body requires.

Not exactly, Add a little Upjohn, LH goes down, cut back, LH concentrations once again rise. And all within physiological range.

The greater the conversion to DHT, the greater the effect on the HPTA.

With lesser degrees on FSH. It is known that there is a selective increase in 5-AR activity in the reproductive tract induced by exposure to exogenously administered T in men maintaining a low rate of spermatogenesis. So in other words this may reflect an adaptive effect within the testis. The relatively greater availability of DHT in the testis may explain minor degrees of spermatogenesis in those men who do not rapidly develop azoospermia despire the suppression of gonadotropin secretion.

Dustin