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

[MANWHORE]

I do 3,000IUs 1st shot,5 days later 2,500IUs,5 days after 1,500IUs and 5 days later 1,500IUs give or take 1 shot .. If it's HRT your looking for i believe 100IUs/day may be fine but not when looking for recovery after heavy andro cycles ..

 

[1cc]

I do 3,000IUs 1st shot,5 days later 2,500IUs,5 days after 1,500IUs and 5 days later 1,500IUs give or take 1 shot ..

Wouldn't this blow your balls away, namely, desensitize them to LH or HCG? Unless, of course they're made of brass.

 

[The_Skeptic]

I do 3,000IUs 1st shot,5 days later 2,500IUs,5 days after 1,500IUs and 5 days later 1,500IUs give or take 1 shot .. If it's HRT your looking for i believe 100IUs/day may be fine but not when looking for recovery after heavy andro cycles ..

How long after a cycle do you begin this? Doesn't this amount cause your E2 levels to soar? Do you take anything to control the E2 with this amount?

 

[jboldman]

Low-Dose Human Chorionic Gonadotropin Maintains Intratesticular Testosterone in Normal Men with Testosterone-Induced Gonadotropin Suppression
Andrea D. Coviello, Alvin M. Matsumoto, William J. Bremner, Karen L. Herbst, John K. Amory, Bradley D. Anawalt, Paul R. Sutton, William W. Wright, Terry R. Brown, Xiaohua Yan, Barry R. Zirkin and Jonathan P. Jarow
Center for Research in Reproduction and Contraception, Geriatric Research Education and Clinical Center, Veteran Affairs Puget Sound Health Care System (A.M.M.), and Department of Medicine, University of Washington School of Medicine (A.D.C., W.J.B., J.K.A., B.D.A., P.R.S.), Seattle, Washington 98195; Department of Medicine, Charles R. Drew University (K.L.H.), Los Angeles, California 90059; Department of Urology, Johns Hopkins University School of Medicine (X.Y., J.P.J.), Baltimore, Maryland 21287; and Division of Reproductive Biology, Department of Biochemistry and Molecular Biology Johns Hopkins University School of Public Health (W.W.W., T.R.B., X.Y., B.R.Z., J.P.J.), Baltimore, Maryland 21205
Address all correspondence and requests for reprints to: Dr. Andrea D. Coviello, Feinberg School of Medicine, Northwestern University, Tarry 15-751, 303 East Chicago Avenue, Chicago, Illinois 60611-3008. E-mail: 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.

 

[DLMCBBB]

After AAS cessation the secretion of LH is nil. It will not be able to initiate T production until a certain stimulus LH level is reached. Studies have shown that the time for this to occur can be lengthy. Thus the idea is to ‘push’ the testicles with hCG and get them started. Once T production is initiated the dependent variable is LH. If the hCG is withdrawn without adequate LH to couple with the testicles return of HPTA functionality will fail.

Dr Mike,

I thought that line of thought was old, and was further perpetrated by the late Dr. Mark O'Connor in the early 90's. Which is why he advocated a movement against the use of hCG or a SERM for that matter.

In one study I have seen cited here countless times (1), normal men were given a fairly light 12 week cycle of a combo of testosterone ( 150 mg/wk), nadrolone (150 mg/wk),Methandrostenolone (15 mg/day), winstrol (5 mg/day). Baseline LH was 6.8 U/L. It fell to a nadir of 4.1 U/L. One month after quitting it had risen to 5.2 U/L. However, 12 weeks after the cycle testosterone was still depressed (14nmol/l vs. a baseline of 21.8 nmol/L), but LH had risen above baseline to 8.0 U/L.


(1) Am J Sports Med 1987 Jul-Aug;15(4):357-61

Androgenic-anabolic steroid effects on serum thyroid, pituitary and steroid hormones in athletes.

Alen M, Rahkila P, Reinila M, Vihko R.

So it seems that low LH post-cycle is not the primary cause of slowed recovery. LH rises to levels above baseline after a cycle much sooner than testosterone production approaches normal, presumably because the pituitary is working overtime to get atrophied Leydig cells to begin producing testosterone again. HCG used during a cycle or at the end of the cycle should help prevent that atrophy. I'm still with SWALE on this that the rate limiting step in post cycle recovery is function of the testes.

Dustin

 

[hackskii]

So often how are you shooting 2,500 IUs? What brand are you using?

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.

 

[wildfox]

I can tell you that 500iu's of HCG a day for 16 days to restore testicular atorphy did not work.
I took a shot of 2500 iu as recomended by Mike and in just one shot I got more size in my testicles than all 16 days of 500iu a day put together.

Would you say that this level of hcg brought you back to your pre-AAS size,
or bigger, or not as big?

WF

 

[jboldman]

this is a routine identical to the one posted at mmonney's site for PCT. Interesting.
http://medibolics.com/ScallyVergelAstractHPGA.pdf

jb

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.

 

[Millard]

this is a routine identical to the one posted at mmonney's site for PCT. Interesting.
http://medibolics.com/ScallyVergelAstractHPGA.pdf

jb

The reason is that Dr. Scally developed, presented and published the PCT protocol in conjunction with PoWeR.

The protocol was developed in response to the medical community's apparent indifference to the HPTA disruption (ASIH) caused by the medical use of AAS in the treatment of LBM wasting seen in individuals with HIV/AIDS

 

[hackskii]

Would you say that this level of hcg brought you back to your pre-AAS size,
or bigger, or not as big?

WF

Yes full size, somtimes I think maybe even bigger.
But depending on time of day or If I am in the shower and its warm they will hang thinner than normal, either that or I have some crazy fixation with my balls now.

Mike did say that size was not an indicatior of testicular recovery, he did mention that a blood test to tell if natural testosterone was being manufactured was the indicator of testicular recovery, he suggested I get my blood work around day 10 of administration of HCG, which would be today.
He mentioned anything over or around 400 was a very good sign.

But outside of the test, my face is greasy, nuts huge, had an awesome workout in the gym and almost a personal best, felt like going of on some stupid people at work (a sign of the androgens), I am willing to bet androgens are pretty high right now.


JB, that PDF does not suprise me as Mike is one of the Docs listed on the first page.
He did say there was a e-book floating around.

I am super optomistic right now about things.
I am quite confidant that I will make a full recovery and wont have to go back on TRT.

 

[MANWHORE]

How long after a cycle do you begin this? Doesn't this amount cause your E2 levels to soar? Do you take anything to control the E2 with this amount?

I don't do HCG for PCT .. During cycle

 

[jboldman]

mike just went up a notch in my book!

jb

 

[hackskii]

mike just went up a notch in my book!

jb

Man, you have know idea how high he is in my book.

Before I talked to him I was doing PCT and my nuts were not comming around, I started to stress hard, Mike reassured me and now I am totally happy. Recovery right now is going better than I had planned.

My only way of repayment twards him is my thanks to him in a public forum.
He took the time to talk to me on the phone and he is a great guy.
I have the upmost respect for him.

 

[Michael Scally MD]

The protocol was worked out over a number of years with many patients. Much lower dosages were first used with no success. One has to remember that this is for an individual who is known to be normal before or at the minimum with no known pathology prior to treatment. So this would be unsuccessful in a patient with a definitive diagnosis of primary or secondary hypogonadism. However, there are a number of individuals given such a diagnosis with a prior history of AAS use that do not really fit the diagnosis given.

In my experience it has been easier to start the testicles producing T rather that the pituitary LH. But this may have more to do with the order in which they need to come online. If one is not successful in coupling the two, pituitary and testicles, but can demonstrate separately their functionality there is no worry about this occurring. In that situation lower doses are usually successful in the HPTA coming online.

Mike

 

[1cc]

Mike,

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

 

[jboldman]

i have been referring people to the pdf on mike mooney's site for quite a while, it owuld be jice if there were some other references for it with labs.

jb

The protocol was worked out over a number of years with many patients. Much lower dosages were first used with no success. One has to remember that this is for an individual who is known to be normal before or at the minimum with no known pathology prior to treatment. So this would be unsuccessful in a patient with a definitive diagnosis of primary or secondary hypogonadism. However, there are a number of individuals given such a diagnosis with a prior history of AAS use that do not really fit the diagnosis given.

In my experience it has been easier to start the testicles producing T rather that the pituitary LH. But this may have more to do with the order in which they need to come online. If one is not successful in coupling the two, pituitary and testicles, but can demonstrate separately their functionality there is no worry about this occurring. In that situation lower doses are usually successful in the HPTA coming online.

Mike

 

[DLMCBBB]

i have been referring people to the pdf on mike mooney's site for quite a while, it owuld be jice if there were some other references for it with labs.

jb

Hey JB, I remember you from CEM back in the days.

This PDF file you posted says the protocol of hCG-clomiphene-tamoxifen was successful in restoring the HPGA within 45 days after androgen cessation, with the mean value for LH being respectively 6.2 and T 458. My question is, how do we know those values are correct given the drugs given. You know it takes about 5 days to excrete just half of the ingested dose of Clomid alone. A more accurate assessment in my book would be how long does it take for values to reach baseline after all drugs are out of the system. Im sure we all thought about this before. What is your take, or any others?

Dustin

 

[Madball99]

"Mike,

Wouldn't HCG shots of 2500iu have a danger of causing leydig desensitization? At what point does this become a concern?"--------------------------------------------------------------------------------------------------------------The protocol seems to work very well and I'm glad someone actually put forth the time and effort to help those w/ ASIH. However I too was wondering about the leydig cell desesitization. Are these doses considered safe because they're only administered for 30 days ? What's the lowest dose you would suggest to try at first , just to be on the safe side, yet still gain results ? I'm thinking maybe the doses were worked up to 2500 iu's and that was the lowest number that garnered success...Am I right ?

Someone posted that leydig cell desensitization was also temporary. Is this true ?

 

[pmgamer18]

This is a copy from the AACE Guildlines.
Gonadal Stimulation in Hypogonadotropic Hypogonadism

Because gonadotropin or GnRH therapy is effective only in hypogonadotropic hypogonadism, this diagnosis must be firmly established before consideration of therapy. Although these agents may also be used to induce puberty in boys and to treat androgen deficiency in hypogonadotropic hypogonadism, the major use of these preparations is in the initiation and maintenance of spermatogenesis in hypogonadotropic men who desire fertility.

Gonadotropin Therapy in Androgen Deficiency

It is known that hCG binds to Leydig cell LH receptors and stimulates the production of testosterone. Peripubertal boys with hypogonadotropic hypogonadism and delayed puberty can be treated with hCG instead of testosterone to induce pubertal development. The initial regimen of hCG is usually 1,000 to 2,000 IU administered intramuscularly two to three times a week. The clinical response is monitored and testosterone levels are measured about every 2 to 3 months. Dosage adjustments of hCG may be needed to determine an optimal schedule. Increasing doses of hCG may reduce testicular stimulation by down-regulating the end-organ; thus, a more optimal result may occur with less frequent or reduced dosing. The half-life of hCG is long.

Gonadotropin Therapy for Induction of Spermatogenesis

Male patients with onset of hypogonadotropic hypogonadism before completion of pubertal development may have testes smaller than 5 mL. These patients usually require therapy with both hCG and human menopausal gonadotropin (or FSH) to induce spermatogenesis. Men with partial gonadotropin deficiency, or who have previously (peripubertally) been stimulated with hCG, may initiate and maintain production of sperm with HCG only. Men with postpubertal-acquired hypogonadotropic hypogonadism and who have previously had normal production of sperm can also generally initiate and maintain production of sperm with hCG therapy only. Fertility may be possible at sperm counts much lower than what would otherwise be considered fertile. Counts of less than 1 million/mL may be associated with pregnancies under these circumstances. It is imperative that the female partner undergo assessment for optimal fertility before or concurrently with consideration of therapy in the man.

Therapy with hCG is generally begun at 1,000 to 2,000 IU intramuscularly two to three times a week, and testosterone levels should be monitored monthly to determine whether any therapeutic adjustments are needed to normalize the levels. It may take 2 to 3 months to achieve normal levels of testosterone. When normal levels of testosterone are produced, examinations should be conducted monthly to determine whether any testicular growth has occurred. Sperm counts should also be conducted monthly during a 1-year period. Because of the high cost of human menopausal gonadotropin (or FSH) preparations, hCG should be the initial therapy of choice for at least 6 to 12 months. Use of hCG, in the absence of exogenous FSH, can often complete spermatogenesis in men with partial gonadotropin deficiency. In general, the response to hCG can be predicted on the basis of the initial testicular volumethe greater the initial testicular volume, the greater the chance of responding to hCG only.

If spermatogenesis has not been initiated by the end of 6 to12 months of therapy with hCG or LH, administration of an FSH-containing preparation is initiated in a dosage of 75 IU intramuscularly three times a week along with the hCG injections. After 6 months, if sperm are not present or are present in very low numbers (<100,000 per mL), the human menopausal gonadotropin (or FSH) dosage can be increased to 150 IU intramuscularly three times a week for another 6 months. If pregnancy occurs, the patients regimen can be switched to only hCG to allow continued spermatogenesis for subsequent potential pregnancies. After delivery, if no further pregnancies are desired, the patient can be switched to testosterone therapy if desired, or long-term hCG therapy can be continued in conjunction with appropriate contraceptive measures, if needed. Rarely, antibodies against hCG may arise and prevent any response to therapy; in such a case, human LH may be effective. Recombinant LH has recently become available and may be of use in selected patients.

Gonadotropin-releasing Hormone (GnRH) Therapy

In patients with an otherwise intact pituitary gland and hypogonadotropic hypogonadism, synthetic gonadotropin-releasing hormone (GnRH) can be given in a pulsatile fashion subcutaneously through a pump every 2 hours. GnRH therapy is monitored by measuring LH, FSH, and testosterone levels every 2 weeks until levels are in the normal range, at which point monitoring can be adjusted to every 2 months. GnRH can be used to initiate pubertal development, maintain virilization and sexual function, and initiate and maintain spermatogenesis. In most patients, these effects may take from 3 to 15 months to achieve sperm production. As with gonadotropin therapy, fertility can be achieved with very low sperm countsoften in the range of 1 million/mL. GnRH may be more effective than gonadotropin stimulation in increasing testicular size and initiating spermatogenesis in many patients with hypogonadotropic hypogonadism.

Other Treatment Considerations

Antiestrogen Therapy in Oligospermia

Currently, the guideline authors do not recommend the general use of clomiphene citrate or tamoxifen for treatment of oligospermia in male patients.

Assisted Reproductive Technology

The ability to perform in vitro fertilization with intracytoplasmic sperm injection directly into the egg has revolutionized the approach to male subfertility. A single sperm or immature form retrieved from the testicle is sufficient to fertilize an egg and provide a reasonable chance at pregnancy. In vitro fertilization with intracytoplasmic sperm injection may be a viable option in many men with hypogonadism who cannot otherwise be induced to produce enough sperm to result in pregnancy as well as in the presence of a female factor that may further make pregnancy by the couple difficult or impossible. The procedure is expensive and seldom covered by health insurance; therefore, this technology will generally not replace conventional gonadal stimulation protocols. Intrauterine insemination may also be a low-cost option in suitable women when the man has mild to moderate oligospermia.

Pituitary Tumors

Patients with acquired hypogonadotropic hypogonadism may require assessment for a possible pituitary tumor with appropriate pituitary imaging studies, such as MRI, and determination of a prolactin level. Depending on the presence or absence of a tumor, other hormonal testing may be indicated, including thyroid and adrenal function tests. Further evaluation and treatment options would depend on what hormonal deficits are present, the size and site of the tumor, the operability of the tumor, and the patients preferences in specific circumstances.

If a prolactinoma is present, therapy would be directed toward correcting this problem before initiation of other therapy. Medical therapy with bromocriptine, pergolide, or cabergoline may effectively reduce prolactin levels sufficiently to allow gonadal function to resume or allow stimulation with gonadotropins. Even when prolactin levels cannot be normalized, hCG therapy alone or in conjunction with human menopausal gonadotropin (or FSH) therapy may stimulate spermatogenesis in treated prolactinomas and result in pregnancies.

Surgical therapy should especially be considered for significant pituitary tumors that are not prolactin-secreting microadenomas. Surgical treatment may also be an option in prolactin-secreting microadenomas if patients have severe side effects from medications or prefer this approach after being appropriately informed of the risks and benefits of medical versus surgical management.

 

[Millard]

However I too was wondering about the leydig cell desesitization. Are these doses considered safe because they're only administered for 30 days ? What's the lowest dose you would suggest to try at first , just to be on the safe side, yet still gain results ?

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.