what do you guys think of this article on hcg?

[mholla]

HCG - Unraveled

By Eric M. Potratz (Email)

Eric M. Potratz has developed his education in the field of endocrinology and performance enhancement through years of research, counseling, and real world experience. Over the past five years he has been a private consultant for hundreds of athletes and bodybuilders alike, and is the founder & president of Primordial Performance.

PCT is a must upon cessation of steroid use . Many great PCT protocols have been outlined over the years, and many individuals have had success with following such protocols. Nevertheless, what works can always work better, and I intend to show you the most effective way to recover from AAS. This is especially the case for those that have had a lack of success following popular advice. In this article I will address the misunderstanding and misuse of Human Chorionic Gonadotropin (hCG) and show you the most efficient way to use hCG for the fastest and most complete recovery.

HCG unraveled –

Human Chorionic Gonadotropin (hCG) is a peptide hormone that mimics the action of luteinizing hormone (LH). LH is the hormone that stimulates the testes to produce testosterone . (1) More specifically LH is the primary signal sent from the pituitary to the testes, which stimulates the leydig cells within the testes to produce testosterone.

When steroids are administered, LH levels rapidly decline. The absence of an LH signal from the pituitary causes the testes to stop producing testosterone, which causes rapid onset of testicular degeneration. The testicular degeneration begins with a reduction of leydig cell volume, and is then followed by rapid reductions in intra-testicular testosterone (ITT), peroxisomes, and Insulin -like factor 3 (INSL3) – All important bio-markers and factors for proper testicular function and testosterone production. (2-6,19) However, this degeneration can be prevented by a small maintenance dose of hCG ran throughout the cycle. Unfortunately, most steroid users have been engrained to believe that hCG should be used after a cycle, during PCT. Upon reviewing the science and basic endocrinology you will see that a faster and more complete recovery is possible if hCG is ran during a cycle.

Firstly, we must understand the clinical history of hCG to understand its purpose and its most efficient application. Many popular “steroid profiles” advocate using hCG at a dose of 2500-5000iu once or twice a week. These were the kind of dosages used in the historical (1960’s) hCG studies for hypogonadal men who had reduced testicular sensitivity due to prolonged LH deficiency. (21,22) A prolonged LH deficiency causes the testes to desensitize, requiring a higher hCG dose for ample stimulation. In men with normal LH levels and normal testicular sensitivity, the maximum increase of testosterone is seen from a dose of only 250iu, with minimal increases obtained from 500iu or even 5000iu. (2,11) (It appears the testes maximum secretion of testosterone is about 140% above their normal capacity.) (12-18) If you have allowed your testes to desensitize over the length of a typical steroid cycle, (8-16 weeks) then you would require a higher dose to elicit a response in an attempt to restore normal testicular size and function – but there is cost to this, and a high probability that you won’t regain full testicular function.

One term that is critical to understand is testosterone secretion capacity which is synonymous to testicular sensitivity. This is the amount of testosterone your testes can produce from any given LH or hCG stimulation. Therefore, if you have reduced testosterone secretion capacity (reduced testicular sensitivity), it will take more LH or hCG stimulation to produce the same result as if you had normal testosterone secretion capacity. If you reduce your testosterone secretion capacity too much, then no amount of LH or hCG stimulation will trigger normal testosterone production – and this leads to permanently reduced testosterone production.

To get an idea of how quickly you can reduce your testosterone secretion capacity from your average steroid cycle, consider this: LH levels are rapidly decreased by the 2nd day of steroid administration. (2,9,10) By shutting down the LH signal and allowing the testis to be non-functional over a 12-16 week period, leydig cell volume decreases 90%, ITT decreases 94%, INSL3 decreases 95%, while the capacity to secrete testosterone decreases as much as 98%. (2-6)

Note: visually analyzing testes size is a poor method of judging your actual testicular function, since testicular size is not directly related to the ability to secrete testosterone. (4) This is because the leydig cells, which are the primary sites of testosterone secretion, only make up about 10% of the total testicular volume. Therefore, when the testes may only appear 5-10% smaller, the testes ability to secrete testosterone upon LH or hCG stimulation can actually be significantly reduced to 98% of their normal production. (3-5) The point here is to not judge testosterone secretion capacity by testicular size.

The decreased testosterone secretion capacity caused by steroid use was well demonstrated in a study on power athletes who used steroids for 16 weeks, and were then administered 4500iu hCG post cycle. It was found that the steroid users were about 20 times less responsive to hCG, when compared to normal men who did not use steroids . (8) In other words, their testosterone secretion capacity was dramatically reduced because they did not receive an LH signal for 16 weeks. The testes essentially became desensitized and crippled. Case studies with steroid using patients show that aggressive long-term treatment with hCG at dosages as high as 10,000iu E3D for 12 weeks were unable to return full testicular size. (7) Another study with men using low dose steroids for 6 weeks showed unsuccessful return of Insulin-like factor-3 (INSL3) concentration in the testes upon 5000iu/wk of HCG treatment for 12 weeks (6) (INSL3 is an important biomarker for testosterone production potential and sperm production. 20)

These studies show that postponing hCG usage until the end of a steroid cycle increases your need for a higher dose of hCG, and decreases your odds of a full recovery. As a consequence to using a higher dose of hCG at the end of a cycle, estrogen will be increased disproportionately to testosterone, which then causes further HPTA suppression (from high estrogen) while increasing the risk of gyno. (11) For example, high doses of hCG have been found to raise estradiol up to 165%, while only raising testosterone 140%. (11) Higher doses of hCG are also known to reduce LH receptor concentration and degrade the enzymes responsible for testosterone synthesis within the testes (12,13,19 ) -- the last thing someone wants during recovery. While these negative effects of hCG can be partly mitigated by the use of a SERM such as tamoxifen , it will create further problems associated with using a toxic SERM (covered in another article).

In light of the above evidence, it becomes obvious that we must take preventative measures to avoid this testicular degeneration. We must protect our testicular sensitivity. Besides, with hCG being so readily available, and such a painless shot, it makes you wonder why anyone wouldn’t use it on cycle.

Based on studies with normal men using steroids, 100iu HCG administered everyday was enough to preserve full testicular function and ITT levels, without causing desensitization typically associated with higher doses of hCG. (2) It is important that low-dose hCG is started before testicular sensitivity is reduced, which appears to rapidly manifest within the first 2-3 weeks of steroid use. Also, it’s important to discontinue the hCG before you start PCT so your leydig cells are given a chance to re-sensitize to your body’s own LH production. (To help further enhance testicular sensitivity, the dietary supplement Toco-8 may be used)

A more convenient alternative to the above recommendation would be a twice a week shot of 200iu hCG, or possibly a once a week shot of 500iu. However, it is most desirable to adhere to a lower more frequent dose of hCG to mimic the body’s natural LH release and minimize estrogen conversion. If you are starting hCG late in the cycle, one could calculate a rough estimate for their required hCG ‘kick starting’ dosage by multiplying 40iu x days of LH absence, since the testes will be desensitized, thus requiring a higher dose. (ie. 40iu x 60 days = 2400iu HCG dose)

Note: If following the on cycle hCG protocol, hCG should NOT be used for PCT.

Recap –

For preservation of testicular sensitivity, use 100iu hCG ED starting 7 days after your first AAS dose. At the end of the cycle, drop the hCG two weeks before the AAS clear the system. For example, you would drop hCG about the same time as your last Testosterone Enanthate shot. Or, if you are ending the cycle with orals, you would drop the hCG about 10 days before your last oral dose. This will allow for a sudden and even clearance in hormone levels, while initiating LH and FSH production from the pituitary, to begin stimulating your testes to produce testosterone. Remember, recovery doesn’t begin until you are off hCG since your body will not release its own LH until the hCG has cleared the system.

In conclusion, we have learned that utilizing hCG during a steroid cycle will significantly prevent testicular degeneration. This helps create a seamless transition from “on cycle” to “off cycle” thus avoiding the post cycle crash.



References -

1. Glycoprotein hormones: structure and function.
Pierce JG, Parsons TF 1981
Annu Rev Biochem 50:466–495

2. Low-Dose Human Chorionic Gonadotropin Maintains Intratesticular Testosterone in Normal Men with Testosterone-Induced Gonadotropin Suppression
Andrea D. Coviello, et al
J. Clin. Endocrinol. Metab., May 2005; 90: 2595 - 2602.

3. Luteinizing hormone on Leydig cell structure and function.
Mendis-Handagama SM
Histol Histopathol 12:869–882 (1997)

4. Leydig cell peroxisomes and sterol carrier protein-2 in luteinizing hormone-deprived rats
SM Mendis-Handagama, et al.
Endocrinology, Dec 1992; 131: 2839.

5. Effect of long term deprivation of luteinizing hormone on Leydig cell volume, Leydig cell number, and steroidogenic capacity of the rat testis.
Keeney DS, et al.
Endocrinology 1988; 123:2906–2915.

6.The Effects of Gonadotropin Suppression and Selective Replacement on Insulin-Like Factor 3 Secretion in Normal Adult Men
Katrine Bay, et al
J. Clin. Endocrinol. Metab., Mar 2006; 91: 1108 - 1111.

7. Successful treatment of anabolic steroid–induced azoospermia with human
chorionic gonadotropin and human menopausal gonadotropin
Dev Kumar Menon, et al.
FERTILITY AND STERILITY VOL. 79, SUPPL. 3, JUNE 2003

8. Testicular responsiveness to human chorionic godadotrophin during transient hypogonadotrophic hypogonadism induced by androgenic /anabolic steroids in power athletes
Hannu et al.
J. Steroid Biochem. Vol. 25, No. 1 pp. 109-112 (1986)

9. Comparison of testosterone, dihydrotestosterone, luteinizing hormone, and follicle-stimulating hormone in serum after injection of testosterone enanthate of testosterone cypionate .
Schulte-Beerbuhl M, et al 1980
Fertil Steril 33:201–203

10. 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.
Matsumoto AM, et al 1990
J Clin Endocrinol Metab 70:282–287

11. Effect of human chorionic gonadotropin on plasma steroid levels in young and old men.
Longcope C et al
Steroids 21:583–590 (1973)

12. Regulation of peptide hormone receptors and gonadal steroidogenesis.
Catt KJ, et al
Rec Prog Horm Res 1980; 36:557–622

13. Effect of human chorionic gonadotropin on the endocrine function of Papio testes
GV Katsiia, et al
Probl Endokrinol (Mosk), Sep 1984; 30(5): 68-71.

14. Reproductive function in young fathers and grandfathers.
Nieschlag E, et al.
J Clin Endocrinol Metab 55:676–681 (1982)

15. The aging Leydig cell III Gonadotropin stimulation in men.
Nankin HR, et al. 1981
J Androl 2:181–189

16. Reproductive hormones in aging men. I. Measurement of sex steroids, basal luteinizing hormone, and Leydig cell response to human chorionic gonadotropin.
Harman SM, et al. 1980
J Clin Endocrinol Metab 51:35–40

17. Prolonged biphasic response of plasma testosterone to single intramuscular injections of human chorionic gonadotropin.
Padron RS, et al. 1980
J Clin Endocrinol Metab 50:1100–1104

18. Gonadotrophins and plasma testosterone in senescence. In: James VHT, Serio M, Martini L, eds. The endocrine function of the human testis.
Mazzi C, et al. 1974
New York: Academic Press, Inc.; 51–66

19. Androgen biosynthesis in Leydig cells after testicular desensitization by luteinizing hormone-releasing hormone and human chorionic gonadotropin.
Dufau ML, et al.
Endocrinology 105 1314–1321 (1979)

20. Insulin-Like Factor 3 Serum Levels in 135 Normal Men and 85 Men with Testicular Disorders: Relationship to the Luteinizing Hormone-Testosterone Axis
K. Bay, S. et al
J. Clin. Endocrinol. Metab., Jun 2005; 90: 3410 - 3418.

21. Stimulation of sperm production by human chorionic gonadotropin after prolonged gonadotropin suppression in normal men.
Matsumoto AM, et al 1985
J Androl 6:137–143

22. Human chorionic gonadotropin and testicular function: stimulation of testosterone, testosterone precursors, and sperm production despite high estradiol levels.
Matsumoto AM, et al. 1983
J Clin Endocrinol Metab 56:720–728

[mholla]

Opioid Modulation for Preventing AAS Induced HPTA Suppression.

By Eric M. Potratz (Email)

Eric M. Potratz has developed his education in the field of endocrinology and performance enhancement through years of research, counseling, and real world experience. Over the past five years he has been a private consultant for hundreds of athletes and bodybuilders alike, and is the founder & president of Primordial Performance.


Suppression of the HPTA (Hypothalamus, Pituitary, Testicular Axis) is seemingly unavoidable during a steroid cycle. What I will be presenting in this article is a new idea to the world of AAS users. This exciting new concept addresses the possibility of limiting and possibly preventing suppression of the (HPTA) during cycle. More specifically, I will show you how to actively modulate the hypothalamus & pituitary pulse generator during cycle and how this can prime our endocrine system for a quicker, smarter, and healthier recovery from anabolic androgenic steroids (AAS).

For a moment, let’s forget the concept of “post cycle therapy ”, and embrace the idea of “on cycle therapy” – active therapy throughout a steroid cycle. The HPTA involves a constant biological interplay of responses and feedback loops that can ultimately become shutdown and degraded during AAS administration. However, research suggests suppression of the hypothalamus and pituitary may be preventable during steroid use . Before we delve into the details, lets first take a quick recap on the HTPA and how it responses to AAS.

HPTA – The basics

When the hypothalamus senses low hormone levels, it secretes gonandotropin releasing hormone (GnRH). This GnRH then travels a short distance to the nearby pituitary gland to stimulate the release of the gonadotrophins -- luteinizing hormone (LH) and follicle stimulating hormone (FSH). These gonadotrophins travel all the way down to the testes, to activate their respective leydig and seritoli cells. LH initiates testosterone production by stimulating the leydig cell receptor (steroidogenesis), while FSH initiates sperm production by stimulating the sertoli cell receptor (spermatogenesis).

AAS’s inhibit hormone production just as your body’s own hormones do. Testosterone interacts with the androgen receptor (AR) and estrogen interacts with the estrogen receptor (ER). When these hormones are in high concentration, they cause the hypothalamus to decrease its release of GnRH, which decreases LH and FSH production from the pituitary. (1) This cuts off the signal to the testis and halts all hormone production. This process is a daily event for the rhythmic endocrine system. Spikes in LH & FSH are followed by spikes in testosterone, and spikes in testosterone result in a reduction of LH & FSH release until testosterone levels decline and LH & FSH is released again. The caveat with most steroids, is that hormone levels remain chronically high (24/7) and do not allow release of LH or FSH, thus leaving the pituitary and testis in a dormant state for as long as the steroids are administered.

While low-dose on-cycle hCG is a good protocol to mimic LH and keep the testes from atrophy, (discussed here) it won’t help prevent pituitary atrophy. We forget that the pituitary is susceptible to the same degradation and atrophy as the testes. That is, when the GnRH secretion from the hypothalamus stops (during a steroid cycle), the pituitary reduces its number of GnRH receptors and becomes less and less responsive to GnRH stimulation as time goes on. (11) This is analogous to atrophy of the testis, during absence of an LH or FSH signal. On the other hand, both the pituitary and testis will decrease receptor concentration during over stimulation as well, as its been found from too much hCG use or too much GnRH stimulation.(12,13) The point here, is that only minor stimulus is required for the preservation of sensitivity in the endocrine organs. Perhaps a completely neglected and suppressed pituitary (or testes) may explain the lack of full and prompt recovery for many steroid users, despite adherence to a “tried and true” PCT regimen. So the question is – How can we prevent suppression of the testes, and better yet, how can we prevent suppression of the pituitary?

A closer look –

There are several ways that steroids can inhibit LH & FSH release from the pituitary based on the receptors they occupy, and this is important to understand if you plan on blocking AAS induced suppression. For instance, it appears that AAS which bind strictly to the AR only inhibit LH & FSH release by suppressing GnRH release from the hypothalamus (ie Primobolan , Proviron , Anavar or Masterontrenbolone and nandrolonemethandrostenolone since they can activate both AR and ER receptors.

Evidence suggests that estradiol is about 200x more suppressive than testosterone on a molar basis (37), and that administration of Arimidex

When it comes to suppression of the hypothalamus, there is more than a simple on/off switch for the hypothalamus control center. Evidence suggests that there isn’t even a direct AR or ER receptor on GnRH secreting neurons. (2-6) Meaning, steroid hormones do not directly influence GnRH release from the hypothalamus, but actually communicate through an intermediary. (7)

It was well summarized here by A. J Tilbrook et al,

“It follows, that the actions of testicular steroids on GnRH neurons must be mediated via neuronal systems that are responsive to steroids and influence the activity of GnRH neurons.”

And again here by FJ Hayes et al,

“It was thus postulated that estrogen-receptive neurons were acting as intermediaries in the non-genomic regulation of GnRH by estrogen”

There is a network of neurogenic intermediaries in the hypothalamus governing GnRH release from steroid hormone influence. More specifically, it is the combined efforts of neuro-active peptides and catecholamines which send the message of “suppression” to the GnRH neurons once activated by steroid hormones. (16) These primary messengers are known as a group of neuro-active peptides called endogenous opioid peptides (EOP’s). (7,16) The EOP’s consist of the three main peptides -- b-endorphin, dynorphin, and enkephalins, which act upon their respective u-opioid, k-opioid, and s-opioid receptors. It appears that the most influential EOP in GnRH modulation is b-endorphin, acting upon the u-opioid receptor. (8-10) For this reason, b-endorphin will be the main focus of the article (although there are other minor intermediates involved.)

When steroid hormones reach the hypophysial portal, they activate the EOP’s, which suppress GnRH and consequently suppress LH & FSH. We know that steroid hormones must communicate with these opioid receptors in order for them to inhibit the release of GnRH from the GnRH neurons, since the GnRH neurons do not have their own AR or ER receptors. What’s most interesting here is that the suppression on GnRH neurons can actually be intercepted by a u-opioid receptor antagonist – such as naloxone, and the orally active congers naltrexone, and nalmefene.

This is accomplished by blocking the u-opioid receptor and preventing the inhibitory effects of b-endorphin upon the GnRH releasing neuron. It should be noted that this “antagonism” of suppression is not due to antagonism of the AR or ER itself, since u-opioid antagonists to not bind to hormone receptors. (15,32)

The effect of a u-opioid receptor antagonist on the HPTA is demonstrated here --

Essentially, a u-opioid antagonist such as naloxone takes the brakes off of GnRH release and allows pulses of GnRH to occur as if no steroid hormones are present. (17) Naloxone, and related u-opioid antagonists have consistently proven to block the suppressive effects of testosterone , DHT, and estrogen administration in both animals and humans. (18-25) It also appears that these drugs have the ability to increase pituitary sensitivity to GnRH. (26,27)

U-opioid antagonists have long been used for treatment of opioid dependence; not only to control cravings of narcotics, but to restore a suppressed endocrine system. (28,29) It’s well known that strong opioid based drugs such as methadone, cocaine, heroin and alcohol can suppress GnRH and therefore suppress LH & FSH. It seems that this decease of GnRH, LH & FSH is due to the same EOP mechanisms seen with AAS induced suppression. (33) In alcoholics, cocaine and heroin users, naltrexone and naloxone have been used to restore LH and testosterone levels. (28,29) Naltrexone has even been proposed as a treatment for male impotence and erectile dysfunction. (30,31)

Naloxone, naltrexone and nalmefene seem progressively more powerful in their potency to block b-endorphin, respectively. (14,18) Naloxone lacks oral bioavailability therefore injection is required. An injectable preparation could easily be made with BA water due to the water solubility of the compound. A 40mg subcutaneous injection would be a typical dose of naloxone. Naltrexone is orally active, with a safe and effective oral dose being about 100mg for a 220lb male. (18) While a lower dose of about 25-50mg of nalmefene would seemingly have the same benefit. (20,24) Increasing the dose of these drugs will surely increase the likelihood of side-effects without notably increasing the benefit. A twice a week dosing protocol would seem appropriate with these drugs, as only to increase GnRH and LH release enough to prevent pituitary and testicular shutdown – Just enough to keep them in the “ball game” so to speak. Also, a twice a week dosing protocol would most likely limit the increased opioid sensitivity induced by the long-term use of the drugs.

A word of caution: The opioid antagonists mentioned in this article are recognized as safe and non-toxic at the given dosages; however they can cause severe withdrawal symptoms in opiate users (methadone, morphine, cocaine, and heroin addicts.) Caution is also advised when using opioid antagonists prior to sedation or surgery as they can reduce effectiveness of anesthetics. Temporary nausea, headache or fatigue, are occasional side-effects associated with the use of these drugs. Naltrexone has been reported to heighten liver enzymes, while naloxone and nalmefene do not appear to have this issue. At any rate, a twice a week protocol for 4-16 weeks is unlikely to cause any liver issues that may be associated with naltrexone. Contrary to popular believe, opioid antagonists do NOT have any addictive properties.

A few point to consider -

For those who choose to embark on an opioid antagonist protocol several things should be considered.




2. As it was pointed out earlier in this article, estrogen has a markedly stronger effect on suppression of LH release compared to androgens since estrogen suppresses the hypothalamus and pituitary. Usage of an AI such as anastrozole, letrozole , or exemestane (Aromasin ) can reduce estrogen and greatly reduce suppression on GnRH, LH and FSH release by preventing excessive ER activation in the hypothalamus and desensitization of the pituitary GnRH receptors. (35,37,38) Anastrozole has ~50% maximal total estrogen suppression at 1mg/day. Exemestane has ~50% maximal total estrogen suppression at 25mg/day. While letrozole has ~60% at 1mg/day. These are averages based on compiled data from several studies. Similar estrogen suppression can also been seen from only twice a week administration of these AI’s. (43-47)



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[Kale]

i also read the article on opioid modulation (i.e. narcan) to prevent hpta suppression. has anyone ever tried that?

btw, dont know if its cool to link articles from other sites that have aas forums.

Its isnt !! It also isnt kewl to talk about opioids either

[bladerunner9]

Whatever, but the Stuff written there seems to be the right thing to do.

[mholla]

Its isnt !! It also isnt kewl to talk about opioids either

sorry ill change it so there is no link, ill copy and paste it. also, the opioid article is about opioid blockers (like narcan and revex) not street opioid drugs.

[Swifto]

Its isnt !! It also isnt kewl to talk about opioids either

Talking about this opoid isnt like talking about the illigal VERY addictive one my friend. Its a very intresting read.

To the poster, this is a repost I believe. I've also read both articles at another board.

I advocate 125-250ius 2-3 times weekly, then bump it up before PCT, then begin PCT without HCG being used (SERMs/AIs).

[mholla]

Talking about this opoid isnt like talking about the illigal VERY addictive one my friend. Its a very intresting read.

To the poster, this is a repost I believe. I've also read both articles at another board.

I advocate 125-250ius 2-3 times weekly, then bump it up before PCT, then begin PCT without HCG being used (SERMs/AIs).

oh i didnt know it was a repost...sorry guys.

the author advocates cutting hcg 2 weeks before aas clears, any experience trying that instead of bumping hcg before pct? thanks for the response.

[jimmyinkedup]

both were a good read ..... the opiod article got me wondering if naubaphine hcl (nubain) has same effects and if that may be an attribution to its popularity in BB circles...just a thought......
(aside from the obvious narcotic type effects associated with it - i wonder if this also applies to it as it also binds to opiod receptor and also is know to cause instant withdrawl symptoms from other opiates much like narcan) alot of speculation but i am curious....

[mholla]

both were a good read ..... the opiod article got me wondering if naubaphine hcl (nubain) has same effects and if that may be an attribution to its popularity in BB circles...just a thought......
(aside from the obvious narcotic type effects associated with it - i wonder if this also applies to it as it also binds to opiod receptor and also is know to cause instant withdrawl symptoms from other opiates much like narcan) alot of speculation but i am curious....

i'm curious too. yes narcan and nubain are chemically similar but narcan can't be used an an analgesic, it's purely an opioid antagonist, so no dependence possible . also, i did a quick search on narcan prices and to run it as the author suggests (0.4mg 2x/wk for cycle length) it could be fairly expensive approx. $300. so, i don't think ill try it out anytime soon unless more concrete evidence comes to light or i become a paramedic.