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HCG - How important is it on cycle?
Before reading this thread, its best to read our article on PCT (Post Cycle Therapy) so you have a basic understanding of the HPTA and understand how natural testosterone becomes first inhibited from the use of anabolic steroids, then eventually "shutdown" when hormone output reaches a very low level (hypogonadism).
The article can be found here: Steroid PCT
First we must distinguish between short-term inhibition and long-term suppression of endogenous testosterone tat occurs from the use of anabolic-androgenic steroids.
Short-term inhibition of testosterone production comes primarily from negative feedback at the pituitary and hypothalamus, which reduces LH output. This could be described as a reduction in the signal to produce testosterone. This LH suppression recovers quickly post cycle in the majority of cases.
However, with time a condition occurs which is called - testicular dysfunction. Without LH from the pituitary, the testes atrophy from disuse and become unresponsive. This testicular dysfunction could be described as a reduction in the responsiveness to a signal to produce testosterone after stimulation from LH (luteinizing hormone) and FSH (follice stimulating hormone).
The hypothalamus and pituitary seem to recover fairly quickly following the use of anabolic steroids but the entire HPTA does not. GnRH (gonadotropin releasing hormone) LH (luteinizing hormone) and FSH (follicle stimulating hormone) rise fairly quickly post cycle when the negative feedback of androgens, estrogens and progesterones declines, but endogenous testosterone levels dont. As shown in this review by William Llewellyn. It indicates that LH levels rise fairly quickly (on the 3rd week) after Testosterone Enanthatee injections of 250mg weekly for 21 weeks. So it seems the hypothalamus and pituitary are not the problem in restarting endogenous testosterone production post anabolic steroids use.
So now we know that GnRH, LH and FSH are not often the problem for why endogenous testosterone does not rise when we’re trying to recover natural testosterone levels post steroid use. So what could be the issue?
If LH levels rise post cycle (in the majority of cases) the reason why endogenous testosterone levels fail to rise is the testes, or the onset of testicular dysfunction. Testicular dysfunction is when the testes become atrophied from disuse or desensitised to gonadotropins, such as LH and FSH. This could also be described as being the onset of primary hypogonadism in males, which is extremely hard to treat if this condition if confirmed. Hormone Replacement Therapy (HRT) is then the most likely treatment.
Primary hypogonadism is when the testes no longer respond to LH or FSH The testes have a lowered sperm concentration/production and endogenous testosterone level, although LH and FSH are above normal levels. This can be due to disease such as, Klinefelter's syndrome, over use of anabolic steroids , as described in this study or overuse of HCG. The simple answer to primary hypogonadism is hormone replacement therapy (HRT) or testosterone replacement therapy (TRT).
Preventing Testicular Dysfunction
So we now know that avoiding testicular dysfunction is our objective when using androgens that cause inhibition or shutdown of natural LH and FSH levels. SERMs and AI’s wont work here as they are simply not strong enough to maintain regular levels of GnRH, LH and FSH when anabolic steroids are used. So what do we have?
Well, we need to address the testes directly and when wishing to do this there are only 2 main peptides that are easily available and work for this action. Both these peptides address the testes directly as they mimic LH in the body.
HMG (human menopausal gonadotropin)
HCG (human chorionic gonadotropin)
Both these peptide agents will mimic LH in the body and HMG will actually maintain FSH as well. This is an advantage as FSH levels are primarily used for sperm production stimulating the germ cells, and LH as its primary action is to stimulate the leydig cells which are responsible for testosterone output. However, HMG is far harder to obtain and is relatively expensive.
HCG mimics LH, but will also cause a low amount of germ cell stimulation as well, is also cheap and widely available, so it gets the green light here. HCG has the ability to maintain endogenous testosterone production and ITT (Intra-Testicular Testosterone) by stimulating the testes directly. This can occur even when shutdown from androgens, such as Testosterone Enathate, shown in this study. By doing this, we will then avoid – testicular dysfunction.
HCG Doses and Duration
HCG used to avoid testicular dysfunction can be done a number of ways, but all are simple and effective.
Firstly, we can use HCG at low doses frequently throughout our anabolic steroid(s) cycle to maintain testicular size and function. Doses ranges from 250-500ius (international units) 2-3 times per week, or 1,000 once per week. Both these methods are effective. A break of 1-3 weeks needs to also be implemented every 10-12 weeks as estrogen levels can build over time. Estrogen needs to also be monitored because the use of HCG will directly increase testicular estrogen levels and the added spike in total testosterone will aromatase and again, raise estrogen. Aromasin 10mg/ED is suggested because of this and is actually always suggested when using steroids that raise levels of circulating estrogen.
The second option, which is effective, but somewhat more risky as testicular dysfunction can begin to appear, is to use larger less infrequent doses of HCG. Larger doses of HCG will be required at around 1,000-2,000ius injected every 6-8 weeks for around 5 shots every 3 days, then take the time off and repeat.
Both methods are effective and HCG doses can be ramped leading to PCT to shock the testes into stimulation if a dormant period has onset. Doubling the dose of the frequent throughout HCG dosing can be done for the final 4 shots leading to PCT. PCT is then conducted with the use of SERMs and support supplements.
The article can be found here: Steroid PCT
First we must distinguish between short-term inhibition and long-term suppression of endogenous testosterone tat occurs from the use of anabolic-androgenic steroids.
Short-term inhibition of testosterone production comes primarily from negative feedback at the pituitary and hypothalamus, which reduces LH output. This could be described as a reduction in the signal to produce testosterone. This LH suppression recovers quickly post cycle in the majority of cases.
However, with time a condition occurs which is called - testicular dysfunction. Without LH from the pituitary, the testes atrophy from disuse and become unresponsive. This testicular dysfunction could be described as a reduction in the responsiveness to a signal to produce testosterone after stimulation from LH (luteinizing hormone) and FSH (follice stimulating hormone).
The hypothalamus and pituitary seem to recover fairly quickly following the use of anabolic steroids but the entire HPTA does not. GnRH (gonadotropin releasing hormone) LH (luteinizing hormone) and FSH (follicle stimulating hormone) rise fairly quickly post cycle when the negative feedback of androgens, estrogens and progesterones declines, but endogenous testosterone levels dont. As shown in this review by William Llewellyn. It indicates that LH levels rise fairly quickly (on the 3rd week) after Testosterone Enanthatee injections of 250mg weekly for 21 weeks. So it seems the hypothalamus and pituitary are not the problem in restarting endogenous testosterone production post anabolic steroids use.
So now we know that GnRH, LH and FSH are not often the problem for why endogenous testosterone does not rise when we’re trying to recover natural testosterone levels post steroid use. So what could be the issue?
If LH levels rise post cycle (in the majority of cases) the reason why endogenous testosterone levels fail to rise is the testes, or the onset of testicular dysfunction. Testicular dysfunction is when the testes become atrophied from disuse or desensitised to gonadotropins, such as LH and FSH. This could also be described as being the onset of primary hypogonadism in males, which is extremely hard to treat if this condition if confirmed. Hormone Replacement Therapy (HRT) is then the most likely treatment.
Primary hypogonadism is when the testes no longer respond to LH or FSH The testes have a lowered sperm concentration/production and endogenous testosterone level, although LH and FSH are above normal levels. This can be due to disease such as, Klinefelter's syndrome, over use of anabolic steroids , as described in this study or overuse of HCG. The simple answer to primary hypogonadism is hormone replacement therapy (HRT) or testosterone replacement therapy (TRT).
Preventing Testicular Dysfunction
So we now know that avoiding testicular dysfunction is our objective when using androgens that cause inhibition or shutdown of natural LH and FSH levels. SERMs and AI’s wont work here as they are simply not strong enough to maintain regular levels of GnRH, LH and FSH when anabolic steroids are used. So what do we have?
Well, we need to address the testes directly and when wishing to do this there are only 2 main peptides that are easily available and work for this action. Both these peptides address the testes directly as they mimic LH in the body.
HMG (human menopausal gonadotropin)
HCG (human chorionic gonadotropin)
Both these peptide agents will mimic LH in the body and HMG will actually maintain FSH as well. This is an advantage as FSH levels are primarily used for sperm production stimulating the germ cells, and LH as its primary action is to stimulate the leydig cells which are responsible for testosterone output. However, HMG is far harder to obtain and is relatively expensive.
HCG mimics LH, but will also cause a low amount of germ cell stimulation as well, is also cheap and widely available, so it gets the green light here. HCG has the ability to maintain endogenous testosterone production and ITT (Intra-Testicular Testosterone) by stimulating the testes directly. This can occur even when shutdown from androgens, such as Testosterone Enathate, shown in this study. By doing this, we will then avoid – testicular dysfunction.
HCG Doses and Duration
HCG used to avoid testicular dysfunction can be done a number of ways, but all are simple and effective.
Firstly, we can use HCG at low doses frequently throughout our anabolic steroid(s) cycle to maintain testicular size and function. Doses ranges from 250-500ius (international units) 2-3 times per week, or 1,000 once per week. Both these methods are effective. A break of 1-3 weeks needs to also be implemented every 10-12 weeks as estrogen levels can build over time. Estrogen needs to also be monitored because the use of HCG will directly increase testicular estrogen levels and the added spike in total testosterone will aromatase and again, raise estrogen. Aromasin 10mg/ED is suggested because of this and is actually always suggested when using steroids that raise levels of circulating estrogen.
The second option, which is effective, but somewhat more risky as testicular dysfunction can begin to appear, is to use larger less infrequent doses of HCG. Larger doses of HCG will be required at around 1,000-2,000ius injected every 6-8 weeks for around 5 shots every 3 days, then take the time off and repeat.
Both methods are effective and HCG doses can be ramped leading to PCT to shock the testes into stimulation if a dormant period has onset. Doubling the dose of the frequent throughout HCG dosing can be done for the final 4 shots leading to PCT. PCT is then conducted with the use of SERMs and support supplements.
