- Joined
- Sep 3, 2006
- Messages
- 4,418
So how important is HCG?
When our HPTA's are "shutdown" we have to distinguish between short-term inhibtion and long-term dysfunction.
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.
However, with time, it leads to testicular dysfunction. Without LH from the pituitary, the testes atrophy from disuse. This testicular dysfunction could be described as a reduction in the responsiveness to a signal to produce testosterone.
The hypothalamus and pituitary seem to recover fairly quickly following the use of androgens. GnRH, LH and FSH rise fairly quickly post cycle, but endogenous testosterone levels dont. As confirmed **broken link removed** by William Llewellyn. It shows that LH levels rise fairly quickly (on the 3rd week) after Testosterone Enanthate injections of 250mg weekly for 21 weeks. So it seems the hypothalamus and pituitary are not the problem in restarting endogenous testosterone production post cycle.
After recent correspondance with Dr.Crisler (Swale) he confirmed ganadotrophin levels were not to blame in restarting the HPTA. So what is?
If LH levels rise post cycle (the majority of the time) the reason why endogenous testosterone levels DONT rise, is the testes. Or testicular dysfunction. Testicular dysfunction is when the testes become atrophied from disuse or desensitised to ganadotrophins, such as LH. This could also be described as being the onset of primary hypogonadism.
Primary hypogonadism is when the testes no longer respond to LH. 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 desease (Klinefelter's syndrome), over use of anabolic steroids, as described in this study or overuse of HCG. The simple answer to primary hypogonadism is HRT.
So if the testes (testicular dysfunction) are the main culprit in restoring testosterone production post cycle how can we maintain testicular function and endogenous testosterone production even when "shutdown" using andorgens? Simple - HCG.
HCG has the ability to maintain endogenous testosterone production and ITT (Intra-Testicular Testosterone) by stimulating the testes (directly) even when shutdown from androgens, such as Testosterone Enathate, shown in this study.
HCG is VERY important in cycles IMHO. It prevents the main reason the HPTA doesnt recover immediately post cycle - testicular dysfunction. It should be a staple of EVERY cycle causing shutdown IMHO.
I suggest HCG be used at 125-250ius 2-3 times weekly (as per Dr.Crisler's advice) with an AI throughout the cycle. This will maintain testicular size and function and prevent testicular dysfunction. It should also be noted that administering over "500ius will cause an increase in estrogen and progesterone, further hindering recovery" - Dr.Crisler.
For those wanting to convert their HCG doses into something more managable. Here's how:
HCG comes in 1500ius and 5000ius amps. Usually from Pregnyl. Chinese suppliers also stock their HCG in these two denominations too.
You need to get some sterile empty 10ML glass serum vials. You can get these from AR-R.
You also need to get some bac. water. If you were to mix 5000ius with 10ML bac. water, 1ML = 500ius. If you were to mix 1500ius with 10ML bac. water, 1ML = 150ius.
Once mixed, refridgerate. I tend to use my mixed HCG within 30-45 days.
Its really that simple.
This thread has been written on correspondance from Dr.Crisler (Swale), Concilliator and my own research gathered.
When our HPTA's are "shutdown" we have to distinguish between short-term inhibtion and long-term dysfunction.
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.
However, with time, it leads to testicular dysfunction. Without LH from the pituitary, the testes atrophy from disuse. This testicular dysfunction could be described as a reduction in the responsiveness to a signal to produce testosterone.
The hypothalamus and pituitary seem to recover fairly quickly following the use of androgens. GnRH, LH and FSH rise fairly quickly post cycle, but endogenous testosterone levels dont. As confirmed **broken link removed** by William Llewellyn. It shows that LH levels rise fairly quickly (on the 3rd week) after Testosterone Enanthate injections of 250mg weekly for 21 weeks. So it seems the hypothalamus and pituitary are not the problem in restarting endogenous testosterone production post cycle.
After recent correspondance with Dr.Crisler (Swale) he confirmed ganadotrophin levels were not to blame in restarting the HPTA. So what is?
If LH levels rise post cycle (the majority of the time) the reason why endogenous testosterone levels DONT rise, is the testes. Or testicular dysfunction. Testicular dysfunction is when the testes become atrophied from disuse or desensitised to ganadotrophins, such as LH. This could also be described as being the onset of primary hypogonadism.
Primary hypogonadism is when the testes no longer respond to LH. 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 desease (Klinefelter's syndrome), over use of anabolic steroids, as described in this study or overuse of HCG. The simple answer to primary hypogonadism is HRT.
So if the testes (testicular dysfunction) are the main culprit in restoring testosterone production post cycle how can we maintain testicular function and endogenous testosterone production even when "shutdown" using andorgens? Simple - HCG.
HCG has the ability to maintain endogenous testosterone production and ITT (Intra-Testicular Testosterone) by stimulating the testes (directly) even when shutdown from androgens, such as Testosterone Enathate, shown in this study.
HCG is VERY important in cycles IMHO. It prevents the main reason the HPTA doesnt recover immediately post cycle - testicular dysfunction. It should be a staple of EVERY cycle causing shutdown IMHO.
I suggest HCG be used at 125-250ius 2-3 times weekly (as per Dr.Crisler's advice) with an AI throughout the cycle. This will maintain testicular size and function and prevent testicular dysfunction. It should also be noted that administering over "500ius will cause an increase in estrogen and progesterone, further hindering recovery" - Dr.Crisler.
For those wanting to convert their HCG doses into something more managable. Here's how:
HCG comes in 1500ius and 5000ius amps. Usually from Pregnyl. Chinese suppliers also stock their HCG in these two denominations too.
You need to get some sterile empty 10ML glass serum vials. You can get these from AR-R.
You also need to get some bac. water. If you were to mix 5000ius with 10ML bac. water, 1ML = 500ius. If you were to mix 1500ius with 10ML bac. water, 1ML = 150ius.
Once mixed, refridgerate. I tend to use my mixed HCG within 30-45 days.
Its really that simple.
This thread has been written on correspondance from Dr.Crisler (Swale), Concilliator and my own research gathered.
