guss
MuscleHead
- Aug 11, 2010
- 380
- 189
There is a lot of information in this section about PCT and protocols. Much of it is sound, based on the science of the day, and has been effective in mitigating estrogen rebound and jump starting natural test production.
But is it right? And is it the most effective way to deal with the shutdown of the HPTA?
I'm going to go against the wind here and make some claims that will give you one more reason to scratch your head.....until you put my protocol into place and see the wisdom in it.
Without recounting the entire science behind AAS use and the effect on the endocrine system that requires intervention, let me go over some basics:
HPTA: Hypothalamic-Pituitary-Testes Axis. This refers to the synergistic relationship of 2 glands (Hypothalamus and Pituitary) and how releases of certain hormones from those two affect the testes, causing them to produce testosterone/sperm. It's called an axis because there is a constant loop of information going between the three. A testosterone to estrogen ratio of less than 2 (less than 2 over 1) signals the "H&P" of the axis to release LH (luteinizing hormone) and FSH (follicle stimulating hormone), which stimulates the testes to produce sperm and testosterone. Once the balance of testosterone to estrogen reaches the 2 to 1 or better, the "H&P" reduce or stop the release of LH and FSH. If testosterone gets too high, the body tries to regulate the ratio by converting more testosterone to estrogen by increasing aromatase enzymes.
The problem with the adjustment in ratio of test to estrogen when one is on cycle is the amount of estrogen available to bind with estrogen receptors all over the body. The higher the number of estrogen receptions, the greater the effect of estrogen on the body, i.e. increasing the size of mammary glands (gyno), increasing prostate tissue (BPH), and water retention.
This is why we use either an AI (aromatase inhibitor), which prevents the aromatase enzyme from converting test to estrogen, or SERM's (Selective estrogen receptor modulator) which competes with estrogen by binding with receptors and preventing estrogen from binding with that site. SERM's are designed to compete at specific sites, rather than at all receptor locations, and the ones we use (Nolvadex, Clomid, and yes...Masteron) are designed to target breast tissue. However, there is some spill-over effect to other areas and that spill-over is different between the 3 SERM's I mentioned....which leads me to my first diversion from standard PCT protocol.
CLOMID vs. NOLVADEX (clomiphene citrate vs. tamoxifen)
It has been common to start PCT with Clomid because it was thought that Clomid acted on the HPTA to force the release of LH and FSH. Once Clomid got the axis working, you would switch to Nolvadex to deal with the increased estrogen brought on by the rise in natural test combined with the AAS still floating around in your system....purely to avoid gyno.
However, it has been more recently understood that the effect Clomid has on the HPTA is through estrogen blocking, specifically competing with the receptors on the hypothalamus and pituitary....which Nolvadex does as well. However, Clomid's effect is more efficient, which is NOT good, because it eventually shuts down the HPTA again, where Nolvadex has a less efficient effect on receptor modulation, not only stimulating the HPTA, but allows the axis to continue producing LH and FSH. I won't bore you with the science behind this for now....and you can research this yourself. What this means is that the much more expensive Clomid is unnecessary in a PCT protocol when the cheaper and more effective Nolvadex works better.
Absorb this for now....and I'll continue towards the proper PCT protocol in following posts.
To reiterate, I believe that Clomid is unnecessary for PCT. Nolvadex acts on the Hypothalamus (binding with estrogen receptors on it) to fool it into a positive feedback loop, inciting it to release GnRH (gonadotropin-releasing hormone) which signals the Pituitary gland to release LH and FSH. Nolvadex alone can be used for PCT following moderate and beginning cycles. The effect is immediate and cumulative. There is a ramp-up of test production over the period of PCT, and if begun at the half life end of the longest ester used, will only allow a small dip in free test as it builds up natural test production.
For a heavy, long cycle, I believe that HCG is necessary to begin PCT. If you have cycled with a total of a gram of AAS or more a week (includes orals), not only are you completely shut down, the drop off after the half life date is significant and catabolism sets in rapidly. Starting a higher dose of Nolvadex along with 3 high dose applications of HCG will do two things. First, I recommend 3-2000IU doses of HCG starting approximately 10 days after the last pinning of the longest ester (test E or C). Those doses are spread evenly over the following 7 days. This will rapidly elevate natural test production to a very high level, with aromatization possible. Starting Nolvadex at the same time at a dose of 40mg/day will deal with aromatization. Then reducing Nolvadex to 20mg/day for the next 2 weeks following HCG administration will kick the Hypothalamus into gear producing GnRH, thus causing the release of LH from the Pituitary and therefore maintaining the test production HCG initiated, but at a normal level.
One caveat to this protocol is that if you are particularly susceptible to gyno, you would double the doses of Nolvadex listed above.
This protocol will give you a straight slide of test levels from the high during cycle to natural test levels rather than a convex curve, where you have a rapid drop-off of strength/energy and then elevated to what natural test can maintain.
It is questionable whether or not a 4 week PCT schedule will bring you back to normal following very high, very long cycles, i.e. 20+ weeks at 1 gram/week or more and I usually recommend cruising after PCT on HRT level AAS for a period at least half as long as the last cycle. HRT levels range from 125mg/week test to 300mg/week. 150mg/week seems to be a good midrange that won't shut you down again and will keep you feeling energetic and strong.
But is it right? And is it the most effective way to deal with the shutdown of the HPTA?
I'm going to go against the wind here and make some claims that will give you one more reason to scratch your head.....until you put my protocol into place and see the wisdom in it.
Without recounting the entire science behind AAS use and the effect on the endocrine system that requires intervention, let me go over some basics:
HPTA: Hypothalamic-Pituitary-Testes Axis. This refers to the synergistic relationship of 2 glands (Hypothalamus and Pituitary) and how releases of certain hormones from those two affect the testes, causing them to produce testosterone/sperm. It's called an axis because there is a constant loop of information going between the three. A testosterone to estrogen ratio of less than 2 (less than 2 over 1) signals the "H&P" of the axis to release LH (luteinizing hormone) and FSH (follicle stimulating hormone), which stimulates the testes to produce sperm and testosterone. Once the balance of testosterone to estrogen reaches the 2 to 1 or better, the "H&P" reduce or stop the release of LH and FSH. If testosterone gets too high, the body tries to regulate the ratio by converting more testosterone to estrogen by increasing aromatase enzymes.
The problem with the adjustment in ratio of test to estrogen when one is on cycle is the amount of estrogen available to bind with estrogen receptors all over the body. The higher the number of estrogen receptions, the greater the effect of estrogen on the body, i.e. increasing the size of mammary glands (gyno), increasing prostate tissue (BPH), and water retention.
This is why we use either an AI (aromatase inhibitor), which prevents the aromatase enzyme from converting test to estrogen, or SERM's (Selective estrogen receptor modulator) which competes with estrogen by binding with receptors and preventing estrogen from binding with that site. SERM's are designed to compete at specific sites, rather than at all receptor locations, and the ones we use (Nolvadex, Clomid, and yes...Masteron) are designed to target breast tissue. However, there is some spill-over effect to other areas and that spill-over is different between the 3 SERM's I mentioned....which leads me to my first diversion from standard PCT protocol.
CLOMID vs. NOLVADEX (clomiphene citrate vs. tamoxifen)
It has been common to start PCT with Clomid because it was thought that Clomid acted on the HPTA to force the release of LH and FSH. Once Clomid got the axis working, you would switch to Nolvadex to deal with the increased estrogen brought on by the rise in natural test combined with the AAS still floating around in your system....purely to avoid gyno.
However, it has been more recently understood that the effect Clomid has on the HPTA is through estrogen blocking, specifically competing with the receptors on the hypothalamus and pituitary....which Nolvadex does as well. However, Clomid's effect is more efficient, which is NOT good, because it eventually shuts down the HPTA again, where Nolvadex has a less efficient effect on receptor modulation, not only stimulating the HPTA, but allows the axis to continue producing LH and FSH. I won't bore you with the science behind this for now....and you can research this yourself. What this means is that the much more expensive Clomid is unnecessary in a PCT protocol when the cheaper and more effective Nolvadex works better.
Absorb this for now....and I'll continue towards the proper PCT protocol in following posts.
To reiterate, I believe that Clomid is unnecessary for PCT. Nolvadex acts on the Hypothalamus (binding with estrogen receptors on it) to fool it into a positive feedback loop, inciting it to release GnRH (gonadotropin-releasing hormone) which signals the Pituitary gland to release LH and FSH. Nolvadex alone can be used for PCT following moderate and beginning cycles. The effect is immediate and cumulative. There is a ramp-up of test production over the period of PCT, and if begun at the half life end of the longest ester used, will only allow a small dip in free test as it builds up natural test production.
For a heavy, long cycle, I believe that HCG is necessary to begin PCT. If you have cycled with a total of a gram of AAS or more a week (includes orals), not only are you completely shut down, the drop off after the half life date is significant and catabolism sets in rapidly. Starting a higher dose of Nolvadex along with 3 high dose applications of HCG will do two things. First, I recommend 3-2000IU doses of HCG starting approximately 10 days after the last pinning of the longest ester (test E or C). Those doses are spread evenly over the following 7 days. This will rapidly elevate natural test production to a very high level, with aromatization possible. Starting Nolvadex at the same time at a dose of 40mg/day will deal with aromatization. Then reducing Nolvadex to 20mg/day for the next 2 weeks following HCG administration will kick the Hypothalamus into gear producing GnRH, thus causing the release of LH from the Pituitary and therefore maintaining the test production HCG initiated, but at a normal level.
One caveat to this protocol is that if you are particularly susceptible to gyno, you would double the doses of Nolvadex listed above.
This protocol will give you a straight slide of test levels from the high during cycle to natural test levels rather than a convex curve, where you have a rapid drop-off of strength/energy and then elevated to what natural test can maintain.
It is questionable whether or not a 4 week PCT schedule will bring you back to normal following very high, very long cycles, i.e. 20+ weeks at 1 gram/week or more and I usually recommend cruising after PCT on HRT level AAS for a period at least half as long as the last cycle. HRT levels range from 125mg/week test to 300mg/week. 150mg/week seems to be a good midrange that won't shut you down again and will keep you feeling energetic and strong.