|
What the hell am I trying to do....
....in running PCT?
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.
__________________
"Everybody wanna be a bodybuilder, but don't nobody wanna lift no heavy-ass weight." Ronnie Coleman.
Last edited by Ironworker; 02-09-2010 at 05:37 AM..
|