Does HCG do what you think it does?
(got this from a different board...but I thought it was a very interesting read)
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To spare the threadjack on another thread, I decided to post my evidence regarding HCG's place in bodybuilding. It has been the common myth that a man's balls shrink during an AAS cycle because they cease producing testosterone. But there are two functional cell groups in the testes, the Leydig cells and the Sertoli cells. Leydigs produce testosterone and Sertoli produce sperm. Only the Sertoli gain or lose mass significantly depending on whether they are producing sperm or not. When producing, they extend "branches" from which sperm cells grow and mature like grapes. As they become "ripe", the sperm are released.
An AAS cycle interrupts the normal HPTA cycle and both the Leydig and Sertoli cells reduce function. It's the reduction of sperm that shrinks the balls.
The Leydig cells are stimulated to produce testosterone by Luteinizing Hormone (LH). The Sertoli cells are stimulated to produce sperm by Follicle Stimulating Hormone (FSH). HCG acts directly on the Leydig cells like LH to cause them to turn out test, and it's very good at doing it. In fact, it can rapidly raise test levels within hours of administration. But Leydig cells don't enlarge or cluster the test it produces. In addition, the sudden increase in test creates a high aromatization environment, creating more estrogen, the very thing PCT is trying to mitigate.
Also, HCG inhibits FSH and LH release. Here's the info:
2.1.3 Human chorionic gonadotropin (hCG)
hCG is a glycoprotein with a molecular weight of about 43.000 daltons, produced by the syncytiotrophoblast. It is a heterodimer composed by two different sub-units: a and b . The specific b sub-unit contains 145 aminoacids and can be distinguished from the b sub-unit of LH only by 30 aminoacids in the C terminal part of the molecule. The whole molecule of hCG is also called holo-hCG, in order to be distinguished from total hCG, currently measured in the labs, (holo-hCG + free b sub-unit). The free b sub-unit circulates also in the blood. A particular form of hCG, called "nicked" hCG, is a holo-hCG or a free b sub-unit, where the bond between the 46th and the 47th aminoacid is broken. This gives rise to a particular tri-dimensional form of the molecule, making it often difficult to be recognised by the antibodies used for its measurement. The immunological recognition of "nicked" forms is specially important when hCG is measured to determine the risk of a mother to carry a trisomy 21 baby ( known as the "What if, double test or triple test"), as in this chromosomal pathology, the "nicked" forms increase significantly. The function of hCG is essential to maintain the corpus luteum of pregnancy and its progesterone secretion. But it has also an anti-gonadotrophic effect, as it inhibits the secretion of LH and FSH. hCG is said to be a "steroidogenic" hormone, not only because it favours the secretion of progesterone by the corpus luteum , but also because it stimulates the steroid secretion from foetal gonads. The regulation of hCG synthesis and secretion is provided by a trophoblastic GnRH.
The whole document is here: http://www.gfmer.ch/Endo/Lectures_08...l_hormones.htm
HCG works directly against restarting the HPTA by inhibiting FSH and LH release, and it does so by altering GnRH's frequency. All HCG does is to resemble LH's action on the Leydig cells and stimulates testosterone production. Just because it does stimulate test production DOES NOT mean that it is ideal. Both Nolvadex and Clomid compete with estrogen receptors on the hypothalamus and pituitary to fool them into thinking estrogen is low. This starts the HPTA cycling to create more testosterone, because it is by aromatizing testosterone into estrogen is how we get our estrogen. Nolva and Clomid essentially kick-start the HPTA into normal function, while HCG blocks it.
Sure, your natural test won't rise as fast as with HCG supplementation, but using HCG keeps the HPTA shut down longer, where Nolva and Clomid bring it back up gradually, but quicker without HCG or the estrogen rebound HCG causes.
Clomid has been shown to be very effective for a two week period, then begins to interrupt the HPTA again with prolonged use. Nolvadex has the same positive effect on the HPTA without the shutdown issue and is cheaper to run. Would I object to 2 weeks of Clomid use followed by 2 weeks of Nolva for PCT? No, except you're wasting money on an expensive drug (Clomid) when the cheaper (Nolva) is just as effective.
My argument that Clomid and HCG are unnecessary in bodybuilding is about efficiency. Why spend money you don't need to, or double efforts unnecessarily, or inhibit recovery ignorantly? Just because it is what we've done for years doesn't make it the correct approach. As science uncovers or discovers new info, we need to consider it in what we're doing. The body has a delicate balance and we're really fucking with it doing AAS. Being smart means being open to new info/ideas.
(got this from a different board...but I thought it was a very interesting read)
--------------------------------------------------------------------------------
To spare the threadjack on another thread, I decided to post my evidence regarding HCG's place in bodybuilding. It has been the common myth that a man's balls shrink during an AAS cycle because they cease producing testosterone. But there are two functional cell groups in the testes, the Leydig cells and the Sertoli cells. Leydigs produce testosterone and Sertoli produce sperm. Only the Sertoli gain or lose mass significantly depending on whether they are producing sperm or not. When producing, they extend "branches" from which sperm cells grow and mature like grapes. As they become "ripe", the sperm are released.
An AAS cycle interrupts the normal HPTA cycle and both the Leydig and Sertoli cells reduce function. It's the reduction of sperm that shrinks the balls.
The Leydig cells are stimulated to produce testosterone by Luteinizing Hormone (LH). The Sertoli cells are stimulated to produce sperm by Follicle Stimulating Hormone (FSH). HCG acts directly on the Leydig cells like LH to cause them to turn out test, and it's very good at doing it. In fact, it can rapidly raise test levels within hours of administration. But Leydig cells don't enlarge or cluster the test it produces. In addition, the sudden increase in test creates a high aromatization environment, creating more estrogen, the very thing PCT is trying to mitigate.
Also, HCG inhibits FSH and LH release. Here's the info:
2.1.3 Human chorionic gonadotropin (hCG)
hCG is a glycoprotein with a molecular weight of about 43.000 daltons, produced by the syncytiotrophoblast. It is a heterodimer composed by two different sub-units: a and b . The specific b sub-unit contains 145 aminoacids and can be distinguished from the b sub-unit of LH only by 30 aminoacids in the C terminal part of the molecule. The whole molecule of hCG is also called holo-hCG, in order to be distinguished from total hCG, currently measured in the labs, (holo-hCG + free b sub-unit). The free b sub-unit circulates also in the blood. A particular form of hCG, called "nicked" hCG, is a holo-hCG or a free b sub-unit, where the bond between the 46th and the 47th aminoacid is broken. This gives rise to a particular tri-dimensional form of the molecule, making it often difficult to be recognised by the antibodies used for its measurement. The immunological recognition of "nicked" forms is specially important when hCG is measured to determine the risk of a mother to carry a trisomy 21 baby ( known as the "What if, double test or triple test"), as in this chromosomal pathology, the "nicked" forms increase significantly. The function of hCG is essential to maintain the corpus luteum of pregnancy and its progesterone secretion. But it has also an anti-gonadotrophic effect, as it inhibits the secretion of LH and FSH. hCG is said to be a "steroidogenic" hormone, not only because it favours the secretion of progesterone by the corpus luteum , but also because it stimulates the steroid secretion from foetal gonads. The regulation of hCG synthesis and secretion is provided by a trophoblastic GnRH.
The whole document is here: http://www.gfmer.ch/Endo/Lectures_08...l_hormones.htm
HCG works directly against restarting the HPTA by inhibiting FSH and LH release, and it does so by altering GnRH's frequency. All HCG does is to resemble LH's action on the Leydig cells and stimulates testosterone production. Just because it does stimulate test production DOES NOT mean that it is ideal. Both Nolvadex and Clomid compete with estrogen receptors on the hypothalamus and pituitary to fool them into thinking estrogen is low. This starts the HPTA cycling to create more testosterone, because it is by aromatizing testosterone into estrogen is how we get our estrogen. Nolva and Clomid essentially kick-start the HPTA into normal function, while HCG blocks it.
Sure, your natural test won't rise as fast as with HCG supplementation, but using HCG keeps the HPTA shut down longer, where Nolva and Clomid bring it back up gradually, but quicker without HCG or the estrogen rebound HCG causes.
Clomid has been shown to be very effective for a two week period, then begins to interrupt the HPTA again with prolonged use. Nolvadex has the same positive effect on the HPTA without the shutdown issue and is cheaper to run. Would I object to 2 weeks of Clomid use followed by 2 weeks of Nolva for PCT? No, except you're wasting money on an expensive drug (Clomid) when the cheaper (Nolva) is just as effective.
My argument that Clomid and HCG are unnecessary in bodybuilding is about efficiency. Why spend money you don't need to, or double efforts unnecessarily, or inhibit recovery ignorantly? Just because it is what we've done for years doesn't make it the correct approach. As science uncovers or discovers new info, we need to consider it in what we're doing. The body has a delicate balance and we're really fucking with it doing AAS. Being smart means being open to new info/ideas.
