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I found this on the net an thought it might be of use in a debate as most I have asked about HCG have all had different views.
HCG: Action and argument for its use by the enhanced athlete
Human chorionic gonadotropin, or HCG for short, is an interesting non-steroidal pharmaceutical product commonly found in the athletes' drug arsenal. For many it has been an ingrained part of the regular steroid regimen, used to enhance endogenous testosterone output during of after a heavy steroid cycle. Recently however, some experts have claimed the practice of using HCG to be completely counterproductive. For those who have taken the time to read the articles of both HCG opponents and proponents, a state of confusion is no doubt going to surround this drug. I likewise thought a closer look at this drug product, as well as the reasoning behind both its good and bad reviews, was called for.
HCG is a natural hormone produced in the female body during pregnancy. The placenta, as a means to "hijack" the fluctuating female hormonal release system and support pregnancy, produces it. This is the same source for pharmaceutically prepared HCG, as this hormone is only currently manufactured by filtering the urine of pregnant women for active compound. The drug of course is purified before sale, and is has been deemed fully same to use. HCG mimics the action of endogenous LH (luteinizing hormone), a pituitary hormone that in men signals the testes to produce testosterone. Upon administration of course HCG will stimulate the Leydig's cells in the testes (by increasing cAMP levels and enhancing cellular activity) to bump up the rate of testosterone release. It is this function that caught to immediate attention of athletes, as clearly more testosterone is a good thing if wishing to increase of maintain muscle mass.
HCG is most commonly used at the conclusion of a steroid cycle, a time when endogenous testosterone levels will likely be suppressed due to the negative feedback inhibition placed on the body by heightened androgen, estrogen or even progestational activity. All three in fact negatively influence testosterone release. The initial method of use was to take HCG in order to restore the natural release of testosterone after steroids have been withdrawn, and avoid a prolonged delay in natural testicular function that otherwise might result. Indeed this is an important concern, as it has been shown to take many weeks, if not months, for the testes to resume normal hormonal production following a suppressive course of steroid therapy. For this purpose many dosage regimens have been suggested, but most call for a weekly or biweekly shot of at least 2500-5000IU.
Now the reasoning behind HCG's recent fall from grace in the eyes of certain researchers is due to both its unique action, as well as a general argument against enhancing testosterone output through direct exogenous stimulation. Its unique action is displayed in its ability to stimulate not only testosterone output, but also the general cellular activity of the Leydig's cells. You see, the Leydig's cells are also a pronounce site of testosterone aromatization. Aromatization is a natural process in which androgens are converted to estrogens in the human body, which (estrogens) of course we know are also inhibitive of testosterone release. When we enhance cellular activity in these cells, aromatization is unavoidably also increased (1). The logical argument is that if we are enhancing our level of estrogens, we will not be supporting a natural return to homeostasis, but preventing it. The general argument against its use is simply that a dramatically heightened release of testosterone is itself inhibitive of endogenous androgen production, and will delay a return to normal state. Those who argue against its use typically recommend anti-estrogens instead, which can support a return to homeostasis by blocking the negative feedback imposed on the body by estrogens. Indeed anti-estrogens can play an important role in this process, however there is no question that they offer less direct, and much weaker, activity in regard to restoring testosterone release.
As you will see also, there is a major flaw in the argument suggesting anti-estrogen use exclusively. Although anti-estrogens may possibly increase the output of endogenous LH, this is likely not going to be enough to stimulate a rapid return to normal testosterone release. This is made clear in a 1975 study (2) charting the balance of hormone levels before, during and after testosterone enanthate therapy (250mg weekly). In this study we notice the expected suppression of both testosterone and LH levels during therapy. However after testosterone was withdrawn, an interesting trend results. Although LH levels rapidly return to normal, testosterone production does not return to this state for months. To spite the normal output of LH, the Leydig's cells, presumably due to a prolonged state of inactivity and atrophy, are not able to resume normal functioning for some time. We therefore must conclude that although anti-estrogens may be able to support LH release after steroid therapy, they are not targeting to site of issue (namely the state of the Leydig's cells).
We likewise must return to the normal argument that HCG can play a vital role in the desired return to homeostasis after steroid therapy. Although HCG simply mimics the action of LH, the use of a periodic bolus dosage may be enough to shock the testes into a more rapid return to normal functioning and volume. This action is clearly supported by the reports of many athletes who have used HCG regularly, despite any bad attention paid to it in recent months. Clearly HCG can accomplish what anti-estrogens are unable, namely overloading the Leydig's cells with the signal needed to restore activity. Otherwise it may be many weeks if not months before the testes catch up to the normal endogenous (or even anti-estrogen supported) LH activity. Indeed there are still drawbacks to the use of HCG (namely enhanced rate of aromatization in the Leydig's cells), and for this reason HCG therapy should be limited to a small course (at a heavy dose of at least 5000IU weekly) for approximately two to three weeks only. To combat the buildup of estrogens during and this time, as well as to support homeostasis though a separate means, anti-estrogens such as Nolvadex or Clomid can still play an important part. In fact it seams quite reasonably to use them at the conclusion of steroid therapy in addition to and after HCG. We however cannot ignore the usefulness of HCG by mistaking a bad argument for a good one; it is still an important if not vital part of the athletes' ancillary drug program.
-William Llewellyn
Author of Anabolics 2000
Bibliography:
1 Acute stimulation of aromatization in Leydig's cells by human chorionic gonadotropin in vitro. Proc Natl Acad Sci USA 76:4460-3, 1979
2 Effect of long-term testosterone enanthate administration on male reproductive function: Clinical evaluation, serum FSH, LH, Testosterone and seminal fluid analysis in normal men. J. Mauss, G. Borsch, K. Bormacher et al. Acta Endocrinologica 78 (1975) 373-384
HCG: Action and argument for its use by the enhanced athlete
Human chorionic gonadotropin, or HCG for short, is an interesting non-steroidal pharmaceutical product commonly found in the athletes' drug arsenal. For many it has been an ingrained part of the regular steroid regimen, used to enhance endogenous testosterone output during of after a heavy steroid cycle. Recently however, some experts have claimed the practice of using HCG to be completely counterproductive. For those who have taken the time to read the articles of both HCG opponents and proponents, a state of confusion is no doubt going to surround this drug. I likewise thought a closer look at this drug product, as well as the reasoning behind both its good and bad reviews, was called for.
HCG is a natural hormone produced in the female body during pregnancy. The placenta, as a means to "hijack" the fluctuating female hormonal release system and support pregnancy, produces it. This is the same source for pharmaceutically prepared HCG, as this hormone is only currently manufactured by filtering the urine of pregnant women for active compound. The drug of course is purified before sale, and is has been deemed fully same to use. HCG mimics the action of endogenous LH (luteinizing hormone), a pituitary hormone that in men signals the testes to produce testosterone. Upon administration of course HCG will stimulate the Leydig's cells in the testes (by increasing cAMP levels and enhancing cellular activity) to bump up the rate of testosterone release. It is this function that caught to immediate attention of athletes, as clearly more testosterone is a good thing if wishing to increase of maintain muscle mass.
HCG is most commonly used at the conclusion of a steroid cycle, a time when endogenous testosterone levels will likely be suppressed due to the negative feedback inhibition placed on the body by heightened androgen, estrogen or even progestational activity. All three in fact negatively influence testosterone release. The initial method of use was to take HCG in order to restore the natural release of testosterone after steroids have been withdrawn, and avoid a prolonged delay in natural testicular function that otherwise might result. Indeed this is an important concern, as it has been shown to take many weeks, if not months, for the testes to resume normal hormonal production following a suppressive course of steroid therapy. For this purpose many dosage regimens have been suggested, but most call for a weekly or biweekly shot of at least 2500-5000IU.
Now the reasoning behind HCG's recent fall from grace in the eyes of certain researchers is due to both its unique action, as well as a general argument against enhancing testosterone output through direct exogenous stimulation. Its unique action is displayed in its ability to stimulate not only testosterone output, but also the general cellular activity of the Leydig's cells. You see, the Leydig's cells are also a pronounce site of testosterone aromatization. Aromatization is a natural process in which androgens are converted to estrogens in the human body, which (estrogens) of course we know are also inhibitive of testosterone release. When we enhance cellular activity in these cells, aromatization is unavoidably also increased (1). The logical argument is that if we are enhancing our level of estrogens, we will not be supporting a natural return to homeostasis, but preventing it. The general argument against its use is simply that a dramatically heightened release of testosterone is itself inhibitive of endogenous androgen production, and will delay a return to normal state. Those who argue against its use typically recommend anti-estrogens instead, which can support a return to homeostasis by blocking the negative feedback imposed on the body by estrogens. Indeed anti-estrogens can play an important role in this process, however there is no question that they offer less direct, and much weaker, activity in regard to restoring testosterone release.
As you will see also, there is a major flaw in the argument suggesting anti-estrogen use exclusively. Although anti-estrogens may possibly increase the output of endogenous LH, this is likely not going to be enough to stimulate a rapid return to normal testosterone release. This is made clear in a 1975 study (2) charting the balance of hormone levels before, during and after testosterone enanthate therapy (250mg weekly). In this study we notice the expected suppression of both testosterone and LH levels during therapy. However after testosterone was withdrawn, an interesting trend results. Although LH levels rapidly return to normal, testosterone production does not return to this state for months. To spite the normal output of LH, the Leydig's cells, presumably due to a prolonged state of inactivity and atrophy, are not able to resume normal functioning for some time. We therefore must conclude that although anti-estrogens may be able to support LH release after steroid therapy, they are not targeting to site of issue (namely the state of the Leydig's cells).
We likewise must return to the normal argument that HCG can play a vital role in the desired return to homeostasis after steroid therapy. Although HCG simply mimics the action of LH, the use of a periodic bolus dosage may be enough to shock the testes into a more rapid return to normal functioning and volume. This action is clearly supported by the reports of many athletes who have used HCG regularly, despite any bad attention paid to it in recent months. Clearly HCG can accomplish what anti-estrogens are unable, namely overloading the Leydig's cells with the signal needed to restore activity. Otherwise it may be many weeks if not months before the testes catch up to the normal endogenous (or even anti-estrogen supported) LH activity. Indeed there are still drawbacks to the use of HCG (namely enhanced rate of aromatization in the Leydig's cells), and for this reason HCG therapy should be limited to a small course (at a heavy dose of at least 5000IU weekly) for approximately two to three weeks only. To combat the buildup of estrogens during and this time, as well as to support homeostasis though a separate means, anti-estrogens such as Nolvadex or Clomid can still play an important part. In fact it seams quite reasonably to use them at the conclusion of steroid therapy in addition to and after HCG. We however cannot ignore the usefulness of HCG by mistaking a bad argument for a good one; it is still an important if not vital part of the athletes' ancillary drug program.
-William Llewellyn
Author of Anabolics 2000
Bibliography:
1 Acute stimulation of aromatization in Leydig's cells by human chorionic gonadotropin in vitro. Proc Natl Acad Sci USA 76:4460-3, 1979
2 Effect of long-term testosterone enanthate administration on male reproductive function: Clinical evaluation, serum FSH, LH, Testosterone and seminal fluid analysis in normal men. J. Mauss, G. Borsch, K. Bormacher et al. Acta Endocrinologica 78 (1975) 373-384
