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We know that some pharmacological derivatives such as trenbolone seem to metabolize into progesterone like steroids in the body. This greatly attenuates the natural production of testosterone.
Consider what would happen at the end of a trenbolone cycle when the patient no longer has testosterone, but instead, tons of progesterones floating around.
Whether its estrogens or progesterones, I suppose we could group these together as "feminizing side effects". These side effects have been documented for many decades now, but still remain poorly understood. Im certain everyone to this web page is familiar with the aromatization of testosterones in the peripheral tissues to estradiol. [The majority of C 19 –steroids with a delta-3-keto configuration can be converted to estrogens leading to various feminizing effects. I think I read a magazine once that suggested that DHT blocked this effect… This isn’t true rather, if the testosterone ester was converted to DHT, then it was unable to become an estrogen]. In people with ‘tired livers’, the condition is worse! (Make note of that!) Moreover, most everyone knows that arimidex is a suitable harbinger to mollify this dilemma.
So now, more and more, the conversations these days turn into, "What about the progesterones..."
Progesterones have a particular antagonism with estrogens. It does this by decreasing estrogen responsiveness in the body. [Its more of an estrogen modifier than an actual antagonist]. By the way, androgenic steroids do this too – which rebuts the theory that theory that exogenous testosterone prematurely abates natural longitudinal bone growth.
Another wave of information circulated out there was that mifepristone (RU 486) blocked the formation of progesterone. This is not true; rather it blocks or competes with the receptor site in uteral tissues.
So what does progesterones do in men? They greatly reduce the production of testosterone by suppressing plasma LH levels. And in some cases, they can compete directly with testosterone at the cellular receptor level. I guess you can refer to it as “Medical Castration”!
I don’t have allot more for you at this time regarding progesterones. It first came to our attention while administering nandrolones to patients. These patients didn’t seem to have an increase in estrogens, but after the treatment cycle, these guys had a real hard time recovering their natural testosterone production. Eventually we concluded that we were dealing with progesterones. Its for that reason, (from experience), that I personally don’t suggest the use of nandrolones nor trenbolones.
I am not aware of the problem between progesterones and anadrol. Not that this problem does not exist. All I can say at this stage is that I’ll look into it later. The metabolites produced from the various testosterone derivatives, and inhibiting that response is paramount in my agenda.
In summary, Progesterone is not particularly good in males. It causes a great deal of ball shrinkage. I am not aware of any progesteronic effects in dbol, testosterone, or winstrol.
There are however, profound progesteronic effects associated with trenbolone acetate. In fact, its those progesteronic effects that make trenbolone a poor choice -- At least in the long run, as the patients balls dwindle away to the size of frozen pea's along with any hope of natural testosterone production following cycle cessation.
If you spend time within this web forum, you can read allot of material about gyno - its causes and its solutions.
In cases of hyperprolactinaemia there is usually no gynaecomastia but milk may be expressed from an entirely normal-sized male breast.
The cause of gyno in males is either due to a the production of allot of estrogen; or, a profound shift in the FREE testosterone:estrogen ratio.
Exogenous testosterone cycles usually cause gyno for all these reasons: 1) the P-450 aromatization of testosterone to estrogens 2) the increase in SHBG (TeBG) - which leads to a decrease in FREE testosterone following the cycle 3) the exogenous testosterone down-regulation of the natural production of testosterone.
Nolvadex (and clomid) will cause rebound gyno, [see previous forum submitals for the citation]. Moreover, they do NOT inhibit the production of estrogens.
The drugs that inhibit estrogen production are arimidex, femara, teslac, and cytadren.
Drugs that help lower TeBG (SHBG) and stimulate the post cycle production of testosterone include growth hormone (first and foremost), and nootropic class medications. That is to say that growth hormone can ameliorate post-cycle functional impairment of the patients endogenous FREE testosterone production.
My advice is to avoid progesterone at all costs because it will delay recovery of natural testosterone production. Furthermore, progesterone is a secondary cause of gyno due to its attenuation of endogenous testosterone production and the resulting shift in balance of free sex steroid levels to estrogen dominance.
Max
Consider what would happen at the end of a trenbolone cycle when the patient no longer has testosterone, but instead, tons of progesterones floating around.
Whether its estrogens or progesterones, I suppose we could group these together as "feminizing side effects". These side effects have been documented for many decades now, but still remain poorly understood. Im certain everyone to this web page is familiar with the aromatization of testosterones in the peripheral tissues to estradiol. [The majority of C 19 –steroids with a delta-3-keto configuration can be converted to estrogens leading to various feminizing effects. I think I read a magazine once that suggested that DHT blocked this effect… This isn’t true rather, if the testosterone ester was converted to DHT, then it was unable to become an estrogen]. In people with ‘tired livers’, the condition is worse! (Make note of that!) Moreover, most everyone knows that arimidex is a suitable harbinger to mollify this dilemma.
So now, more and more, the conversations these days turn into, "What about the progesterones..."
Progesterones have a particular antagonism with estrogens. It does this by decreasing estrogen responsiveness in the body. [Its more of an estrogen modifier than an actual antagonist]. By the way, androgenic steroids do this too – which rebuts the theory that theory that exogenous testosterone prematurely abates natural longitudinal bone growth.
Another wave of information circulated out there was that mifepristone (RU 486) blocked the formation of progesterone. This is not true; rather it blocks or competes with the receptor site in uteral tissues.
So what does progesterones do in men? They greatly reduce the production of testosterone by suppressing plasma LH levels. And in some cases, they can compete directly with testosterone at the cellular receptor level. I guess you can refer to it as “Medical Castration”!
I don’t have allot more for you at this time regarding progesterones. It first came to our attention while administering nandrolones to patients. These patients didn’t seem to have an increase in estrogens, but after the treatment cycle, these guys had a real hard time recovering their natural testosterone production. Eventually we concluded that we were dealing with progesterones. Its for that reason, (from experience), that I personally don’t suggest the use of nandrolones nor trenbolones.
I am not aware of the problem between progesterones and anadrol. Not that this problem does not exist. All I can say at this stage is that I’ll look into it later. The metabolites produced from the various testosterone derivatives, and inhibiting that response is paramount in my agenda.
In summary, Progesterone is not particularly good in males. It causes a great deal of ball shrinkage. I am not aware of any progesteronic effects in dbol, testosterone, or winstrol.
There are however, profound progesteronic effects associated with trenbolone acetate. In fact, its those progesteronic effects that make trenbolone a poor choice -- At least in the long run, as the patients balls dwindle away to the size of frozen pea's along with any hope of natural testosterone production following cycle cessation.
If you spend time within this web forum, you can read allot of material about gyno - its causes and its solutions.
In cases of hyperprolactinaemia there is usually no gynaecomastia but milk may be expressed from an entirely normal-sized male breast.
The cause of gyno in males is either due to a the production of allot of estrogen; or, a profound shift in the FREE testosterone:estrogen ratio.
Exogenous testosterone cycles usually cause gyno for all these reasons: 1) the P-450 aromatization of testosterone to estrogens 2) the increase in SHBG (TeBG) - which leads to a decrease in FREE testosterone following the cycle 3) the exogenous testosterone down-regulation of the natural production of testosterone.
Nolvadex (and clomid) will cause rebound gyno, [see previous forum submitals for the citation]. Moreover, they do NOT inhibit the production of estrogens.
The drugs that inhibit estrogen production are arimidex, femara, teslac, and cytadren.
Drugs that help lower TeBG (SHBG) and stimulate the post cycle production of testosterone include growth hormone (first and foremost), and nootropic class medications. That is to say that growth hormone can ameliorate post-cycle functional impairment of the patients endogenous FREE testosterone production.
My advice is to avoid progesterone at all costs because it will delay recovery of natural testosterone production. Furthermore, progesterone is a secondary cause of gyno due to its attenuation of endogenous testosterone production and the resulting shift in balance of free sex steroid levels to estrogen dominance.
Max
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