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Some notes on Oxymetholone:
Although the mechanism of Anadrol action hasn?t been studied very well, it?s one of the few compounds that has been tested in so many studies, on so many people, for so many different things, in such wildly varying doses (usually 1-5 mg/kg bodyweight)
Anadrol is not a very potent anabolic. People don?t like to hear that, since its commonly used as a mass drug, but it?s a very poor ligand for the androgen receptor because of its bulky 2-methylene group, and there is a reason its run at such high doses, even in clinical studies. Common bodybuilding doses are 50-200 mg per day, but the 1-5 mg per kg used in clinical studies, amounts to 91-455 mg per day for a 200 lbs person. That means if any of us here were partaking in a clinical study with anadrol, none of us would be taking less than 75 mg, most no less than 100 mg, provided you were in the LOWEST dose group. Not a single androgen was ever used in such doses clinically, which speaks a lot to its weaker anabolic activity, relative to other AAS.
The main issue with fully elucidating Anadrol?s effect is that it metabolizes into a wild array of compounds that may all have some biological activity at type I nuclear receptors, and therefore we can?t go just by its own structure and say it should behave like this?, like we can for most AAS. It even has some unusual secosteroid metabolites that are entirely unique. But we can make a number of deductions based on both experience and the main metabolites.
One such is that Anadrol may actually be more androgenic than it is anabolic. The other is that Anadrol is most definitely estrogenic BUT IS VERY UNLIKELY TO CAUSE GYNO. Let?s start with the androgenic part. The parent steroid will bind as weakly in androgenically sensitive tissues as in muscle, so you would expect its androgenic potential to be on par with its anabolic potential. But one key metabolite of oxymetholone is mestanolone (methyl-DHT, it basically loses its 2-hydroxymethylene group) and like DHT, mestanolone is readily metabolized to its 3alpha-hydroxy form in muscle, but not in scalp, skin, prostate and so on. Of course the metabolisation to mestanolone is only a portion, so even in the high doses, its unlikely to rival taking pure mestanolone (excretion studies suggest about 1/5th is converted)
On the estrogenic front things get interesting. First of all we have conclusive evidence that Anadrol DOES NOT AROMATIZE (so to the person taking an AI, that?s sort of pointless) and does NOT bind the progesterone receptor AT ALL. Renowned organic chemist Patrick Arnold once noted it could bind the ER directly because it has an acidic A-ring, and the data seems to confirm this. Mestanolone, the metabolite, readily converts, especially in muscle, to methyl-androstanediol, and the parent oxymetholone could behave exactly like methyl-androstanediol because the hydroxymethylone group extends far enough to pass for a 3-hydroxyl group. Androstanediol is a physiological estrogen, known to selectively bind the Estrogen receptor, especially in the brain. HOWEVER (and this is a big one) androstanediol is directly created, physiologically, from DHT. Neither DHT nor mestanolone, nor any such product has ever been known to cause gyno. Indeed, it does not appear that androstanediols (saturated A-ring steroids with a C19 and a 3alpha-hydroxy group) are estrogenic in the breast.
In fact some of you may have directly taken these products since both androstanediol (3-alpha) and methyl-androstanediol (Methyl-3-alpha) were available as prohormones at some time or another. If you did, you know they were not believed to be estrogenic in the sense an AAS user considers something estrogenic, despite the fact that they are known physiologically active estrogens. Hence it is extremely unlikely that oxymetholone or its major metabolites can cause or aggravate gyno. The plethora of studies seems to confirm this, as one study in 1985 used it to TREAT gyno, and a wide range of studies never once remarked on the appearance of gyno as a possible side-effect, even in doses in excess of 300 mg (including studies using 200 mg for 20 weeks). However since it is distinctly estrogenic in other tissues, it is likely some of its effects are mediated by the estrogen receptor.
In regards to water retention, it is unclear if there is a link to its estrogenic nature, but oxymetholone is known to drastically increase blood pressure, an effect likely mediated downstream of ACE causing increased mineralocorticoid action. Use of an ACE inhibitor can alleviate most symptoms associated with oxymetholone use, including water retention and high blood pressure. This is likely why its garnering some attention as a prep drug, since people in prep often use ACE inhibitors and/or diuretics, which nullify increased blood pressure and bloat, allowing the strength effects (since it’s a known neuro-estrogen this could directly relate to its amazing strength effects) to help you without any real side-effects, even in relatively high doses.
Many studies remark the liver toxicity of anadrol, but its hard to get an actual read on just how bad it is, and it may be that different individuals respond differently. In some studies lower doses over short periods of time already alarmingly raise liver enzyme levels, while a study with 200 mg for 20 weeks seemed to not have a higher incidence of liver problems than those other studies.
Although the mechanism of Anadrol action hasn?t been studied very well, it?s one of the few compounds that has been tested in so many studies, on so many people, for so many different things, in such wildly varying doses (usually 1-5 mg/kg bodyweight)
Anadrol is not a very potent anabolic. People don?t like to hear that, since its commonly used as a mass drug, but it?s a very poor ligand for the androgen receptor because of its bulky 2-methylene group, and there is a reason its run at such high doses, even in clinical studies. Common bodybuilding doses are 50-200 mg per day, but the 1-5 mg per kg used in clinical studies, amounts to 91-455 mg per day for a 200 lbs person. That means if any of us here were partaking in a clinical study with anadrol, none of us would be taking less than 75 mg, most no less than 100 mg, provided you were in the LOWEST dose group. Not a single androgen was ever used in such doses clinically, which speaks a lot to its weaker anabolic activity, relative to other AAS.
The main issue with fully elucidating Anadrol?s effect is that it metabolizes into a wild array of compounds that may all have some biological activity at type I nuclear receptors, and therefore we can?t go just by its own structure and say it should behave like this?, like we can for most AAS. It even has some unusual secosteroid metabolites that are entirely unique. But we can make a number of deductions based on both experience and the main metabolites.
One such is that Anadrol may actually be more androgenic than it is anabolic. The other is that Anadrol is most definitely estrogenic BUT IS VERY UNLIKELY TO CAUSE GYNO. Let?s start with the androgenic part. The parent steroid will bind as weakly in androgenically sensitive tissues as in muscle, so you would expect its androgenic potential to be on par with its anabolic potential. But one key metabolite of oxymetholone is mestanolone (methyl-DHT, it basically loses its 2-hydroxymethylene group) and like DHT, mestanolone is readily metabolized to its 3alpha-hydroxy form in muscle, but not in scalp, skin, prostate and so on. Of course the metabolisation to mestanolone is only a portion, so even in the high doses, its unlikely to rival taking pure mestanolone (excretion studies suggest about 1/5th is converted)
On the estrogenic front things get interesting. First of all we have conclusive evidence that Anadrol DOES NOT AROMATIZE (so to the person taking an AI, that?s sort of pointless) and does NOT bind the progesterone receptor AT ALL. Renowned organic chemist Patrick Arnold once noted it could bind the ER directly because it has an acidic A-ring, and the data seems to confirm this. Mestanolone, the metabolite, readily converts, especially in muscle, to methyl-androstanediol, and the parent oxymetholone could behave exactly like methyl-androstanediol because the hydroxymethylone group extends far enough to pass for a 3-hydroxyl group. Androstanediol is a physiological estrogen, known to selectively bind the Estrogen receptor, especially in the brain. HOWEVER (and this is a big one) androstanediol is directly created, physiologically, from DHT. Neither DHT nor mestanolone, nor any such product has ever been known to cause gyno. Indeed, it does not appear that androstanediols (saturated A-ring steroids with a C19 and a 3alpha-hydroxy group) are estrogenic in the breast.
In fact some of you may have directly taken these products since both androstanediol (3-alpha) and methyl-androstanediol (Methyl-3-alpha) were available as prohormones at some time or another. If you did, you know they were not believed to be estrogenic in the sense an AAS user considers something estrogenic, despite the fact that they are known physiologically active estrogens. Hence it is extremely unlikely that oxymetholone or its major metabolites can cause or aggravate gyno. The plethora of studies seems to confirm this, as one study in 1985 used it to TREAT gyno, and a wide range of studies never once remarked on the appearance of gyno as a possible side-effect, even in doses in excess of 300 mg (including studies using 200 mg for 20 weeks). However since it is distinctly estrogenic in other tissues, it is likely some of its effects are mediated by the estrogen receptor.
In regards to water retention, it is unclear if there is a link to its estrogenic nature, but oxymetholone is known to drastically increase blood pressure, an effect likely mediated downstream of ACE causing increased mineralocorticoid action. Use of an ACE inhibitor can alleviate most symptoms associated with oxymetholone use, including water retention and high blood pressure. This is likely why its garnering some attention as a prep drug, since people in prep often use ACE inhibitors and/or diuretics, which nullify increased blood pressure and bloat, allowing the strength effects (since it’s a known neuro-estrogen this could directly relate to its amazing strength effects) to help you without any real side-effects, even in relatively high doses.
Many studies remark the liver toxicity of anadrol, but its hard to get an actual read on just how bad it is, and it may be that different individuals respond differently. In some studies lower doses over short periods of time already alarmingly raise liver enzyme levels, while a study with 200 mg for 20 weeks seemed to not have a higher incidence of liver problems than those other studies.
