Does methandienone aromatize less than testosterone?

With respect to aromatase rate, less (~35% that of T), because the 17α-methyl group sterically hinders aromatization in vivo. However, it aromatizes to a more potent estrogen than T.

With respect to aromatic potency, more. Since its aromatic product is heretofore unidentified, but is very likely 17α-methyl-estrogen (17α-methyl-E), identical to methyltestosterone's potent aromatic product, and essentially functionally equivalent in aromatic potency to MT given their similarly sterically hindered rate of aromatization.

17α-methyl-E's efficacy, or potency to transactivate the ER-α is ~ 36.5% more potent than estradiol's (E2's).

We might, theoretically, use the formula rate of aromatization* EC50 * RBA, but we wouldn't be accounting for (a) uncertainty in the identity of the aromatic product, (b) rate of breakdown of the produced 7a-methylestradiol, nor (c) the estrogenic potency of the resulting metabolites.
 
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the science this guy said above.

As far as my experience, it seems like dbol gives off “e2 like” sides way harder.

I can take 350mg of test a week and stay tight. 50mg of dbol a day, and you might wanna spear me because I look like a water buffalo. Also get the itchy nippers
 
With respect to aromatase rate, less (~35% that of T), because the 17α-methyl group sterically hinders aromatization in vivo. However, it aromatizes to a more potent estrogen than T.

With respect to aromatic potency, more. Since its aromatic product is heretofore unidentified, but is very likely 17α-methyl-estrogen (17α-methyl-E), identical to methyltestosterone's potent aromatic product, and essentially functionally equivalent in aromatic potency to MT given their similarly sterically hindered rate of aromatization.

17α-methyl-E's efficacy, or potency to transactivate the ER-α is ~ 36.5% more potent than estradiol's (E2's).

We might, theoretically, use the formula rate of aromatization* EC50 * RBA, but we wouldn't be accounting for (a) uncertainty in the identity of the aromatic product, (b) rate of breakdown of the produced 7a-methylestradiol, nor (c) the estrogenic potency of the resulting metabolites.
Now that is a response, holy hell
 
With respect to aromatase rate, less (~35% that of T), because the 17α-methyl group sterically hinders aromatization in vivo. However, it aromatizes to a more potent estrogen than T.

With respect to aromatic potency, more. Since its aromatic product is heretofore unidentified, but is very likely 17α-methyl-estrogen (17α-methyl-E), identical to methyltestosterone's potent aromatic product, and essentially functionally equivalent in aromatic potency to MT given their similarly sterically hindered rate of aromatization.

17α-methyl-E's efficacy, or potency to transactivate the ER-α is ~ 36.5% more potent than estradiol's (E2's).

We might, theoretically, use the formula rate of aromatization* EC50 * RBA, but we wouldn't be accounting for (a) uncertainty in the identity of the aromatic product, (b) rate of breakdown of the produced 7a-methylestradiol, nor (c) the estrogenic potency of the resulting metabolites.
In other words, 500 mg testosterone a week will cause less aromatization or will produce less potent estradiol compared to 400 mg testosterone and 100 mg dianabol a week?
 
In other words, 500 mg testosterone a week will cause less aromatization or will produce less potent estradiol compared to 400 mg testosterone and 100 mg dianabol a week?
400 mg T & 100 mg metandienone will produce slightly more symptoms of estrogenicity (e.g., gynecomastia) than 500 mg T q.w.
 
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