dice404
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i used to have pubertal gyno (just got it removed), that means a hard painful lump behind puffed up nips. needless to say, I am very gyno prone. before I had it removed, i ran 3 superdrol cycles, and the gyno actually got SMALLER while on the cycle. however, it did flare up after pct was finished (pct consisted of nolva, 6oxo, and diff cort control). So i dont think that gyno while on superdrol should be much of a concern. A friend of mine actually got some rebound gyno after his second cycle of superdrol (he ran the same pct as me). he noticed that his gyno shruk as well while on his next cycle of superdrol, and then rebounded after pct,so this reaction was not only limited to myself.
This got me thinking, superdrol is essentially methyl masteron, and masteron has been shown to have some antiestrogenic properties. now, yes, the 17aa does change the reaction the body has to the chemical, but i believe that this characteristic has remained. Anyone ever notice how they lose a lot of water after starting a superdrol cycle? (absence of this effect and consequently bloating may be due to an improperly synthesized clone, made from anadrol, and may still may contain some anadrol) This leads me to belive that superdrol has some anti-estrogenic properties as well. As far a increased prolactin, i believe this is a combination of its anti-estrogenic properties (supression of natty test plus an anti-estrogen leads to low estrogen. supressing E2 too much causes prolactin to rise) and superdrol's similarities to anadrol. Some people forget that superdrol is not simply methyl masteron, but also a "super saturated anadrol" as the original write up suggests. This means that instead of the 2a-hydroxymethylene that anadrol posess, superdrol (like masteron) has a 2a-methyl group. This gives superdrol some characteristics similar to anadrol, in my belief, namely the abillity to directly stimulate progesterone receptors. This combination leads to the prolactin induced sides.
Another thing to consider is the use of an AI in conjunction with a serm. think about it, when there is little estrogen present in the body, there is little need to further supress it in pct, like thesinner states, the object of pct(which causes hpta rebound) is not to iradicate estrogen, but control it. For superdrol, a serm alone is enough to achieve this. the prolonged suppression of estrogen only leads to increased prolactin and a greater chance for rebound gyno due to estrogen rebound after pct.
This is just a thought, but if anyone else has any input or sees I made a mistake, please say so
This got me thinking, superdrol is essentially methyl masteron, and masteron has been shown to have some antiestrogenic properties. now, yes, the 17aa does change the reaction the body has to the chemical, but i believe that this characteristic has remained. Anyone ever notice how they lose a lot of water after starting a superdrol cycle? (absence of this effect and consequently bloating may be due to an improperly synthesized clone, made from anadrol, and may still may contain some anadrol) This leads me to belive that superdrol has some anti-estrogenic properties as well. As far a increased prolactin, i believe this is a combination of its anti-estrogenic properties (supression of natty test plus an anti-estrogen leads to low estrogen. supressing E2 too much causes prolactin to rise) and superdrol's similarities to anadrol. Some people forget that superdrol is not simply methyl masteron, but also a "super saturated anadrol" as the original write up suggests. This means that instead of the 2a-hydroxymethylene that anadrol posess, superdrol (like masteron) has a 2a-methyl group. This gives superdrol some characteristics similar to anadrol, in my belief, namely the abillity to directly stimulate progesterone receptors. This combination leads to the prolactin induced sides.
Another thing to consider is the use of an AI in conjunction with a serm. think about it, when there is little estrogen present in the body, there is little need to further supress it in pct, like thesinner states, the object of pct(which causes hpta rebound) is not to iradicate estrogen, but control it. For superdrol, a serm alone is enough to achieve this. the prolonged suppression of estrogen only leads to increased prolactin and a greater chance for rebound gyno due to estrogen rebound after pct.
This is just a thought, but if anyone else has any input or sees I made a mistake, please say so