russianstar
New member
Anyone who knows anything about chemical structures will see that superdrol is not a progestin, and shouldnt cause prolactin like side effects.
The problem is everyone is different and eveyone has different amounts of progestin receptors, wich can cause worse sides in some users than others, one guy can use deca and get no bloat, another with the same dose will get bloat and gyno, because of this one reason alone. Now Beastsrol or superdrol is in itself not that androgenic, and as its structure suggests its not that different to other dht based steroids, now an action takes place that explains how it works... its doesnt act like a typical androgenic, but acts a little like oxymetholone, in that it doesnt show any real affinity for the 5AR enzyme, so you get weaker affinty for the androgen receptor than dht, but you get stronger androgenic effects as the enzyme 3beta hydroxysteroid dehydrogenase has little effect on the androgen affinity of superdrol.
The problem is this same enzyme 3beta hydroxysteroid dehydrogenase, is used in the conversion of many metaobiles in the body, Superdrol produces a lot of metabolites that dont get bound by the androgen receptor like we just saw, it cant aromatize, so it doesnt bind to the estrogen receptor, but it circulates, as its also a di methyl, it is very biovailable so a lot of the product circulates in the blood, and these extra metabolites dont bind specificly...not in the way they should.. so i will explain in a detailed way then make it much easier to understand.
Prolactin is normaly caused by progestins, but can also be caused by dht, how?
For example, it is currently understood that when testosterone enters the cell cytoplasm it is subsequently converted to the more "active" androgen, dihydrotestosterone, DHT, by reduction at the 5alpha position, This is normal. Dihydrotestosterone is then either bound to a cytoplasmic "receptor" protein Rc, or is further metabolized to either 5alpha-androstane-3alpha,17beta-diol or 5alpha-androstane-3beta,17beta-diol ,DIOL. The binding of DHT to its cytoplasmic receptor protein results in translocation of the steroid-receptor complex into the nucleus where presumably the complex dissociates and DHT exerts its androgenic effects. The transport of DHT to the nucleus can also result from the conversion of testosterone to DHT by nuclear membrane-bound 5alpha-reductase. Prolactin augmentation of DHT effects is envisioned as resulting from interaction of prolactin with its receptor, which due to the large size of the prolactin molecule is probably located in or on the plasma membrane.
Because superdrol is androgenic, but lacks the ability to show affinity via 5ar, it circulates, and this causes the large amounts of androgens to look for a transporter, so that it can bind to the androgen recptor, so it uses prolactin wich has a high affinity to cytoplasmic receptor protein, allowing the androgens, testosterone, to be carried and allowing them to convert to dht, only problem is prolactin hormone or luteotropic hormone is synthesised and secreted by sex binding lactotrope cells in the adenohypophysis (anterior pituitary gland, And this gland now produces more prolactin to help deal with the large amount of testosterone circulating that hasnt bound to the estrogen of androgen receptor, Part of the reason why superdol is so anabolic, So instead of binding to the androgen receptors in the scalp and the prostrate it converts to dht through this unique process, using prolactin to enter the cytoplasmic receptror protein, and allowing it to convert to dht and then bind to the androgen receptors in the muscle, causing its distinct hardening effects, it still cant bind to the scalp or prostrate via 5ar as the form of dht it has converted too doesnt allow for that affinity.
So more prolactin is produced to allow for the superdol to find a receptor ,this excess prolactin triggers a process that fills the breast with milk via a process called lactogenesis, in men however it causes a distinct enlargment of the mammary gland and can even cause a man to lactate.
If superdrol had better binding to the androgen receptor via 5AR then this problem would be prevented, the other thing is that prolactin production can remain elevated for months after a cycle has finished, and once the androgen has been removed, ( the cycle is over) the cytoplasmic receptor proteins have nothing to do other than to allow the prolactin to proceed with its hormonal action within the body, causing the male mammary gland to enlarge ready to produce milk... Hence the REBOUND gyno, this is why proper post cycle therapy (pct) is needed for superdrol, and the use of something to prevent prolactin.
R.S
The problem is everyone is different and eveyone has different amounts of progestin receptors, wich can cause worse sides in some users than others, one guy can use deca and get no bloat, another with the same dose will get bloat and gyno, because of this one reason alone. Now Beastsrol or superdrol is in itself not that androgenic, and as its structure suggests its not that different to other dht based steroids, now an action takes place that explains how it works... its doesnt act like a typical androgenic, but acts a little like oxymetholone, in that it doesnt show any real affinity for the 5AR enzyme, so you get weaker affinty for the androgen receptor than dht, but you get stronger androgenic effects as the enzyme 3beta hydroxysteroid dehydrogenase has little effect on the androgen affinity of superdrol.
The problem is this same enzyme 3beta hydroxysteroid dehydrogenase, is used in the conversion of many metaobiles in the body, Superdrol produces a lot of metabolites that dont get bound by the androgen receptor like we just saw, it cant aromatize, so it doesnt bind to the estrogen receptor, but it circulates, as its also a di methyl, it is very biovailable so a lot of the product circulates in the blood, and these extra metabolites dont bind specificly...not in the way they should.. so i will explain in a detailed way then make it much easier to understand.
Prolactin is normaly caused by progestins, but can also be caused by dht, how?
For example, it is currently understood that when testosterone enters the cell cytoplasm it is subsequently converted to the more "active" androgen, dihydrotestosterone, DHT, by reduction at the 5alpha position, This is normal. Dihydrotestosterone is then either bound to a cytoplasmic "receptor" protein Rc, or is further metabolized to either 5alpha-androstane-3alpha,17beta-diol or 5alpha-androstane-3beta,17beta-diol ,DIOL. The binding of DHT to its cytoplasmic receptor protein results in translocation of the steroid-receptor complex into the nucleus where presumably the complex dissociates and DHT exerts its androgenic effects. The transport of DHT to the nucleus can also result from the conversion of testosterone to DHT by nuclear membrane-bound 5alpha-reductase. Prolactin augmentation of DHT effects is envisioned as resulting from interaction of prolactin with its receptor, which due to the large size of the prolactin molecule is probably located in or on the plasma membrane.
Because superdrol is androgenic, but lacks the ability to show affinity via 5ar, it circulates, and this causes the large amounts of androgens to look for a transporter, so that it can bind to the androgen recptor, so it uses prolactin wich has a high affinity to cytoplasmic receptor protein, allowing the androgens, testosterone, to be carried and allowing them to convert to dht, only problem is prolactin hormone or luteotropic hormone is synthesised and secreted by sex binding lactotrope cells in the adenohypophysis (anterior pituitary gland, And this gland now produces more prolactin to help deal with the large amount of testosterone circulating that hasnt bound to the estrogen of androgen receptor, Part of the reason why superdol is so anabolic, So instead of binding to the androgen receptors in the scalp and the prostrate it converts to dht through this unique process, using prolactin to enter the cytoplasmic receptror protein, and allowing it to convert to dht and then bind to the androgen receptors in the muscle, causing its distinct hardening effects, it still cant bind to the scalp or prostrate via 5ar as the form of dht it has converted too doesnt allow for that affinity.
So more prolactin is produced to allow for the superdol to find a receptor ,this excess prolactin triggers a process that fills the breast with milk via a process called lactogenesis, in men however it causes a distinct enlargment of the mammary gland and can even cause a man to lactate.
If superdrol had better binding to the androgen receptor via 5AR then this problem would be prevented, the other thing is that prolactin production can remain elevated for months after a cycle has finished, and once the androgen has been removed, ( the cycle is over) the cytoplasmic receptor proteins have nothing to do other than to allow the prolactin to proceed with its hormonal action within the body, causing the male mammary gland to enlarge ready to produce milk... Hence the REBOUND gyno, this is why proper post cycle therapy (pct) is needed for superdrol, and the use of something to prevent prolactin.
R.S
