Originally Posted by
Atomini
Everyone can react differently to different compounds. Some people do not have prolactin increases with trenbolone just as many people do not have gyno issues despite aromatizing steroids converting to estrogen (myself being one of them, at least for the time being - knock on wood). When we get into far deeper detail, we see that for prolactin levels to increase, there must be high estrogens and also high progesterone levels, which then result in prolactin being released by the anterior pituitary. While reducing estrogen to lower than normal levels does resolve the issue of prolactin increases, I don't consider such to be healthy. I have also seen reports of normal estrogen levels and lactation occurring.
The interesting thing is, that high progestersone levels actually inhibit prolactin production. With this being said, note that 19-nors such as nandrolone and trenbolone are classified as progestins. One would now think that trenbolone should actually suppress prolactin secretion. It makes logical sense considering the evidence.
So in theory, tren should NOT raise prolactin levels, however it absolutely does in most people. I can unequivocally say that tren rasies prolactin levels because I have the bloodwork to prove it, and i've seen others too. And from the successful prevention/reduction of sides many others have experienced from using prolactin-antagonists, it would seem that all of these people are not the exception. Now, when we delve into the world of AAS, we know that when modifications are made to the chemical strucutres of hormones to create different and more powerful anabolic steroids with different attributes, we end up with compounds that are supposed to act a certain way when they absolutely in real practicality show exactly the opposite! One such compound as an example is Anadrol! Anadrol is a DHT-derivative, which makes it highly androgenic and unable to convert into estrogen - yet it produces heavy estrogenic side effects without aromatization. Other strange anomalies that have been found with other AAS is, for example, Anavar which has been found to cause gyno in a very small amount of people because it somehow has a binding affinity for the estradiol receptor!
The fact is, even if it was true that winstrol acted as a prolactin-antagonist, I would still not use it for this purpose because of the fact that I have not seen any data describing its effectiveness at doing so. And with proven and true prolactin-antagonists out there such as Pramiprexole and Cabergoline, why take this chance?
