
Originally Posted by
Atomini
Metalject,
According to research cited here (1), prolactin may have a direct stimulatory effect on mammary tissue development, but only in the presence of high estrogen levels. Regarding prolactin, androgens decrease prolactin levels whereas estrogens increase prolactin. Non-aromatizing androgens have never been shown to elevate prolactin levels in humans, but testosterone has, due to its aromatization to estradiol (2). Prolactin secreting tumors, or prolactinomas, are often associated with gyno. But in these cases the prolactin is believed to induce gyno by suppressing testosterone production: “Prolactinomas that are sufficiently large to cause gynecomastia do so as a result of impairment of gonadotropin secretion and secondary hypogonadism”. (1)
The causation of gyno is largely complex and its precise specifics are largely unknown, and a number of agents including estrogens, progestins, GH, IGF -1, and prolactin may be involved. However, most authorities believe that a decreased (T+DHT)/E ratio is central to the development of gyno, and that blocking the effects of estrogen, or increasing T + DHT levels, is central to amending the problem.
Trenbolone plays a part in its role in causing gyno by signaling the pituitary to secrete and release prolactin, which then activates prolactin receptors in breast tissue. As well, due to the nature of trenbolone itself being a progestin, there are progesterone receptors on breast tissue as well that it binds to in order to contribute to the overall complex mechanism that produces gyno. If we can eliminate one of the gears in the machine that is responsible for the formulation of gyno, you can effectively have a high chance of stopping, blocking, and preventing it. In the case of trenbolone, prolactin does play a large role in it. This is why I advise running a prolactin antagonist, and keeping estrogen in check.
REFERENCES:
1. Ismail AA, Barth JH.Ann Clin Biochem 2001 Nov;38(Pt 6):596-607
2. Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F Acta Endocrinol (Copenh) 1984 Feb;105(2):167-72