- Joined
- Feb 4, 2003
- Messages
- 18
Progestins & Gyno
Before you decide that blocking progesterone is the solution to gyno, consider a few things. There is not one case of progesterone induced gyno in the medical literature EXCEPT in those cases where strong synthetic progestins, like medroxyprogesterone, were administered. In these cases the gyno is due to suppression of LH and testosterone by the progestin, NOT by a direct effect on breast tissue. On a cycle your LH is already suppressed by the AAS anyway.
Breasts have two components: alveoli and ducts. The alveoli are what secrete milk; they drain into ducts. Gynecomastia is the result of ductal hyperplasia, not alveolar hyperplasia. Estrogen stimulates the ductal tissue, while progesterone stimulates the alveoli. Alveolar hyperplasia does not contribute to gyno. If you want to read more on breast development, I suggest visiting this site:
**broken link removed**
In various tissues throughout the body, including cultured neoplastic breast tissue, progestins downregulate the estrogen receptor (1). Progesterone receptor blockers like RU-486 upregulate the estrogen receptor (1). This is consistent with the fact that RU-486 CAUSES gyno in patients in whom it is used to treat Cushing's disease and meningiomas (2).
Progestins are also anti-estrogenic in that they induce the enzyme 17-hydroxysteroid dehydrogenase, which catalyzes the oxidation of estradiol to the less potent estrone. Progestins also induce estrogen sulfotransferase, the enzyme which catalyzes the sulfation and inactivation of estrogens.
So do progestins contribute to gyno, and if yes, how so? If you visit the link above you will see that progestins increase IGF-1 levels. As that article indicated, IGF-1 is essential to the the development of mammary tissue. This is also how it is believed that progestins in HRT or oral contraceptives contribute to breast cancer: by increasing IGF-1 levels. But as bodybuilders we are always trying to maximize IGF-1. Hence the futility of trying to lower IGF-1 by blocking progestins. The other anabolics we use will elevate (hopefully) IGF-1, while blocking the progesterone receptor will only increase the levels and activity of estrogen by the mechanisms outlined above.
Two drugs have shown the greatest efficacy in treating gyno: Nolvadex, and Raloxifene, another SERM. Nolvadex has the longest track record, but a recent trial with Raloxifene showed it to be superior to Nolvadex. With these drugs you attack the problem at its source: the estrogen receptor. You get the added benefit of lowering IGF-1. Not a good thing for making gains, but important for treating gyno.
Before you decide that blocking progesterone is the solution to gyno, consider a few things. There is not one case of progesterone induced gyno in the medical literature EXCEPT in those cases where strong synthetic progestins, like medroxyprogesterone, were administered. In these cases the gyno is due to suppression of LH and testosterone by the progestin, NOT by a direct effect on breast tissue. On a cycle your LH is already suppressed by the AAS anyway.
Breasts have two components: alveoli and ducts. The alveoli are what secrete milk; they drain into ducts. Gynecomastia is the result of ductal hyperplasia, not alveolar hyperplasia. Estrogen stimulates the ductal tissue, while progesterone stimulates the alveoli. Alveolar hyperplasia does not contribute to gyno. If you want to read more on breast development, I suggest visiting this site:
**broken link removed**
In various tissues throughout the body, including cultured neoplastic breast tissue, progestins downregulate the estrogen receptor (1). Progesterone receptor blockers like RU-486 upregulate the estrogen receptor (1). This is consistent with the fact that RU-486 CAUSES gyno in patients in whom it is used to treat Cushing's disease and meningiomas (2).
Progestins are also anti-estrogenic in that they induce the enzyme 17-hydroxysteroid dehydrogenase, which catalyzes the oxidation of estradiol to the less potent estrone. Progestins also induce estrogen sulfotransferase, the enzyme which catalyzes the sulfation and inactivation of estrogens.
So do progestins contribute to gyno, and if yes, how so? If you visit the link above you will see that progestins increase IGF-1 levels. As that article indicated, IGF-1 is essential to the the development of mammary tissue. This is also how it is believed that progestins in HRT or oral contraceptives contribute to breast cancer: by increasing IGF-1 levels. But as bodybuilders we are always trying to maximize IGF-1. Hence the futility of trying to lower IGF-1 by blocking progestins. The other anabolics we use will elevate (hopefully) IGF-1, while blocking the progesterone receptor will only increase the levels and activity of estrogen by the mechanisms outlined above.
Two drugs have shown the greatest efficacy in treating gyno: Nolvadex, and Raloxifene, another SERM. Nolvadex has the longest track record, but a recent trial with Raloxifene showed it to be superior to Nolvadex. With these drugs you attack the problem at its source: the estrogen receptor. You get the added benefit of lowering IGF-1. Not a good thing for making gains, but important for treating gyno.
