? for Prolangtum on Fina & Novadex

[SJR7674]

some of the board members said that you had some interseting information on how Novadex can prevent gyno from Fina. I am wondering how since 1 mg of Arimidex has failed to do so. If this is true, how come and how much would I need to combat the effects of Fina

Thanks

SJR

[CJWolf]

i would reccomend dostinex instead of nolvadex for gyno from fina, but to each his own ...

[SJR7674]

Does dostinex block estrogen conversion or progesterone conversion. Why do you think dostinex?

Thanks

[CJWolf]

dostinex is just bromocriptine which stops the prolactin side effects from the fina ...

[SJR7674]

I have to act stupid for a minute here - Prolactin? What is that.

I'm trying to get all the facts so that I can call my doctor. He will give me what ever I need as long as I can explain why I need it. He will have no idea even what Fina is or Prolactin, so I need to be very clear on understanding these terms so I can explain them to him. If he will give me Dostinex, what mg amount do they come in and how many will I need?

Thanks

[prolangtum]

I always refer to Nandi on this one:
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:

http://www.endotext.org/male/male14/male14.htm

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.

(1) Int J Biol Markers 1995 Jan-Mar;10(1):47-54
Progesterone agonists and antagonists induce down- and up-regulation of estrogen receptors and estrogen inducible genes in human breast cancer cell lines.

(2) J Neurosurg 1991 Jun;74(6):861-6
Treatment of unresectable meningiomas with the antiprogesterone agent mifepristone.
Grunberg SM, Weiss MH, Spitz IM, Ahmadi J, Sadun A, Russell CA, Lucci L, Stevenson LL.
Department of Neurosurgery, University of Southern California School of Medicine, Los Angeles.