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i'm in the middle of a deca/winnie cycle. I know it's not really for bulking but after 4 weeks I'm up 8 pounds (shoulders got big, man). i was always very lean and cut but now it seems that i'm getting a little fluffy around the hips (belt got tighter too). I'll just melt some away.
tks, bro.
yea, winnie's oral. i went from 200deca/ew + winnie 40mged to 300ew + 50mged and round maybe off by throwing some oxandrolone at the end after the winnie.
i'll pause 10 weeks and plan a boldenone/ oxandrolone cycle after. never did any test since i was afraid to bulk too much, during my kickboxing days. love my cuts too much... but might be wrong.
Nandi:
Virtually all androgens bind to the progesterone receptor to some degree; similarly progestins (and antiprogestins) bind to the androgen receptor. RU 486 binds to the androgen receptor as an antiandrogen, rendering it useless for bodybuilders.
As far as the winstrol article goes, has anyone bothered to actually read the whole study? Presumably we are supposed to believe winstrol has some kind of antiprogestin capability because it blocked FGF stimulated DNA synthesis.
The effect on DNA synthesis was measured by thymidine uptake. Less thymidine uptake means less DNA synthesis. Quoting from page 38 of the article,
" A significant inhibition of thymidine uptake was seen in response to stanozolol in both cell types. The steroids nortestosterone, oxymetholone, and progesterone itself were also tested for their effect on thymidine uptake to determine whether the effects of stanozolol on DNA synthesis were unique. These other compounds also inhibited DNA synthesis in both cell types"
In other words, winstrol has THE SAME effect as progesterone on progesterone receptor mediated DNA synthesis: they both block it. So rather than acting as an antiprogesterone in this study, winstrol, as well as nandrolone and oxymetholone, act in the same manner as progesterone.
Ellis AJ, Cawston TE, Mackie EJ.
Rheumatology Research Unit, Addenbrooke's Hospital, Cambridge, UK.
The anabolic steroid stanozolol stimulates the production of prostaglandin E2 (PGE2) and the matrix metalloproteinases collagenase and stromelysin in human skin fibroblasts but not in rheumatoid synovial fibroblasts. The basis for these differential responses was investigated at the levels of DNA synthesis and steroid receptor binding. Stanozolol inhibited fibroblast growth factor (FGF)-stimulated DNA synthesis in both the skin and synovial fibroblasts, showing that both cell types were capable of responding to the compound. Competitive binding assays indicated that stanozolol bound specifically to both the skin and synovial fibroblasts. Binding of stanozolol to both cell types could be partially displaced by progesterone, indicating that stanozolol binds to the progesterone receptor. Immunocytochemical studies confirmed the presence of progesterone receptors on skin and synovial fibroblasts. However, progesterone failed to elicit any response with respect to collagenase production in either cell type. Nortestosterone, dexamethasone and 17 beta-oestradiol had no effect on binding of stanozolol to either cell type. These results indicate that the inhibition of DNA synthesis by stanozolol is elicited through the progesterone receptor. The effects of stanozolol on collagenase and PGE2 production are mediated by a different receptor, present on skin but not synovial fibroblasts, and as yet unidentified.
I eat at least 6 times a day to build my body
I pray at least 6 times a day to build my soul
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:
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
I eat at least 6 times a day to build my body
I pray at least 6 times a day to build my soul
damn pro, good stuff. i actually thought taking proviron simultaneously should do the trick since it prevents conversion into estrogen...(?) appreciate the time you take to bring this over to us laymen, really! now i'm confused with my cycle...
You should be aware that Proviron is also an estrogen antagonist which prevents the aromatization of steroids. Unlike the antiestrogen Nolvadex which only blocks the estrogen receptors (see Nolvadex) Proviron already prevents the aromatizing of steroids. Therefore gynecomastia and increased water retention are successfully blocked. Since Proviron strongly suppresses the forming of estrogens no rebound effect occurs after discontinuation of use of the compound as is the case with, for example, Nolvadex where an aromatization of the steroids is not prevented. One can say that Nolvadex cures the problem of aromatization at its root while Nolvadex simply cures the symptoms. For this reason male athletes should prefer Proviron to Nolvadex. With Proviron the athlete obtains more muscle hardness since the androgen level is increased and the estrogen concentration remains low. This, in particular, is noted positively during the preparation for a competition when used in combination with a diet. (quoted from steroidtips.com).
Originally posted by monroe You should be aware that Proviron is also an estrogen antagonist which prevents the aromatization of steroids. Unlike the antiestrogen Nolvadex which only blocks the estrogen receptors (see Nolvadex) Proviron already prevents the aromatizing of steroids. Therefore gynecomastia and increased water retention are successfully blocked. Since Proviron strongly suppresses the forming of estrogens no rebound effect occurs after discontinuation of use of the compound as is the case with, for example, Nolvadex where an aromatization of the steroids is not prevented. One can say that Nolvadex cures the problem of aromatization at its root while Nolvadex simply cures the symptoms. For this reason male athletes should prefer Proviron to Nolvadex. With Proviron the athlete obtains more muscle hardness since the androgen level is increased and the estrogen concentration remains low. This, in particular, is noted positively during the preparation for a competition when used in combination with a diet. (quoted from steroidtips.com).
there you go CJ.
I was saying Proviron sucks IMO. Liquidex/Femera are a much better choice for keeping the sides away.
But since you're only running deca/winny proviron won't really do anything at all for you ...
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