Bignick
New member
Winstrol
The use of Winstrol is also an effective method of controlling progesterone-induced gyno, as it is anti-progestagenic. An effective dose appears to be in the vicinity of 50mg eod (depot) or 30 to 35mg/day (tabs) although this dose may require increasing depending on the doses being employed in the stack.
One important point worth mentioning is, although generally the progestins do not aromatise, there is an exception to this rule: Deca, as well as being a progestin also aromatises, only very slightly, but nevertheless, still does to some extent. Although this is not nearly enough to cause the large majority any problems at all, for those extremely sensitive to gyno, this small amount of aromatisation to oestrogen can be enough of an elevation to activate the progesterone. Very few people are likely to suffer this, but we feel it is a point worth mentioning.
MEDICAL ARTICLE ABSTRACT: (translation....winny is a anti ProG)
Stanozolol (winny) 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.
THIS IS ANOTHER EXCERPT TALKING ABOUT THE RU486 AND WINNY (RU486 is the abortion pill)
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.
****what to make of all this*******
The theory goes that Winny can bind and compete for a position at the progesterone receptor much like Clomid of Nolvadex would at the estrogen receptor, thereby inhibiting progestagenic effects. Now, progesterone can aggravate estrogenic side-effects by agonizing estrogen and it does play a role in gyno.
We also discussed that certain steroids may indeed stimulate and act at the height of the progesterone receptor including nandrolone and Norethandrolone. These hormones are also altered by it inducing a decrease in libido and a sense of lethargy and such, and eventhough they aromatize in lesser rates than some other steroids, they show an equal capability to cause estrogenic side-effects, particularly when stacked with other aromatizable compounds.
***Now there is evidence that Winny does indeed bind to the progesterone receptor1 and its users do not indicate the normal characteristics of progesterone stimulation, which bodes well for these anti-progestagenic properties. There is also some clinical data that it does aid in symptoms that require progesterone suppression2. Much in the way danazol was also successfully used.
The one thing we shouldn't lose sight of however is in what rate it binds to the progesterone reception. There is no data on this. For all we know it couldn't bind strong enough to compete with nandrolone or norethandrolone. So its not wise to state that Winny is an anti-progestagin per se, but it does make Winny a good match for these products in stacks in any case
Winny is agood stack for alot fo cycles, and my opinion on its progesterone blocking capabilities is unsure...but my advice is that it truly cannot hurt so why not give it a shot
The use of Winstrol is also an effective method of controlling progesterone-induced gyno, as it is anti-progestagenic. An effective dose appears to be in the vicinity of 50mg eod (depot) or 30 to 35mg/day (tabs) although this dose may require increasing depending on the doses being employed in the stack.
One important point worth mentioning is, although generally the progestins do not aromatise, there is an exception to this rule: Deca, as well as being a progestin also aromatises, only very slightly, but nevertheless, still does to some extent. Although this is not nearly enough to cause the large majority any problems at all, for those extremely sensitive to gyno, this small amount of aromatisation to oestrogen can be enough of an elevation to activate the progesterone. Very few people are likely to suffer this, but we feel it is a point worth mentioning.
MEDICAL ARTICLE ABSTRACT: (translation....winny is a anti ProG)
Stanozolol (winny) 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.
THIS IS ANOTHER EXCERPT TALKING ABOUT THE RU486 AND WINNY (RU486 is the abortion pill)
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.
****what to make of all this*******
The theory goes that Winny can bind and compete for a position at the progesterone receptor much like Clomid of Nolvadex would at the estrogen receptor, thereby inhibiting progestagenic effects. Now, progesterone can aggravate estrogenic side-effects by agonizing estrogen and it does play a role in gyno.
We also discussed that certain steroids may indeed stimulate and act at the height of the progesterone receptor including nandrolone and Norethandrolone. These hormones are also altered by it inducing a decrease in libido and a sense of lethargy and such, and eventhough they aromatize in lesser rates than some other steroids, they show an equal capability to cause estrogenic side-effects, particularly when stacked with other aromatizable compounds.
***Now there is evidence that Winny does indeed bind to the progesterone receptor1 and its users do not indicate the normal characteristics of progesterone stimulation, which bodes well for these anti-progestagenic properties. There is also some clinical data that it does aid in symptoms that require progesterone suppression2. Much in the way danazol was also successfully used.
The one thing we shouldn't lose sight of however is in what rate it binds to the progesterone reception. There is no data on this. For all we know it couldn't bind strong enough to compete with nandrolone or norethandrolone. So its not wise to state that Winny is an anti-progestagin per se, but it does make Winny a good match for these products in stacks in any case
Winny is agood stack for alot fo cycles, and my opinion on its progesterone blocking capabilities is unsure...but my advice is that it truly cannot hurt so why not give it a shot
