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  1. #1
    Dr.Evil's Avatar
    Dr.Evil is offline Retired Moderator
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    Winny is Anti-Progestenic. Some Evidence

    there aren't a lot of things to take to prevent gyno induced by progesterone such as the case with deca and anadrol other than ru-486 (impossible to get). there are rumors that winny may be effective too. the following abstracts show signs that winny (stanozolol ) bind to progesterone receptors and compete for binding with progesterone and possibly lowering serum progesterone levels. there is no telling how effective this would be at preventing progesterone induced gyno in men though, but a fun read none-the-less.


    Agents Actions 1994 Mar;41(1-2):37-43

    The differential effects of stanozolol on human skin and synovial fibroblasts in vitro: DNA synthesis and receptor binding.

    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.


    J Allergy Clin Immunol 1981 Sep;68(3):181-7

    Clinical and biochemical effects of stanozolol therapy for hereditary angioedema.

    Sheffer AL, Fearon DT, Austen KF.

    Stanozolol, an inexpensive anabolic steroid with a 30:1 anabolic:androgenic ratio, was administered to 12 male and 15 female patients with biochemically proven hereditary angioedema over a 2-yr period to obtain a systematic assessment of the relationship between drug dosage and clinical response, incidence of side effects, and amelioration of complement abnormalities. All 27 patients attained the minimal effective dose, ranging from 0.5 to 2 mg daily, which controlled the frequency and intensity of symptoms with minimal side effects. At daily maintenance doses of 2, 1, and 0.5 mg the frequencies of attacks per weeks of therapy were 1/14.6, 1/7.2, and 1/8.2 wk, respectively. Side effects with maintenance therapy included menstrual abnormalities and virilization in four females and elevation of serum creatinine phosphokinase (CPK) in five males. In six patients on maintenance doses of stanozolol, serum levels of testosterone , free thyroxin (T4), and thyroxin binding globulin (TBG) (four males), and of estradiol, progesterone, T4, and TBG (two females) were normal. Slightly low serum levels of progesterone and TBG were found in two females who had normal menstrual cycles. Statistically significant elevations above pretherapy levels of serum inhibitor to the activated first component of complement function and C4 protein and function occurred when patients were on maintenance therapy, but these measurements remained below the lower limit of normal range. Higher doses of stanozolol (4 mg/day), which caused greater immunochemical responses, were unnecessary for control of clinical disease and were unjustified for chronic therapy because of more frequent side effects.



    J Pharmacol Exp Ther 1996 Dec;279(3):1123-9

    Identification of a specific binding site for the anabolic steroid stanozolol in male rat liver microsomes.

    Boada LD, Fernandez L, Zumbado M, Luzardo OP, Chirino R, Diaz-Chico BN.

    Departamento de Ciencias Clinicas, Universidad de Las Palmas de Gran Canaria, Spain.

    Male rat liver microsomes contain a [3H]dexamethasone binding site, capable of binding glucocorticoids and progesterone. We have shown previously that the 17 alpha-alkylated androgen, stanozolol, can inhibit the [3H]dexamethasone binding to microsomes through a negative allosteric mechanism, which gives rise to the possibility of its interaction with a different binding site. In this study, the existence of a single-saturating binding site, capable of binding the radioactive steroid with a maximum number of the specific binding site of 49 +/- 2 pmol/mg of protein and a Kd of 37 +/- 1.3 nM was demonstrated by using [3H]stanozolol. In competition experiments, only stanozolol and danazol were able to compete with [3H]stanozolol for its binding to microsomes, among more than 60 steroids and other compounds tested. The binding of [3H]stanozolol was depressed after protease treatment of the microsomes, or after the administration of cycloheximide to adult male rats for 24 hr, which suggest its proteic nature. The [3H]stanozolol binding site was detected in many tissues of the rat, with the highest concentrations being found in the liver. It was detected from birth, increasing afterward in concentration and reaching a peak at 2 to 3 months of age. This is the first experimental verification of the existence in liver microsomes of a specific binding site for some 17 alpha-alkylate androgens, such as stanozolol and danazol, different from the androgen receptor or the [3H]dexamethasone binding site.

  2. #2
    Shredder's Avatar
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    awesome post ! you did a good deed!

  3. #3
    NightOp is offline Member
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    hmm, good post, but I want to see what Mike has to say... there is a big thread on progesterone unveiled which is certainly worth a look

  4. #4
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    I did't know ru-486 was so hard to get. GREAT POST!

  5. #5
    Sicilian30's Avatar
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    I knew this already, but awesome post Dr. Evil..

  6. #6
    Mike's Avatar
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    Hmmm...no offense Doc but I don't see anything in there that really states that winny will prevent deca gyno....

    In fact all it says is that winny will bind to the progesterone receptor....not even that it decreases progesterone levels if thats what the second one was supposed to prove.

    Deca and anadrol etc, dont actually elevate progesterone levels so that isn't the key to combatting deca gyno.

    M

  7. #7
    jon
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    good post

  8. #8
    Dr.Evil's Avatar
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    Originally posted by Mike
    Hmmm...no offense Doc but I don't see anything in there that really states that winny will prevent deca gyno....

    In fact all it says is that winny will bind to the progesterone receptor....not even that it decreases progesterone levels if thats what the second one was supposed to prove.

    Deca and anadrol etc, dont actually elevate progesterone levels so that isn't the key to combatting deca gyno.

    M
    winny does not reduce progesterone levels, but it decreases the amount of progesterone receptors available to bind to deca. if less deca can bind to PR then there will be less progestenic effect from deca.

  9. #9
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    Good to see someone finding,... scientific data on the questions we present. Well done Dr.E

  10. #10
    dosXX's Avatar
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    ^^xx reported

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