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Thread: Stanozolol injections cycle for women

  1. #46
    Member XMAN's Avatar
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    Quote Originally Posted by Jbigdog69 View Post
    Good to hear Xman please post weight gain "If Any" post cycle....thanks
    after 2 weeks on cycle and today the beginning of the 3rd week she went on the scale on an empty stomach and she's now 47.5 kg, she started at 50 kg, it's mostly fat as it shows but i think she went a little extreme on her diet cuz i notice that her muscles r not so pumped and a little blurred , she did loose some muscles in the process dunno exactly how much but it's visible, and now we're fighting about increasing calories a bit but she deosn't want to, so i'm going to force feed her lol


  2. #47
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    another thing, the issue of AI use in pre-menopausal women still unclear, i used to know that it's only for post-menopausal women cuz their only estro source is from andro conversion, but sassy told me that there's an aromatase activity in the ovaries too, andro or prog aromatisation dunno the exact mechanism but i read this article now and it really did confused me a lot. here's the link :
    Dr. Susan Love Research Foundation | I am a premenopausal woman with early stage breast cancer. Can I use an aromatase inhibitor?

    and this is a copy paste in case the link didn't work :

    Dr. Susan Love (Research Foundation)
    ER-Positive Tumors and Hormone Therapy

    I am a premenopausal woman with early stage breast cancer. Can I use an aromatase inhibitor?

    Aromatase inhibitors are hormone therapies that are used to treat women with hormone-positive (estrogen receptor [ER]-positive and/or progesterone receptor [PR]-positive) tumors. Aromatase inhibitors work by blocking the aromatase enzyme, which converts androgens into estrogen. Although pre- and postmenopausal women can use tamoxifen as hormonal therapy, only postmenopausal women can use an aromatase inhibitor. That's because postmenopausal women get most of their estrogen from the conversion of androgens into estrogen by the aromatase enzyme. In contrast, premenopausal women get most of their estrogen directly from their ovaries (and aromatase inhibitors aren't able to block this estrogen).

    Currently three aromatase inhibitors are approved for use by the US Food and Drug Administration (FDA): anastrozole (brand name Arimidex), letrozole (brand name Femara), and exemestane (brand name Aromasin).

    In December 2004, the American Society of Clinical Oncology (ASCO) issued new guidelines on hormonal therapy. ASCO now recommends that most postmenopausal women be treated with an aromatase inhibitor. This means that tamoxifen, which has been used in the adjuvant setting since the 1980s, is no longer the standard of care for postmenopausal women. Tamoxifen does, however, remain the standard of care for premenopausal women.

    For a premenopausal (still menstruating post chemotherapy) woman to take an aromatase inhibitor, she must have her ovaries removed (oophorectomy) or take a drug that will suppress ovarian functioning and decrease estrogen levels, putting her into menopause. The drugs most commonly used for this purpose are goserelin (brand name Zoladex), leuprolide (brand name Lupron), and triptorelin (brand name Trelstar).

    Theoretically, an aromatase inhibitor should be as effective in a woman who is put into temporary menopause via one of these drugs as it is in a woman who has gone into menopause naturally. But we can't just assume that, which is why three important studies are now underway in Europe and the US to determine the optimal hormone treatment for, and the effectiveness of aromatase inhibitors in, premenopausal women. The three trials are called SOFT, TEXT, and PERCHE, or STP.

    Investigators hope to recruit more than 6,000 women over the next five to seven years for these studies, which will play a critical role in determining which hormone therapies are recommended to premenopausal women in the future. Investigators expect to report preliminary data from these studies in 2008.

    All three trials will use tamoxifen or the aromatase inhibitor exemestane along with triptorelin. Exemestane differs from the other aromatase inhibitors in that it stops the aromatase enzyme's production process permanently. This is why exemestane is often referred to as an aromatase "inactivator" rather than as an aromatase "inhibitor." Exemestane was selected because there are data from small studies that indicate it may be less likely to cause osteoporosis.

    If you are interested in trying an aromatase inhibitor, I would suggest that you speak with your oncologist about enrolling in one of these trials. If there is no trial that is right for you, you and your doctor will need to discuss your risk for recurrence and the fact that we currently have no data on this treatment. This may be true for women whose tumors are HER2-positive, as there is some evidence that women who are both HER2-positive and ER-positive may have tumors that are resistant to tamoxifen but will respond to an aromatase inhibitor. (HER2 is also sometimes referred to as HER-2 or Her-2/neu or erb-b2.)

    If you do decide to use an aromatase inhibitor as adjuvant therapy, you should have your bone density monitored during your treatment. Some oncologists recommend that premenopausal women try to decrease their risk of bone loss by also taking a bisphosphonate, a drug used to treat osteoporosis. You should speak with your oncologist about this as well. Whether you take tamoxifen or an aromatase inhibitor, I would encourage you to try to maintain your bone health by doing weight-bearing exercises. You should also make sure that you get adequate amounts of vitamin D and calcium in your diet, taking supplements if necessary.

  3. #48
    Weasel Hunting Moderator SHINE's Avatar
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    AI's like letro or Faslo are strong enuff to slow estro conversion in the ovaries and they do block P450scc there as well (dose dependant)just not as strongly as other parts of the body and that's why the medical community never mentions the use OF AI's for stoping all estro conversion of the Ovaries which they don't, Ovaries don't produce direct estro. Her statements need to be a bit more clear but she is speaking to medical community and patients . With breast cancer nolva is always a part of the protocol since it reduces IGF as well as blocking any available estro at the site. Reason aromatase inhibitors are not normaly used in premenopausal women, the decrease in estrogen activates the hypothalamus and pituitary axis to increase gonadotropin secretion, which in turn stimulates the ovary to increase androgen/hormone production .
    That and some of the AI's again like letro stimulate Aromatase protein which can lead to an imbalance of higher estrogen later.

    Your supressing ovarian function with Stanazolol slowing estrogen production do to that fact and Stano doesn't convert to estrogen.
    Your over thinking things IMO. Good article though.
    Last edited by SHINE; 11-21-2011 at 01:52 PM.

  4. #49
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    Quote Originally Posted by SHINE View Post
    AI's like letro or Faslo are strong enuff to slow estro conversion in the ovaries and they do block P450scc there as well (dose dependant)just not as strongly as other parts of the body and that's why the medical community never mentions the use OF AI's for stoping all estro conversion of the Ovaries which they don't, Ovaries don't produce direct estro. Her statements need to be a bit more clear but she is speaking to medical community and patients . With breast cancer nolva is always a part of the protocol since it reduces IGF as well as blocking any available estro at the site. Reason aromatase inhibitors are not normaly used in premenopausal women, the decrease in estrogen activates the hypothalamus and pituitary axis to increase gonadotropin secretion, which in turn stimulates the ovary to increase androgen/hormone production .
    That and some of the AI's again like letro stimulate Aromatase protein which can lead to an imbalance of higher estrogen later.

    Your supressing ovarian function with Stanazolol slowing estrogen production do to that fact and Stano doesn't convert to estrogen.
    Your over thinking things IMO. Good article though.
    thx for the clarification , sounds logic.

  5. #50
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    Hi there! I am new here as of today...I have a question...I took winstrol IM a few years ago and loved it...I am going to do another 1/2 cycle now...Tho before I took 1/2 cc everyother day, is this the best schedule? I have read also to do it every day??....Just looking to lean out and increase muscle...I am already eating pretty clean and this time around am taking supps too. (BCAA's, mutli V, CLA, protein powder)...also, do you know if it's OK to take a them on the days that I don't take an injection? Or maybe even the same day? Any input would be greatly appreciated!

  6. #51
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    Quote Originally Posted by sfina View Post
    Hi there! I am new here as of today...I have a question...I took winstrol IM a few years ago and loved it...I am going to do another 1/2 cycle now...Tho before I took 1/2 cc everyother day, is this the best schedule? I have read also to do it every day??....Just looking to lean out and increase muscle...I am already eating pretty clean and this time around am taking supps too. (BCAA's, mutli V, CLA, protein powder)...also, do you know if it's OK to take a them on the days that I don't take an injection? Or maybe even the same day? Any input would be greatly appreciated!
    How much is 1cc? I.e. what is the mg/ml on the bottle? Typically if you're using tabs, people do it every day at 5-10 mg/day. If you're using injectible, you can go E3D at like 25-30 mg. Or you can just measure out the 10 mg/day and ingest it orally (i.e. you can drink the winny because it is water-based). At the end of the day - just look at your total dosing/week. If tabs @ 10mg/day = 70mg/week. If inject E3D@ 25 mg/day - averages out to about 70mg/week.

    There's no interaction between your injections and your OTC supps. In all cases what usually matters most is just consistency in dosing. It doesn't matter if you take them on the same day or different days of the injection.

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