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Progesterone and Prolactin

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    Quote Originally Posted by sethroberts View Post
    Actually, they are considered progestins because of the lack of a carbon at the C-19 position.

    Vites has been shown to have estrogenic and progestational effects in addition to its prolactin lowering potential. With this mix of activities, it is difficutl to say what effect it is having and if it may be causing more harm than good.
    Correct, it is the lack of carbon in the 19 position, my typo.

    Im not sure what your implying by saying Vitex has “estrogenic” or “progestational” effects. Im not aware of any research that shows any constituent of Vitex having agonistic action at the PR or ER.

    If you are referring to a stimulus effect at the female hypothalamus/pituitary of estrogen or progesterone, I hope you’re not assuming this stimulatory effect applies to males.

    -Eric

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    Quote Originally Posted by sethroberts View Post
    Vites has been shown to have estrogenic and progestational effects in addition to its prolactin lowering potential. With this mix of activities, it is difficutl to say what effect it is having and if it may be causing more harm than good.
    There is a 1-to-1 relationship with gyno and tren in some individuals, however with the introduction of something like vitex, these gyno symptoms go away. There is a connection with “sore, sensitive and puffy” nipples in males and the reduction with subsequent vitex supplementation.

    -Eric
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    Quote Originally Posted by sethroberts View Post
    Dienolone is actually more similar to nandrolone than to trenbolone in terms of binding affinity (trenbolone = 134AR, 74PR, dienolone 134AR, 17PR, nandrolone 154AR, 20PR) especially towards the progesterone receptor. Additionally, whereas trenbolone does not convert to estrogen, nandrolone does and it is possible that dienolone does as well. They are all strong androgens. Being a chemical intermediate is irrelevent.
    Actually, it’s the double bond the 9th position that prevents the aromatization of dienolone. It simply cannot bind with aromatase.

    I have plenty of experience with Trenbolone, nandrolone and dienolone base and I can say without a doubt that dienolone has characteristics closer related to Trenbolone than nandrolone. The dry gains, hot flashes, potent CNS activation, insomnia, ect… (Even the compounds characteristics are similar - yellowish hue, burns the mucous membranes, ect)
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    Quote Originally Posted by sethroberts View Post
    I posted a comment in that thread. That is a classic case of misinterpretation of the literature. Nolvadex may increase progesterone receptors in the uterus but not likely in the breast. Just because something happens in one tissue type does not mean it will happen in all types -- that is what makes different tissues and organs different! Also, most papers I see show tamoxifen downregulating estrogen receptors in the breast so a slight increase in progesterone receptors would likely not be a problem.

    I can also tell you from personal experience that Nolva is a very poor choice for combating progestin related gyno. It simply doesn’t work.

    I wouldn’t call it misinterpretation of the literature either. Nolva up regulates progesterone receptor. If it does it in the endometrium, this is enough reason for me to suspect it also does it in breast tissue. (but of course, I can’t force anyone to adopt my logic)

    I also suspect (although have no references) that other SERM’s may up-regulate the progesterone receptor similar to nolvadex. I simply have fallen out of favor of using SERMs for the treatment of gyno, especially progestin based gyno.

    As I have said already, I have most success with suppressing prolactin or estrogen, and reducing the total stimulatory action on mammary gland via these mechanisms.

    You have some interesting theory’s and I can agree with most of what you are saying, but I have to make it clear to the members that there other point of views on this subject… simply because I have a vested interest that my customer don’t have gyno symptoms when using our products.

    I say use Vitex if you are using 19-nor, and an possibly an AI if an aromatizable steroid is used.

    -Eric



    Effects of tamoxifen on steroid hormone receptors and hormone concentration and the results of DNA analysis by flow cytometry in endometrial carcinoma.
    M Nola, et al
    Gynecol Oncol, Mar 1999; 72(3): 331-6.

    Tamoxifen increases the plasma estrogen-binding equivalents and has an estradiol agonistic effect on histologically normal premenopausal and postmenopausal
    Gorodeski, G.I., et al.
    endometrium. Fertil. Steril, 57, 320-327. (1992)

    Estrogen and progesterone receptor expressors o£ decidual endometrium in a postmenopausal woman treated with tamoxifen and megestrol acetate.
    Cohen, I., Shulman, A., Altaras, M., Tepper, R., Cordoba, M. and Beyth, Y.
    Gynecol. Obstet. Invest., 38, 127-129. (1994)
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    Quote Originally Posted by Primordial Perf View Post
    Correct, it is the lack of carbon in the 19 position, my typo.

    Im not sure what your implying by saying Vitex has “estrogenic” or “progestational” effects. Im not aware of any research that shows any constituent of Vitex having agonistic action at the PR or ER.

    If you are referring to a stimulus effect at the female hypothalamus/pituitary of estrogen or progesterone, I hope you’re not assuming this stimulatory effect applies to males.

    -Eric
    1: J Agric Food Chem. 2001 May;49(5):2472-9. Links
    Evaluation of estrogenic activity of plant extracts for the potential treatment of menopausal symptoms.Liu J, Burdette JE, Xu H, Gu C, van Breemen RB, Bhat KP, Booth N, Constantinou AI, Pezzuto JM, Fong HH, Farnsworth NR, Bolton JL.
    Department of Medicinal Chemistry and Pharmacognosy, UIC/NIH Center for Botanical Dietary Supplements Research, College of Pharmacy, M/C 781, University of Illinois at Chicago, 833 South Wood Street, Chicago, Illinois 60612, USA.

    Eight botanical preparations that are commonly used for the treatment of menopausal symptoms were tested for estrogenic activity. Methanol extracts of red clover (Trifolium pratense L.), chasteberry (Vitex agnus-castus L.), and hops (Humulus lupulus L.) showed significant competitive binding to estrogen receptors alpha (ER alpha) and beta (ER beta). With cultured Ishikawa (endometrial) cells, red clover and hops exhibited estrogenic activity as indicated by induction of alkaline phosphatase (AP) activity and up-regulation of progesterone receptor (PR) mRNA. Chasteberry also stimulated PR expression, but no induction of AP activity was observed. In S30 breast cancer cells, pS2 (presenelin-2), another estrogen-inducible gene, was up-regulated in the presence of red clover, hops, and chasteberry. Interestingly, extracts of Asian ginseng (Panax ginseng C.A. Meyer) and North American ginseng (Panax quinquefolius L.) induced pS2 mRNA expression in S30 cells, but no significant ER binding affinity, AP induction, or PR expression was noted in Ishikawa cells. Dong quai [Angelica sinensis (Oliv.) Diels] and licorice (Glycyrrhiza glabra L.) showed only weak ER binding and PR and pS2 mRNA induction. Black cohosh [Cimicifuga racemosa (L.) Nutt.] showed no activity in any of the above in vitro assays. Bioassay-guided isolation utilizing ER competitive binding as a monitor and screening using ultrafiltration LC-MS revealed that genistein was the most active component of red clover. Consistent with this observation, genistein was found to be the most effective of four red clover isoflavones tested in the above in vitro assays. Therefore, estrogenic components of plant extracts can be identified using assays for estrogenic activity along with screening and identification of the active components using ultrafiltration LC-MS. These data suggest a potential use for some dietary supplements, ingested by human beings, in the treatment of menopausal symptoms.

    1: Pak J Biol Sci. 2007 Jul 15;10(14):2300-7.Links
    The effects of Vitex agnus castus extract and its interaction with dopaminergic system on LH and testosterone in male mice.Nasri S, Oryan S, Rohani AH, Amin GR.
    Department of Biology, Parand Branch, Azad University, Tehran, Iran.

    The purpose of this study was to evaluate the probable effects of Vitex agnus castus (Vac.) on the male reproductive physiology. It is a well known fact that LH secretion from the anterior pituitary of mammals is controlled by many neurotransmiters such as dopamine. In this experiment, we have studied the effect of Vac. extract on the LH and testosterone hormones and its interaction with the dopaminergic system on male mice. In order to evaluate these effects, we used the hydroalcoholic Vac. extract (for extraction we used percolation technique) injection with the following doses: 65, 165, 265, 365 and 465 mg kg-', bromocriptine as a dopamine receptor agonist (5, 10, 20 mg kg(-1)) and haloperidol as a dopamine receptor antagonist (1, 1.5, 2, 2.5, 3 mg kg(-1)). To study the interaction between Vac. extract and dopaminergic system, we injected the optimum doses of Vac. with bromocriptine or haloperidol at the same time. Intraperitoneal injections were applied in all experiments, once a day for 30 days. The control group remained intact and the sham group received vehicle. After the last injection, we collected the animal blood serums for hormonal assays. LH and testosterone were measured by Radio Immuno Assay (RIA). LH and testosterone, showed significant decrease in bromocriptine group and haloperidol increased these hormones. Vac. extract decreased significantly the LH and testosterone levels. The coadministration of Vac. extract and bromocriptine decreased LH and testosterone. Coadministration of Vac. extract and haloperidol decreased LH and testosterone levels. These results suggest: dopamine regulates the gonadotroph-leydig cells axis. It appears that Vac. exertes effects through dopaminergic system and other pathways. The findings of this study show we can use Vac. extract for pathological cases of increasing LH and testosterone.
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    Quote Originally Posted by Primordial Perf View Post
    There is a 1-to-1 relationship with gyno and tren in some individuals, however with the introduction of something like vitex, these gyno symptoms go away. There is a connection with “sore, sensitive and puffy” nipples in males and the reduction with subsequent vitex supplementation.

    -Eric
    So if there is a 1:1 ratio then everyone who takes tren gets gyno?
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    Quote Originally Posted by sethroberts View Post
    Is this what you were on before the bridge with phera/mdrol?

    I just came back from work and addressed almost all the posts since then so go back to the first page to catch up
    nope i got gyno about 3 months after that cycle then started my other one (that im still on and will be for a lil while), long history,
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    Quote Originally Posted by Primordial Perf View Post
    Actually, it’s the double bond the 9th position that prevents the aromatization of dienolone. It simply cannot bind with aromatase.

    I have plenty of experience with Trenbolone, nandrolone and dienolone base and I can say without a doubt that dienolone has characteristics closer related to Trenbolone than nandrolone. The dry gains, hot flashes, potent CNS activation, insomnia, ect… (Even the compounds characteristics are similar - yellowish hue, burns the mucous membranes, ect)
    Do you have any data to back up your assertion that the double bond in the 9th position prevents aromatization of dienolone? The 4,9,11 conjugated system makes it impossible for trenbolone to convert to estrogen but the lack of the 11 double bond in dienolone could allow the electron density of the double bond at the 9-position to actually aid in the formation of the conjugated a-ring system -- i.e. the formatin of estrogen.

    Your personal experience of the end effects means nothing in the face of binding data to the contrary. Anecdotal information is useful but does not trump controlled scientific data. Oh, so it has a yellowish hue and burns the musuc membranes -- you just described probably >10,000 unrelated compounds.
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    Quote Originally Posted by Primordial Perf View Post
    I can also tell you from personal experience that Nolva is a very poor choice for combating progestin related gyno. It simply doesn’t work.

    I wouldn’t call it misinterpretation of the literature either. Nolva up regulates progesterone receptor. If it does it in the endometrium, this is enough reason for me to suspect it also does it in breast tissue. (but of course, I can’t force anyone to adopt my logic)

    I also suspect (although have no references) that other SERM’s may up-regulate the progesterone receptor similar to nolvadex. I simply have fallen out of favor of using SERMs for the treatment of gyno, especially progestin based gyno.

    As I have said already, I have most success with suppressing prolactin or estrogen, and reducing the total stimulatory action on mammary gland via these mechanisms.

    You have some interesting theory’s and I can agree with most of what you are saying, but I have to make it clear to the members that there other point of views on this subject… simply because I have a vested interest that my customer don’t have gyno symptoms when using our products.

    I say use Vitex if you are using 19-nor, and an possibly an AI if an aromatizable steroid is used.

    -Eric



    Effects of tamoxifen on steroid hormone receptors and hormone concentration and the results of DNA analysis by flow cytometry in endometrial carcinoma.
    M Nola, et al
    Gynecol Oncol, Mar 1999; 72(3): 331-6.

    Tamoxifen increases the plasma estrogen-binding equivalents and has an estradiol agonistic effect on histologically normal premenopausal and postmenopausal
    Gorodeski, G.I., et al.
    endometrium. Fertil. Steril, 57, 320-327. (1992)

    Estrogen and progesterone receptor expressors o£ decidual endometrium in a postmenopausal woman treated with tamoxifen and megestrol acetate.
    Cohen, I., Shulman, A., Altaras, M., Tepper, R., Cordoba, M. and Beyth, Y.
    Gynecol. Obstet. Invest., 38, 127-129. (1994)
    You speak as if noone else has anecdotal information -- what you are also lacking is the education and experience in interpretting pharmacological data to formulate a hypothesis that is based on anything but conjecture. You company owners crack me up when you think that somehow you are qualified to make these determinations. If you knew anything about physiology and the action of estrogen you would know that endometrium and breast are very different tissues with very different responses to estrogens and SERMS. When those science type fellows talk about selective estrogen receptor modulators do you realize that they are talking about tissue selectivity and that while tamoxifen is used to fight breast cancer because it acts as an antagonist (with slight partial agonist activity) in the breast that those patients are at an increased risk of endometrial cancer because tamoxifen acts as an agonist in that tissue? You are certainly entitled to your opinion but just realize that it is an unqualified opinion of someone who is trying to defend a product that noone was bashing.
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    Quote Originally Posted by crazyfool405 View Post
    nope i got gyno about 3 months after that cycle then started my other one (that im still on and will be for a lil while), long history,
    your previous quote:
    i was on epi as well as npp, and test, i stopped the epi and im still on npp and test and within 24 hours, my gyno came back

    Ok, you said you were on epi, mpp and test you stopped epi and within 24 hours gyno came back, so this was three months after what?
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    Quote Originally Posted by Primordial Perf View Post

    You have some interesting theory’s and I can agree with most of what you are saying, but I have to make it clear to the members that there other point of views on this subject… simply because I have a vested interest that my customer don’t have gyno symptoms when using our products.
    I don't mean to be crabby, but my "interesting theory's" are built on 19+ years of personal experience combined with an extensive knowledge of physiology and pharmacology as well as 10+ years in the lab so when someone comes along asserting somethign to be fact based on personal experience alone and question my knowledge, I get a little miffed.

    quotes like this one "If you are referring to a stimulus effect at the female hypothalamus/pituitary of estrogen or progesterone, I hope you’re not assuming this stimulatory effect applies to males." don't help.
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    Quote Originally Posted by sethroberts View Post
    your previous quote:
    i was on epi as well as npp, and test, i stopped the epi and im still on npp and test and within 24 hours, my gyno came back

    Ok, you said you were on epi, mpp and test you stopped epi and within 24 hours gyno came back, so this was three months after what?
    alright ill give you the scoop lol ill just post it all in here,

    i ran PPlex mdrol bridge as you know and i ended up geting gyno about 1 week before my next cycle which was and still is....


    My History and current status
    For all of you who have followed my previous log you know whats going on. I havent posted in there for a while so im going to start a discussion, not a flame, nothing of the sort but explain what i did (which you should not do), and the current stack i am doing

    History: (here goes another one thread)

    Week 1-5 test E 500mg
    Week 6-12 .6 mL ST450 (260mg), 1.4mL Test E (350mg)
    Week 12-17 .6mL ST450 (260mg), 1.4mL Test C (350mg), 3mL NPP (300mg)
    Week 18-25/26 .6mL ST450 (260mg), 1.4mL Test C (350mg), 2 mL Tren A (200mg)
    week 1-3 EQT2 (3 caps)
    week 3-5 Hdrol (3 caps)
    week 2-5 Trenadrol (2/2/3/3)
    Week 10-13 Epithin E (3/3/3/4)


    ob viously long yadda yadda, i know how everyone will react, im going from bulk to cut....

    i havent started tren yet
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    Quote Originally Posted by crazyfool405 View Post
    alright ill give you the scoop lol ill just post it all in here,

    i ran PPlex mdrol bridge as you know and i ended up geting gyno about 1 week before my next cycle which was and still is....


    My History and current status
    For all of you who have followed my previous log you know whats going on. I havent posted in there for a while so im going to start a discussion, not a flame, nothing of the sort but explain what i did (which you should not do), and the current stack i am doing

    History: (here goes another one thread)

    Week 1-5 test E 500mg
    Week 6-12 .6 mL ST450 (260mg), 1.4mL Test E (350mg)
    Week 12-17 .6mL ST450 (260mg), 1.4mL Test C (350mg), 3mL NPP (300mg)
    Week 18-25/26 .6mL ST450 (260mg), 1.4mL Test C (350mg), 2 mL Tren A (200mg)
    week 1-3 EQT2 (3 caps)
    week 3-5 Hdrol (3 caps)
    week 2-5 Trenadrol (2/2/3/3)
    Week 10-13 Epithin E (3/3/3/4)


    ob viously long yadda yadda, i know how everyone will react, im going from bulk to cut....

    i havent started tren yet
    so you got gyno while you were still on the bridge it went away on the EQT2 and then when you went off it came back? Sorry -- difficult to follow
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    Quote Originally Posted by sethroberts View Post
    so you got gyno while you were still on the bridge it went away on the EQT2 and then when you went off it came back? Sorry -- difficult to follow
    got gyno 1 week before EQT2, treated with adex through my cycle up until epithin E, (5a reduced has an atangonist effect on e2 from what i read mild AI prop) and within 1 day of stopping it, it came back full force, now im treating again with adex,

    hope that cleared it up

    BTW you need anyguinie pigs to help do any studies lol im down
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    yeah...i cant really keep up either crazy....
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    Quote Originally Posted by mooch2321 View Post
    yeah...i cant really keep up either crazy....
    AHHH i hate not being understood lol

    my last post didnt clear it up?
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    Quote Originally Posted by crazyfool405 View Post
    got gyno 1 week before EQT2, treated with adex through my cycle up until epithin E, (5a reduced has an atangonist effect on e2 from what i read mild AI prop) and within 1 day of stopping it, it came back full force, now im treating again with adex,

    hope that cleared it up

    BTW you need anyguinie pigs to help do any studies lol im down
    Clears it up for me I think. It seems to be nothing outside of normal estrogen related gyno. The phera and superdrol suppresss SHBG levels freeing up estradiol and estrone as well as removing the protective effect of SHBG and probably stimulating DHEA production in the adrenal which can have some estrogneic activity of its own without conversion. So this initiated the gyno one week before starting. the epithiostanol probably has some AI ability but likely also acts as an estrogen receptor antagonist which is why you saw symptoms as soon as you went off. The AI will help with the production of estrogen, but it does nothing for the circulating pool of estrogen, especially in the form of estrone sulfate which can be very long lived.
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    Quote Originally Posted by sethroberts View Post
    Clears it up for me I think. It seems to be nothing outside of normal estrogen related gyno. The phera and superdrol suppresss SHBG levels freeing up estradiol and estrone as well as removing the protective effect of SHBG and probably stimulating DHEA production in the adrenal which can have some estrogneic activity of its own without conversion. So this initiated the gyno one week before starting. the epithiostanol probably has some AI ability but likely also acts as an estrogen receptor antagonist which is why you saw symptoms as soon as you went off. The AI will help with the production of estrogen, but it does nothing for the circulating pool of estrogen, especially in the form of estrone sulfate which can be very long lived.
    soo some I3C later on can help in that area right>
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    Quote Originally Posted by crazyfool405 View Post
    soo some I3C later on can help in that area right>
    I doubt it is potent enough.
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    Quote Originally Posted by crazyfool405 View Post
    AHHH i hate not being understood lol

    my last post didnt clear it up?
    we posted at the same time....i didnt see that last one....oh and im scrolling impaired..
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    so in crazy's case seth would you recomend a combination like adex/nolva in low doses?...or something elase entirely
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    Quote Originally Posted by sethroberts View Post
    I would caution against "reducing" estrogen as I do think that AIs may be partially to blame. "Controlling" estrogen is preferable and I am partial to SERMS for this purpose. Especially for non-aromatizing or low aromatizing compounds because the reduction in SHBG and the increased "free" estrogens will not be helped by AI's.
    I got 2 small lumps under my nipple after a month of my PCT using Nolvadex. (cycle was tren/hdrol) I never been prone to gyno nor had it before. I have no clue what happened, but i just came up with my own conclusion that estrogen elevated again...

    So you think if i used a low dose of AI after i stopped that SERM would have brought me different results?
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    People started invoking "new" mechanisms for the induction of gyno in the late 1990's -- As far as I know, I was one of the first people proposing progesterone receptor activation as a potential cause of gyno back then. I have changed my mind since then as I have accumulated knowledge over the years. There is no evidence that progesterone or prolactin intitiate gynecomastia but plenty of evidence that estrogen does. All of this stemmed fro mthe fact that people were complaining of gyno from anadrol but also fron tren and nandrolone none of which were supposed to convert to estrogen. What I realized a while ago is that there is no need to invoke exotic mechanisms. Pher and superdrol do not convert to estrogen (nor does tren or anadrol) but they do suppress SHBG. SHBG is actually protective against breast tissue growth beyond just sequestering estrogens (you can read more about this in my book ). The removal of this protective effect as weel as the increase in "free" estrogen from the reduction in SHBG can explain some of the propensity for forming gyno with these compounds. With nandrolone, trenbolone, and other 19-norsteroids, there is also the added production of 5-alpha reduced metabolites that are weak androgens (there is some evidence that tren is metabolized in this fashion) which upstes the androgen to estrogen rati and further contributes to the ability to produce gyno.
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    Quote Originally Posted by mooch2321 View Post
    so in crazy's case seth would you recomend a combination like adex/nolva in low doses?...or something elase entirely
    I am not a fan of AIs - they tend to suppress estrogen too low and SHBG with it not to mention the effects on cholesterol etc.

    In that situation, I would probably have used nolva throughout and into PCT.
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    Quote Originally Posted by sethroberts View Post
    I doubt it is potent enough.

    what else can lower estrone sulfate levels....
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    When I was on a sust/deca cycle I had some first signs of gyno like symptoms. Note I say signs as there were never a lump or discharge that developed. What I do know is that nolva took care of ALL of the symptoms in quick fashion. I also used it along with clomid for pct. This was a year ago and never had issue since.

    That said I am week 3 into m-drol cycle and am using a-dex at very low dose and am taking low dose vitex and am have zero sensations in nipple area. I make sure bodyfat is always below 12 percent before starting any cycle as I think this helps.

    Just shows that there are a few ways to skin a cat.
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    Quote Originally Posted by mooch2321 View Post
    we posted at the same time....i didnt see that last one....oh and im scrolling impaired..
    LOL!

    This thread is awesome BTW..
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    what about the study showing nolva causes sperm damage? im still young when i recover i dont want that to recover and have poor sperm
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    Quote Originally Posted by Problem View Post
    I got 2 small lumps under my nipple after a month of my PCT using Nolvadex. (cycle was tren/hdrol) I never been prone to gyno nor had it before. I have no clue what happened, but i just came up with my own conclusion that estrogen elevated again...

    So you think if i used a low dose of AI after i stopped that SERM would have brought me different results?
    You may have needed a longer course of nolva since your SHBG levels probably had not recovered by the time you came off. I doubt an AI would have helped since it was probably not production of estrogen that was the problem. I generally believe that 20 mg of nolva is enough but there are circumstances where 40 or 60 mg would be appropriate. These strong androgen cycles are sometimes worst than aromatizing androgens because they can suppress SHBG levels so low.
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    Quote Originally Posted by crazyfool405 View Post
    what else can lower estrone sulfate levels....
    a sulfotransferase inhibitor or a 17 beta hydroxysteroid dehydrogenase inhibitor to prevent the back conversion of estrone to estradiol -- both of which are in development for breast cancer.
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    Quote Originally Posted by sethroberts View Post
    People started invoking "new" mechanisms for the induction of gyno in the late 1990's -- As far as I know, I was one of the first people proposing progesterone receptor activation as a potential cause of gyno back then. I have changed my mind since then as I have accumulated knowledge over the years. There is no evidence that progesterone or prolactin intitiate gynecomastia but plenty of evidence that estrogen does. All of this stemmed fro mthe fact that people were complaining of gyno from anadrol but also fron tren and nandrolone none of which were supposed to convert to estrogen. What I realized a while ago is that there is no need to invoke exotic mechanisms. Pher and superdrol do not convert to estrogen (nor does tren or anadrol) but they do suppress SHBG. SHBG is actually protective against breast tissue growth beyond just sequestering estrogens (you can read more about this in my book ). The removal of this protective effect as weel as the increase in "free" estrogen from the reduction in SHBG can explain some of the propensity for forming gyno with these compounds. With nandrolone, trenbolone, and other 19-norsteroids, there is also the added production of 5-alpha reduced metabolites that are weak androgens (there is some evidence that tren is metabolized in this fashion) which upstes the androgen to estrogen rati and further contributes to the ability to produce gyno.
    I wonder about all these people claiming gyno while using Nolva, and how this would all change if people used PHARM GRADE medicines rather then these research chems.
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    Quote Originally Posted by animaleater2 View Post
    When I was on a sust/deca cycle I had some first signs of gyno like symptoms. Note I say signs as there were never a lump or discharge that developed. What I do know is that nolva took care of ALL of the symptoms in quick fashion. I also used it along with clomid for pct. This was a year ago and never had issue since.

    That said I am week 3 into m-drol cycle and am using a-dex at very low dose and am taking low dose vitex and am have zero sensations in nipple area. I make sure bodyfat is always below 12 percent before starting any cycle as I think this helps.

    Just shows that there are a few ways to skin a cat.
    That is true and it is true that in men the majority of aromatase activity comes from adipose (but not all). I am concerned that opamine manipulation may be contributing to the increased incidence of "gyno" and "lactating" though.
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    Quote Originally Posted by crazyfool405 View Post
    what about the study showing nolva causes sperm damage? im still young when i recover i dont want that to recover and have poor sperm
    It also inhibits cholesterol side chain cleavage. Don't you think androgens have the potential to cause sperm damage. There are risks involeved to using all of these medications.
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    Quote Originally Posted by imprezivr6 View Post
    I wonder about all these people claiming gyno while using Nolva, and how this would all change if people used PHARM GRADE medicines rather then these research chems.
    Very good point. Even the "legal" OTC stuff has the potential to be contaminated. How many of these cases of tren gyno are the result of contamination or substitution?
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    Quote Originally Posted by sethroberts View Post
    It also inhibits cholesterol side chain cleavage. Don't you think androgens have the potential to cause sperm damage. There are risks involeved to using all of these medications.
    o of course!!! but in recovery i dont want to be damaging my sperm i did enough on cycle.
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    This thread is very informative and confusing at the same time. There are so many different theories that once you think you have a good understanding on how to prevent certain things, you read a different (yet still legit) opinion.
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    Quote Originally Posted by crazyfool405 View Post
    o of course!!! but in recovery i dont want to be damaging my sperm i did enough on cycle.
    It's funny. I never worried about sperm damage. That is not to say that it can't happen but sperm are made constantly and I had 3 kids without issue.
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    Quote Originally Posted by sethroberts View Post
    It's funny. I never worried about sperm damage. That is not to say that it can't happen but sperm are made constantly and I had 3 kids without issue.
    congrats man!

    when i get married thats the number im shooting for .
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    Quote Originally Posted by sethroberts View Post
    1: J Agric Food Chem. 2001 May;49(5):2472-9. Links
    Evaluation of estrogenic activity of plant extracts for the potential treatment of menopausal symptoms.Liu J, Burdette JE, Xu H, Gu C, van Breemen RB, Bhat KP, Booth N, Constantinou AI, Pezzuto JM, Fong HH, Farnsworth NR, Bolton JL.
    Department of Medicinal Chemistry and Pharmacognosy, UIC/NIH Center for Botanical Dietary Supplements Research, College of Pharmacy, M/C 781, University of Illinois at Chicago, 833 South Wood Street, Chicago, Illinois 60612, USA.

    Eight botanical preparations that are commonly used for the treatment of menopausal symptoms were tested for estrogenic activity. Methanol extracts of red clover (Trifolium pratense L.), chasteberry (Vitex agnus-castus L.), and hops (Humulus lupulus L.) showed significant competitive binding to estrogen receptors alpha (ER alpha) and beta (ER beta). With cultured Ishikawa (endometrial) cells, red clover and hops exhibited estrogenic activity as indicated by induction of alkaline phosphatase (AP) activity and up-regulation of progesterone receptor (PR) mRNA. Chasteberry also stimulated PR expression, but no induction of AP activity was observed. In S30 breast cancer cells, pS2 (presenelin-2), another estrogen-inducible gene, was up-regulated in the presence of red clover, hops, and chasteberry. Interestingly, extracts of Asian ginseng (Panax ginseng C.A. Meyer) and North American ginseng (Panax quinquefolius L.) induced pS2 mRNA expression in S30 cells, but no significant ER binding affinity, AP induction, or PR expression was noted in Ishikawa cells. Dong quai [Angelica sinensis (Oliv.) Diels] and licorice (Glycyrrhiza glabra L.) showed only weak ER binding and PR and pS2 mRNA induction. Black cohosh [Cimicifuga racemosa (L.) Nutt.] showed no activity in any of the above in vitro assays. Bioassay-guided isolation utilizing ER competitive binding as a monitor and screening using ultrafiltration LC-MS revealed that genistein was the most active component of red clover. Consistent with this observation, genistein was found to be the most effective of four red clover isoflavones tested in the above in vitro assays. Therefore, estrogenic components of plant extracts can be identified using assays for estrogenic activity along with screening and identification of the active components using ultrafiltration LC-MS. These data suggest a potential use for some dietary supplements, ingested by human beings, in the treatment of menopausal symptoms.

    1: Pak J Biol Sci. 2007 Jul 15;10(14):2300-7.Links
    The effects of Vitex agnus castus extract and its interaction with dopaminergic system on LH and testosterone in male mice.Nasri S, Oryan S, Rohani AH, Amin GR.
    Department of Biology, Parand Branch, Azad University, Tehran, Iran.

    The purpose of this study was to evaluate the probable effects of Vitex agnus castus (Vac.) on the male reproductive physiology. It is a well known fact that LH secretion from the anterior pituitary of mammals is controlled by many neurotransmiters such as dopamine. In this experiment, we have studied the effect of Vac. extract on the LH and testosterone hormones and its interaction with the dopaminergic system on male mice. In order to evaluate these effects, we used the hydroalcoholic Vac. extract (for extraction we used percolation technique) injection with the following doses: 65, 165, 265, 365 and 465 mg kg-', bromocriptine as a dopamine receptor agonist (5, 10, 20 mg kg(-1)) and haloperidol as a dopamine receptor antagonist (1, 1.5, 2, 2.5, 3 mg kg(-1)). To study the interaction between Vac. extract and dopaminergic system, we injected the optimum doses of Vac. with bromocriptine or haloperidol at the same time. Intraperitoneal injections were applied in all experiments, once a day for 30 days. The control group remained intact and the sham group received vehicle. After the last injection, we collected the animal blood serums for hormonal assays. LH and testosterone were measured by Radio Immuno Assay (RIA). LH and testosterone, showed significant decrease in bromocriptine group and haloperidol increased these hormones. Vac. extract decreased significantly the LH and testosterone levels. The coadministration of Vac. extract and bromocriptine decreased LH and testosterone. Coadministration of Vac. extract and haloperidol decreased LH and testosterone levels. These results suggest: dopamine regulates the gonadotroph-leydig cells axis. It appears that Vac. exertes effects through dopaminergic system and other pathways. The findings of this study show we can use Vac. extract for pathological cases of increasing LH and testosterone.
    Interesting study. Sounds like vitex may even be an progesterone/estrogen antagonist in certain settings by competitively binding. (It certainly doesn’t look like it has any potency even remotely close to estrogen or progesterone itself)

    Im not sure the second study has much relevance. I’m not recommending vitex for PCT.

    -Eric
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    Quote Originally Posted by sethroberts View Post
    Do you have any data to back up your assertion that the double bond in the 9th position prevents aromatization of dienolone? The 4,9,11 conjugated system makes it impossible for trenbolone to convert to estrogen but the lack of the 11 double bond in dienolone could allow the electron density of the double bond at the 9-position to actually aid in the formation of the conjugated a-ring system -- i.e. the formatin of estrogen.

    Your personal experience of the end effects means nothing in the face of binding data to the contrary. Anecdotal information is useful but does not trump controlled scientific data. Oh, so it has a yellowish hue and burns the musuc membranes -- you just described probably >10,000 unrelated compounds.
    Yeah, it should’nt be aromatizing. I’ll have to find a reference for this. Upon a quick search, I pulled this up –

    http://www.mesomorphosis.com/article...trenbolone.htm

    AR binding data is the ultimate tell all of a steroids effects eh? Interesting...

    -Eric
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