Progesterone and Prolactin

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    Quote Originally Posted by crazyfool405 View Post
    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
    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

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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.
    Got ya..

    This is interesting as i have probably read "don't use nolva with tren(progestins) as it will cause gyno/make gyno worse" a thousand times..
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    Quote Originally Posted by imprezivr6 View Post
    Got ya..

    This is interesting as i have probably read "don't use nolva with tren(progestins) as it will cause gyno/make gyno worse" a thousand times..
    I would love to see the argument behind that.
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    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.
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    so seth...if lactation is occuring, its not neccesarily high levels of prolactin but the difference in the levels of estrogen and prolactin....how should this be treated at this point....let estrogen levels raise or take a prolactin antagonist? Couldnt we be causing other problems by letting estrogen rebound?
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    Quote Originally Posted by mooch2321 View Post
    so seth...if lactation is occuring, its not neccesarily high levels of prolactin but the difference in the levels of estrogen and prolactin....how should this be treated at this point....let estrogen levels raise or take a prolactin antagonist? Couldnt we be causing other problems by letting estrogen rebound?
    If lactation is truly occuring then at that point I would get a blood test to confirm elevated prolactin or severly suppressed estrogen and then I would take caber. I cannot stress how bad it is to supress estrogen to very low levels.

    Obviously the idea would be to not get to the point of either getting gyno or lactating but I think sometimes people get too overzealous in the other direction and wind up causing themselves harm through polypharmacy.
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    can you define truly occuring....if a nipple is squeezed and beads of liquid are excreted would you consider this true lactation or are we looking for more discharge?
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    Quote Originally Posted by mooch2321 View Post
    can you define truly occuring....if a nipple is squeezed and beads of liquid are excreted would you consider this true lactation or are we looking for more discharge?
    I would likely classify that under "stop squeezing your nipples". It would need to be more of a discharge. Did you see the reference above to self-manipulation and lactation?
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    sorry i missed that post....
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    Quote Originally Posted by mooch2321 View Post
    sorry i missed that post....
    for the scrolling-impaired

    Benign galactorrhea/breast discharge in adolescent males probably due to breast self-manipulation.Rohn RD.
    Three adolescent males presented with nipple discharge. In two boys, the expressed secretion was clinically consistent with galactorrhea. Galactorrhea/breast discharge is a rare complaint in males of any age. Although galactorrhea is commonly associated with a neuroendocrine disorder or drug ingestion, the work-up in each, including basal prolactin level, was normal. Reluctantly, each by admitted to breast self-manipulation to reduce gynecomastia. When the behavior was discontinued, the galactorrhea/breast secretion ceased. Clinicians should be aware of this heretofore undescribed and apparently benign phenomenon. If basal hyperprolactinemia is absent in a male with a breast discharge and a history of breast manipulation, then an extensive work-up is not usually indicated.

    PMID: 6429109 [PubMed - indexed for MEDLINE
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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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