Progesterone and Prolactin

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    Quote Originally Posted by sethroberts View Post
    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.
    Your right, I don’t know anything about science or SERMs…

    BTW, I notice you’re quick to recommend nolva. Here is a piece that some members might want to consider when choosing this drug for gyno related issues -

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    Quote Originally Posted by sethroberts View Post
    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.

    I’m sorry your miffed and crabby… you shouldn’t be … ya know, with all this free advertising for your book you are getting.

    Anyway, Ive made the points I wanted to make.

    Good luck.

    -Eric
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    Quote Originally Posted by Primordial Perf View Post
    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
    So you reference an article about trenbolone as a support for dienolone not aromatizing?

    AR binding is not the ultimate tell all of a steroids effects, but it means a hell of a lot more than what you anecdotally "feel" from a steroid.
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    Quote Originally Posted by Primordial Perf View Post
    Your right, I don’t know anything about science or SERMs…

    BTW, I notice you’re quick to recommend nolva. Here is a piece that some members might want to consider when choosing this drug for gyno related issues -
    Where was that paper published and who peer reviewed it?
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    Quote Originally Posted by Primordial Perf View Post
    I’m sorry your miffed and crabby… you shouldn’t be … ya know, with all this free advertising for your book you are getting.

    Anyway, Ive made the points I wanted to make.

    Good luck.

    -Eric
    I have been posting on message boards since 1997 and have only had a book published for the past few months. Obviously my motivation for posting goes beyond advertising my book. Does yours go beyond selling/defending your products? I explained why I get crabby -- people who think that they are qualified to dispute the science because they own a supplement company. Does everyone know what qualifications it takes to start a supplement company and put products onto the market that you ingest?
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    Quote Originally Posted by Primordial Perf View Post
    Your right, I don’t know anything about science or SERMs…

    BTW, I notice you’re quick to recommend nolva. Here is a piece that some members might want to consider when choosing this drug for gyno related issues -
    You may know something about SERMS but you lack the knowledge to understand something as basic as the fact that endometrium and breast are very different when it comes to estrogen response. That is probably the biggest problem on these boards is that people start reading articles in pubmed without the basic understanding of human physiology, pharmacology, pharmacokinetics and chemistry and start to make assertions that are dead wrong. And then they fight for these assertions to the death because their "guru"-hood is built on those assertions. Just like you cannot become a medical doctor by reading medical books, it is difficult if not impossible to become an expert in pharmacology or endocrinology by just reading books or articles - especially if you don't have the baseline education in the topics above.
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    sethroberts said,

    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
    Other than keeping dosages and length of cycle reasonable, is there any way of limiting these sides while on a SD-clone?

    Or, in your opinion, what would be the best way to run an Mdrol cycle, including PCT?
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    Quote Originally Posted by marco wolf View Post
    sethroberts said,



    Other than keeping dosages and length of cycle reasonable, is there any way of limiting these sides while on a SD-clone?

    Or, in your opinion, what would be the best way to run an Mdrol cycle, including PCT?
    whos seth roberts....
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    Quote Originally Posted by mooch2321 View Post
    whos seth roberts....


    i must be scrollically impaired, though.
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    Quote Originally Posted by sethroberts View Post
    You may know something about SERMS but you lack the knowledge to understand something as basic as the fact that endometrium and breast are very different when it comes to estrogen response. That is probably the biggest problem on these boards is that people start reading articles in pubmed without the basic understanding of human physiology, pharmacology, pharmacokinetics and chemistry and start to make assertions that are dead wrong...
    Seth, according to literature I've read in the past, tamoxifen increases PgRs initially, and then they go back to baseline after around 2 weeks. I was able to dig up a couple of the articles. I do not claim to be an expert in pharmacology or endocrinology, and would be interested in your input regarding my interpretation of these.


    (Full article attached)
    U. Karck and F. Kommoss
    Does tamoxifen change oestrogen and progesterone receptor expression in the endometrium and breast?
    Department of Obstetrics and Gynaecology, University of Freiburg, Hugstetter Straβe 55, 79106 Freiburg, Germany
    Institute of Pathology, University of Mainz, 55101 Mainz, Germany
    http://www.sciencedirect.com/science...9609ec32b2dc7c


    1: Cancer. 1993 Feb 15;71(4):1266-72.Links
    Up-regulation of estrogen receptor by tamoxifen in human breast cancer.
    Noguchi S, Motomura K, Inaji H, Imaoka S, Koyama H.
    Department of Surgery, Center for Adult Diseases, Osaka, Japan.
    http://www.ncbi.nlm.nih.gov/pubmed/8382104
    Attached Images Attached Images
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    I have a seemingly simple question in all this that I believe is the crux of the whole argument (at least it is for me, as I've researched this quite a bit). Maybe Seth can answer it.

    Does binding the progesterone receptor have any effect whatsoever on prolactin levels?

    Or even more simply: other than a concurrent rise in estrogen, what other stimuli can raise prolactin?

    If anyone can answer these, I think I'll have a pretty good grasp of what happens with so-called prolactin gyno.
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    Quote Originally Posted by sethroberts View Post
    Where was that paper published and who peer reviewed it?
    And what peer reviewed journal published “anabolic pharmacology”?
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    Quote Originally Posted by sethroberts View Post
    You may know something about SERMS but you lack the knowledge to understand something as basic as the fact that endometrium and breast are very different when it comes to estrogen response. That is probably the biggest problem on these boards is that people start reading articles in pubmed without the basic understanding of human physiology, pharmacology, pharmacokinetics and chemistry and start to make assertions that are dead wrong. And then they fight for these assertions to the death because their "guru"-hood is built on those assertions. Just like you cannot become a medical doctor by reading medical books, it is difficult if not impossible to become an expert in pharmacology or endocrinology by just reading books or articles - especially if you don't have the baseline education in the topics above.
    Anyway…

    You recommended Nolva for progestin based gyno. I’m sorry, but in my experience this doesn’t work. I’ve provided my recommendations for something that does work. No need for personal insults…
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    Quote Originally Posted by Primordial Perf View Post
    And what peer reviewed journal published “anabolic pharmacology”?
    Ha ha. Touche.
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    Quote Originally Posted by Primordial Perf View Post
    And what peer reviewed journal published “anabolic pharmacology”?
    Very true. However, I did not reference my book as support at any point in this discussion. You referenced a rather silly article written by yourself and posted on your company web site. Sorry if that doesn't carry much weight in my opinion. Nor does your personal experience.
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    Quote Originally Posted by Primordial Perf View Post
    Anyway…

    You recommended Nolva for progestin based gyno. I’m sorry, but in my experience this doesn’t work. I’ve provided my recommendations for something that does work. No need for personal insults…
    Show me one shred of evidence that stimulation of the progesterone receptor causes gynecomastia.
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    Quote Originally Posted by Mass_69 View Post
    Seth, according to literature I've read in the past, tamoxifen increases PgRs initially, and then they go back to baseline after around 2 weeks. I was able to dig up a couple of the articles. I do not claim to be an expert in pharmacology or endocrinology, and would be interested in your input regarding my interpretation of these.


    (Full article attached)
    U. Karck and F. Kommoss
    Does tamoxifen change oestrogen and progesterone receptor expression in the endometrium and breast?
    Department of Obstetrics and Gynaecology, University of Freiburg, Hugstetter Straβe 55, 79106 Freiburg, Germany
    Institute of Pathology, University of Mainz, 55101 Mainz, Germany
    http://www.sciencedirect.com/science...9609ec32b2dc7c


    1: Cancer. 1993 Feb 15;71(4):1266-72.Links
    Up-regulation of estrogen receptor by tamoxifen in human breast cancer.
    Noguchi S, Motomura K, Inaji H, Imaoka S, Koyama H.
    Department of Surgery, Center for Adult Diseases, Osaka, Japan.
    http://www.ncbi.nlm.nih.gov/pubmed/8382104
    Those were the papers I was referring to when I mentioned in one of my posts that tamoxifen may cause a slight upregulation or no change in progesterone receptor.
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    sethroberts said,

    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
    marco asked:

    Other than keeping dosages and length of cycle reasonable, is there any way of limiting these sides while on a SD-clone?

    Or, in your opinion, what would be the best way to run an Mdrol cycle, including PCT?
    I'm not trying to put you on the spot, or anything, but you've stated that you're "not a fan" of AI's. I was wondering what you would recommend instead of AI's, if anything at all.
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    Quote Originally Posted by Dragon13 View Post
    I have a seemingly simple question in all this that I believe is the crux of the whole argument (at least it is for me, as I've researched this quite a bit). Maybe Seth can answer it.

    Does binding the progesterone receptor have any effect whatsoever on prolactin levels?

    Or even more simply: other than a concurrent rise in estrogen, what other stimuli can raise prolactin?

    If anyone can answer these, I think I'll have a pretty good grasp of what happens with so-called prolactin gyno.
    There are quite a few papers showing progesterone to reduce prolactin levels -- likely through its suppressive effects on estrogen receptor activation. I pasted abstracts from a couple below. Even medroxyprogesterone, a very potent porgesterone, causes a decease in prolactin receptor levels.

    Drugs that interfere with the production or release of dopamine. Antipsychotic medications are well known for causing increased prolactin levels.


    1: Biol Reprod. 1988 Dec;39(5):1067-73. Links
    Antagonism of estrogen-induced prolactin release by progesterone.Brann DW, Rao IM, Mahesh VB.
    Department of Physiology and Endocrinology, Medical College of Georgia, Augusta 30912-3000.

    Previous work from our laboratory has shown that during the process of nuclear occupancy of the progesterone receptor complex (1-2 h), nuclear estradiol receptors of the anterior pituitary are depleted. The purpose of this study was to determine whether the depletion of nuclear estradiol receptors by progesterone had functional biological significance. The ovariectomized (26 days of age) immature rat was used as the model for analysis of this question. The ability of estradiol to release prolactin from the anterior pituitary was the function chosen to determine the biological significance of the progesterone and estradiol interactions. In response to estradiol exposure (2 micrograms/rat), prolactin release reached peak values from 8 h to 12 h and returned to control levels by 24 h. A second injection of estradiol 13 h after the initial injection stimulated a second increase in serum prolactin at 25 h. This model of two injections of estradiol 13 h apart served to provide adequate levels of anterior pituitary progesterone receptors and elevated serum prolactin levels upon which superimposed progestin modulation could be examined. A single injection of progesterone (0.8 mg/kg BW) 1 h before the second estradiol injection blocked the increase in serum prolactin. This action was a receptor-mediated event because progesterone had no effect without estrogen priming or when the progesterone antagonist RU486 was used. Finally, when the interval between the progesterone and second estradiol injection was extended to 4 h, a time period when progesterone does not deplete pituitary nuclear estrogen receptors, the estrogen-induced increase in serum prolactin was not blocked.(ABSTRACT TRUNCATED AT 250 WORDS)

    1: Pharmacol Res Commun. 1988 Aug;20(8):719-30.Links
    Effects of medroxyprogesterone acetate on serum prolactin levels and liver prolactin binding capacity in the rat.Muccioli G, Racca S, Ricci Gamalero S, Di Carlo F.
    Institute of Pharmacology, Faculty of Medicine, University of Turin, Italy.

    Modifications in liver prolactin (PRL) receptor levels and serum PRL concentration induced by administration of medroxyprogesterone acetate (MPA) were investigated in rats of both sexes. MPA induced a reduction both of the levels of PRL in the serum and of liver PRL receptors in the female rat. The reduction of the number of PRL receptors caused by MPA was rapid and almost complete after 10 days of treatment and appeared earlier than that of serum PRL levels. Furthermore the MPA-induced decrease in PRL receptors was specific, since insulin binding to the same liver membranes was not affected. MPA given simultaneously with oestradiol (which increases both the number of liver PRL receptors and the serum PRL levels in the male rats) was able to counteract the increase in PRL binding induced by oestradiol. On the contrary, the oestrogen-induced increase in serum PRL was not affected by MPA treatment. Similar results were obtained using tamoxifen, a well known antioestrogenic drug. In conclusion, our results show that the reduction of PRL receptor levels induced by MPA in rat liver is specific, not correlated to serum PRL concentration, and seems to depend on the antioestrogenic activity of the drug.
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    I got to say that I agree with Seth in everything he says, it make a lot a sense and for my research , experience and readings on anabolics its all true
    reps and I`M going to the store and buy the book, I`ll pay a lot in taxes but what the hell its well worth
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    Quote Originally Posted by marco wolf View Post
    sethroberts said,



    marco asked:



    I'm not trying to put you on the spot, or anything, but you've stated that you're "not a fan" of AI's. I was wondering what you would recommend instead of AI's, if anything at all.
    Sorry -- trying to respond to everything. Of course keeping doses as low as needed to have an effect will help. Other than that, I would use nolvadex. Nolvadex reduces estrogen receptor stimulation, keeps SHBG levels up and helps with blood lipids a little.
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    Seth- I know you don't agree with PP's article, but do YOU feel there is considerable risk using nolva for extended periods of time(ie.16-20wks)? Or are they over stated in that sort of time frame, and generally only an issue in prolonged use?
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    Quote Originally Posted by imprezivr6 View Post
    Seth- I know you don't agree with PP's article, but do YOU feel there is considerable risk using nolva for extended periods of time(ie.16-20wks)? Or are they over stated in that sort of time frame, and generally only an issue in prolonged use?
    I think the dangers of nolva are largely overstated -- mostly by people trying to sell something as a dietary supplement for on or post-cycle therapy. That being said, the risk of adverse events generally goes up in frequency as the dose and duration are increased. I would not use Nolva for 20 weeks -- I would also be cautious about combining it with oral AAS since nolva can cause some liver tox.
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    Quote Originally Posted by sethroberts View Post
    I think the dangers of nolva are largely overstated -- mostly by people trying to sell something as a dietary supplement for on or post-cycle therapy. That being said, the risk of adverse events generally goes up in frequency as the dose and duration are increased. I would not use Nolva for 20 weeks -- I would also be cautious about combining it with oral AAS since nolva can cause some liver tox.
    I hear ya, it is hard for me to wrap my head around an article, with such scare tactics, when advertising a generally unproven, over the counter supplement to do the job of actual pharmaceuticals.

    As for the 20wks, i was figuring if you ran a 14-16wk cycle while using nolva, then ran it for an additional 4wk pct, that would put you up in that range. Maybey longer factoring in any long esters clearing prior to PCT.

    Even a 12wk cycle would put you at 16wk min.
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    Quote Originally Posted by imprezivr6 View Post
    I hear ya, it is hard for me to wrap my head around an article, with such scare tactics, when advertising a generally unproven, over the counter supplement to do the job of actual pharmaceuticals.

    As for the 20wks, i was figuring if you ran a 14-16wk cycle while using nolva, then ran it for an additional 4wk pct, that would put you up in that range. Maybey longer factoring in any long esters clearing prior to PCT.

    Even a 12wk cycle would put you at 16wk min.
    True and I am sure that nolva is being used for very long periods of time by some users. I probably wouldn't run nolva at the same dose for an entire cycle and then into PCT. But then again, I tend towards more moderate doses which reduces the need for ancillaries. I think there is (perhaps rightfully so) a paranoia about developing gynecomastia so people go overboard and throw everything but the kitchen sink at it in the hopes of warding it off. How many posts do you see with people saying "I just took my third dose of X and my nipples are tingling, itching, sore, full, puffy, leaking when i apply enough pressure to pop my nipple off"
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    Good thread. Good info. Cheers.
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    Quote Originally Posted by sethroberts View Post
    Show me one shred of evidence that stimulation of the progesterone receptor causes gynecomastia.
    Reducing prolactin will reduce stimulation and growth of the mammary gland. (whether it’s PR or ER mediated growth) This is why I advice vitex while on cycle. Vitex also doesn’t carry the same toxic properties as Nolva.

    -Eric
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    Quote Originally Posted by sethroberts View Post
    I think the dangers of nolva are largely overstated -- mostly by people trying to sell something as a dietary supplement for on or post-cycle therapy. That being said, the risk of adverse events generally goes up in frequency as the dose and duration are increased. I would not use Nolva for 20 weeks -- I would also be cautious about combining it with oral AAS since nolva can cause some liver tox.

    The dangers from Nolva are equally expressed by articles coming from peer reviewed journals too… Not just from my silly supplement company… the dangers are a reality.

    Interesting that you say the “dangers are overstated”, yet you say “I would not use nolva for 20 weeks”…

    Contradictory no?

    Let me just ask..

    Do you think Vitex is ineffective for combating gyno coming from the use of a progestin based anabolic?

    -Eric
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    Quote Originally Posted by nunes View Post
    I got to say that I agree with Seth in everything he says, it make a lot a sense and for my research , experience and readings on anabolics its all true
    reps and I`M going to the store and buy the book, I`ll pay a lot in taxes but what the hell its well worth
    I agree with most of what he says too… except his prescription of nolva…

    -Eric
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    statements like nolva makes gyno worse while on nandrolone are over all the boards. do you recommend using nolva if symptoms of gynecomastia appear while on nandrolone?
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    Quote Originally Posted by Primordial Perf View Post
    Reducing prolactin will reduce stimulation and growth of the mammary gland. (whether it’s PR or ER mediated growth) This is why I advice vitex while on cycle. Vitex also doesn’t carry the same toxic properties as Nolva.

    -Eric
    There is simply no evidence that prolactin plays a role in gynecomastia -- i.e. the growth of breast tissue. The Williams Text of Endocrinology states and I quote "Prolactin does not play a direct role in gynecomastia" and "this conclusion is in keeping with the fact that prolactin is not a growth hormone for the breast".

    Vitex does not carry the same toxic properties as nolva but that does not mean that it is free from potential side effects. Any substance that alters dopamine signalling has the potential to desensitive dopaminergic neurons to dopamine which could result in levated prolactin levels upon cessation due to the loss of inhibitory control.

    Do you have any evdiece to the contrary?
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    Quote Originally Posted by Primordial Perf View Post
    The dangers from Nolva are equally expressed by articles coming from peer reviewed journals too… Not just from my silly supplement company… the dangers are a reality.

    Interesting that you say the “dangers are overstated”, yet you say “I would not use nolva for 20 weeks”…

    Contradictory no?

    Let me just ask..

    Do you think Vitex is ineffective for combating gyno coming from the use of a progestin based anabolic?

    -Eric

    "The dangers are overstated" does not mean that there are not potential risks with its use. These risks increase with dose and duration as I have previously stated. The greatest dangers from nolva - in my opinion - are liver toxicity and endometrial cancer -- and I don't have a uterus.

    I do not think vitex is effective for combating gyno coming from the use of progestin based anabolics because there is not evidence that it is the progesterone receptor activity or the prolactin that is causing the gyno. What are you proposing to be the mechanism of action of vitex efficacy in progestin based gyno? I am open to discussion and new evidence must always be considered if theories are to evolve over time but I am not going to go round and round with you in a circular argument -- either provide evidence outside of anecdotal observations or give us all a break.
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    Quote Originally Posted by repmks View Post
    statements like nolva makes gyno worse while on nandrolone are over all the boards. do you recommend using nolva if symptoms of gynecomastia appear while on nandrolone?
    There is a lot of bologni all over the boards. Somebody says something and then everyone repeats it over and over again to appear as if they know something. If gyno symptoms appear, then it may be too late. Do I recommend nolva over treating with something to reduce prolactin in the absence of elevated prolactin? yes.

    The statements about nolva are based on the following premises: 1) progesterone receptor stimulation causes gyno 2) nolvadex upregulates progesterone receptors. There is no evidence for #1 and although # 2 may occur in the short term, nolva has been shown to decrease progesterone receptor concentration in the longer term.
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    Quote Originally Posted by sethroberts View Post
    There is a lot of bologni all over the boards. Somebody says something and then everyone repeats it over and over again to appear as if they know something. If gyno symptoms appear, then it may be too late. Do I recommend nolva over treating with something to reduce prolactin in the absence of elevated prolactin? yes.

    The statements about nolva are based on the following premises: 1) progesterone receptor stimulation causes gyno 2) nolvadex upregulates progesterone receptors. There is no evidence for #1 and although # 2 may occur in the short term, nolva has been shown to decrease progesterone receptor concentration in the longer term.

    http://www.aafp.org/afp/20050901/821.html

    dont we always use nolva short term anyway, so the long term decrease in PR concentration doesnt apply to how we use it correct?
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    Quote Originally Posted by crazyfool405 View Post
    http://www.aafp.org/afp/20050901/821.html

    dont we always use nolva short term anyway, so the long term decrease in PR concentration doesnt apply to how we use it correct?
    Depends on how you define short and long term and how you define increased PR expression. I would actually argue that PR downregulation is not desired. Treatment with the progesterone receptor antagonist Mifepristine actually results in gynecomastia probably through the loss of the suppressive effects of progesterone receptor activation on estrogen.
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    Quote Originally Posted by crazyfool405 View Post
    http://www.aafp.org/afp/20050901/821.html

    dont we always use nolva short term anyway, so the long term decrease in PR concentration doesnt apply to how we use it correct?
    That is an interesting article that you linked to. Did you see these quotes?

    A small study involving 20 healthy men showed increased prolactin levels in those receiving a low dose of chasteberry (120 mg per day) but a decrease of prolactin secretion with higher doses (480 mg per day).

    Chasteberry also has been used to modify libido, most often to reduce sexual desire but sometimes to improve decreased libido.

    Also, did you notice absolutely no mention of treatment of gynecomastia in that article. Additionally, there is no evidence in the scientiific/medical literature of its use for gynecomastia.
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    Yea I just thought I'd put that out there because there was a small discussion on it and you can take from it what u can
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    Quote Originally Posted by crazyfool405 View Post
    Yea I just thought I'd put that out there because there was a small discussion on it and you can take from it what u can
    Yeah. And I am not telling people to not use vitex or AIs or some combination of those and whatever else you want to take that makes you feel like you are doing the best thing for you. There are risks associated with every substance you put into your body, including over the counter supps and herbs. Everybody has to weigh these risks versus the potential benefits and make an informed decision. I just have not seen any convincing evidence that progesterone or prolactin cause the symptoms of gynecomastia in the absence of elevated estrogen and if elevated estrogen is the root cause, then that is what I want to treat.
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    Quote Originally Posted by sethroberts View Post
    Yeah. And I am not telling people to not use vitex or AIs or some combination of those and whatever else you want to take that makes you feel like you are doing the best thing for you. There are risks associated with every substance you put into your body, including over the counter supps and herbs. Everybody has to weigh these risks versus the potential benefits and make an informed decision. I just have not seen any convincing evidence that progesterone or prolactin cause the symptoms of gynecomastia in the absence of elevated estrogen and if elevated estrogen is the root cause, then that is what I want to treat.
    Fair statement here.

    I’d love to spend the next few hours of my day hunting down abstracts that show prolactin or progestin induce mammary gland growth… but I simply don’t have the opportunity at the moment. (pregnancy = prolactin = breast growth, hello!?)

    Trenbolone would theoretically lower circulating estrogen during a cycle by way of negative feedback upon T production, yet gyno is a common occurrence with high doses of this Trenbolone. (obviously, I propose this is related to a direct action on the PR). I think your theory is that sulfate bound E2 is being released over the term of this cycle, and thus stimulating gyno by a lack of ER antagonism from trenbolone?

    I suppose this is a possibility (and probably explains part of the problem), but you would be just as hard pressed to find a single silver bullet study to support that statement as I would have trying to find a study showing male gyno being induced by a progestin or a prolactin/progestin combination.

    -Eric
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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.
    whats your opinion on running low dosed- two pumps 2xday td formestane on a tren cycle? formestane is different than most ai's as you well know.
  

  
 

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