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Progesterone and Prolactin

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    Quote Originally Posted by Primordial Perf View Post
    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
    That is pretty close. Back conversion of estrone sulfate to estradiol. The estrogen sulfate would be elevated due to decreases in SHBG that accompanies strong androgenic stimulation in the absence of estrogen. This decrease in SHBG also removes the protective effect of SHBG against breast tissue gorwth. Everyone is keen on decreasing SHBG but there are some good papers showing that SHBG actually protects against breast tissue growth beyond its ability to sequestor estrogens.

    As I stated earlier in the thread, I was one of the first to put the idea out there that progesterone receptor stimulation may be causing gyno. It was only later that I realized that this is incorrect. Breast growth in pregnancy is probably not a good model for gynecomastia because there are so many hormonal changes going on simultaneously. Prolactin is not a growth factor in the breast and progesterone not only decrease prolactin but also decreases estrogen receptor expression. This is further driven home by the fact that the progesterone antagonist, mifepristone, actually results in gynecomastia. You don't have to search now and this shouldn't be some kind of contest. I have searched extensively on this topic over the years and I am very well-versed in the body of knowledge on the subject but you never know, you may pick a set of search terms that turns up something I haven't.

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    Quote Originally Posted by thebigt View Post
    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.
    I am not sure if suicidal AIs are better or worse when it comes down to it. The end result is generally the same, too low levels of estrogen, horrible HDL levels and potential rebound gynecomastia.
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    Quote Originally Posted by sethroberts View Post
    I am not sure if suicidal AIs are better or worse when it comes down to it. The end result is generally the same, too low levels of estrogen, horrible HDL levels and potential rebound gynecomastia.
    but by it boosting igf-1 secretion, upregulating hpta and decreasing shbg doesn't this make formestane different than most other suicide ai's. and i am talking low dosed.
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    Quote Originally Posted by thebigt View Post
    but by it boosting igf-1 secretion, upregulating hpta and decreasing shbg doesn't this make formestane different than most other suicide ai's. and i am talking low dosed.
    Maybe but it makes it similar to some competitive AI's
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    Quote Originally Posted by sethroberts View Post
    Maybe but it makes it similar to some competitive AI's
    i have to disagree, i feel adding td formestane to my cycles is the best decision ive made regarding ph cycles. ive done propadrol before and many different cycles with formestane included and have no signs of any gyno/prolatin issues. i guess results speak for themselves. nice information though, very interesting.
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    Quote Originally Posted by thebigt View Post
    i have to disagree, i feel adding td formestane to my cycles is the best decision ive made regarding ph cycles. ive done propadrol before and many different cycles with formestane included and have no signs of any gyno/prolatin issues. i guess results speak for themselves. nice information though, very interesting.
    To each his own. If the reduced HDL levels don't bother you and you don't sufer from rebound gyno then do what works for you.
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    Quote Originally Posted by sethroberts View Post
    To each his own. If the reduced HDL levels don't bother you and you don't sufer from rebound gyno then do what works for you.
    well my lipids are just fine, and looking at my join date i guess ive been doing ph cycles for about 3 years now. not that i don't value your information, just it seems inconclusive, imo. i see all these guys with all these symptoms that i don't have, and ive ran a lot more cycles than most of them. the difference is td formestane-i swear by the stuff and it's treated me very well. my bro-science theory is keep estrogen low not dead on cycle and prevent most of these symptoms if not all. low dosed td formestane for the win.
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    Quote Originally Posted by thebigt View Post
    well my lipids are just fine, and looking at my join date i guess ive been doing ph cycles for about 3 years now. not that i don't value your information, just it seems inconclusive, imo. i see all these guys with all these symptoms that i don't have, and ive ran a lot more cycles than most of them. the difference is td formestane-i swear by the stuff and it's treated me very well. my bro-science theory is keep estrogen low not dead on cycle and prevent most of these symptoms if not all. low dosed td formestane for the win.
    What is your HDL post cycle if you don't mind sharing?

    What is your on cycle Estradiol? I assume you know since you say "keep it low, not dead"

    What is your history with gyno, if any, prior to using TD form?
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    Quote Originally Posted by imprezivr6 View Post
    What is your HDL post cycle if you don't mind sharing?

    What is your on cycle Estradiol? I assume you know since you say "keep it low, not dead"

    What is your history with gyno, if any, prior to using TD form?
    i don't keep my medical history on hand but i get tested for liver values and lipids 2 times a year, my doc has never raised a concern so i assume they are within normal range- i have been tested while on cycle, post cycle and off cycle and never once have the varied enough for my doc to be concerned. i have test and estrogen tested once a year-all my insurance will pay for and again no concern by my doc-these tests have been done for last 7 years and i have been doing ph's for 3 of them. never had gyno and i use td formestane to keep it that way. sorry if i seem abrassive but i really feel the formestane is why i have none of the symptoms others seem to be having.
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    Quote Originally Posted by thebigt View Post
    i don't keep my medical history on hand but i get tested for liver values and lipids 2 times a year, my doc has never raised a concern so i assume they are within normal range- i have been tested while on cycle, post cycle and off cycle and never once have the varied enough for my doc to be concerned. i have test and estrogen tested once a year-all my insurance will pay for and again no concern by my doc-these tests have been done for last 7 years and i have been doing ph's for 3 of them. never had gyno and i use td formestane to keep it that way. sorry if i seem abrassive but i really feel the formestane is why i have none of the symptoms others seem to be having.
    1. Just because your Dr didn't express concern doesn't mean you are in optimal range. My HDL was in the 20's and my dr didn't say ****, as my total choles, and trigs were fine.

    2. I have never seen any on-cycle form bloodwork.. How do we even know to what degree it is effecting E2?

    3. I am glad to hear you have never gotten gyno symptoms, but since you never had them before TD Form, is it possible you are one of the few to be pretty resilient to gyno?



    I can personally say i have ran 500mg test/300mg deca, and 750mg(think i actually touched 1k at one point) test/400mg deca, no AI, or anything to combat estro, and didn't have any gyno symptoms.. Does that mean everyone will have that experience?
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    Quote Originally Posted by imprezivr6 View Post
    1. Just because your Dr didn't express concern doesn't mean you are in optimal range. My HDL was in the 20's and my dr didn't say ****, as my total choles, and trigs were fine.

    2. I have never seen any on-cycle form bloodwork.. How do we even know to what degree it is effecting E2?

    3. I am glad to hear you have never gotten gyno symptoms, but since you never had them before TD Form, is it possible you are one of the few to be pretty resilient to gyno?



    I can personally say i have ran 500mg test/300mg deca, and 750mg(think i actually touched 1k at one point) test/400mg deca, no AI, or anything to combat estro, and didn't have any gyno symptoms.. Does that mean everyone will have that experience?
    look, i never claimed to have science or medical background, but since this is a forum for sharing our experiences i shared mine. all i can say is ive been using ph's for awhile now and i have no symtoms others are reporting, the difference imo is the formestane on cycle. i did not stumble upon formestane, there is a ton of research on it and it has been used for decades for cycles like you have mentioned. take it for what it's worth but i believe in the stuff and will never run a cycle without it.
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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.
    Progesterone:

    1) http://www.endotext.org/male/male14/male14.html

    2) http://cat.inist.fr/?aModele=afficheN&cpsidt=1525645 (sort of, in a round-about way; abstract seems to conclude presence of elevated E and PR receptors contributes to severity of condition)

    3) http://www.springerlink.com/content/235p1612528vk68t/

    Now here's the thing. All of the above and every other study I could find (of the few out there) also had estrogen linked in in some manner. Also, some of the above are admittedly tenuous links. But the bottom line seems to be estrogen and progesterone work synergistically when it comes to breast growth. IOW, I agree with you that estrogen is the key... sort of. I have concluded that elevated progesterone itself cannot cause gyno, but it can (in a round-about way) in the presence of enough estrogen. I don't think you disagree, seeing as how estrogen is still the key, so here's where I'm going with this.

    We've been talking about the Tren compounds here; from what I understand they have an incredible binding affinity for the progesterone receptor. My theory: 1 part of the Tren gyno issue is that the tremendous surge in progesterone can trigger gyno in the presence of normal estrogen levels. You mentioned the breakdwon of SHBG and how it would increase circulating E; this would only serve to exacerbate the problem. So yes, E is the key, but saying progesterone has no role is misleading IMO.

    Now on to prolactin. You said this earlier in the thread: "There is no evidence that controlling prolactin will prevent or treat gynecomastia. Many of the issues that are being attributed to prolactin can be explained through other mechanisms."

    If this is true please explain why the first 2 links below indicate prolactin is a growth factor for breast enlargement, while the 3rd and 4th, which provide an overview of the symptoms of clinical prolactinoma, list gynecomastia as a symptom (albeit "uncommonly" on the Mayo Clinic link), and the last 3 all list gyno as a symptom of simple hyperprolactinemia.

    Prolactin:

    1) http://www.springerlink.com/content/nn1424748054t0w4/

    2) http://www.pubmedcentral.nih.gov/art...?artid=1869171

    3) http://neurosurgery.ucla.edu/body.cfm?id=212

    4) http://www.mayoclinic.com/health/pro...CTION=symptoms

    5) http://www.vivo.colostate.edu/hbooks...prolactin.html

    6) http://en.wikipedia.org/wiki/Hyperpr...aemia#Symptoms

    7) http://www.wrongdiagnosis.com/h/hype...a/symptoms.htm

    Finally, here's a quote from MedicineNet.com by author Dr. Robert Ferry Jr., MD and his Medical Editor, Dr. Ruchi Mathur, MD, FRCP(C).

    What is the normal function of prolactin?

    "Prolactin stimulates the breast tissues to enlarge during pregnancy."

    I flat-out don't buy the fact the elevated prolactin can't cause gyno. I've run across enough evidence, both anecdotal and not, to not believe otherwise. Perhaps there is a relatiuonship similar to progesterone with E in that eswtrogen is needed in some degree to cause actual breast growth - I don't know. My question from earlier, about whether or not binding the PR receptor could affect prolactin levels, would fit perfectly if it were true. (Tren binding PR = rise in prolactin = part 2 of potential gyno (along with normal E and E+PR issues). Alas, you posted evidence to the contrary - thanks by the way. Now I'm kind of back in the same place I was before: I think prolactin can stimulate gyno (and if not classical gynecomastia in all cases, then certainly nipple discharge, and who wants that either), but I can't explain why prolactin would go up so high on a designer Tren cycle.

    I rambled a bit here, hope this all makes sense. Hoping you can respond here, maybe there's something I'm missing.
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    Quote Originally Posted by thebigt View Post
    look, i never claimed to have science or medical background, but since this is a forum for sharing our experiences i shared mine. all i can say is ive been using ph's for awhile now and i have no symtoms others are reporting, the difference imo is the formestane on cycle. i did not stumble upon formestane, there is a ton of research on it and it has been used for decades for cycles like you have mentioned. take it for what it's worth but i believe in the stuff and will never run a cycle without it.
    I understand, but you are giving no info, while making claims like"my bro-science theory is keep estrogen low not dead on cycle and prevent most of these symptoms if not all. low dosed td formestane for the win"

    How can you even say that when you don't even know what it is doing to your estradiol?

    I have yet to see any bloodwork with Form. Please show me any labs you have found over the years..

    Lastly what ph's have you run, while using TD form?

    I am not knocking the stuff, as i have used it a few times myself, just to be clear.
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    Quote Originally Posted by sethroberts View Post
    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.
    Yeah, I knew these latter ones, was kind of hoping for info on PR activation. Very interesting that progesterone reduces prolactin. My theory still has one hole (see above post).
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    Quote Originally Posted by Dragon13 View Post
    Progesterone:

    1) http://www.endotext.org/male/male14/male14.html

    2) http://cat.inist.fr/?aModele=afficheN&cpsidt=1525645 (sort of, in a round-about way; abstract seems to conclude presence of elevated E and PR receptors contributes to severity of condition)

    3) http://www.springerlink.com/content/235p1612528vk68t/

    Now here's the thing. All of the above and every other study I could find (of the few out there) also had estrogen linked in in some manner. Also, some of the above are admittedly tenuous links. But the bottom line seems to be estrogen and progesterone work synergistically when it comes to breast growth. IOW, I agree with you that estrogen is the key... sort of. I have concluded that elevated progesterone itself cannot cause gyno, but it can (in a round-about way) in the presence of enough estrogen. I don't think you disagree, seeing as how estrogen is still the key, so here's where I'm going with this.

    We've been talking about the Tren compounds here; from what I understand they have an incredible binding affinity for the progesterone receptor. My theory: 1 part of the Tren gyno issue is that the tremendous surge in progesterone can trigger gyno in the presence of normal estrogen levels. You mentioned the breakdwon of SHBG and how it would increase circulating E; this would only serve to exacerbate the problem. So yes, E is the key, but saying progesterone has no role is misleading IMO.

    Now on to prolactin. You said this earlier in the thread: "There is no evidence that controlling prolactin will prevent or treat gynecomastia. Many of the issues that are being attributed to prolactin can be explained through other mechanisms."

    If this is true please explain why the first 2 links below indicate prolactin is a growth factor for breast enlargement, while the 3rd and 4th, which provide an overview of the symptoms of clinical prolactinoma, list gynecomastia as a symptom (albeit "uncommonly" on the Mayo Clinic link), and the last 3 all list gyno as a symptom of simple hyperprolactinemia.

    Prolactin:

    1) http://www.springerlink.com/content/nn1424748054t0w4/

    2) http://www.pubmedcentral.nih.gov/art...?artid=1869171

    3) http://neurosurgery.ucla.edu/body.cfm?id=212

    4) http://www.mayoclinic.com/health/pro...CTION=symptoms

    5) http://www.vivo.colostate.edu/hbooks...prolactin.html

    6) http://en.wikipedia.org/wiki/Hyperpr...aemia#Symptoms

    7) http://www.wrongdiagnosis.com/h/hype...a/symptoms.htm

    Finally, here's a quote from MedicineNet.com by author Dr. Robert Ferry Jr., MD and his Medical Editor, Dr. Ruchi Mathur, MD, FRCP(C).

    What is the normal function of prolactin?

    "Prolactin stimulates the breast tissues to enlarge during pregnancy."

    I flat-out don't buy the fact the elevated prolactin can't cause gyno. I've run across enough evidence, both anecdotal and not, to not believe otherwise. Perhaps there is a relatiuonship similar to progesterone with E in that eswtrogen is needed in some degree to cause actual breast growth - I don't know. My question from earlier, about whether or not binding the PR receptor could affect prolactin levels, would fit perfectly if it were true. (Tren binding PR = rise in prolactin = part 2 of potential gyno (along with normal E and E+PR issues). Alas, you posted evidence to the contrary - thanks by the way. Now I'm kind of back in the same place I was before: I think prolactin can stimulate gyno (and if not classical gynecomastia in all cases, then certainly nipple discharge, and who wants that either), but I can't explain why prolactin would go up so high on a designer Tren cycle.

    I rambled a bit here, hope this all makes sense. Hoping you can respond here, maybe there's something I'm missing.
    Firstly, only trenbolone is a strong PR binder, dienolone and nandrolone are not -- they bind but are actually quite weak. The rest of what you wrote (I can address more fully in a little while -- I am heading out at the moment) is more or less correct (there are some things that I will take issue with later) but the whole ball of wax can be summed up by saying that in the absence of elevated estrogen, prolactin and progesterone will not cause gynecomastia so I go back to my original statement that if you control estrogen, then you will limit gyno. If prolactin and or gyno cannot cause gyno in the absence of elevated estrogen then they are not the root cause.
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    ^ that's similar to what Bill Roberts has mentioned... tren has a binding affinity for PRs but does not activate them.

    Great thread. Appreciate everybody's input.
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    Quote Originally Posted by sethroberts View Post
    Firstly, only trenbolone is a strong PR binder, dienolone and nandrolone are not -- they bind but are actually quite weak. The rest of what you wrote (I can address more fully in a little while -- I am heading out at the moment) is more or less correct (there are some things that I will take issue with later) but the whole ball of wax can be summed up by saying that in the absence of elevated estrogen, prolactin and progesterone will not cause gynecomastia so I go back to my original statement that if you control estrogen, then you will limit gyno. If prolactin and or gyno cannot cause gyno in the absence of elevated estrogen then they are not the root cause.
    Interesting, thanks seth. However, I'm sure everyone here has seen this post from "guru" Big Cat regarding 19-Norandrosta-4,9-diene-3,17-dione (the active in the Tren designers):

    "prohormone that converts to 9-unsaturated nandrolone's. 4,9-diene-19-nor steroids are discussed as a group in the two studies I reference often by Ojasoo and Raynaud, and compared against 4-ene-19-nor and 4,9,11-trien-19-nor steroids. By comparison they are almost as potent progestagenically as the trienes, but their androgenic component is actually lower than that of the 4-ene steroids. That makes them, for a dose that yields equal anabolic effect, considerably more progestagenic and supressive. Its mostly crap. If you want I can probably post some RBA data when I get home."

    He would seem to disagree with you.

    Secondly, part of what I was saying was that perhaps "Tren gyno" may not necessarily need elevated estrogen to induce it. However, if what you are saying about the 19-nor compound only weakly binding is true... I'm back at square one.
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    Quote Originally Posted by Dragon13 View Post
    Interesting, thanks seth. However, I'm sure everyone here has seen this post from "guru" Big Cat regarding 19-Norandrosta-4,9-diene-3,17-dione (the active in the Tren designers):

    "prohormone that converts to 9-unsaturated nandrolone's. 4,9-diene-19-nor steroids are discussed as a group in the two studies I reference often by Ojasoo and Raynaud, and compared against 4-ene-19-nor and 4,9,11-trien-19-nor steroids. By comparison they are almost as potent progestagenically as the trienes, but their androgenic component is actually lower than that of the 4-ene steroids. That makes them, for a dose that yields equal anabolic effect, considerably more progestagenic and supressive. Its mostly crap. If you want I can probably post some RBA data when I get home."

    He would seem to disagree with you.

    Secondly, part of what I was saying was that perhaps "Tren gyno" may not necessarily need elevated estrogen to induce it. However, if what you are saying about the 19-nor compound only weakly binding is true... I'm back at square one.

    The Ojasoo Raynaud paper I am most familiar with(J Steroid Biochem. 1987;27(1-3):255-69) shows dienolone to have an androgen receptor binding affinity equal to tren (and both significantly greater than testosterone) but with 1/6th the binding affinity of the progesterone receptor as trenbolone. I have seen him refer to a 1984 paper but the only paper they published in 1984 (Clin Neuropharmacol. 1984;7(4):325-31.) does not mention dienolone at all.

    Another paper (J Comput Aided Mol Des. 1992 Dec;6(6):569-81.) confirms this level of progesterone receptor affinity but shows trenbolone to have much greater AR affintiy that the ojasoo raynaud paper. In this paper, dienolone still has much higher AR activity than testosterone.

    Also, as PP pointed out earlier, binding affinity isn't everything. However, I am not aware of any functional assyas published for dienolone that show the level of activity at the progesterone receptor. However, in my opinion it seems very likely that it is not acting as a full agonist.
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    Quote Originally Posted by imprezivr6 View Post
    I understand, but you are giving no info, while making claims like"my bro-science theory is keep estrogen low not dead on cycle and prevent most of these symptoms if not all. low dosed td formestane for the win"

    How can you even say that when you don't even know what it is doing to your estradiol?

    I have yet to see any bloodwork with Form. Please show me any labs you have found over the years..

    Lastly what ph's have you run, while using TD form?

    I am not knocking the stuff, as i have used it a few times myself, just to be clear.
    ok, first of all if your hdl were that low and your doctor didn't say anything i would find a new doctor ASAP. second how can you say you can't find find any blood work on how it effects estradiol? my GOD man, it was a prescription anti-estrogen breast cancer drug. it was replaced by 2nd generation drugs like nolvadex becuase of poor bio-availability not because it didn't work in iv form. transdermal delivery solved this problem. do some research, it's all over the place, i suggest something called google. btw don't take my word on it, form is recommended for on cycle use by DR.D, DINOII, AND ARTUR L. REA WHO WROTE THE DEFINATIVE ARTICLE ON IT. IT SEEMS APPARENT YOU POSTED TO DISCREDIT ME, BUT I AM NOT ALONE IN ADVOCATING THE USE OF TRANSDERMAL FORM ON CYCLE.
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    Quote Originally Posted by thebigt View Post
    ok, first of all if your hdl were that low and your doctor didn't say anything i would find a new doctor ASAP. second how can you say you can't find find any blood work on how it effects estradiol? my GOD man, it was a prescription anti-estrogen breast cancer drug. it was replaced by 2nd generation drugs like nolvadex becuase of poor bio-availability not because it didn't work in iv form. transdermal delivery solved this problem. do some research, it's all over the place, i suggest something called google. btw don't take my word on it, form is recommended for on cycle use by DR.D, DINOII, AND ARTUR L. REA WHO WROTE THE DEFINATIVE ARTICLE ON IT. IT SEEMS APPARENT YOU POSTED TO DISCREDIT ME, BUT I AM NOT ALONE IN ADVOCATING THE USE OF TRANSDERMAL FORM ON CYCLE.
    Big-T, i actually had some respect for you, but you're sounding like a big fat cry-baby..lol Seems like the form isn't lowering your estrogen enough..

    Try READING what i wrote.
    2. I have never seen any on-cycle form bloodwork.. How do we even know to what degree it is effecting E2?
    I have yet to see any bloodwork with Form. Please show me any labs you have found over the years..
    I said i have yet to see any blood work..I didn't say it doesn't exist, or i looked specifically for it.. I asked you to post what you have found, since you are the self appointed Form. guru, and clearly have seen bloodwork.. I just want to see bloodwork on an CYCLE, not on some women with breast cancer. I would love to see the impact it has on E2, at certain doses.


    Discredit you? When did i ever say form shouldn't be used on cycle? NEVER, said that. I asked you to quantify your claims.. You talk about not driving E2 to low, and then said your E2 is in good range, and i asked what your numbers were, is that too much to ask, when you make claims like that?

    I asked perfectly valid questions, per the info you posted. It seems like you got butt hurt, and felt my questions were some sort of attack, rather then just answering the questions.

    I never said anything against using an AI on cycle, at all..lol We are not fighting on opposing sides here, I just asked you some simple questions, and rather then answer them, you go on some tangent..

    Seems like you are on the defensive.. Seriously, get off the rag dude... It is obvious you can't carry on a mature discussion, without getting defensive, and acting like people are against you. We are all trying to learn here, the more info the better..
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    Quote Originally Posted by imprezivr6 View Post
    Big-T, i actually had some respect for you, but your sounding like a big fat cry-baby..lol Seems like the form isn't lowering your estrogen enough..

    Try READING what i wrote. I said i have yet to see any blood work..I didn't say it doesn't exist.. I asked you to post what you have found, since you are the self appointed Form. guru. I just want to see bloodwork on an CYCLE, not on some women with breast cancer. I would love to see the impact it has on E2, at certain doses.

    Discredit you? When did i ever say form shouldn't be used on cycle? NEVER, said that. I asked you to quantify your claims.. You talk about not driving E2 to low, and then said your E2 is in good range, and i asked for proof, is that too much to ask, when you make claims like that?

    I asked perfectly valid questions, per the info you posted. It seems like you got butt hurt, and felt my questions were some sort of attack, rather then just answering the questions.

    I never said anything against using an AI on cycle, at all..lol Seems like you are on the defensive.. Seriously, get off the rag dude...
    ok, i admit to being a little defensive. i am on a xtren/formestane cycle right now. just know what my results have been like. as for being a formestane guru-i found something that is more effective by far than the higher priced stuff or 'hard to get stuff chems', and just passing along how great it's results have been for me.
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    Quote Originally Posted by thebigt View Post
    ok, i admit to being a little defensive. i am on a xtren/formestane cycle right now. just know what my results have been like. as for being a formestane guru-i found something that is more effective by far than the higher priced stuff or 'hard to get stuff chems', and just passing along how great it's results have been for me.
    I just hope you understand, i never got an attitude with you, or had any intention of arguing, and was genuinely asking relevant questions, so we can all get a better idea of what is happening with on cycle form use.. I am not doubting your experiences at all, but trying to get as much of the picture as i can.. Again, the more info we have the better.

    I am not against FORM at all, and stated i have used it myself. I just wish i knew more about it in regards to on cycle bloodwork.. From looking at all the HRT threads with people using Adex, we can get an idea of what doses to start at/use, in order to get estradiol where we want it, without squashing it.
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    maybe a good on cycle mix would be DIM/I3C mix ED with 6bromo EOD?

    keep estradiol low aswell as the freed up estrone sulfate hopefully more undercontrol?
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    Quote Originally Posted by imprezivr6 View Post
    I just hope you understand, i never got an attitude with you, or had any intention of arguing, and was genuinely asking relevant questions, so we can all get a better idea of what is happening with on cycle form use.. I am not doubting your experiences at all, but trying to get as much of the picture as i can.. Again, the more info we have the better.

    I am not against FORM at all, and stated i have used it myself. I just wish i knew more about it in regards to on cycle bloodwork.. From looking at all the HRT threads with people using Adex, we can get an idea of what doses to start at/use, in order to get estradiol where we want it, without squashing it.
    sorry, between working 12's and the tren kicking in, i have been a little on edge.
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    Quote Originally Posted by Dragon13 View Post
    Progesterone:

    1) http://www.endotext.org/male/male14/male14.html

    2) http://cat.inist.fr/?aModele=afficheN&cpsidt=1525645 (sort of, in a round-about way; abstract seems to conclude presence of elevated E and PR receptors contributes to severity of condition)

    3) http://www.springerlink.com/content/235p1612528vk68t/

    Now here's the thing. All of the above and every other study I could find (of the few out there) also had estrogen linked in in some manner. Also, some of the above are admittedly tenuous links. But the bottom line seems to be estrogen and progesterone work synergistically when it comes to breast growth. IOW, I agree with you that estrogen is the key... sort of. I have concluded that elevated progesterone itself cannot cause gyno, but it can (in a round-about way) in the presence of enough estrogen. I don't think you disagree, seeing as how estrogen is still the key, so here's where I'm going with this.

    We've been talking about the Tren compounds here; from what I understand they have an incredible binding affinity for the progesterone receptor. My theory: 1 part of the Tren gyno issue is that the tremendous surge in progesterone can trigger gyno in the presence of normal estrogen levels. You mentioned the breakdwon of SHBG and how it would increase circulating E; this would only serve to exacerbate the problem. So yes, E is the key, but saying progesterone has no role is misleading IMO.

    Now on to prolactin. You said this earlier in the thread: "There is no evidence that controlling prolactin will prevent or treat gynecomastia. Many of the issues that are being attributed to prolactin can be explained through other mechanisms."

    If this is true please explain why the first 2 links below indicate prolactin is a growth factor for breast enlargement, while the 3rd and 4th, which provide an overview of the symptoms of clinical prolactinoma, list gynecomastia as a symptom (albeit "uncommonly" on the Mayo Clinic link), and the last 3 all list gyno as a symptom of simple hyperprolactinemia.

    Prolactin:

    1) http://www.springerlink.com/content/nn1424748054t0w4/

    2) http://www.pubmedcentral.nih.gov/art...?artid=1869171

    3) http://neurosurgery.ucla.edu/body.cfm?id=212

    4) http://www.mayoclinic.com/health/pro...CTION=symptoms

    5) http://www.vivo.colostate.edu/hbooks...prolactin.html

    6) http://en.wikipedia.org/wiki/Hyperpr...aemia#Symptoms

    7) http://www.wrongdiagnosis.com/h/hype...a/symptoms.htm

    Finally, here's a quote from MedicineNet.com by author Dr. Robert Ferry Jr., MD and his Medical Editor, Dr. Ruchi Mathur, MD, FRCP(C).

    What is the normal function of prolactin?

    "Prolactin stimulates the breast tissues to enlarge during pregnancy."

    I flat-out don't buy the fact the elevated prolactin can't cause gyno. I've run across enough evidence, both anecdotal and not, to not believe otherwise. Perhaps there is a relatiuonship similar to progesterone with E in that eswtrogen is needed in some degree to cause actual breast growth - I don't know. My question from earlier, about whether or not binding the PR receptor could affect prolactin levels, would fit perfectly if it were true. (Tren binding PR = rise in prolactin = part 2 of potential gyno (along with normal E and E+PR issues). Alas, you posted evidence to the contrary - thanks by the way. Now I'm kind of back in the same place I was before: I think prolactin can stimulate gyno (and if not classical gynecomastia in all cases, then certainly nipple discharge, and who wants that either), but I can't explain why prolactin would go up so high on a designer Tren cycle.

    I rambled a bit here, hope this all makes sense. Hoping you can respond here, maybe there's something I'm missing.

    Thanks for doin my searching for me...
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    Quote Originally Posted by sethroberts View Post
    Firstly, only trenbolone is a strong PR binder, dienolone and nandrolone are not -- they bind but are actually quite weak. The rest of what you wrote (I can address more fully in a little while -- I am heading out at the moment) is more or less correct (there are some things that I will take issue with later) but the whole ball of wax can be summed up by saying that in the absence of elevated estrogen, prolactin and progesterone will not cause gynecomastia so I go back to my original statement that if you control estrogen, then you will limit gyno. If prolactin and or gyno cannot cause gyno in the absence of elevated estrogen then they are not the root cause.
    Im still standing by my recommendation of vitex and possibly an AI for the control of progestin based gyno. (perhaps even in cases of non-progestin based gyno)

    I think it’s obvious that prolactin is a contributing growth factor, although it may not be the “root” of the cause. But who cares.

    Rather than administering a toxic SERM, or an AI that may push HDL down to unfavorable levels, it seems most logical (to me) to simply suppress prolactin for period and thus handicap gyno growth through this mechanism.

    BTW, Ive worked with AAS/GH using athletes who have had gyno issues. In this case, where further estrogen suppression is undesirable, I simply recommend they reduce their hGH therapy. Guess what, the gyno stops.

    By simply by reducing a co-factor (eg, GH, prolactin, IGF-1, ect) you can manage gyno issues. That’s my approach.

    -Eric
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    Quote Originally Posted by sethroberts View Post
    The Ojasoo Raynaud paper I am most familiar with(J Steroid Biochem. 1987;27(1-3):255-69) shows dienolone to have an androgen receptor binding affinity equal to tren (and both significantly greater than testosterone) but with 1/6th the binding affinity of the progesterone receptor as trenbolone. I have seen him refer to a 1984 paper but the only paper they published in 1984 (Clin Neuropharmacol. 1984;7(4):325-31.) does not mention dienolone at all.

    Another paper (J Comput Aided Mol Des. 1992 Dec;6(6):569-81.) confirms this level of progesterone receptor affinity but shows trenbolone to have much greater AR affintiy that the ojasoo raynaud paper. In this paper, dienolone still has much higher AR activity than testosterone.

    Also, as PP pointed out earlier, binding affinity isn't everything. However, I am not aware of any functional assyas published for dienolone that show the level of activity at the progesterone receptor. However, in my opinion it seems very likely that it is not acting as a full agonist.
    Very interesting. I never was foolish enough to take everything that guy said as gospel truth, but he did seem to know his stuff and everyone else considered him "the" authority. This is the first time I've ever seen anyone directly contradict his conclusion. You just never know with these "gurus"; after all, how do we know what their background is and how knowledgable they really are? (Hmmm, same could be said for you Seth. No offense, I just don't know much about you)

    Back to the topic at hand: if what you say is true, then I am at a loss to explain why the Tren designers can give prolactin-related sides such as leaky nips and (possibly) gyno. And I am still at a loss to explain why prolactin becomes elevated when using these compounds. Despite what you've posted, I do not believe elevated or even rebound estrogen alone can cause lactation in men, despite the E - prolactin relationship.

    Great thread, but the ditch is getting deeper.
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    Quote Originally Posted by Primordial Perf View Post
    Im still standing by my recommendation of vitex and possibly an AI for the control of progestin based gyno. (perhaps even in cases of non-progestin based gyno)

    I think it’s obvious that prolactin is a contributing growth factor, although it may not be the “root” of the cause. But who cares.
    Exactly.

    Rather than administering a toxic SERM, or an AI that may push HDL down to unfavorable levels, it seems most logical (to me) to simply suppress prolactin for period and thus handicap gyno growth through this mechanism.
    Both need to be controlled, as supressing prolactin alone still leaves estrogenic effects to be dealt with. While I agree prolactin is a contributing growth factor, when using an aromatizing compound (which I suspect the Tren designers to be, despite manufacturer claims), I'd still go AI. HDL is likely going to be in the ****ter anyways.

    BTW, Ive worked with AAS/GH using athletes who have had gyno issues. In this case, where further estrogen suppression is undesirable, I simply recommend they reduce their hGH therapy. Guess what, the gyno stops.

    By simply by reducing a co-factor (eg, GH, prolactin, IGF-1, ect) you can manage gyno issues. That’s my approach.

    -Eric
    Eric, question for you: the Tren designers, of which 1-T Tren is one, all obviously market as being very similar to trenbolone. Yet the chemical structure of the end hormone after enzymatic conversion may (from what I understand) actually be closer to nandrolone. Any insight on this?

    Also - I can't really find any info on dienolone itself, does anybody have Vida #s on it?
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    Quote Originally Posted by Dragon13 View Post
    Very interesting. I never was foolish enough to take everything that guy said as gospel truth, but he did seem to know his stuff and everyone else considered him "the" authority. This is the first time I've ever seen anyone directly contradict his conclusion. You just never know with these "gurus"; after all, how do we know what their background is and how knowledgable they really are? (Hmmm, same could be said for you Seth. No offense, I just don't know much about you)
    If you are referring to Big Cat, you're not alone. He's a smart guy, but sometimes seems to either not think out of the box or have some agenda against certain steroids (particularly 2nd-Gen. OTC ones). I've watched other "gurus" (Patrick Arnold, Dr. D, etc.) rip apart his "theories" on BB.com over the years. I have not considered him a guru or "the final word" on endocrine physiology for years. He loves to quote Vida text (which is a very valuable resource), but doesn't seem to venture too far for other sources.

    Quote Originally Posted by Dragon13 View Post
    Back to the topic at hand: if what you say is true, then I am at a loss to explain why the Tren designers can give prolactin-related sides such as leaky nips and (possibly) gyno. And I am still at a loss to explain why prolactin becomes elevated when using these compounds. Despite what you've posted, I do not believe elevated or even rebound estrogen alone can cause lactation in men, despite the E - prolactin relationship.

    Great thread, but the ditch is getting deeper.
    Elevated E2 causes the prolactin receptors to become more sensitive, therefor possibly not requiring a rise in serum prolactin to cause a "prolactin effect." Is that enough to cause lactation in a human male? I don't know, but I don't discount it either.
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    Quote Originally Posted by Mass_69 View Post
    If you are referring to Big Cat, you're not alone. He's a smart guy, but sometimes seems to either not think out of the box or have some agenda against certain steroids (particularly 2nd-Gen. OTC ones). I've watched other "gurus" (Patrick Arnold, Dr. D, etc.) rip apart his "theories" on BB.com over the years. I have not considered him a guru or "the final word" on endocrine physiology for years. He loves to quote Vida text (which is a very valuable resource), but doesn't seem to venture too far for other sources.
    I was, and I agree. Although did not witness the bb.com shredding as I avoid that board usually. Only reason I referenced him was b/c that quote on the Tren compounds is parroted on the boards as gospel truth with no one contradiciting it, so much so that I more or less believed it, as much for a lack of contradictory evidence as anything else.

    Elevated E2 causes the prolactin receptors to become more sensitive, therefor possibly not requiring a rise in serum prolactin to cause a "prolactin effect." Is that enough to cause lactation in a human male? I don't know, but I don't discount it either.
    I'll buy that, E and PRO have a converse relationship - but what's causing elevated E2? Just regular suppression + SHBG offset? Wouldn't think this would be enough. Or... if the compound is not binding the progesterone receptor (or not very strongly), are we looking at simple aromatization issues here? Everything could be avoided by simply adding an AI? Sounds too easy, although I don't think I've seen anyone run a Tren designer with an AI (although I admit I haven't searched).
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    wow guys a whole host of info here!

    right now i am 4 weeks after a course of superdrol and it has cause some gyno, now i have been all over the boards and came to the conclusion that i need to do get hold of cabaser (carbogoline) to supress my prolactin levels... i have done this but with no effect!

    i currently have cabaser and nolva on hand and i was scared to use the nolva as it was considered bad for this type of gyno.

    now from what i have read it would be best for me to run a low dose of nolva for an extended period of time so that my SHBG levels would be up after a while... my question is if i took cabaser at the same time would this have me coverd or surpress my SHGB

    i want to bring up letro as a hot potato here and what role that would play as iv not seen it mentioned yet....

    from all the boards i have read it seems this is the most knowledgeable and i woud greatly respect your opinion on this matter thanks lee
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    Quote Originally Posted by Mass_69 View Post
    If you are referring to Big Cat, you're not alone. He's a smart guy, but sometimes seems to either not think out of the box or have some agenda against certain steroids (particularly 2nd-Gen. OTC ones). I've watched other "gurus" (Patrick Arnold, Dr. D, etc.) rip apart his "theories" on BB.com over the years. I have not considered him a guru or "the final word" on endocrine physiology for years. He loves to quote Vida text (which is a very valuable resource), but doesn't seem to venture too far for other sources.

    Elevated E2 causes the prolactin receptors to become more sensitive, therefor possibly not requiring a rise in serum prolactin to cause a "prolactin effect." Is that enough to cause lactation in a human male? I don't know, but I don't discount it either.
    Nobody, not even myself, should be considered the final word on anything. I am not perfect and I do not know everything. There are too many people on these boards who refuse to admit that they are ever wrong because they are afraid that if they are ever wrong that they somehow lose credibility. if noone ever questions the status quo, our knowledge will never grow.

    Now, I will say that a qualified opinion always carries more weight than an unqualified one (that is why they have experts testify in court) but good ideas can come from anywhere. It is easy from me. I can stay here and state my theories and answer questions or I can not. My expertise is recognized outside of these boards. The difficult part is for the guys looking for answers because they have to weed through the bullsh-t and make a determination as to who is believable and what is a good idea.
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    Quote Originally Posted by Primordial Perf View Post
    Im still standing by my recommendation of vitex and possibly an AI for the control of progestin based gyno. (perhaps even in cases of non-progestin based gyno)

    I think it’s obvious that prolactin is a contributing growth factor, although it may not be the “root” of the cause. But who cares.

    Rather than administering a toxic SERM, or an AI that may push HDL down to unfavorable levels, it seems most logical (to me) to simply suppress prolactin for period and thus handicap gyno growth through this mechanism.

    BTW, Ive worked with AAS/GH using athletes who have had gyno issues. In this case, where further estrogen suppression is undesirable, I simply recommend they reduce their hGH therapy. Guess what, the gyno stops.

    By simply by reducing a co-factor (eg, GH, prolactin, IGF-1, ect) you can manage gyno issues. That’s my approach.

    -Eric
    The only issue I have with that is that you might be overlooking the potential dangers of dopaminergic modulation while you malign "toxic" nolva. GH is known to be mitogenic in the breast so your conlcusion about reducing dose in those cases is spot on.
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    Quote Originally Posted by Dragon13 View Post
    I was, and I agree. Although did not witness the bb.com shredding as I avoid that board usually. Only reason I referenced him was b/c that quote on the Tren compounds is parroted on the boards as gospel truth with no one contradiciting it, so much so that I more or less believed it, as much for a lack of contradictory evidence as anything else.



    I'll buy that, E and PRO have a converse relationship - but what's causing elevated E2? Just regular suppression + SHBG offset? Wouldn't think this would be enough. Or... if the compound is not binding the progesterone receptor (or not very strongly), are we looking at simple aromatization issues here? Everything could be avoided by simply adding an AI? Sounds too easy, although I don't think I've seen anyone run a Tren designer with an AI (although I admit I haven't searched).
    look at cel's xtren/formestane log in the review section, no sides related to estrogen/prolactin so far.
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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 did not know this. Very interesting.
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    Quote Originally Posted by Heracles25 View Post
    I did not know this. Very interesting.
    It is very interesting and is unknown in the message board (and dare i say) the steroid using community.
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    Quote Originally Posted by sethroberts View Post
    It is very interesting and is unknown in the message board (and dare i say) the steroid using community.
    I always knew that most steroids suppressed SHBG to some extinct, others like DHT, Winny and so on did a better job but never knew about the other effectst that you listed.

    Great thread and thanks for taking the time to do this. Maybe post this at bb.com. I post there the most, but there are ALOT of questions in regards to prolactin, progesterone, gyno and so forth.
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    Quote Originally Posted by sethroberts View Post
    The only issue I have with that is that you might be overlooking the potential dangers of dopaminergic modulation while you malign "toxic" nolva. GH is known to be mitogenic in the breast so your conlcusion about reducing dose in those cases is spot on.
    I was under the impression Caber had was "toxic" to the liver as well, no?
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    Quote Originally Posted by imprezivr6 View Post
    I was under the impression Caber had was "toxic" to the liver as well, no?
    Hepatic Impairment: Since Cabergoline is extensively metabolized by the liver, caution should be used, and careful monitoring exercised, when administering Cabergoline to patients with hepatic impairment.

    There is also some potential for cardiac valvulopathy but that is generally with longer term use.

    The larger concern is not even listed as a potential side effect. In the lab we used dopamine agonists to desensitize dopamine receptors. We did it to mimic parkinson's and though i doubt that is a concern here, the desensitization is a concern because the loss of dopaminergic suppression of lactotropes could actually result in prolactin excess.
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    Quote Originally Posted by Dragon13 View Post

    Eric, question for you: the Tren designers, of which 1-T Tren is one, all obviously market as being very similar to trenbolone. Yet the chemical structure of the end hormone after enzymatic conversion may (from what I understand) actually be closer to nandrolone. Any insight on this?
    If you look at the molecule structure of dienolone you can see it's somewhere between nandrolone and Trenbolone, but since it doesn’t aromatize (and considering its overall effects) I’d say it much closer to trenbolone.

    -Eric
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