Progesterone and Prolactin

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  1. Quote Originally Posted by sethroberts View Post
    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.
    so are you saying that you could get a prolactin 'rebound' effect after stopping cabergoline treatment?


  2. Quote Originally Posted by Primordial Perf View Post
    If these steroids are causing gyno by releasing E2 through SHBG down-regulation or competitive binding then an AI wonít do anything to prevent gyno from the circulating E2. (or the low levels of antagonistic DHT) Therefore, Seth suggests a SERM to block the action of estrogen.

    The theory makes sense, but I would still caution against the SERM administration and instead opt for prolactin control. (Being a potent co-factor in breast growth, perhaps keeping it in the sub-physiological range will partly cripple estrogens ability to induce mammary growth)

    -Eric
    The only problem is that prolactin control wil ldo nothing for the elevated estrogen and with a reduction in prolactin, estrogen is likely to go higher.
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  3. Quote Originally Posted by samadhismiles View Post
    so are you saying that you could get a prolactin 'rebound' effect after stopping cabergoline treatment?
    Absolutely. Possibly long term depending on how severe the desensitization in dopaminergic neurons.

  4. Quote Originally Posted by fueledpassion View Post
    The only problem is, I still have this feeling of "iffiness". I dont really see a conclusion or a general agreement in theory. I see one very educated man in this thread in the matters of hormones and everyone else either 1) sharing results, or 2) asking questions like myself. Heck, I'm gonna get all of these products and keeping searching for a perfect way to combine the dosages in PCT. So far, I have this:

    Formex
    Nolva
    ZMA


    and I might consider buying the Vitrix stuff, since I've heard good results in libido enhancements, or I might opt for Hydrotest. So if anyone on here has experience with the same or similar PCT please chime in on how to use them together in regards to Tren or Trenlike PH's. Thanks.
    When there is a perfect consensus, that is when you should be very skeptical.

  5. Quote Originally Posted by fueledpassion View Post
    The only problem is, I still have this feeling of "iffiness". I dont really see a conclusion or a general agreement in theory. I see one very educated man in this thread in the matters of hormones and everyone else either 1) sharing results, or 2) asking questions like myself. Heck, I'm gonna get all of these products and keeping searching for a perfect way to combine the dosages in PCT. So far, I have this:

    Formex
    Nolva
    ZMA


    and I might consider buying the Vitrix stuff, since I've heard good results in libido enhancements, or I might opt for Hydrotest. So if anyone on here has experience with the same or similar PCT please chime in on how to use them together in regards to Tren or Trenlike PH's. Thanks.
    Just FYI, Im just talking about 460mg/day of the generic vitex... not all the fancy stuff on the market.

    -Eric
    •   
       


  6. Quote Originally Posted by sethroberts View Post
    with a reduction in prolactin, estrogen is likely to go higher.
    How do you propose?

  7. Excellent thread everyone, absolutely riveting!

    I have a complicated question about PRE-Cycle therapy, based on my limited knowledge. i.e. Setting up a good environment for avoiding gyno. Ideally, I'd rather avoid it than deal with it.

    From the reading of this thread, I gleaned this: Tren, Tren desigers and possible Anadrol etc. cause a lowering of SHBG, which releases bound Estrone Sulfate, which in the presence of raised PG or PG sensitivity = possible gyno. Or maybe the Estrone Sulfate alone causes it.

    The question is thus:
    Would a low-dosed AI for a month or so before a cycle help avoid the arising of Gyno symptoms once on a cycle of Tren or the "Tren" designers?

    My thinking (however dimly lit) is like this: By suicidal inhibition of Aromatase for a month, most aromatase is inhibited. During this time, SHBG bound Estrone Sulfate clears the body by regular enzymatic process. New SHBG is produced, but is not bound to Estrone Sulfate as there would be little to bind to due to the AI. So when the Tren Designer is introduced, there is no Estrone Sulfate to be released, so less gyno risk. Follow up by taking Nolva on cycle to avoid whatever problems may arise from the DS/AAS

    I ask about a month period as I've heard that it is roughly the enzymatic turnover time for aromatase. (Journal of Broscience et. al 2009).

    Or by doing the above, would we just be setting up a major estro-rebound in PCT?

    Is there any way to set up the body for a cycle of Tren/Designers?

    Thanks again for the excellent read!

  8. Quote Originally Posted by Brenn View Post
    Excellent thread everyone, absolutely riveting!

    I have a complicated question about PRE-Cycle therapy, based on my limited knowledge. i.e. Setting up a good environment for avoiding gyno. Ideally, I'd rather avoid it than deal with it.

    From the reading of this thread, I gleaned this: Tren, Tren desigers and possible Anadrol etc. cause a lowering of SHBG, which releases bound Estrone Sulfate, which in the presence of raised PG or PG sensitivity = possible gyno. Or maybe the Estrone Sulfate alone causes it.

    The question is thus:
    Would a low-dosed AI for a month or so before a cycle help avoid the arising of Gyno symptoms once on a cycle of Tren or the "Tren" designers?

    My thinking (however dimly lit) is like this: By suicidal inhibition of Aromatase for a month, most aromatase is inhibited. During this time, SHBG bound Estrone Sulfate clears the body by regular enzymatic process. New SHBG is produced, but is not bound to Estrone Sulfate as there would be little to bind to due to the AI. So when the Tren Designer is introduced, there is no Estrone Sulfate to be released, so less gyno risk. Follow up by taking Nolva on cycle to avoid whatever problems may arise from the DS/AAS

    I ask about a month period as I've heard that it is roughly the enzymatic turnover time for aromatase. (Journal of Broscience et. al 2009).

    Or by doing the above, would we just be setting up a major estro-rebound in PCT?

    Is there any way to set up the body for a cycle of Tren/Designers?

    Thanks again for the excellent read!
    Thats a really good question and I too would like to hear some educated opinions on the matter.

  9. Quote Originally Posted by sethroberts View Post
    The only problem is that prolactin control wil ldo nothing for the elevated estrogen and with a reduction in prolactin, estrogen is likely to go higher.
    Which makes an even more compelling case for an on-cycle AI or SERM.

  10. Quote Originally Posted by Brenn View Post
    From the reading of this thread, I gleaned this: Tren, Tren desigers and possible Anadrol etc. cause a lowering of SHBG, which releases bound Estrone Sulfate, which in the presence of raised PG or PG sensitivity = possible gyno. Or maybe the Estrone Sulfate alone causes it.
    FYI - Elevated androgens in general cause a lowering of SHBG (as do elevated insulin, cortisol, among other things). Estrogens & thyroid hormones, among other things, raise SHBG. I'm not sure if there are specific androgens that do not lower SHBG, but my guess would be the less androgenic (the androgen) is, the less of a lowering effect it has on SHBG.

  11. Very interesting thread on another site. See:

    http://www.t-nation.com/free_online_...85069&pageNo=0

    Read through the whole thing, but about 25% down on page 2 you'll see the tie-in with the this topic.

  12. Hey Mass69, Roger that, very true. I mentioned those Trens and Anadrol as they seem to lower SHBG AND result in problems for many folks. (AD50 I really enjoyed when I was younger BTW). For some reason, other SHBG lowering AAS don't seem to have the same nasty reputation. I wish I knew why.

    I'm really curious to find the differences between AAS's that affect SHBG the same way, as Tren and Anadrol (Superdrol), but don't cause nearly the same amount of Gyno hassle.

    For example: Winni and Proviron are so great at lowering SHBG, and are often taken to enhance the effectiveness of a Test cycle, raise free test etc. But I've never heard of Winnie or Proviron causing this problem, as we know they are taken to offset gyno risk! Tendons that snap like dry twigs, yes! But not the Gyno so much. Something else is going on there that doesn't seem to depend solely on SHBG being down. So it must be in combination with PG being up? But then what about Anadrol, wheres the PG? I'd love to know.

    With 19-nors and Tren, we can say they are progesterones and, that the action on PG and PG sensitivity is to blame, in combo with the SHBG lowering. But Interestingly, in another thread on this here board, there was a discussion about SD and Gyno.

    One member interviewed many users and the ones that reported Gyno after SD almost always included and AI in their PCT. The ones who used SERM only, far less Gyno.

    They theorized that it was because of supressed E for too long (on cycle, then into PCT) then came off the AI after PCT, the AI cycles out of the system, then WHAM! Estrogen sensitivity + raised E2 = "delayed gyno"...seemed convincing.

    However, if the info in this thread is on target, perhaps it works like this: With a Clomid protocol for example, in basic terms Test rises, but so does E2 to a lesser degree. With a rise in E2 from the Clomid therapy, SHBG rises with it, giving (as Seth said) protective effects in the breast tisue = no gyno.

    Alternatively:
    Post cycle CLOMID + AI would suppress this E2 rise from the clomid and also the SHBG rise with it, also further enhance E2 sensitivity, then a few weeks/months later...delayed gyno. So when PCT is finished: Low SHBG, rising E2, E2 sensitivity...gyno

    Much like IKEA furniture however, after making this (cough) "theory" there is still an extra part left out...Progesterone. Where does it fit with the Lowered SHBG + E2 sensitivity/rise? Dunno. As hormones normalise, is there a rise in PG also?

    Ok guys, (taking of my Broscientist Lab coat and hat with the mirror thing), off to work.

    Fun thread...I got a bottle SD that I'm keen to use, but I gotta work this out beforehand!

  13. Quote Originally Posted by Brenn View Post
    Hey Mass69, Roger that, very true. I mentioned those Trens and Anadrol as they seem to lower SHBG AND result in problems for many folks. (AD50 I really enjoyed when I was younger BTW). For some reason, other SHBG lowering AAS don't seem to have the same nasty reputation. I wish I knew why.

    I'm really curious to find the differences between AAS's that affect SHBG the same way, as Tren and Anadrol (Superdrol), but don't cause nearly the same amount of Gyno hassle.

    For example: Winni and Proviron are so great at lowering SHBG, and are often taken to enhance the effectiveness of a Test cycle, raise free test etc. But I've never heard of Winnie or Proviron causing this problem, as we know they are taken to offset gyno risk! Tendons that snap like dry twigs, yes! But not the Gyno so much. Something else is going on there that doesn't seem to depend solely on SHBG being down. So it must be in combination with PG being up? But then what about Anadrol, wheres the PG? I'd love to know.

    With 19-nors and Tren, we can say they are progesterones and, that the action on PG and PG sensitivity is to blame, in combo with the SHBG lowering. But Interestingly, in another thread on this here board, there was a discussion about SD and Gyno.

    One member interviewed many users and the ones that reported Gyno after SD almost always included and AI in their PCT. The ones who used SERM only, far less Gyno.

    They theorized that it was because of supressed E for too long (on cycle, then into PCT) then came off the AI after PCT, the AI cycles out of the system, then WHAM! Estrogen sensitivity + raised E2 = "delayed gyno"...seemed convincing.
    Bingo. Exactly what I think causes the "delayed gyno" phenomenon. This is especially true with all the OTC PCT users out there. You can't get a true SERM OTC. All the products guys get OTC- Reversitol, Novedex, etc etc - are AIs. You run 4 weeks at a steady dose, estrogen has been killed, test has recovered somewhat, you have a heightened sensitivity to E... That's why if you use an AI in PCT, you absolutle MUST taper down.

    However, if the info in this thread is on target, perhaps it works like this: With a Clomid protocol for example, in basic terms Test rises, but so does E2 to a lesser degree. With a rise in E2 from the Clomid therapy, SHBG rises with it, giving (as Seth said) protective effects in the breast tisue = no gyno.
    Hmmm, I'll buy that.

    Alternatively:
    Post cycle CLOMID + AI would suppress this E2 rise from the clomid and also the SHBG rise with it, also further enhance E2 sensitivity, then a few weeks/months later...delayed gyno. So when PCT is finished: Low SHBG, rising E2, E2 sensitivity...gyno
    Exactly.

    Much like IKEA furniture however, after making this (cough) "theory" there is still an extra part left out...Progesterone. Where does it fit with the Lowered SHBG + E2 sensitivity/rise? Dunno. As hormones normalise, is there a rise in PG also?

    Ok guys, (taking of my Broscientist Lab coat and hat with the mirror thing), off to work.

    Fun thread...I got a bottle SD that I'm keen to use, but I gotta work this out beforehand!
    Progesterone can only cause gyno in the presence of E, so it's a player but only secondarily. However, part of my thinking is that perhaps compounds with strong affinity for the PR receptor can cause gyno in the presence of normal E levels simply because the PR receptor is being activated so strongly - although based on Seth's direct refutation of the Big Cat Tren Theory, maybe Tren compunds don't have this issue. Some others may, however.

    Finally, don't forget about prolactin! I still believe it can be a growth factor, similar to PR above. High prolactin can cause lactation/breast growth even in the presence of "normal" levels of E. Check out the link I posted above. Obviously anecdotal, but interesting nontheless.

    Great post, BTW.

  14. Hey Dragon,
    Good stuff there. Especially the bit about the Prolactin. I read the post you linked to as well, interesting reading. Here's a question: Is prolactin always estrogen induced, or is it (as the T-nation article mentions) possibly a separate action of a mal-functioning pituitary? I hope by addressing E2 we are addressing MOST of the problem.

    All this leaves me wondering about alternative methods of controlling this gyno problem. Perhaps including low-dosed AAS like Winstrol in a Tren or Tren-like stack would impart some of it's "moob"-protective benefits on-cycle? Or will this drive SHBG into a deep and dangerous hole, that results in Double-D's. Wish I knew!

    I've always been old-school with this stuff: I use the lowest dose necessarry to get the result I want. Stop when the weight I want is achieved or continue a bit longer if it is not. I'd love to try these Tren designers, but need more answers. Nothing is worth wrecked pecs, IMO. It takes away from the look I'm going for

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  16. Quote Originally Posted by Dragon13 View Post
    Progesterone can only cause gyno in the presence of E, so it's a player but only secondarily. However, part of my thinking is that perhaps compounds with strong affinity for the PR receptor can cause gyno in the presence of normal E levels simply because the PR receptor is being activated so strongly - although based on Seth's direct refutation of the Big Cat Tren Theory, maybe Tren compunds don't have this issue. Some others may, however.

    Finally, don't forget about prolactin! I still believe it can be a growth factor, similar to PR above. High prolactin can cause lactation/breast growth even in the presence of "normal" levels of E. Check out the link I posted above. Obviously anecdotal, but interesting nontheless.

    Great post, BTW.
    There is no evidence that progesterone causes gyno, even in the presence of estrogen. That is not to say that it is not possible. High prolactin levels will cause problems -- possibly even in the presence of "normal" levels of estrogen but unless you have a blood test showing elevated prolactin levels, I would assume estrogen first, prolactin last. At this point we have a ton of people blindly using caber and bromo (and even profilactively in some cases) with no evidence of prolactin elevation which has the possibility of seriously screwing up your pituitary.

  17. Quote Originally Posted by Brenn View Post
    Hey Mass69, Roger that, very true. I mentioned those Trens and Anadrol as they seem to lower SHBG AND result in problems for many folks. (AD50 I really enjoyed when I was younger BTW). For some reason, other SHBG lowering AAS don't seem to have the same nasty reputation. I wish I knew why.

    I'm really curious to find the differences between AAS's that affect SHBG the same way, as Tren and Anadrol (Superdrol), but don't cause nearly the same amount of Gyno hassle.

    For example: Winni and Proviron are so great at lowering SHBG, and are often taken to enhance the effectiveness of a Test cycle, raise free test etc. But I've never heard of Winnie or Proviron causing this problem, as we know they are taken to offset gyno risk! Tendons that snap like dry twigs, yes! But not the Gyno so much. Something else is going on there that doesn't seem to depend solely on SHBG being down. So it must be in combination with PG being up? But then what about Anadrol, wheres the PG? I'd love to know.

    With 19-nors and Tren, we can say they are progesterones and, that the action on PG and PG sensitivity is to blame, in combo with the SHBG lowering. But Interestingly, in another thread on this here board, there was a discussion about SD and Gyno.

    One member interviewed many users and the ones that reported Gyno after SD almost always included and AI in their PCT. The ones who used SERM only, far less Gyno.

    They theorized that it was because of supressed E for too long (on cycle, then into PCT) then came off the AI after PCT, the AI cycles out of the system, then WHAM! Estrogen sensitivity + raised E2 = "delayed gyno"...seemed convincing.

    However, if the info in this thread is on target, perhaps it works like this: With a Clomid protocol for example, in basic terms Test rises, but so does E2 to a lesser degree. With a rise in E2 from the Clomid therapy, SHBG rises with it, giving (as Seth said) protective effects in the breast tisue = no gyno.

    Alternatively:
    Post cycle CLOMID + AI would suppress this E2 rise from the clomid and also the SHBG rise with it, also further enhance E2 sensitivity, then a few weeks/months later...delayed gyno. So when PCT is finished: Low SHBG, rising E2, E2 sensitivity...gyno

    Much like IKEA furniture however, after making this (cough) "theory" there is still an extra part left out...Progesterone. Where does it fit with the Lowered SHBG + E2 sensitivity/rise? Dunno. As hormones normalise, is there a rise in PG also?

    Ok guys, (taking of my Broscientist Lab coat and hat with the mirror thing), off to work.

    Fun thread...I got a bottle SD that I'm keen to use, but I gotta work this out beforehand!
    You should pick up a copy of my book. I think it does a pretty good job of laying all of this out and gives several reasons for the difference in activity of different AAS.

    Commercials aside Proviron is a really strong binder of SHBG but I have never seen any evidence that proviron decreases SHBG levels. But then again, people tend to stack mesterolone with aromatizing steroids. Winstrol reduces SHBG and we see that in the literature, but the reduction is not that severe -- only about 50%. Stronger androgens can decreases SHBG levels to only about 10% of control values - In one study, Anadrol reduced SHBG levels by 55 nmol/L which is a major decrease.

  18. Hi Seth,
    I'm already on it! Looking into getting a copy now.

    Ah, correct sir, I mis-spoke!...Proviron binds SHBG, not lowers it. Winnie lowers it, but not like Anadrol. Check.

    Does bound SHBG have any protective benefit in the breast or otherwise?

    Until this thread, I wasn't aware that SHBG had any role at all in gyno. I always thought SHBG was a biological verison of pure-evil, put on us by an angry God.

    Thanks for taking the time, Seth. Looking forward to your book.

  19. Quote Originally Posted by Brenn View Post
    Hi Seth,
    I'm already on it! Looking into getting a copy now.

    Ah, correct sir, I mis-spoke!...Proviron binds SHBG, not lowers it. Winnie lowers it, but not like Anadrol. Check.

    Does bound SHBG have any protective benefit in the breast or otherwise?

    Until this thread, I wasn't aware that SHBG had any role at all in gyno. I always thought SHBG was a biological verison of pure-evil, put on us by an angry God.

    Thanks for taking the time, Seth. Looking forward to your book.
    Until recently, that is pretty much what I thought too. You have to realize that SHBG is not "bound" per se. It is in flux between being bound and unbound in an equilibrium state.

  20. Quote Originally Posted by sethroberts View Post
    There is no evidence that progesterone causes gyno, even in the presence of estrogen. That is not to say that it is not possible. High prolactin levels will cause problems -- possibly even in the presence of "normal" levels of estrogen but unless you have a blood test showing elevated prolactin levels, I would assume estrogen first, prolactin last. At this point we have a ton of people blindly using caber and bromo (and even profilactively in some cases) with no evidence of prolactin elevation which has the possibility of seriously screwing up your pituitary.
    Say Joe blow has estrogen levels within the normal range, then introduces a progestin and starts seeing gyno symptoms within the first 2 weeks

    Would you say the estrogen or progestin caused that gyno?

    I say it’s silly to say it was either, since they are both cofactors.

    Whether or not a progestin will initiate gyno in the total absence of estrogen I couldn’t say, but estrogen, progestin, prolactin, GH, and IGF-1 are all contributors to the growth of mammary tissue. Thus reducing any of them will reduce the chance of experiencing gyno symptoms... I think this is important to keep in mind.

    -Eric

  21. Quote Originally Posted by Primordial Perf View Post
    Say Joe blow has estrogen levels within the normal range, then introduces a progestin and starts seeing gyno symptoms within the first 2 weeks

    Would you say the estrogen or progestin caused that gyno?

    I say it’s silly to say it was either, since they are both cofactors.

    Whether or not a progestin will initiate gyno in the total absence of estrogen I couldn’t say, but estrogen, progestin, prolactin, GH, and IGF-1 are all contributors to the growth of mammary tissue. Thus reducing any of them will reduce the chance of experiencing gyno symptoms... I think this is important to keep in mind.

    -Eric
    I was looking a board on your website and noticed that your not too fond of SERM usage? What would you propose to normalizing libido/test/estrogen?

    As far as this thread goes I've come to a conclusion that controlling estrogen is key as well as prolactin. But I'm not trying to kill estrogen during PCT, as it is already killed during cycle for me. So I almost feel reluctant to use anything more than a low dose of AI tapering to EOD dosages during PCT. What do you think?

    I also plan on using Clomid first few weeks then jumping on perhaps TRS afterwards, if I can come off my hip for that stack.

  22. Quote Originally Posted by fueledpassion View Post
    I was looking a board on your website and noticed that your not too fond of SERM usage? What would you propose to normalizing libido/test/estrogen?

    As far as this thread goes I've come to a conclusion that controlling estrogen is key as well as prolactin. But I'm not trying to kill estrogen during PCT, as it is already killed during cycle for me. So I almost feel reluctant to use anything more than a low dose of AI tapering to EOD dosages during PCT. What do you think?

    I also plan on using Clomid first few weeks then jumping on perhaps TRS afterwards, if I can come off my hip for that stack.
    Yep, not a fan of SERMís. In my experience they high doses can lower libido and raise estrogen to the point where rebound problems can occur when you discontinue them. If you are going to use a SERM I suggest sticking with lower than traditional doses. (eg, 10mg/day nolva, 25mg/day clomid)

    I donít advise using steroid AIís for PCT simply because they are steroid hormones that may interfere with the HPTA and natural T production.

    Of course, I propose the TRS for PCT. It wonít cause estrogen to rise out of the normal range, nor will it overly suppress estrogen.

    -Eric

  23. Quote Originally Posted by Primordial Perf View Post
    If these steroids are causing gyno by releasing E2 through SHBG down-regulation or competitive binding then an AI wonít do anything to prevent gyno from the circulating E2. (or the low levels of antagonistic DHT) Therefore, Seth suggests a SERM to block the action of estrogen.

    The theory makes sense, but I would still caution against the SERM administration and instead opt for prolactin control. (Being a potent co-factor in breast growth, perhaps keeping it in the sub-physiological range will partly cripple estrogens ability to induce mammary growth)

    -Eric
    Eric, to test your theory regarding prolactin being the MAJOR player in gyno

    why dont I take Pramipexole high dose and zap out PRL first

    then i will take synthetic estradiol

    will I develope gyno then?

    I think Estrogen needs to be addressed first. it is clear estrogen makes boobies grow i mean look at some boobies carrying homosapiens, namely women, they have high ass E level not high PRL, co factor is a co factor, why not take out the source?

    also SERM is, as the name states, selective, meaning its not a full on antagonist of ER, therefore it is partially agnoistic, your HPTA will be 'happy' to see some estrogen like activity happening somwehre (liver or whatever)...which wont freak out and ramp up estrone build up or aromatase build up. Using AI will however cause rebound in some cases, I personally think SERM is better for PCT and even during cycle (nolva).


    unrelated, but how about use progesterone cream to lower ER LOL,,,you will be shutdown anyways during cycle, taper off progesterone while tapering off test, run low dose test for awhile then start PCT? no gyno during cycle due to lowered ER? this sounds bad but someone should try it ahhaha

    Seth, you should start a thread explaining how progestins work with GR and cause joint pain relief or sore joints depending on structure (nandrolone and winny) and how cortisol, progesterone and glucocorticoid all can interact with same receptors of each...why do i get acne only from progestin based gear? and do they increase cortisol? and yet anti catabolic WTF?

  24. Quote Originally Posted by comacho View Post
    Eric, to test your theory regarding prolactin being the MAJOR player in gyno

    why dont I take Pramipexole high dose and zap out PRL first

    then i will take synthetic estradiol

    will I develope gyno then?

    I think Estrogen needs to be addressed first. it is clear estrogen makes boobies grow i mean look at some boobies carrying homosapiens, namely women, they have high ass E level not high PRL, co factor is a co factor, why not take out the source?

    also SERM is, as the name states, selective, meaning its not a full on antagonist of ER, therefore it is partially agnoistic, your HPTA will be 'happy' to see some estrogen like activity happening somwehre (liver or whatever)...which wont freak out and ramp up estrone build up or aromatase build up. Using AI will however cause rebound in some cases, I personally think SERM is better for PCT and even during cycle (nolva).


    unrelated, but how about use progesterone cream to lower ER LOL,,,you will be shutdown anyways during cycle, taper off progesterone while tapering off test, run low dose test for awhile then start PCT? no gyno during cycle due to lowered ER? this sounds bad but someone should try it ahhaha

    Seth, you should start a thread explaining how progestins work with GR and cause joint pain relief or sore joints depending on structure (nandrolone and winny) and how cortisol, progesterone and glucocorticoid all can interact with same receptors of each...why do i get acne only from progestin based gear? and do they increase cortisol? and yet anti catabolic WTF?
    I actually found a rellay good paper on estrogen and the joints but my f--king computer crashed so I have to refind it. But the points you bring up are good ones that I will look into.

  25. Ok seth bloods are back I remember my e2 levels but not all I will try and gt the rest up soon

  26. Quote Originally Posted by crazyfool405 View Post
    Ok seth bloods are back I remember my e2 levels but not all I will try and gt the rest up soon
    cool -- just no more pics of your ass unless you have a real abcess.

  27. U got it bro. Lol I thought u really liked it soooo...... Anyway e2 before cycle in dec was less thn 20 then a week later gyno popped up. March e2 was 29 and I was on 40mg epi 300mg npp and test 610mg

  28. U got it bro. Lol I thought u really liked it soooo...... Anyway e2 before cycle in dec was less thn 20 then a week later gyno popped up. March e2 was 29 and I was on 40mg epi 300mg npp and test 610mg

  29. Quote Originally Posted by comacho View Post
    Eric, to test your theory regarding prolactin being the MAJOR player in gyno

    why dont I take Pramipexole high dose and zap out PRL first

    then i will take synthetic estradiol

    will I develope gyno then?

    I think Estrogen needs to be addressed first. it is clear estrogen makes boobies grow i mean look at some boobies carrying homosapiens, namely women, they have high ass E level not high PRL, co factor is a co factor, why not take out the source?

    also SERM is, as the name states, selective, meaning its not a full on antagonist of ER, therefore it is partially agnoistic, your HPTA will be 'happy' to see some estrogen like activity happening somwehre (liver or whatever)...which wont freak out and ramp up estrone build up or aromatase build up. Using AI will however cause rebound in some cases, I personally think SERM is better for PCT and even during cycle (nolva).


    unrelated, but how about use progesterone cream to lower ER LOL,,,you will be shutdown anyways during cycle, taper off progesterone while tapering off test, run low dose test for awhile then start PCT? no gyno during cycle due to lowered ER? this sounds bad but someone should try it ahhaha

    Seth, you should start a thread explaining how progestins work with GR and cause joint pain relief or sore joints depending on structure (nandrolone and winny) and how cortisol, progesterone and glucocorticoid all can interact with same receptors of each...why do i get acne only from progestin based gear? and do they increase cortisol? and yet anti catabolic WTF?
    Eric is simply stating that prolactin (as progesterone) are cofactors in the overall development of mammary tissue and milk production. Nothing more, and this really isn't a novelty at this point. Nobody here is denying the prevalence of estrogen in the overall stimulation and/or development of mammary tissue, however the whole issue goes way beyond that. Even in the presence of a normal estrogen level, if your cofactors are elevated to any degree the risk is there to potentiate an issue; not to mention there is the possiblity of so many unknown underlying factors playing a part at times (i.e. underlying hormonal disorders, dopaminergic factors, disease process.)

    Just as an example, look at the hormonal/development algorhythm women experience during their menses or pregnancy. Progesterone and prolactin without-a-doubt play a part in the development of glandular tissue and lactation. As in puberty, estrogen controls the growth of the ducts and progesterone controls the growth of the glandular buds. It's all relative here in the end, and that's what really matters.

    I can see what you're getting at overall, and i don't disagree per se, but this issue is far more complicated than just estrogen alone in many instances. We could go on for hours discussing each cofactor and the different scenarios that could play a role in any given individual issue. I'm not Anti-Serm myself, and i do think they play an important role, but in general i don't think many people realize how complex endocrinology really is. Without blood work to correlate with each individual presenting case, there is no way to prove any specific treatment modality effective; or even warranted for that matter.

    Evolutionary Muse - Inspire to Evolve
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