Progesterone and Prolactin

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  1. 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


  2. 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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  3. 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.

  4. 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.
    GOD, FAMILY, COUNTRY!!!

  5. 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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  6. 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.

  7. 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.

  8. 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?

  9. 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.

  10. 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

  11. Quote Originally Posted by Primordial Perf View Post
    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
    Their is no proof one way or the other as to whether it aromatizes and the binding affinities say that it is closer to nandrolone.

    Nandrolone Dienolone Trenbolone
    AR 154 134 197
    PR 20 17 74

  12. Quote Originally Posted by sethroberts View Post
    Their is no proof one way or the other as to whether it aromatizes and the binding affinities say that it is closer to nandrolone.

    Nandrolone Dienolone Trenbolone
    AR 154 134 197
    PR 20 17 74
    Yeah, based on info in this thread - I'm kinda leaning towards maybe it does. That would explain a whole heck of a lot, and make running an AI with the Trens the simple solution.

  13. 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.
    do you feel .5 mg of Caber will do more harm then good at 1 dose per week? will it be ok to use it especially on npp and test, and soon to be test and Tren?

  14. seth, eric: what are your views on Bromocriptine in the event of prolactin problems? will it be effective against 1-t tren gyno? (if any occurs) im also confused about its long term effects, will there be any effects of a short 1.25mg ED sort of course if I needed it to cure issues on/after 1-t tren? Do either of you also have views on running it on cycle, or is it just overkill?

  15. Seth,

    I’d appreciate it if you could touch on the anadrol-winstrol relationship. It’s got me a little confused.

    Anadrol doesn’t aromatize obviously… Historically its sides have been attributed to progestins, as it binds PR but not AR. Now, you’ve stated that the release of bound estrogens due to lowered SHBG levels, as well as the loss of the general protective effects of SHBG can explain gyno with certain compounds such as SD, phera, anadrol and tren. That makes sense to me so far.

    Running winny alongside anadrol seems to cut down on sides. Yet winny supposedly knocks down SHBG levels greatly. It’s also been said that winny has “anti-progestagenic” effects. I don’t know what that really entails. If anadrol’s sides are indeed due to freed estrogen and a lowered SHBG environment, can you explain what happens when winny is added to the model? Why aren't anadrol's sides more pronounced? TIA.

  16. Quote Originally Posted by crazyfool405 View Post
    do you feel .5 mg of Caber will do more harm then good at 1 dose per week? will it be ok to use it especially on npp and test, and soon to be test and Tren?
    The only appropriate use of bromocriptine is in the presence of clinically elevated prolactin levels (and of course as prescribed and under the supervision of a physician) -- imo there is no reason to use it otherwise.

  17. Quote Originally Posted by gelin View Post
    Seth,

    I’d appreciate it if you could touch on the anadrol-winstrol relationship. It’s got me a little confused.

    Anadrol doesn’t aromatize obviously… Historically its sides have been attributed to progestins, as it binds PR but not AR. Now, you’ve stated that the release of bound estrogens due to lowered SHBG levels, as well as the loss of the general protective effects of SHBG can explain gyno with certain compounds such as SD, phera, anadrol and tren. That makes sense to me so far.

    Running winny alongside anadrol seems to cut down on sides. Yet winny supposedly knocks down SHBG levels greatly. It’s also been said that winny has “anti-progestagenic” effects. I don’t know what that really entails. If anadrol’s sides are indeed due to freed estrogen and a lowered SHBG environment, can you explain what happens when winny is added to the model? Why aren't anadrol's sides more pronounced? TIA.
    There is no evidence that oxymetholone binds to the PR and though its AR binding is low, its has been shown that its effects are mediated through the AR. Running winny may seem to cut down on the sides but this is not in controlled tests -- only through anecdotal reports. I suggested its use as such back in 1997 or 1998. Winstrol is a strange molecule -- it binds receptors for which there is no known function (or whose function is still being elucidated). I also talk a lot in my book about how different steroids alter adrenal function and how this may have a role in producing gynecomastia.

  18. Quote Originally Posted by sethroberts View Post
    The only appropriate use of bromocriptine is in the presence of clinically elevated prolactin levels (and of course as prescribed and under the supervision of a physician) -- imo there is no reason to use it otherwise.
    libido purposes, seems to help me a little in that area when i take it. just wondered if it would be more more harm then good while on test and progestins, im using adex EOD though

  19. Quote Originally Posted by crazyfool405 View Post
    libido purposes, seems to help me a little in that area when i take it. just wondered if it would be more more harm then good while on test and progestins, im using adex EOD though
    If prolactin is elevated and is causing decreased libido then it would be valid to use it for that purpose. Do you have any evidence that prolactin is elevated?

  20. Quote Originally Posted by sethroberts View Post
    If prolactin is elevated and is causing decreased libido then it would be valid to use it for that purpose. Do you have any evidence that prolactin is elevated?
    im using it 1x a week for protective measure, because i need to pick up my labs from my last blood test.

    but i still have a little gyno so i know my e2 is a tad high or higher then it should be as well as my growth factors which may lead to that prolactin increase.

  21. Quote Originally Posted by crazyfool405 View Post
    im using it 1x a week for protective measure, because i need to pick up my labs from my last blood test.

    but i still have a little gyno so i know my e2 is a tad high or higher then it should be as well as my growth factors which may lead to that prolactin increase.
    The only question then is, if prolactin is not elevated, would there be any point to using caber?
    but, since you are already taking it, it may confound the test results (if you were taking it before the blood test)

  22. Quote Originally Posted by sethroberts View Post
    The only question then is, if prolactin is not elevated, would there be any point to using caber?
    but, since you are already taking it, it may confound the test results (if you were taking it before the blood test)
    i cant remember, i dont think soo i think i started the next day

  23. Quote Originally Posted by crazyfool405 View Post
    i cant remember, i dont think soo i think i started the next day
    Well then it may be enlightneing to see your prolactin level when it comes back. Please share. I just wonder how many people are treating "elevated" prolactin when there is, in fact, no real elevation.

  24. Damn - It looks like a missed quite a bit in the week i was gone. I have some catching up to do with reading.

    I have some good endocrine/pathophysiology info to add to this discussion.

    Evolutionary Muse - Inspire to Evolve
    Legendary


  25. Quote Originally Posted by sethroberts View Post
    Well then it may be enlightneing to see your prolactin level when it comes back. Please share. I just wonder how many people are treating "elevated" prolactin when there is, in fact, no real elevation.
    i can call and try having them fax my labs over, its a 40min drive to go there just tp pick them up.;
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