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  1. #1
    Shut up and squat ! g1234's Avatar
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    Progesterone and prolactin levels
    Quote Originally Posted by GymLift View Post
    My understanding which may be wrong is that nandrolone and trenbolone are progestins in that they attach to the progestin receptor but at the same time they are of course NOT progesterone. I've seen it suggested that with the nor-19 drugs attaching to the progestin receptor, serum progesterone levels decrease. And as you said, progesterone inhibits prolactin so with the lowered progesterone levels, serum prolactin increases.

    I probably researched this at one point in time but I don't remember. And I no longer have full access to published study data.

    What I do know is that when I use tren, my prolactin levels definitely increase and I definitely lactate.
    Quote Originally Posted by FerrariF50 View Post
    there's no data to suggest progesterone increases prolactin
    they are two separate hormones that happen to start with the letter P

    in fact there is studies showing progesterone decreases and has inhibitory effects on serum prolactin levels

    as well nandrolone and tren are androgens, which typically decrease prolactin levels

    prolactin is being raised somehow but i've yet to see any reasonable explanation as to why or how
    This link between progesterone and prolactins is something weird, does anyone have a physiological explanation? I found this link Human Reproduction, Lectures: Prolactin

    After reading it seems to me that for prolactin levels to increase, there must be high estrogens and also high progesterone levels, then prolactin is released by the anterior pituitary. Could be correct??

  2. #2
    Olympian Bodybuilder Ozzy27's Avatar
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    You be researching......good for you. Maybe
    Last edited by StoneColdNTO; 01-10-2009 at 04:26 PM.

  3. #3
    - FerrariF50's Avatar
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    limit circulating estrogen and there will be no progestagen or prolactin issues

  4. #4
    A Legend GymLift's Avatar
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    Quote Originally Posted by FerrariF50 View Post
    limit circulating estrogen and there will be no need for an anti-prolactin
    perhaps, but regardless it would be nice to better understand the cause->effect of tren/nandrolone->increased prolactin.

    Also, I've seen reports of normal estrogen levels and lactation. While reducing estrogen to below-normal levels does resolve the issue, I don't consider such to be healthy.

    But I suppose I'm getting off topic myself.

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    Quote Originally Posted by FerrariF50 View Post
    limit circulating estrogen and there will be no progestagen or prolactin issues
    So you are saying if you run an Aromatase inhibitor (AI), you should not get gyno symptoms from Nandrolone or Tren ?

    Speaking from experience, that certainly does NOT hold true for me.

    1mg Arimedex/day (from SBC, in case you were going to question it's dosing or potency)

    I've heard that theory plently of times on the boards over the years. Maybe on paper it works, but in reality .....????
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  6. #6
    - FerrariF50's Avatar
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    Quote Originally Posted by StoneColdNTO View Post
    So you are saying if you run an Aromatase inhibitor (AI), you should not get gyno symptoms from Nandrolone or Tren ?

    Speaking from experience, that certainly does NOT hold true for me.

    1mg Arimedex/day (from SBC, in case you were going to question it's dosing or potency)

    I've heard that theory plently of times on the boards over the years. Maybe on paper it works, but in reality .....????
    its exactly what I believe. there is only 1 type of gyno, and 9 out of 10 times it needs estrogen to form. even in the presence of prolactin.

    to support the theory, not many people complain about prolactin issues while running tren alone.

    deca aromatises slightly, so although it binds to the PgR with less affinity than tren it could still cause problems without the addition of an aromatising steroid.

  7. #7
    Shut up and squat ! g1234's Avatar
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    I think so aswel, i think gyno only happens if both estrogens and prolactins are high, and high estrogen levels increase secretion of prolactin. Thats why some reports show testosterone itself increase prolactins and causes gyno.

    Check this:

    PROGESTERONE AND PROLACTIN INDUCED GYNECOMASTIA

    Before delving into this subject, I***8217;d like to say first and foremost, that in users of anabolic/androgenic steroids (AAS) the first step in combating the development of gynecomastia, or male breast enlargement, is to eliminate the causative agent: the anabolic steroid. Drug-induced gynecomastia almost invariably resolves on its own when a person quits taking the drugs responsible for it, if caught before permanent fibrosis develops. Unfortunately, most AAS users don***8217;t want to employ this simple approach, for obvious reasons, so the foregoing will all be under the assumption that a person wants to prevent or treat gyno and still continue steroid use.

    In the belief that certain anabolic steroids increase prolactin levels as well as act as agonists at the progesterone receptor, some have advocated the use of antiprolactin agents, like bromocriptine, or progesterone receptor blockers like RU-486 to treat AAS related gynecomastia, in lieu of more traditional drugs like tamoxifen.

    In truth, the etiology of gynecomastia is unknown and a number of agents including estrogens, progestins, GH, IGF-1, and prolactin may be involved. However, most authorities believe that a decreased (T+DHT)/E ratio is central to the development of gyno, and that blocking the effects of estrogen, or increasing T + DHT levels, is central to ameliorating the problem.

    Regarding prolactin, androgens decrease prolactin levels whereas estrogens increase prolactin. Non-aromatizing androgens have never been shown to elevate prolactin levels in humans, but testosterone has, due to its aromatization to estradiol (19). Prolactin secreting tumors, or prolactinomas, are often associated with gyno. But in these cases the prolactin is believed to induce gyno by suppressing testosterone production: ***8220;Prolactinomas that are sufficiently large to cause gynecomastia do so as a result of impairment of gonadotropin secretion and secondary hypogonadism***8221;. (20). However, this is a moot issue in AAS users whose gonadotropin secretion is already blunted.

    According to research cited in (20), prolactin may have a direct stimulatory effect on mammary tissue development, but only in the presence of high estrogen levels:

    The presence of mild hyperprolactinaemia is therefore not uncommon in patients with estrogen excess. Significant primary hyperprolactinaemia, on the other hand, may directly stimulate epithelial cell proliferation in an estrogen-primed breast, causing epithelial cell proliferation and gynaecomastia.

    So rather than focusing solely on lowering prolactin levels which may be elevated in users of aromatizing androgens, attacking estrogen should be the first line of action.

    GH and IGF-1 are considered critical to the proliferation of mammary tissue. An excellent review of the role played by these hormones, as well as a general overview of gynecomastia can be found here:

    Since elevated GH and IGF-1 are considered important to the anabolic effect of AAS, it would be impractical and counterproductive to attempt to prevent gynecomastia by blocking GH/IGF.

    Progesterone acts in concert with estrogen to promote breast development, and at least part of any role played by synthetic progestins may be to stimulate IGF-1 production in the breast. But again, blocking the action of progesterone or synthetic progestins is not practical. Specific progesterone receptor antagonists like RU-486 block not only the progesterone receptor, but the androgen receptor as well, and have actually been associated with the development of gynecomastia (21). In any case, progesterone is thought to act on the breast to enhance the effects of estrogen (22) so once again, attacking estrogen is the easiest and most logical approach.

    DHT gel (Andractim) or a generic knockoff might help as well. DHT is thought to act as an aromatase inhibitor (23) and perhaps compete directly with estrogen for binding at the estrogen receptor (24). DHT has been used in several case reports and controlled trials to successfully treat gynecomastia. So perhaps a viable strategy would be to combine DHT gel with tamoxifen. I would recommend tamoxifen rather than an aromatase inhibitor due to the simple fact that tamoxifen has been widely used in numerous controlled studies to succesfully treat gynecomastia, whereas the evidence to support the efficacy of aromatase inhibitors is scanty at best.

    Undoubtedly, due to space limitations, I have left out a number of what are surely many readers***8217; pet myths. Perhaps in a future issue we can address more of these myths and questionable notions. Feedback is always welcome, and if readers wish to submit their ideas for myths that need to be examined in the future, please feel free to contact Mind & Muscle with your ideas.



    References:

    (1) Price TM, O'Brien SN, Welter BH, George R, Anandjiwala J, Kilgore M. Am J Obstet Gynecol 1998 Jan;178(1 Pt 1):101-7

    (2) Bjorntorp P. Hum Reprod 1997 Oct;12 Suppl 1:21-5

    (3) Ramirez ME, McMurry MP, Wiebke GA, Felten KJ, Ren K, Meikle AW, Iverius PH Metabolism 1997 Feb;46(2):179-85

    (4) Zmuda JM, Fahrenbach MC, Younkin BT, Bausserman LL, Terry RB, Catlin DH, Thompson PD. Metabolism 1993 Apr;42(4):446-50

    (5) Tomita T, Yonekura I, Okada T, Hayashi E
    Horm Metab Res 1984 Oct;16(10):525-8

    (6) Mystkowski P, Seeley RJ, Hahn TM, Baskin DG, Havel PJ, Matsumoto AM, Wilkinson CW, Peacock-Kinzig K, Blake KA, Schwartz MW. J Neurosci 2000 Nov 15;20(22):8637-42

    (7) Greer,M. N Engl J Med 244:385, 1951

    (8) Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH. N Engl J Med 1975 Oct 2;293(14):681-4

    (9) Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN J Clin Endocrinol Metab 1975 Jul;41(1):70-80

    (10) Liva SM, Voskuhl RR J Immunol 2001 Aug 15;167(4):2060-7

    (11) Ulloa-Aguirre A, Blizzard RM, Garcia-Rubi E, Rogol AD, Link K, Christie CM, Johnson ML, Veldhuis J Clin Endocrinol Metab 1990 Oct;71(4):846-54

    (12) Hochman IH, Laron Z Horm Metab Res 1970 Sep;2(5):260-4
    .
    (13) Steinetz BG, Giannina T, Butler M, Popick F
    Endocrinology 1972 May;90(5):1396-8

    (14) Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.
    Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7

    (15) Sheffield-Moore M, Urban RJ, Wolf SE, Jiang J, Catlin DH, Herndon DN, Wolfe RR,
    Ferrando AA
    J Clin Endocrinol Metab 1999 Aug;84(8):2705-11

    (16) Doumit ME, Cook DR, Merkel RA..Endocrinology 1996 Apr;137(4):1385-94

    (17) Bricout VA, Germain PS, Serrurier BD, Guezennec CY.Cell Mol Biol (Noisy-le-grand) 1994 May;40(3):291-4

    (18) Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.
    Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7

    (19) Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F
    Acta Endocrinol (Copenh) 1984 Feb;105(2):167-72

    (20) Ismail AA, Barth JH.Ann Clin Biochem 2001 Nov;38(Pt 6):596-607

    (21) Grunberg SM, Weiss MH, Spitz IM, Ahmadi J, Sadun A, Russell CA, Lucci L, Stevenson LL J Neurosurg 1991 Jun;74(6):861-6

    (22) Nomura K, Suzuki H, Saji M, Horiba N, Ujihara M, Tsushima T, Demura H, Shizume K
    J Clin Endocrinol Metab 1988 Jan;66(1):230-2

    (23) Perel E, Stolee KH, Kharlip L, Blackstein ME, Killinger DW
    J Clin Endocrinol Metab 1984 Mar;58(3):467-72

    (24) Casey RW, Wilson JD.
    J Clin Invest 1984 Dec;74(6):2272-8

  8. #8
    Shut up and squat ! g1234's Avatar
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    "In any case, progesterone is thought to act on the breast to enhance the effects of estrogen (22) so once again, attacking estrogen is the easiest and most logical approach."

    What did you experience stone ? You got gyno even when running the Aromatase inhibitor (AI) ? how did you fix it? caber/bromo?

  9. #9
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    Quote Originally Posted by g1234 View Post
    What did you experience stone ? You got gyno even when running the Aromatase inhibitor (AI) ? how did you fix it? caber/bromo?
    Vitamin B6.......which certainly does not work for everyone, but it solved my symptoms.
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  10. #10
    Moderator dialtone's Avatar
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    Quote Originally Posted by StoneColdNTO View Post
    Vitamin B6.......which certainly does not work for everyone, but it solved my symptoms.
    in what doses did you run the b6?

  11. #11
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    Quote Originally Posted by detone01 View Post
    in what doses did you run the b6?
    600mg/day until gyno symptoms subsided, then 200mg/day for the duration.
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  12. #12
    Shut up and squat ! g1234's Avatar
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    wow... the recommended dietary allowance for vitamin B6 is between 1 and 2mg/day??

  13. #13
    Moderator Kane_Red_Machine's Avatar
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    NRC... 0.7-2.2mg/day... yes i've seen that.... these are the minimal. doses.

    could be increase without sides to 200mg/day/4 weeks.

    and supplementation of pirydoxin chlorid about 250mg/twice-a-day/4weeks. some times more longer.

    Anyway. prolactin never proceed from anything but to high level of progest.

  14. #14
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    Quote Originally Posted by g1234 View Post
    wow... the recommended dietary allowance for vitamin B6 is between 1 and 2mg/day??
    Considering they are OTC and come in 100mg tabs, I find that kinda hard to beleive.
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  15. #15
    Moderator juced_porkchop's Avatar
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    Quote Originally Posted by StoneColdNTO View Post
    Vitamin B6.......which certainly does not work for everyone, but it solved my symptoms.
    BUMPP!
    it helped me also.
    i took aabout 400 ed for a few weeks and then just kept up with 200-300 for the duration.
    "was also on an AI"
    Follow me on Twitter for advanced in-depth peptide, supplement and AAS knowledge, along with all things bodybuilding! Follow me-> @Juced_porkchop

  16. #16
    Moderator Kane_Red_Machine's Avatar
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    Quote Originally Posted by StoneColdNTO View Post
    Considering they are OTC and come in 100mg tabs, I find that kinda hard to beleive.
    You are right both.

    they are NRC reglementatiion, but all all tabs are at least 100 and several times 250, mg...

    So...

    But def it works...

  17. #17
    Shut up and squat ! g1234's Avatar
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    Quote Originally Posted by StoneColdNTO View Post
    Considering they are OTC and come in 100mg tabs, I find that kinda hard to beleive.
    seriously, the recommened normal dose is between 1 and 2 mg per day. But therapeutic doses in case of troubles can be much higher.. i'm just surprised to see how much higher.

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    Quote Originally Posted by FerrariF50 View Post
    limit circulating estrogen and there will be no progestagen or prolactin issues

    nope. you might think this and it might be logical, but NOPE.

    there are about a dozen reasons why, but a couple are breast tissue produces aromatase, even when plasma levels of E are extremely low aromatase is still produced to some extent in this tissue. Actually this goes for many tissues. Some more so than others. its the whole local vs. systemic dilemna.

    you dont need E. ERKO lab animal variants still produce prolactin and still can develop breast tissue (its fucked up breast tissue, but still breast tissue)

    promiscous ligands, there are lots of things that can bind to the ER. Including but not limited too metabolites of 5-androstanes (DHT), many methylated steroids (particularly di-methyls), a lot of exogenous and even endogenous chemicals, hormones metabolites, etc... sometimes there action is very weak, sometimes like say with 3-beta-diol its EXTREMELY potent.


    as a note- anastrozole and letrozole are more likely than other AI's to increase 3-beta-diol synthesis (at least in theory, since 3-beta has only been really looked at recently and not extensively) because of their tissue specific actions

  19. #19
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    am generally opposed to high dose b-6, its only effective in a limited number of cases. It has side effects, including abrogation of AAS anabolic effects (so might as well not have cycled), and it can cause nerve damage.

    cabaser tablets or pramipexole (liquid or tabs) are better options for prolactin suppression

    neither of which is particularly expensive, when purchased from the right places (note- as of this time all liquid cabergoline is not reccomended- for a variety of reasons from degradation issues to the clear indications that material is either substandard or fake-- though again even in the cases where good material is used, appropriate suspensions are not)

  20. #20
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    not sure who wrote that article, but there are a number of errors in it. Some of it is quite relevant but obviously understanding of ER/PgR/PrlR interactions and ligands is not up to par or speed.

    the reccomendation of tamoxifen is pure idiocy and well borne out, that its upregulation of the PgR can cause aggravation and/or even precipate gynecomastia flare and growth cycle. when will people realize that tamoxifen is a dirty SERM, and its estrogenic actions are far more prevalant than its anti-estrogenic ones. Particularly when it comes to allosteric and non-genomic binding sites as well as its actions in the hypothalamus and pituitary, because of the receptor subtypes densities and isoforms present there.

    lay explanation: tamoxifen is a common CAUSATIVE factor in post cycle gynecomastia, its use during cycle with these compounds MAY reduce aggravation/pain but not significantly limit proliferation, though generally not. ie. this is why some people, say that it works, not putting together the fact that after cycle when it "blows up" that they were just masking the symptoms.

    moderation of E synthesis, even high level suppression of aromatase does help. Its just not necessarily enough.

    Direct PRL suppression is generally also needed, keeping in mind still reccomend E suppresion as E/pgr activation can still present issues even if PRL is highly suppressed.

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    to answer the first post ER and PgR are both regulators/modulators of PRL-RH and PRLR as well as PRL itself. Of course PRL is a modulator of ER and PgR action as well.

    so these systems are inter-related but their interplay is lot more complicated than those statement lay out. And there are numerous other factors involved, not to mention the influence of promiscuous ligands or non traditional ligands.

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    So much different information. Macro your saying B6 might reduce the effectiveness of the cycle you are taking?

    And for those that have used it, I am sure you did not notice any hindrance am I right?

    I ask because it was a toss up to get caber or B6 for my test deca cycle......

  23. #23
    "Resident BadAss" RichGenetics's Avatar
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    PRAMI is the key. Ask Mac.

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    I don't know if it helps, but I did a blood check 1 year ago because I slightly have some gyno, and my prolactin levels were through the roof.

  25. #25
    Junior Bodybuilder coquito's Avatar
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    Whats prami ?

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