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  1. #1
    Mavilia is offline New Member
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    what is prolactin? causes sex problems?

    I recently posted asking about some sex problems im having while on a cycle. here is the cycle
    weeks 1-12 500mg test e
    weeks 1-7 50mg dbol
    weeks 6-10 100mg tren ace eod

    experienced a loss of random erections, still having alot of sex drive but it just wasnt functioning right, and like i always have on my 4 or 5 previous cycles. people told me it was the prolactin from the tren. but i just stopped the dbol and it seems to be getting better, having morning wood again ect... so im not sure what prolactin even is, is it also in dbol like it is tren? only other cycles ive done are test and dbol. but ive never done as much dbol as i did this time. 50 to 60mg a day. its liquid dbol so couldnt be as exact as i have in the past with 5mg tabs. im almost done with the tren as well so i just have one more 10ml bottle of test e 250. guess my question is could have it been the dbol? and what exactly is prolactin and what can be done to combat it in the future? thanks

  2. #2
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    You had to jump right into the tren huh? Yeah so you ignored all the other 1000s of post telling people and you if you asked about Tren that it's NOT a good 1st, 2nd or 3rd cycle for most people Why would you listen to advice now?

    OK expect more brow beating, you deserve it.

    What is your planned PCT? If you say NON then you deserve to have more problems in the immediate future.....

    What do you have on hand for AI? Nothing, right? Get some liquidex or Stane from Lion, use it as noted and it should take care of the problem. Your estrogen is probably out of whack.

  3. #3
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    Lol way to do your research smart guy. Prolactin isn't IN a compound....The compound causes an increase in the PRODUCTION of prolactin...Which is a hormone secreted by the pituitary...It counteracts the effects of dopamine which is partly responsible for sexual arousal...Learn to research and take advice before starting a cycle.

  4. #4
    Mavilia is offline New Member
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    i had aromasin on hand havent used it. pct is torem and nolva. and yes out of 4 or 5 cycles this is first time im using a pct. never had any issues in the past. im not sure if people understand or arent willing to except that most people who use steroids from time to time arent experts and dont cycle properly. i just got flamed for what? asking what is prolactin and does dbol cause it. alot of people use this site as research, as im using it for. i know plenty of people who have used tren n their 1st cycle. it seems alot of people on this site want steroids to be their own underground thing but anyone who has money and a connection can use them if they want weather they are doing it the right or wrong way. as i said since stopping the dbol everything seems like it went back to normal so it doesnt seem to be the tren. in any case thanks for the advice, kinda. i just wanted to know what prolactin was, i never said or said i thought it was a compound, smart guy. was just curious to what it was and what it does to your body. and yeah people who dont do any research and then have problems have themselves to blame.

  5. #5
    Mavilia is offline New Member
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    seriously easy20 where do you see me saying prolactin was a compund? smart guy

  6. #6
    Mavilia is offline New Member
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    and lovbyts tell me exactly why i deserve more brow beating, whatever that means? because i asked what prolactin was. i clearly stated it my post the issue went away when stopping the dbol , so yeah i should have never taken that tren

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    Yah, I don't know why people are giving you a hard time.

    How do you know it's a prolactin problem? Sounds like an elevated Estrogen problem to me.

    I'd start using the stane at 10mg EOD and see how that works.

    Here's a good read for you: http://forums.steroid.com/showthread...d-gynecomastia

  8. #8
    Mavilia is offline New Member
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    ok my bad i read where i asked if its in dbol like its in tren . i meant does dbol cause it like tren does. thats my bad

  9. #9
    Mavilia is offline New Member
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    i dont know its a prolcatin problem. when i had the issue i posted asking about it, got flamed and then people said it was the prolactin from the tren .

  10. #10
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    no, prolactin increase is attributed to 19nor's like tren and deca

  11. #11
    Mavilia is offline New Member
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    and thanks d7m, good read

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    Quote Originally Posted by Mavilia View Post
    ok my bad i read where i asked if its in dbol like its in tren. i meant does dbol cause it like tren does. thats my bad
    So who's the "smart guy?" FYI you're always going to get heat from a good bit of members for not knowing the potential side effects of the compounds you run. Especially when you jump right into tren .

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    Quote Originally Posted by MBMETC View Post
    no, prolactin increase is attributed to 19nor's like tren and deca
    Its actually attributed to estrogen, or compounds that interact (one way or another) with the estrogen receptor, not 19-Nor's solely.

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    Mavilia is offline New Member
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    still im not sure why the smart guy comment was called for or why people give other people looking for answers so much heat. and again i didnt just jump right into tren . yeah I have only done 4 or 5 cycles in the past. and i do research side effects. i thought that was why everyone says make sure you run test with tren, or anything else for that matter. its not lile i didnt know that sexual problems are a possible side effect of most cycles. again when i posted the question when this issue was happening to me i was told that its probably prolactin from the tren. so im curious if there is a way to combat it in the future if i ever run tren again. but like i said the issue seems to have gone away after stopping the dbols.

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    Quote Originally Posted by Mavilia View Post
    still im not sure why the smart guy comment was called for or why people give other people looking for answers so much heat. and again i didnt just jump right into tren . yeah I have only done 4 or 5 cycles in the past. and i do research side effects. i thought that was why everyone says make sure you run test with tren, or anything else for that matter. its not lile i didnt know that sexual problems are a possible side effect of most cycles. again when i posted the question when this issue was happening to me i was told that its probably prolactin from the tren. so im curious if there is a way to combat it in the future if i ever run tren again. but like i said the issue seems to have gone away after stopping the dbols.
    Read the link I gave you in post #7.

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    Quote Originally Posted by Mavilia View Post
    still im not sure why the smart guy comment was called for or why people give other people looking for answers so much heat. and again i didnt just jump right into tren. yeah I have only done 4 or 5 cycles in the past. and i do research side effects. i thought that was why everyone says make sure you run test with tren, or anything else for that matter. its not lile i didnt know that sexual problems are a possible side effect of most cycles. again when i posted the question when this issue was happening to me i was told that its probably prolactin from the tren. so im curious if there is a way to combat it in the future if i ever run tren again. but like i said the issue seems to have gone away after stopping the dbols.
    Elevated prolactin is a common side effect from tren which is why when you didn't even know what prolactin is it makes me question your research. Anyway, if the issue has resolved after the cessation of dbol , your issue was more than likely an estrogen imbalance, not prolactin.

    As for keeping prolactin levels in check for next time, anything that aids the releasing of dopamine will counter-act the secretion of prolactin (dopamine's primary function is to inhibit the secretion of prolactin). Ar-r has "liquid prami" which I've heard works great. However, if you want to go the more "old school" route you can take Vitamin B6. This is a less effective way to control prolactin and needs to be taken for a good bit of time prior to cycle in order to have a decent effect.

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    Quote Originally Posted by Eazy20 View Post
    Elevated prolactin is a common side effect from tren which is why when you didn't even know what prolactin is it makes me question your research. Anyway, if the issue has resolved after the cessation of dbol , your issue was more than likely an estrogen imbalance, not prolactin.

    As for keeping prolactin levels in check for next time, anything that aids the releasing of dopamine will counter-act the secretion of prolactin (dopamine's primary function is to inhibit the secretion of prolactin). Ar-r has "liquid prami" which I've heard works great. However, if you want to go the more "old school" route you can take Vitamin B6. This is a less effective way to control prolactin and needs to be taken for a good bit of time prior to cycle in order to have a decent effect.
    No, its not.

    Where is the evidence Tren increases PRL in the majority of user's. It doesnt and is no where near as big as a problem as people think.

    An AI will also help control PRL as its regulated by estrogen.

    Vit-B6 can be used to lower PRL, but too much will cause CNS damage. Stick to a maximum of 150mg/ED IMHO, Vit-B6 will also lower AR gene transcription.

  18. #18
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    Quote Originally Posted by Swifto View Post
    No, its not.

    Where is the evidence Tren increases PRL in the majority of user's. It doesnt and is no where near as big as a problem as people think.

    An AI will also help control PRL as its regulated by estrogen.

    Vit-B6 can be used to lower PRL, but too much will cause CNS damage. Stick to a maximum of 150mg/ED IMHO, Vit-B6 will also lower AR gene transcription.
    Quote Originally Posted by steroid.com
    In sensitive steroid .com members this can lead to bloat and breast growth worse still, trenbolones active metabolite17beta-trenbolone has a binding affinity to the progesterone receptor (PgR) that is actually greater than progesterone itself (18). No need to panic though, the anti-estrogens letrzole or fulvestrant can lower progesterone levels, and combat any progestenic sides. The use of a 19-nor compound like trenbolone also increases prolactin& . bromocriptine or cabergoline are often recommended to lower prolatin levels (20). Testicular atrophy (shrunken balls) may also occur; HCG used intermittently throughout a cycle can prevent this. (21) It is also wise for Tren users to closely monitor their cholesterol levels, as well as kidney function and liver enzymes, as Tren has the potential to negatively affect all of those functions.
    In all of my research I cannot find a single correlation to elevated estrogen levels and Hyperprolactinemia.
    Last edited by Eazy20; 03-08-2011 at 03:39 PM.

  19. #19
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    Quote Originally Posted by Swifto View Post
    No, its not.

    Where is the evidence Tren increases PRL in the majority of user's. It doesnt and is no where near as big as a problem as people think.

    An AI will also help control PRL as its regulated by estrogen.

    Vit-B6 can be used to lower PRL, but too much will cause CNS damage. Stick to a maximum of 150mg/ED IMHO, Vit-B6 will also lower AR gene transcription.
    Quote Originally Posted by steroid.com
    In sensitive steroid .com members this can lead to bloat and breast growth worse still, trenbolones active metabolite17beta-trenbolone has a binding affinity to the progesterone receptor (PgR) that is actually greater than progesterone itself (18). No need to panic though, the anti-estrogens letrzole or fulvestrant can lower progesterone levels, and combat any progestenic sides. The use of a 19-nor compound like trenbolone also increases prolactin& . bromocriptine or cabergoline are often recommended to lower prolatin levels (20). Testicular atrophy (shrunken balls) may also occur; HCG used intermittently throughout a cycle can prevent this. (21) It is also wise for Tren users to closely monitor their cholesterol levels, as well as kidney function and liver enzymes, as Tren has the potential to negatively affect all of those functions.
    Also:
    Interestingly, there is a neuroendorcine link between dopamine secretion, progestins and prolactin secretion in the brain. In the arcuate nucleus of the hypothalamus there is a group of dopaminonergic neurons that are responsive to progesterones. Progenstins bind to neurons in this region and reduces dopamine secretion locally leading to increased prolactin secretion and decreased secretion of GnRH (and thus LH and FSH) into the hypophysial portal blood. This series of physiologic responses may explain the loss of sexual function in nandrolone and trenbolone users.
    ^An AI will not help with that.


    Sorry for the double post, my browser went crazy on me


    I'm not saying that OP's sides were because of elevated prolactin levels, I stated that in a previous post. I also agree that an AI should be run during cycle, however, you also should have some form of a prolactin inhibitor as well for any 19-nor compound.
    Last edited by Eazy20; 03-08-2011 at 04:28 PM.

  20. #20
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    OP, are you experiencing any milky discharge from your nipples? If so, you may have elevated prolactin levels. If not, I'd be more incline to agree with D7M's opinion. You could always try Caber or Prami and see if they help. By the way with something like tren , you probably should've at the very least had some prami on hand.

  21. #21
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    Quote Originally Posted by Mavilia View Post
    still im not sure why the smart guy comment was called for or why people give other people looking for answers so much heat. and again i didnt just jump right into tren. yeah I have only done 4 or 5 cycles in the past. and i do research side effects. i thought that was why everyone says make sure you run test with tren, or anything else for that matter. its not lile i didnt know that sexual problems are a possible side effect of most cycles. again when i posted the question when this issue was happening to me i was told that its probably prolactin from the tren. so im curious if there is a way to combat it in the future if i ever run tren again. but like i said the issue seems to have gone away after stopping the dbols.
    Honestly I'm not sure if it was edited or somehow I missed the "i always have on my 4 or 5 previous cycles" because I swear it said or something lead me to believe it was your first cycle and started after you had been here reading already so a BAD choice and thus deserve the brow beating. In retrospect if I missed the 4-5 previous cycles then it's not an issue except for needing to continue the research on what sides to expect and how to combat them. As I had said previously, sound like estrogen related sides but D7M and Swifto would know best.

  22. #22
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    Quote Originally Posted by Eazy20 View Post
    Also:
    ^An AI will not help with that.


    Sorry for the double post, my browser went crazy on me


    I'm not saying that OP's sides were because of elevated prolactin levels, I stated that in a previous post. I also agree that an AI should be run during cycle, however, you also should have some form of a prolactin inhibitor as well for any 19-nor compound.
    Progesterone becomes more active when estrogen is present, using SERMS will lower estorgen thus blocking progesterone related sides aswell. From my understanding prolactin and estrogen have some kind of feedback with each other so if you reduce or block estrogen prolatcin cant increase.

    If prolactin is out of control then you need a dopamine agonist but for prevention methods you can use a SERM to hopefully stop this issue before it does get out of control.

    I will leave swifto to post study after study on this subject so you can update your knowledge.
    *Anyone wanting a source check from a willing vet/mod must first acquire 100 posts and 45 days of activity*

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    Edited by marcus

    Quote Originally Posted by Eazy20 View Post
    In all of my research I cannot find a single correlation to elevated estrogen levels and Hyperprolactinemia.
    The below is a discussion I had with Dr. Scally.


    Swifto-
    I know this is a somewhat greay area, but is there any evidence confirming andorgens (19-Nors or others) increase PRL (prolactin) in males?

    AAS seem to lower T3. Therfore prolactin seems to increase, but apart from that I cannot find anything on it.

    Does PgR binding in the hypothalamus increase prolactin levels?

    Why do user-s of 19-Nor's experience lactation? I know lactation in males is not solely attributed to prolactin, as hypoongondal males also experience this side effect. I have also read that an out of balance androgen:estrogen ratio can contribute or be a causative factor.

    BigCat says no.

    Conciliator, Bill Roberts, Dr. Michael Scally, please share your input...

    Thank-you.



    bigrobbie-
    Yes, T3 is lowered and contributes to Prolactin production, but at the same time if you, as a male, keep your estrogen levels under control Prolactin production and lactation in men

    won't happen. But it is hard to find anything spacific on 19-Nor's and prolactin production, I think

    this is because it is still being debated. I've read both sides and the more I read, the more I realize I have to learn....Sorry I wasn't much help bro.....Anyone else??


    Swifto-
    Not many of the greater minds in our community have come to a conclusion on this. Yet research companies openly sell dopamine agonists to reduce "prolactin gyno". I wonder if it even exists. In the research put forward by BigCat, it doesn't.

    But thanks.



    Bill Roberts-
    Yes, it's been measured on occasion.

    One study I read a while back was interesting in that, among other parameters, it measured prolactin levels both for male athletes using a testosterone ester and those using a nandrolone ester each at individual dosage levels, and gave results for each subject rather than simply a combined statistic.

    Some of the men using testosterone had large increases in prolactin; many had no increase.

    Among those using nandrolone, increase in prolactin seemed more frequent (I didn't run statistics on it and don't recall any conclusion given in the article on it) but there were still many subjects who showed no increase.

    Or as another finding in this area, not that it must necessarily be the same for man, but I found at least one veterinary study demonstrating no prolactin increase from trenbolone . I was looking for this specifically because of claims of increasing prolactin.

    Many claims in bb'ing regarding prolactin are made without evidence.

    However, if an individual finds cabergoline to help him, then very good. It would be nice for the sake of knowledge if he actually had had prolactin tested beforehand, but this seems at best rarely to be done.

    But in conclusion, is it a fact that for example Deca must raise prolactin in all users? No.

    Is it a fact that both testosterone (for example) and Deca can raise prolactin in some users? Yes.



    Swifto-
    Do you have this paper to hand? I'd like to read it.

    Would you say its more common for AAS user's to experience raised PRL levels when using exogenous testosterone WITH a 19-Nor?

    This agrees with my stance on the subject. That it is very subjective. There is no real reason to always use some sort of PRL control using 19-Nors. But one should keep it on hand.

    Do you agree that PRL is not solely responsible for lactation in males? But a contributing factor?

    Thank-you.


    bigrobbie-
    Am I wrong in my thought that in order for PRL to become a problem for the male AAS user, that

    male must first have elevated estrogen levels...in other words, keep the estrogen in check, and

    prolactin shouldn't be a problem. If I'm way off base please correct, thanks!


    Dr Scally-
    I am quite busy with a current project that if successful will be of great and enormous benefit to countless men. I will provide more information later, but it has to do with HPTA restoration. [Note: No matter what your faith or inclination, I believe in collective karma � so think good thoughts!] The following abstracts and attachments will get you on your way regarding anabolic steroids and prolactin.


    Sodi R, Fikri R, Diver M, Ranganath L, Vora J. Testosterone replacement -induced hyperprolactinaemia: case report and review of the literature. Ann Clin Biochem 2005;42(Pt 2):153-9.

    Half of all men with prolactin (PRL)-producing macroadenomas present with hypogonadism, decreased libido and impotence, and therefore require testosterone replacement. However, very little is known about the effect of testosterone on prolactinomas. We report a case of an 18-year-old obese man who presented with hypogonadism and hyperprolactinaemia and underwent a transphenoidal hypophysectomy after a computer tomography scan showed the presence of a suprasellar macroadenoma. On separate occasions, we documented a rise in PRL when testosterone replacement was started and a fall in PRL when testosterone replacement was stopped (r = 0.6090, P = 0.0095). Furthermore, imaging studies suggested the possibility of tumour re-growth after testosterone therapy . We hypothesize that the exogenous testosterone was aromatized to oestradiol, which stimulated the release of PRL by the anterior pituitary. This was supported by the increase in oestradiol levels after testosterone replacement, although statistical significance was not achieved due to the availability of only a few data points. This case highlights the need to be aware of testosterone-replacement-induced hyperprolactinaemia, an under-recognized complication of androgen replacement in this setting. The use of aromatase inhibitors together with testosterone-replacement therapy or the use of non-aromatizable androgens might be indicated in such patients. Taken together, this report and previous studies show that dopamine agonists apparently do not suppress the hyperprolactinaemia induced by testosterone replacement.


    Gill-Sharma MK. Prolactin and male fertility: the long and short feedback regulation. Int J Endocrinol 2009;2009:687259.

    In the last 20 years, a pituitary-hypothalamus tissue culture system with intact neural and portal connections has been developed in our lab and used to understand the feedback mechanisms that regulate the secretions of adenohypophyseal hormones and fertility of male rats. In the last decade, several in vivo rat models have also been developed in our lab with a view to substantiate the in vitro findings, in order to delineate the role of pituitary hormones in the regulation of fertility of male rats. These studies have relied on both surgical and pharmacological interventions to modulate the secretions of gonadotropins and testosterone. The interrelationship between the circadian release of reproductive hormones has also been ascertained in normal men. Our studies suggest that testosterone regulates the secretion of prolactin through a long feedback mechanism, which appears to have been conserved from rats to humans. These studies have filled in a major lacuna pertaining to the role of prolactin in male reproductive physiology by demonstrating the interdependence between testosterone and prolactin. Systemic levels of prolactin play a deterministic role in the mechanism of chromatin condensation during spermiogenesis.


    Gillam MP, Middler S, Freed DJ, Molitch ME. The novel use of very high doses of cabergoline and a combination of testosterone and an aromatase inhibitor in the treatment of a giant prolactinoma J Clin Endocrinol Metab 2002;87(10):4447-51.

    Most prolactinomas respond rapidly to low doses of dopamine agonists. Occasionally, stepwise increases in doses of these agents are needed to achieve gradual prolactin (PRL) reductions. Approximately 50% of treated men remain hypogonadal, yet testosterone replacement may stimulate hyperprolactinemia. A 34-yr-old male with a pituitary macroadenoma was found to have a PRL level of 10,362 micro g/liter and testosterone level of 3.5 nmol/liter. Eleven months of dopamine agonist therapy at standard doses lowered PRL levels to 299 micro g/liter. Subsequent stepwise increases in cabergoline (3 mg daily) further lowered PRL levels to 71 micro g/liter, but hypogonadism persisted. Initiation of testosterone replacement resulted in a rise and discontinuation in a fall of PRL levels. Aromatization of exogenous testosterone to estradiol and subsequent estrogen-stimulated PRL release was suspected. Concomitant use of cabergoline with the aromatase inhibitor anastrozole after resuming testosterone replacement resulted in the maintenance of testosterone levels and restoration of normal sexual function, without increasing PRL. Ultimately, further reduction in PRL on this therapy permitted endogenous testosterone production. Thus, novel pharmacological maneuvers may permit successful medical treatment of some patients with invasive macroprolactinomas.


    Prior JC, Cox TA, Fairholm D, Kostashuk E, Nugent R. Testosterone-related exacerbation of a prolactin-producing macroadenoma: possible role for estrogen. J Clin Endocrinol Metab 1987;64(2):391-4.

    Men with PRL-producing macroadenomas often present with hypogonadism and impotence. This report documents exacerbation of a PRL-secreting tumor after two separate 200-mg testosterone enanthate (T) injections despite continued bromocriptine (BRC) therapy. A 37-yr-old man with a 60-mm invasive tumor and a serum PRL level of 13,969 +/- 332 ng/ml (mean +/- SD) responded to BRC therapy with rapid disappearance of visual field defect, headache, and facial pain as well as decrease in serum PRL to 5,103 +/- 1,446 ng/ml. T injection was followed by severe headache, facial pain, and increase in PRL to 13,471 ng/ml. Visual field deterioration and increased tumor size (height, 40-43 mm) by computed tomography were documented. A relationship between T injection and exacerbation of the prolactinoma was not recognized until after a second T injection 3 months later. After that therapy, baseline PRL increased from 6,900 to 12,995 ng/ml. The hypothesis that T was aromatized to estradiol, directly stimulating lactotrophs, was supported by an increase in serum estradiol from 24 to 51 pg/ml after the second T injection. Although T treatment is accepted as appropriate therapy for hypogonadism in men with prolactinomas, it may not only interfere with the response of the tumor to BRC therapy, but even stimulate tumor growth and secretion.


    swifto-
    Thank-you.

    But doesn't this have limited applicability because there not healthy eugondal males?

    From what I understand. PRL is regulated by testosterone (long feedback) and also estrogen at the anterior pituitary.

    Do you have any information on 19-Nors and PRL? Would they raise PRL moreso, than, for example, a compound that aromotases, such as Testosterone?

    Is estrogen that important for PRL synthesis? From what I understand, it seems so as Arimidex (when introduced to to exogenous T) reduced PRL.


    Dr Scally-
    The answers to your questions are fairly obvious. If the compound aromatizes, interacts with the estradiol receptor, then there will be an effect on prolactin secretion. The same effects would be expected in a "healthy" person taking AAS. The abstracts above address the questions directly. The estradiol produced from testosterone in TRT will "overpower" the negative dopamine agonist effect of cabergoline, therefore the use of an aromatization inhibitor.

    An overview of the regulation of prolactin secretion. Prolactin secretion is paced by a light-entrained circadian rhythm, which is modified by environmental input, with the internal milieu and reproductive stimuli affecting the inhibitory or stimulatory elements of the hypothalamic regulatory circuit. The final common pathways of the central stimulatory and inhibitory control of prolactin secretion are the neuroendocrine neurons producing prolactin inhibiting factors (PIF), such as dopamine (DA), somatostatin (SST), and gamma-aminobutyric acid (GABA), or prolactin releasing factors (PRF), such as thyrotropin releasing hormone (TRH), oxytocin (OT), and neurotensin (NT).

    PIF and PRF from the neuroendocrine neurons can be released either at the median eminence into the long portal veins or at the neurointermediate lobe, which is connected to the anterior lobe of the pituitary gland by the short portal vessels. Thus lactotrophs are regulated by blood-borne agents of central nervous system or pituitary origin (alpha-melanocyte stimulating hormone) delivered to the anterior lobe by the long or short portal veins. Lactotrophs are also influenced by PRF and PIF released from neighboring cells (paracrine regulation) or from the lactotrophs themselves (autocrine regulation).



    Direct effects of neurotransmitters, neuromodulators, and peripheral hormones on the activity of tuberoinfundibular dopaminergic system (TIDA). The inhibitory agents (left) will promote an increase of prolactin secretion as a result of diminishing TIDA activity. On the other hand, the stimulatory neurotransmitters and progesterone (right) will tend to decrease prolactin secretion as a result of increasing output of TIDA neurons.

    It should be noted, however, that many of these agents have multiple levels of action, often with opposing biological effect. Therefore, in some cases (*), effects on PRF and/or directly at the lactotrophs will prevail over the influence on TIDA activity.

    Key: 5-HT, serotonin; NE, norepinephrine; HA, histamine; EOP, endogenous opioid peptides (endorphin, enkephalin, dynorphin, nociceptin/orphanin); GAL, galanin; SST, somatostatin; CCK8, cholecystokinin-8; GABA, gamma-aminobutyric acid; NO, nitric oxide; ACh, acetylcholine; TRH, thyrotropin releasing hormone; OT, oxytocin; VP, vasopressin; VIP, vasoactive intestinal polypeptide; PACAP, pituitary adenylate cyclase-activating peptide; ANG II, angiotensin II; NT, neurotensin; NPY, neuropeptide Y; CT, calcitonin; BOM, bombesin-like peptides (gastrin-releasing peptide, neuromedin B, neuromedin C); ANP, atrial natriuretic peptides.




    Trenbolne review by Dr Scally-
    Trenbolone – A summary from the article, “Yarrow JF, McCoy SC, Borst SE. Tissue selectivity and potential clinical applications of trenbolone (17[beta]-hydroxyestra-4,9,11-trien-3-one): A potent anabolic steroid with reduced androgenic and estrogenic activity. Steroids;In Press, Accepted Manuscript.”

    Androgens exert both genomic and rapid non-genomic actions. The genomic actions primarily occur following classic androgen receptor (AR) mediated signaling pathways. The non-genomic actions are mediated by androgen interaction with cell surface G-protein coupled receptors. Testosterone dose-dependently augments skeletal muscle mass and bone mineral density (BMD), reduces adiposity, and elevates red blood cell production (erythropoiesis) in men either directly, via AR activation, or indirectly, via AR and estradiol receptor (ER) activation, following its conversion to dihydrotestosterone (DHT) and estradiol (E2), respectively.

    Many of the side-effects associated with supraphysiological testosterone administration appear to be primarily mediated by the more potent testosterone metabolites, DHT and E2. The metabolism and the biological effects of testosterone are influenced by the tissue-specific localization and expression of the 5alpha reductase isoenzymes and the aromatase enzyme. These considerations have led to the development of selective androgen receptor modulators (SARM), steroidal and non-steroidal, aimed at inducing anabolic effects in skeletal muscle and bone without inducing adverse effects.

    17β –TBOH (trenbolone) has a low oral bioavailability (not methylated at the 17α position), it is not a substrate for 5α reductase and may not be a substrate for aromatase. The toxicity of 17β –TBOH has not been scientifically studied in humans, but anecdotally has been reported to have a low potential for liver toxicity because this drug is generally administered intramuscularly.

    The metabolism of 17β –TBOH differs from that of testosterone because 17β –TBOH is neither 5α reducible nor aromatizable. The primary metabolites of 17β –TBOH are the less potent androgens 17α –TBOH and Trendione (TBO) in humans. Due to the reduced potency of its metabolites, 17β –TBOH appears to induce fewer systemic and tissue-specific androgenic and estrogenic side-effects than testosterone.

    Some variation in the in vivo metabolism of 17β –TBOH exists among mammalian species, but the primary metabolites are 17β-hydroxy- and 17- oxo- metabolites of trenbolone in rodents or 17α-hydroxy- metabolites of trenbolone in ruminants (various hoofed, even-toed, usually horned mammals of the suborder Ruminantia, such as cattle, sheep, goats, deer, and giraffes, characteristically having a stomach divided into four compartments and chewing a cud consisting of regurgitated, partially digested food).

    In humans, ingested 6,7-3H labeled 17β –TBOH is primarily excreted intact, as 17β –TBOH, as the 17α epimer (epitrenbolone; 17α –TBOH ) or as trendione (TBO). Several yet to be identified polar metabolites of 17β –TBOH have also been detected in human urine. 17β –TBOH has a greater affinity for the AR than any of its primary metabolites, suggesting that biotransformation of 17β –TBOH reduces the biological activity of this steroid. [Schanzer W. Metabolism of anabolic androgenic steroids. Clin Chem 1996;42(7):1001-20. Link: http://www.clinchem.org/cgi/reprint/42/7/1001.pdf ]

    17β –TBOH-acetate (17β-acetoxyestra-4,9,11-trien-3-one) is a highly potent anabolic androgenic steroid which is primarily used legally as a growth promoting agent in domestic livestock production either alone, as Finaplix or in combination with E2, as Revalor, or E2-benzoate, as Synovex. Following administration, 17β –TBOH-acetate is rapidly converted to the biologically active steroid 17β –TBOH.

    5α Reductase: Despite its structural similarities to testosterone, 17β –TBOH does not undergo 5α reduction due to the presence of a 3-oxotriene structure, which prevents A ring reduction. 17β –TBOH undergoes biotransformation to less biologically active androgens, similar to other anabolic androgenic steroids, such as 19-nortestosterone.

    17β –TBOH administration has been shown to reduce prostate mass in growing male rodents when compared with control animals. 17β –TBOH exerts less pronounced effects than testosterone in androgen-sensitive tissues which express the 5α reductase enzyme including the prostate and accessory sex-organs, despite the fact that 17β –TBOH binds to the human AR, along with ARs of various model species, with approximately three times the affinity of testosterone.

    17β –TBOH remains highly anabolic, evidenced by equal or greater growth in the levator ani skeletal muscle (an androgen responsive tissue which lacks the 5α reductase enzymes), compared to testosterone. Reports indicate that 17β –TBOH produces a ratio of anabolic/androgenic effects that may be favorable compared to the effects of testosterone.

    Aromatase: 17β –TBOH and other C19 norandrogens are reported to not be substrates for the aromatase enzyme and to be relatively non-estrogenic; although some debate exists regarding 19-nortestosterone to undergo aromatization and induce estrogenic effects. In vitro bioassays and cell culture experiments demonstrate that 17β – TBOH and its metabolites have a very low binding affinity for ERs and have low estrogenic activity with approximately 20% of the efficacy of E2. Reports also suggest that 17β – TBOH reduces serum E2 concentrations in vivo and exerts a variety of anti-estrogenic effects, perhaps through hypothalamic feedback inhibition of the production of testosterone (a substrate necessary for endogenous E2 biosynthesis).

    Body Growth/Skeletal Muscle: Trenbolone, 17β –TBOH, a potent synthetic testosterone analogue, promotes gains in skeletal muscle mass and BMD and reduces adiposity in various model species. The use of 17β – TBOH in athletics suggests that this steroid is capable of producing potent anabolic effects in muscle.

    The administration of 17β –TBOH or its acetate ester enhance total body growth and skeletal muscle mass in various rodent and livestock models when administered alone or when administered in combination with E2. Several studies have reported that administration of 17β –TBOH in combination with E2 results in greater body growth and skeletal muscle mass than either steroid alone; indicating that E2 enhances the anabolic effects of 17β –TBOH.

    The presence of E2 is not required for 17β –TBOH to augment skeletal muscle mass as demonstrated in rodent models which experience significant growth of the levator ani muscle and other skeletal muscles following 17β –TBOH administration, despite lacking the primary source of endogenous E2.

    5α reduction of testosterone is not required for skeletal muscle maintenance in hypogonadal animals or humans. E2 administration has been shown to protect against loss of muscle strength in ovariectomized female rodents suggesting that aromatization might contribute to the effects of testosterone on skeletal muscle in males.

    The anabolic responses appear to be related to the direct activation of tissue-specific AR mediated signaling pathways, alterations in endogenous growth factors, and reductions in glucocorticoid activity.

    Human myonuclei are approximately 50% AR positive and ruminants are highly sensitive to androgen induced myotropic stimuli due to high concentrations of ARs in bovine skeletal muscle and skeletal muscle satellite cells. The androgen sensitive levator ani muscle in rodents contains approximately 74% AR positive myonuclei and experiences robust atrophic responses to castration and hypertrophic responses to androgen administration.

    It is suspected that 17β –TBOH exerts direct anabolic effects on skeletal muscle primarily via AR activation and associated nuclear translocation and transcription or via modulation of the Wnt/β-catenin pathway, similar to other androgens. In vitro evidence indicates that 17β –TBOH induces translocation of human ARs to the nucleus in a dose-dependent manner and induces gene transcription to at least the same extent as DHT. 17β –TBOH treatment of cultured bovine satellite cells upregulates AR mRNA expression.

    17β –TBOH may induce anabolic effects via mechanisms associated with alterations in endogenous growth factor concentrations or the responsiveness of skeletal muscle to such growth factors. 17β –TBOH alone or in combination with 17β –E2 upregulates insulin -like growth factor (IGF-1) mRNA in a variety of tissues. The upregulation of IGF-1 mRNA translates into increased serum IGF-1 in 17β –TBOH treated animals. It seems likely that increased growth factor expression resulting from 17β –TBOH administration is one mechanism underlying the anabolic responses to this steroid in skeletal muscle, especially considering that binding of IGF-1 to the type 1 IGF receptor is required for proliferation of satellite cells.

    17β –TBOH may also preserve or increase lean mass by reducing via anti-catabolic effects associated with reductions in endogenous glucocorticoid activity or with the suppression of amino acid degradation within the liver. 17β –TBOH administration has been shown to reduce circulating corticosterone concentrations in rodents and resting cortisol in cattle. Evidence indicates that 17β –TBOH works in the adrenals to suppress adrenocorticotropic hormone (ACTH)-stimulated cortisol synthesis and to suppress cortisol release.

    17β –TBOH has been shown to reduce the ability of cortisol to bind to skeletal muscle glucocorticoid receptors (GR) and to down regulate skeletal muscle GR expression. The multiple anti-glucocorticoid actions induced by 17β –TBOH explain, in part, the 17β –TBOH-mediated increase in total body nitrogen retention and the reductions in total and myofibrillar protein degradation in several species. As a result of its anti-glucocorticoid actions, 17β –TBOH produces a more robust inhibition of protein degradation than does testosterone, which only slightly reduces protein degradation while increasing protein synthesis.

    Fat Mass: 17β –TBOH administration alone or in combination with E2 also reduces subcutaneous fat, intramuscular fat, and muscle marbling (a gross measurement of intramuscular fat content), along with other stores of body fat in various livestock species. 17β – TBOH-enanthate administration reduces retroperitoneal fat mass, perirenal fat mass, and perhaps other fat depots, in male rodents in a dose-dependent manner. The lipolytic effects of 17β –TBOH-enanthate appear even more potent than that of supraphysiological testosterone-enanthate.

    HPTA: Disruptions of the HPG axis, including reductions in serum luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone, DHT, and E2 have been observed in a variety of species following 17β –TBOH exposure. Indirect evidence indicates disruptions of the HPG axis are present in livestock which experience reduced testicular circumference and weight and delayed puberty following administration of 17β –TBOH.

    Erythropoiesis: Testosterone administration results in dose-dependent increases in both hematocrit and hemoglobin. The aromatization of testosterone does not appear to be required for erythropoiesis as administration of DHT (a non-aromatizable endogenous androgen) augments erythropoiesis in men, while exogenous testosterone, but not E2 administration, increases hematocrit in aromatase deficient men. The 5α reduction of testosterone may not be required for erythropoiesis as high-dose testosterone administration in combination with finasteride increases hematocrit and hemoglobin concentrations in hypogonadal men to the same extent as testosterone alone, despite a nearly 65% lower serum DHT concentrations in the finasteride group. The conclusion from these studies is androgens directly elevate erythropoiesis via AR-mediated mechanisms. 17β –TBOH increases hemoglobin concentrations in orchiectomized male rodents in a dose-dependent manner and to a greater extent than supraphysiological testosterone, even though circulating DHT is suppressed by over 50% following 17β –TBOH administration

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    Thanks mate.

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    so based off the articles, its safe to say, that adding test to a deca cycle(without the use of an AI) will actually make the progesterone sides worse?

    awesome research above, thanks!

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    Quote Originally Posted by D7M View Post
    Yah, I don't know why people are giving you a hard time.

    How do you know it's a prolactin problem? Sounds like an elevated Estrogen problem to me.

    I'd start using the stane at 10mg EOD and see how that works.

    Here's a good read for you: http://forums.steroid.com/showthread...d-gynecomastia
    Awesome link, great read...

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    Quote Originally Posted by 5x10 View Post
    so based off the articles, its safe to say, that adding test to a deca cycle(without the use of an AI) will actually make the progesterone sides worse?

    awesome research above, thanks!
    Use an AI and keep a dopamine agonist on hand IN CASE prolactin is a problem.

    F*ck progesterone, its not a problem IMHO when estrogen is controlled + Tamoxifen or a SERM can address that problem.

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    Sorry for bringing up a dead thread, but my internet was out for a few days. Great read. Very interesting. So, what I gathered from that is that an AI is more-so a preventative precaution rather than a fix if the problem is already there, correct? Also, I don't understand why prolactin can be a problem in a compound that doesn't aromatize (or does so very minimally) like tren if there is no correlation between 19-nor's and prolactin levels other than estrogen. Did I miss that explanation in the reading?

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    bump

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    Thanks for the bump,

    Im actually on test and deca now. Ive been running 12.5 of Aromasin since day one but added caber .5 every 3.5. days when I added deca.

    From this im getting that i can stop the caber since ive been on an AI and kept estrogen at bay?

    Also what sides would i get from high prolactin if i did decide to stop the caber... Just so i would know when to start again?

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    hey guys was just wondering if anyone knows the conversions for miu/l to ng/ml need 147 miu's to ng/mls
    its for prolactin im aussie an thats what they measured bloods in..thanks
    Last edited by shorty09; 04-18-2012 at 09:53 PM.

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    Bumping this again since its a great discussion

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