^^ ROFL you are delusional.. and you need a course in basic mathematics. The members can decide. Other than you and your clown car friends, I'm sure all of them understand ratios.
MESO-Rx
Anabolic Steroids
Myth Buster - Prolactin Tren/Deca
- Thread starter Sworder
- Start date
Is that jealousy in your tone? Would you like an invitation to the clown car? Just come clean about your affiliation with superior peptides......
Sworder
Member
You really don't understand that just because something attaches to the PR doesn't mean it acts the same as progesterone. That's the expression I was talking about and you still don't understand it.. To make it simple for you, but what effect did the compounds have? Can't find it? Guess a little? Correlate that to this topic? You can't..
Jimmyinkedup
New Member
This Should Cover It, By the late Nandi:
PROGESTERONE AND PROLACTIN INDUCED GYNECOMASTIA
Before delving into this subject, I’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’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: “Prolactinomas that are sufficiently large to cause gynecomastia do so as a result of impairment of gonadotropin secretion and secondary hypogonadism”. (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.
PROGESTERONE AND PROLACTIN INDUCED GYNECOMASTIA
Before delving into this subject, I’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’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: “Prolactinomas that are sufficiently large to cause gynecomastia do so as a result of impairment of gonadotropin secretion and secondary hypogonadism”. (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.
Ostrich
New Member
Any updates regarding this myth/broscience?
"PROGESTERONE AND prolactin INDUCED GYNECOMASTIA "
"omg I'm lactating when I ran deca/tren and when I dropped them everything went back normal". No bloods, no analyze on the compound and no ai......everything UG.
"PROGESTERONE AND prolactin INDUCED GYNECOMASTIA "
"omg I'm lactating when I ran deca/tren and when I dropped them everything went back normal". No bloods, no analyze on the compound and no ai......everything UG.
Any updates regarding this myth/broscience?
"PROGESTERONE AND prolactin INDUCED GYNECOMASTIA "
"omg I'm lactating when I ran deca/tren and when I dropped them everything went back normal". No bloods, no analyze on the compound and no ai......everything UG.
Yes, there's no such thing as prolactin gyno
Ostrich
New Member
Yes I know doc its sad all the myths keep circulating everywhere.
But there have been plenty of guys that lactate from 19-nors, and have it cleared up with the use of caber
Lactation is not gynecomastia.
jackthegripper2
Member
Never for gyro. But am sure as hell the prolactin build up from 19nor's turned me into a diff. Person. Cabers a must for me as well
I had lactation on normal prolactin level. My e2 were like 133. Fixed e2 level lactation stopped. No caber needed.
instant.muscle
New Member
I've run deca and tren quite a few times and never got gyno.
Maybe i'm just lucky.
BTW deca + tren = amazing.
Maybe i'm just lucky.
BTW deca + tren = amazing.
johntt44
Member
I cycled 250mg test Cyp and 700mg tren ace a week. Kept my e2 in check with an ai and had no prolactin/lactation/gyno issues.
I must say, I just read this from the very first post. Even though there was obvious disagreeing theories, I have learned more from this thread than any other thread, or book I have read. Thank you to everyone who invested the time to "debate" this topic.
Armani212
New Member
How do you keep your E2 in check? my left gland is starting to feel sore, it barley looks even puffy but i can tell something is going on... 250 Test prop, 400mg Tren E and 250mg Tren Ace. I will be replacing one of the Trens with Primobolan next week plus 80mg of Anavar for the next 7 weeks.
blood work needs to be done to check your E2. It would benefit you to find the proper bllod work thread and read it fully to learn what blood work to order.
Dude, you take 650 mg a week of tren and now you ask how to keep e2 in check? GTFO
johntt44
Member
I had been on that test dosage for 2yrs, so I knew how my body reacted. I took .5mg anastrazole every 3 days. Then I just added 1 thing, tren. Next cycle will be equal test/tren. I don't convert to estrogen much anyway. I did have the caber on hand just in case but didnt need it. Just add one thing at a time to see how you react and be conservative. Theres no reason to have bad sides if you're careful.
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