Progesterone and Prolactin
- 04-23-2009, 01:48 PM
As I stated earlier in the thread, I was one of the first to put the idea out there that progesterone receptor stimulation may be causing gyno. It was only later that I realized that this is incorrect. Breast growth in pregnancy is probably not a good model for gynecomastia because there are so many hormonal changes going on simultaneously. Prolactin is not a growth factor in the breast and progesterone not only decrease prolactin but also decreases estrogen receptor expression. This is further driven home by the fact that the progesterone antagonist, mifepristone, actually results in gynecomastia. You don't have to search now and this shouldn't be some kind of contest. I have searched extensively on this topic over the years and I am very well-versed in the body of knowledge on the subject but you never know, you may pick a set of search terms that turns up something I haven't.
- 04-23-2009, 01:50 PM
- 04-23-2009, 02:05 PM
04-23-2009, 02:31 PM
04-23-2009, 02:38 PM
04-23-2009, 02:42 PM
04-23-2009, 02:48 PM
04-23-2009, 02:54 PM
04-23-2009, 03:12 PM
04-23-2009, 03:22 PM
2. I have never seen any on-cycle form bloodwork.. How do we even know to what degree it is effecting E2?
3. I am glad to hear you have never gotten gyno symptoms, but since you never had them before TD Form, is it possible you are one of the few to be pretty resilient to gyno?
I can personally say i have ran 500mg test/300mg deca, and 750mg(think i actually touched 1k at one point) test/400mg deca, no AI, or anything to combat estro, and didn't have any gyno symptoms.. Does that mean everyone will have that experience?
04-23-2009, 03:30 PM
04-23-2009, 03:44 PM
2) http://cat.inist.fr/?aModele=afficheN&cpsidt=1525645 (sort of, in a round-about way; abstract seems to conclude presence of elevated E and PR receptors contributes to severity of condition)
Now here's the thing. All of the above and every other study I could find (of the few out there) also had estrogen linked in in some manner. Also, some of the above are admittedly tenuous links. But the bottom line seems to be estrogen and progesterone work synergistically when it comes to breast growth. IOW, I agree with you that estrogen is the key... sort of. I have concluded that elevated progesterone itself cannot cause gyno, but it can (in a round-about way) in the presence of enough estrogen. I don't think you disagree, seeing as how estrogen is still the key, so here's where I'm going with this.
We've been talking about the Tren compounds here; from what I understand they have an incredible binding affinity for the progesterone receptor. My theory: 1 part of the Tren gyno issue is that the tremendous surge in progesterone can trigger gyno in the presence of normal estrogen levels. You mentioned the breakdwon of SHBG and how it would increase circulating E; this would only serve to exacerbate the problem. So yes, E is the key, but saying progesterone has no role is misleading IMO.
Now on to prolactin. You said this earlier in the thread: "There is no evidence that controlling prolactin will prevent or treat gynecomastia. Many of the issues that are being attributed to prolactin can be explained through other mechanisms."
If this is true please explain why the first 2 links below indicate prolactin is a growth factor for breast enlargement, while the 3rd and 4th, which provide an overview of the symptoms of clinical prolactinoma, list gynecomastia as a symptom (albeit "uncommonly" on the Mayo Clinic link), and the last 3 all list gyno as a symptom of simple hyperprolactinemia.
Finally, here's a quote from MedicineNet.com by author Dr. Robert Ferry Jr., MD and his Medical Editor, Dr. Ruchi Mathur, MD, FRCP(C).
What is the normal function of prolactin?
"Prolactin stimulates the breast tissues to enlarge during pregnancy."
I flat-out don't buy the fact the elevated prolactin can't cause gyno. I've run across enough evidence, both anecdotal and not, to not believe otherwise. Perhaps there is a relatiuonship similar to progesterone with E in that eswtrogen is needed in some degree to cause actual breast growth - I don't know. My question from earlier, about whether or not binding the PR receptor could affect prolactin levels, would fit perfectly if it were true. (Tren binding PR = rise in prolactin = part 2 of potential gyno (along with normal E and E+PR issues). Alas, you posted evidence to the contrary - thanks by the way. Now I'm kind of back in the same place I was before: I think prolactin can stimulate gyno (and if not classical gynecomastia in all cases, then certainly nipple discharge, and who wants that either), but I can't explain why prolactin would go up so high on a designer Tren cycle.
I rambled a bit here, hope this all makes sense. Hoping you can respond here, maybe there's something I'm missing.
04-23-2009, 03:45 PM
How can you even say that when you don't even know what it is doing to your estradiol?
I have yet to see any bloodwork with Form. Please show me any labs you have found over the years..
Lastly what ph's have you run, while using TD form?
I am not knocking the stuff, as i have used it a few times myself, just to be clear.
04-23-2009, 03:52 PM
04-23-2009, 03:55 PM
04-23-2009, 04:00 PM
^ that's similar to what Bill Roberts has mentioned... tren has a binding affinity for PRs but does not activate them.
Great thread. Appreciate everybody's input.
04-23-2009, 04:18 PM
"prohormone that converts to 9-unsaturated nandrolone's. 4,9-diene-19-nor steroids are discussed as a group in the two studies I reference often by Ojasoo and Raynaud, and compared against 4-ene-19-nor and 4,9,11-trien-19-nor steroids. By comparison they are almost as potent progestagenically as the trienes, but their androgenic component is actually lower than that of the 4-ene steroids. That makes them, for a dose that yields equal anabolic effect, considerably more progestagenic and supressive. Its mostly crap. If you want I can probably post some RBA data when I get home."
He would seem to disagree with you.
Secondly, part of what I was saying was that perhaps "Tren gyno" may not necessarily need elevated estrogen to induce it. However, if what you are saying about the 19-nor compound only weakly binding is true... I'm back at square one.
04-23-2009, 06:52 PM
The Ojasoo Raynaud paper I am most familiar with(J Steroid Biochem. 1987;27(1-3):255-69) shows dienolone to have an androgen receptor binding affinity equal to tren (and both significantly greater than testosterone) but with 1/6th the binding affinity of the progesterone receptor as trenbolone. I have seen him refer to a 1984 paper but the only paper they published in 1984 (Clin Neuropharmacol. 1984;7(4):325-31.) does not mention dienolone at all.
Another paper (J Comput Aided Mol Des. 1992 Dec;6(6):569-81.) confirms this level of progesterone receptor affinity but shows trenbolone to have much greater AR affintiy that the ojasoo raynaud paper. In this paper, dienolone still has much higher AR activity than testosterone.
Also, as PP pointed out earlier, binding affinity isn't everything. However, I am not aware of any functional assyas published for dienolone that show the level of activity at the progesterone receptor. However, in my opinion it seems very likely that it is not acting as a full agonist.
04-23-2009, 09:12 PM
04-23-2009, 09:37 PM
Try READING what i wrote.
2. I have never seen any on-cycle form bloodwork.. How do we even know to what degree it is effecting E2?I said i have yet to see any blood work..I didn't say it doesn't exist, or i looked specifically for it.. I asked you to post what you have found, since you are the self appointed Form. guru, and clearly have seen bloodwork.. I just want to see bloodwork on an CYCLE, not on some women with breast cancer. I would love to see the impact it has on E2, at certain doses.I have yet to see any bloodwork with Form. Please show me any labs you have found over the years..
Discredit you? When did i ever say form shouldn't be used on cycle? NEVER, said that. I asked you to quantify your claims.. You talk about not driving E2 to low, and then said your E2 is in good range, and i asked what your numbers were, is that too much to ask, when you make claims like that?
I asked perfectly valid questions, per the info you posted. It seems like you got butt hurt, and felt my questions were some sort of attack, rather then just answering the questions.
I never said anything against using an AI on cycle, at all..lol We are not fighting on opposing sides here, I just asked you some simple questions, and rather then answer them, you go on some tangent..
Seems like you are on the defensive.. Seriously, get off the rag dude... It is obvious you can't carry on a mature discussion, without getting defensive, and acting like people are against you. We are all trying to learn here, the more info the better..
04-23-2009, 09:44 PM
04-23-2009, 09:52 PM
I am not against FORM at all, and stated i have used it myself. I just wish i knew more about it in regards to on cycle bloodwork.. From looking at all the HRT threads with people using Adex, we can get an idea of what doses to start at/use, in order to get estradiol where we want it, without squashing it.
04-23-2009, 09:57 PM
maybe a good on cycle mix would be DIM/I3C mix ED with 6bromo EOD?
keep estradiol low aswell as the freed up estrone sulfate hopefully more undercontrol?
04-24-2009, 08:04 AM
04-24-2009, 12:18 PM
04-24-2009, 12:23 PM
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.
04-24-2009, 12:59 PM
Back to the topic at hand: if what you say is true, then I am at a loss to explain why the Tren designers can give prolactin-related sides such as leaky nips and (possibly) gyno. And I am still at a loss to explain why prolactin becomes elevated when using these compounds. Despite what you've posted, I do not believe elevated or even rebound estrogen alone can cause lactation in men, despite the E - prolactin relationship.
Great thread, but the ditch is getting deeper.
04-24-2009, 01:35 PM
Both need to be controlled, as supressing prolactin alone still leaves estrogenic effects to be dealt with. While I agree prolactin is a contributing growth factor, when using an aromatizing compound (which I suspect the Tren designers to be, despite manufacturer claims), I'd still go AI. HDL is likely going to be in the ****ter anyways.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.
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?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.
Also - I can't really find any info on dienolone itself, does anybody have Vida #s on it?
04-24-2009, 01:45 PM
04-24-2009, 02:08 PM
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).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.
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