Sorry -- trying to respond to everything. Of course keeping doses as low as needed to have an effect will help. Other than that, I would use nolvadex. Nolvadex reduces estrogen receptor stimulation, keeps SHBG levels up and helps with blood lipids a little.
I think the dangers of nolva are largely overstated -- mostly by people trying to sell something as a dietary supplement for on or post-cycle therapy. That being said, the risk of adverse events generally goes up in frequency as the dose and duration are increased. I would not use Nolva for 20 weeks -- I would also be cautious about combining it with oral AAS since nolva can cause some liver tox.
I hear ya, it is hard for me to wrap my head around an article, with such scare tactics, when advertising a generally unproven, over the counter supplement to do the job of actual pharmaceuticals.
True and I am sure that nolva is being used for very long periods of time by some users. I probably wouldn't run nolva at the same dose for an entire cycle and then into PCT. But then again, I tend towards more moderate doses which reduces the need for ancillaries. I think there is (perhaps rightfully so) a paranoia about developing gynecomastia so people go overboard and throw everything but the kitchen sink at it in the hopes of warding it off. How many posts do you see with people saying "I just took my third dose of X and my nipples are tingling, itching, sore, full, puffy, leaking when i apply enough pressure to pop my nipple off"
Reducing prolactin will reduce stimulation and growth of the mammary gland. (whether it’s PR or ER mediated growth) This is why I advice vitex while on cycle. Vitex also doesn’t carry the same toxic properties as Nolva.
There is simply no evidence that prolactin plays a role in gynecomastia -- i.e. the growth of breast tissue. The Williams Text of Endocrinology states and I quote "Prolactin does not play a direct role in gynecomastia" and "this conclusion is in keeping with the fact that prolactin is not a growth hormone for the breast".
There is a lot of bologni all over the boards. Somebody says something and then everyone repeats it over and over again to appear as if they know something. If gyno symptoms appear, then it may be too late. Do I recommend nolva over treating with something to reduce prolactin in the absence of elevated prolactin? yes.
Depends on how you define short and long term and how you define increased PR expression. I would actually argue that PR downregulation is not desired. Treatment with the progesterone receptor antagonist Mifepristine actually results in gynecomastia probably through the loss of the suppressive effects of progesterone receptor activation on estrogen.
That is an interesting article that you linked to. Did you see these quotes?
Yeah. And I am not telling people to not use vitex or AIs or some combination of those and whatever else you want to take that makes you feel like you are doing the best thing for you. There are risks associated with every substance you put into your body, including over the counter supps and herbs. Everybody has to weigh these risks versus the potential benefits and make an informed decision. I just have not seen any convincing evidence that progesterone or prolactin cause the symptoms of gynecomastia in the absence of elevated estrogen and if elevated estrogen is the root cause, then that is what I want to treat.
Fair statement here.
whats your opinion on running low dosed- two pumps 2xday td formestane on a tren cycle? formestane is different than most ai's as you well know.
That is pretty close. Back conversion of estrone sulfate to estradiol. The estrogen sulfate would be elevated due to decreases in SHBG that accompanies strong androgenic stimulation in the absence of estrogen. This decrease in SHBG also removes the protective effect of SHBG against breast tissue gorwth. Everyone is keen on decreasing SHBG but there are some good papers showing that SHBG actually protects against breast tissue growth beyond its ability to sequestor estrogens.
I am not sure if suicidal AIs are better or worse when it comes down to it. The end result is generally the same, too low levels of estrogen, horrible HDL levels and potential rebound gynecomastia.
but by it boosting igf-1 secretion, upregulating hpta and decreasing shbg doesn't this make formestane different than most other suicide ai's. and i am talking low dosed.
Maybe but it makes it similar to some competitive AI's
i have to disagree, i feel adding td formestane to my cycles is the best decision ive made regarding ph cycles. ive done propadrol before and many different cycles with formestane included and have no signs of any gyno/prolatin issues. i guess results speak for themselves. nice information though, very interesting.
To each his own. If the reduced HDL levels don't bother you and you don't sufer from rebound gyno then do what works for you.
well my lipids are just fine, and looking at my join date i guess ive been doing ph cycles for about 3 years now. not that i don't value your information, just it seems inconclusive, imo. i see all these guys with all these symptoms that i don't have, and ive ran a lot more cycles than most of them. the difference is td formestane-i swear by the stuff and it's treated me very well. my bro-science theory is keep estrogen low not dead on cycle and prevent most of these symptoms if not all. low dosed td formestane for the win.
What is your HDL post cycle if you don't mind sharing?
i don't keep my medical history on hand but i get tested for liver values and lipids 2 times a year, my doc has never raised a concern so i assume they are within normal range- i have been tested while on cycle, post cycle and off cycle and never once have the varied enough for my doc to be concerned. i have test and estrogen tested once a year-all my insurance will pay for and again no concern by my doc-these tests have been done for last 7 years and i have been doing ph's for 3 of them. never had gyno and i use td formestane to keep it that way. sorry if i seem abrassive but i really feel the formestane is why i have none of the symptoms others seem to be having.
1. Just because your Dr didn't express concern doesn't mean you are in optimal range. My HDL was in the 20's and my dr didn't say ****, as my total choles, and trigs were fine.
look, i never claimed to have science or medical background, but since this is a forum for sharing our experiences i shared mine. all i can say is ive been using ph's for awhile now and i have no symtoms others are reporting, the difference imo is the formestane on cycle. i did not stumble upon formestane, there is a ton of research on it and it has been used for decades for cycles like you have mentioned. take it for what it's worth but i believe in the stuff and will never run a cycle without it.
Progesterone:
I understand, but you are giving no info, while making claims like"my bro-science theory is keep estrogen low not dead on cycle and prevent most of these symptoms if not all. low dosed td formestane for the win"
Yeah, I knew these latter ones, was kind of hoping for info on PR activation. Very interesting that progesterone reduces prolactin. My theory still has one hole (see above post).
Firstly, only trenbolone is a strong PR binder, dienolone and nandrolone are not -- they bind but are actually quite weak. The rest of what you wrote (I can address more fully in a little while -- I am heading out at the moment) is more or less correct (there are some things that I will take issue with later) but the whole ball of wax can be summed up by saying that in the absence of elevated estrogen, prolactin and progesterone will not cause gynecomastia so I go back to my original statement that if you control estrogen, then you will limit gyno. If prolactin and or gyno cannot cause gyno in the absence of elevated estrogen then they are not the root cause.
Interesting, thanks seth. However, I'm sure everyone here has seen this post from "guru" Big Cat regarding 19-Norandrosta-4,9-diene-3,17-dione (the active in the Tren designers):
ok, first of all if your hdl were that low and your doctor didn't say anything i would find a new doctor ASAP. second how can you say you can't find find any blood work on how it effects estradiol? my GOD man, it was a prescription anti-estrogen breast cancer drug. it was replaced by 2nd generation drugs like nolvadex becuase of poor bio-availability not because it didn't work in iv form. transdermal delivery solved this problem. do some research, it's all over the place, i suggest something called google. btw don't take my word on it, form is recommended for on cycle use by DR.D, DINOII, AND ARTUR L. REA WHO WROTE THE DEFINATIVE ARTICLE ON IT. IT SEEMS APPARENT YOU POSTED TO DISCREDIT ME, BUT I AM NOT ALONE IN ADVOCATING THE USE OF TRANSDERMAL FORM ON CYCLE.
Big-T, i actually had some respect for you, but you're sounding like a big fat cry-baby..lol Seems like the form isn't lowering your estrogen enough..
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.
ok, i admit to being a little defensive. i am on a xtren/formestane cycle right now. just know what my results have been like. as for being a formestane guru-i found something that is more effective by far than the higher priced stuff or 'hard to get stuff chems', and just passing along how great it's results have been for me.
I just hope you understand, i never got an attitude with you, or had any intention of arguing, and was genuinely asking relevant questions, so we can all get a better idea of what is happening with on cycle form use.. I am not doubting your experiences at all, but trying to get as much of the picture as i can.. Again, the more info we have the better.
sorry, between working 12's and the tren kicking in, i have been a little on edge.
Im still standing by my recommendation of vitex and possibly an AI for the control of progestin based gyno. (perhaps even in cases of non-progestin based gyno)
Very interesting. I never was foolish enough to take everything that guy said as gospel truth, but he did seem to know his stuff and everyone else considered him "the" authority. This is the first time I've ever seen anyone directly contradict his conclusion. You just never know with these "gurus"; after all, how do we know what their background is and how knowledgable they really are? (Hmmm, same could be said for you Seth. No offense, I just don't know much about you)
Exactly.
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 shitter anyways. :worried:
Eric, question for you: the Tren designers, of which 1-T Tren is one, all obviously market as being very similar to trenbolone. Yet the chemical structure of the end hormone after enzymatic conversion may (from what I understand) actually be closer to nandrolone. Any insight on this?
If you are referring to Big Cat, you're not alone. He's a smart guy, but sometimes seems to either not think out of the box or have some agenda against certain steroids (particularly 2nd-Gen. OTC ones). I've watched other "gurus" (Patrick Arnold, Dr. D, etc.) rip apart his "theories" on BB.com over the years. I have not considered him a guru or "the final word" on endocrine physiology for years. He loves to quote Vida text (which is a very valuable resource), but doesn't seem to venture too far for other sources.
Elevated E2 causes the prolactin receptors to become more sensitive, therefor possibly not requiring a rise in serum prolactin to cause a "prolactin effect." Is that enough to cause lactation in a human male? I don't know, but I don't discount it either.
I was, and I agree. Although did not witness the bb.com shredding as I avoid that board usually. Only reason I referenced him was b/c that quote on the Tren compounds is parroted on the boards as gospel truth with no one contradiciting it, so much so that I more or less believed it, as much for a lack of contradictory evidence as anything else.
I'll buy that, E and PRO have a converse relationship - but what's causing elevated E2? Just regular suppression + SHBG offset? Wouldn't think this would be enough. Or... if the compound is not binding the progesterone receptor (or not very strongly), are we looking at simple aromatization issues here? Everything could be avoided by simply adding an AI? Sounds too easy, although I don't think I've seen anyone run a Tren designer with an AI (although I admit I haven't searched).