Tren & Progesterone Receptor Activation

I can’t remember what thread it was on that Bill was asking for a ref that showed PR activation with Tren…I was reading a piece of marketing for a new product from another company that is very similar in structure to Tren (almost the same molecule and doesn’t even require reduction to get to an anabolic so I assume it will take about 10 mins to get banned) but they did a litttle bio on REAL trenbolone which referenced the fact that Tren has a strong affinity for and will activiate the progesterone receptor…the ref they listed is below…

  1. Characterisation of the affinity of different anabolics and synthetic hormones to the human androgen receptor, human sex hormone binding globulin and to the bovine progestin receptor.
    Bauer, Meyer et al.
    Acta Pathol Microbiol Imunol Scand Suppl 108 (2000) 838-46

Thought you guys may be interested to read it.

FG

I know that I discussed the difference between having affinity, as the only thing measured, and being an agonist in the other thread.

I really just have to write something that (hopefully) would be made a sticky, so that things like this don’t just keep rising from the grave again and again and again and again and again

Sure there’s definitely a big difference, but isn’t that study (assuming it’s well done of course) at least a sort of circumstantial evidence? I mean if the data lines up with the supposed anecdotal reports then it’s at least plausible right?

I’m well aware of the huge difference between having an affinity for simply binding to a receptor and actually being a true agonist, but people generally have so little to go off of in the way of true scholarly research when regarding AAS–because of the ethical difficulties and red tape involved in in vivo human studies–that it’s worth a “plausibility” rating at least, right? Especially if (and again I haven’t read the study itself yet) it’s well done and conforms with anecdotal evidence.

That’s like saying the fact that flutamide having high affinity for the androgen receptor is “sort of circumstantial evidence” that it has androgenic activity, or that the fact that tamoxifen and clomiphene have high affinity for the estrogen receptor in breast tissue is “sort of circumstantial evidence” that it has estrogenic activity there.

Why not instead look for a study that actually seeks to measure progestagenic activity? It’s not that it doesn’t exist – and the activity found was none.

Or why not read the previous fucking thread where all this was hashed out before, and even then hardly for the first time? :wink:

As for “confirmed with anecdotal evidence” that is no more correct and also would bear reading the previous threads.

I just gotta write a sticky: some things are just absolutely “beating your head against the wall” type things that no amount of repetition EVER succeeds in overcoming the mass of statements to be found elsewhere and therefore it is bothersome writing the same things out again, never to any lasting avail.

Not even just a couple of weeks, in this case, for example.

[quote]Bill Roberts wrote:
I know that I discussed the difference between having affinity, as the only thing measured, and being an agonist in the other thread.

I really just have to write something that (hopefully) would be made a sticky, so that things like this don’t just keep rising from the grave again and again and again and again and again[/quote]

Please Please do! :slight_smile:

Thanks! I will try to get started on it.

[quote] Brook wrote:
Bill Roberts wrote:
I know that I discussed the difference between having affinity, as the only thing measured, and being an agonist in the other thread.

I really just have to write something that (hopefully) would be made a sticky, so that things like this don’t just keep rising from the grave again and again and again and again and again

Please Please do! :)[/quote]

2x that Bill! If it is any motivation, just know that while some of us on here never learn anything, I know myself and plenty of other people who actually appreciate and apply what knowledge you offer. I quote you in the gym more than I quote Ronnie or Arnold! lol and thats saying something!! Though I dont think you cant beat Ronnies “LIGHT WEIGHT BABY!” you should try!! ; )

[quote]Bill Roberts wrote:
Thanks! I will try to get started on it.[/quote]

Awesome

ok, i see your point, sorry, i only very briefly read your original argument and so i was confused about the differentiation between afinity and activation. I thought you were just looking for a ref for affinity.

I see your point about Nolva…very high affinity with breast tissue ER but very low activation…you are asserting that Tren is similar in that the affinity with the PR is high but the activation is low making it a non-issue.

OK, i re-read the article I got the ref from and see why i posted it…they do say directly that Tren ACTIVATES the PR…here is the write up copy and pasted from the source…not saying this guy is correct Bill…just saying he said it.

Side effects

Trenbolone does have one downfall or upside, depending on how you look at it.

Trenbolone is a progestin based anabolic, which means it activates the progesterone receptor [PR]. (1) The combination of a high affinity for the androgen & progesterone receptor makes Trenbolone especially prone to cause individuals to “Hulk out” with aggression and anger. [A great thing for the gym, but a problem for the people that irritate you]

Aside from the possible emotional episodes, the PR action of Trenbolone can also stimulate gyno by directly activating the progesterone receptor [PR]. (1) This makes Trenbolone problematic when stacked with highly estrogenic compounds, since it appears that activation of the PR increases estrogen’s proliferative ability on breast tissue. (2) Therefore, to avoid gyno symptoms it is best to use Trenbolone [or related steroids] with compounds that have low estrogenic activity.

Even though Trenbolone lacks the ability to convert to DHT, it can encourage temporary hair loss because of its direct action on the androgen receptor [AR]. However, the possible hair shedding from Trenbolone could be considered less than the hair loss associated with high DHT producing compounds. [eg, testosterone]

Oh, so someone being a steroid dealer makes what they say correct then. (I assume that this is from popular steroid book author, most or all of whom have as their only qualification being steroid dealers or ex-steroid dealers.)

Do not assume that simply because someone puts a number after their statement, with a reference, that the reference must say what they are saying, or that the conclusion they draw from it is a conclusion that actually does follow.

If you are going to argue on this subject provide the actual literature statements, not what some non-scientist has to say on pharmacological matters that they claim follows from the literature. We are supposed to accept this unnamed person as authoritative? Obviously you don’t accept my statements as such, and deny the accuracy of my reports of what the literature shows: why do you or why should we accept his statements as authoritative and buy into his interpretation of the meaning of the literature?

I have already thoroughly treated this subject already. I have provided literature citations according to what they actually say, as well as responded to each literature citation anyone else has provided according to what each actually said. Obviously I completely wasted my time.

As stated before I have already treated this thoroughly. Go back and re-read. End of thread (so far as I am concerned.)

This was actually taken from the Primordial Performance site…it’s part of the marketing piece for 1-Tren…I assume they had one of their marketers grab a profile from a steroid book or maybe one of their own guys did a write up on it…i don’t know.

To be clear, I am in no way arguing with you or saying that what this guy is saying is correct…I’m simply saying that it was said and he gave that as a ref to back up what he was saying…I haven’t gone in and read the article from Pubmed or wherever…I was just sharing what I read so people could read it and critique what was being said.

I don’t think this is a waste of time because I think it is an important point of distinction and if what you are saying is correct there is a lot of parrotting of bad information going on (which I myself am guilty of).

Well the article does not say that, according to its own abstract. Only affinity was shown, not activity: as per the recent thread on the subject.

I admit to it being an idiosyncratic thing: there are a handful of things that I just find tedious and boring, while there are many other things that remain interesting and there is no problem discussing lots of times. There’s no way another person could predict what things it is that just tire me out. I guess it it is taper, tren-is-a-progestin, and SHBG as the three that stand out at the moment as being just dreadfully dull and Chinese-water-torture repetitive.

Speaking of, actually I cannot imagine how Chinese water torture could be effective. I believe I would like it. In fact, with my ex-fiancee that tended to drag me with her for clothes-shopping, many times I expressed that I wished they would install a Chinese water torture booth in the store so as to have something to do while waiting.

So I guess there just is no predicting what repetitive things a given person will find no problem at all, or just torture. Could be the reverse of what another person would guess :slight_smile:

[quote]Bill Roberts wrote:
That’s like saying the fact that flutamide having high affinity for the androgen receptor is “sort of circumstantial evidence” that it has androgenic activity, or that the fact that tamoxifen and clomiphene have high affinity for the estrogen receptor in breast tissue is “sort of circumstantial evidence” that it has estrogenic activity there.

Why not instead look for a study that actually seeks to measure progestagenic activity? It’s not that it doesn’t exist – and the activity found was none.

Or why not read the previous fucking thread where all this was hashed out before, and even then hardly for the first time? :wink:

As for “confirmed with anecdotal evidence” that is no more correct and also would bear reading the previous threads.

I just gotta write a sticky: some things are just absolutely “beating your head against the wall” type things that no amount of repetition EVER succeeds in overcoming the mass of statements to be found elsewhere and therefore it is bothersome writing the same things out again, never to any lasting avail.

Not even just a couple of weeks, in this case, for example.[/quote]

Damn. 2 am bites me in the ass again.

I didn’t look for another study because it was 2 am and I was tired/lazy/out of my mind. I searched through the last 5 pages of your posts Bill but didn’t see the old thread. I had assumed it was fairly new but I guess it wasn’t. Search function ho!

EDIT–I have either epic failed again, or the search function isn’t bringing this old thread back up. Searched a variety of terms, also included a name search for Bill. What was it FG?

EDIT 2 — was it this thread? https://www.T-Nation.com/free_online_forum/sports_training_performance_bodybuilding_gear/the_trenprogesteroneprolactin_thread

That was the most recent, yes. There was another one not very much earlier than that.

The search engine indeed does not turn up everything, unfortunately.

That one was fairly new: March 6th. However it seems that various posts that are nothing but one-liners and so forth have run up the number of threads I’ve been on so high that that winds up being page 9, which is further than I’d thought. The board does wind up listing the same threads dozens of times if dozens of OTHER people have posted as well, so that does expand the thing.

So that was unintentionally-bad advice on how to find it. I should have said just go back a couple of pages on the Steroid forum: it’s on page 3.

There was another one very recently before that, too. That was the one where I went more in depth.

It is a shame that it’s so hard to find past posts – definitely not your fault of missing something that could have been found in 30 seconds, even though it may have been within 30 days and certainly no more than 90. Probably 2 months as a guess.

You know, I think the site has completely lost the thread I’m referring to.

I know for sure when I was responding to the thread you mention I was saying to myself, “Geez, why a new thread on this, I just did this thoroughly maybe a month ago” and distinctly remembered how that thread had gone and what sorts of posts I’d made on it.

Now not even Google turns anything up. It apparently doesn’t exist anymore.

Anyway, as I had had to spend some time on that previous posts to provide the references as I did not have them at hand and certainly couldn’t give the exact citations from memory, this time around I would rather just say HOW to find these things.

At PubMed do a search for, for example,

trenbolone AND (progestin OR progestagenic OR progesterone OR prolactin) and then read every single thing! :slight_smile:

Then to be extra sure, use Google Scholar, which will be much more time consuming as various quite useless hits will come up, but when, as I was saying, stating definitely that something is not in the literature and there having been a possibility that something new, hypothetically, could have turned up, one cannot stint.

Hey guys,

I have the folowing references saved in a file:

(In response to my question as to whether it is necessary to run Test longer than Tren on ?Adding Winny? Thread March 2, 2009-03-02
http://www.T-Nation.com/free_online_forum/sports_training_performance_bodybuilding_gear/adding_winny_1?pageNo=0#2844868 )
Bill Roberts: Yes, I meant in general it is not necessary to stop trenbolone sooner than testosterone. Not for “sexual side effects” or any other reason.

(In response to my question as to whether test should be run longer than Deca)
Bill Roberts: Deca is very inhibitory due to progestagenic effect and for good recovery use should be ended well before the end of the cycle, if used at all. There seems to be a quite long-lasting effect to inhibition resulting from this mechanism.

If one doesn’t personally benefit from and need its effect on joints, the logical reason why someone would want to take a progestagenic steroid instead of other anabolic steroids not having that problem seems a real puzzler. Additionally, from the practical standpoint there’s no real reason but the above to do so, either. It is surely not necessary to outstanding results nor is it key to maximal results.

(I’m not, above, referring to possible reasons such as having a vial already and, having paid for it, wanting to use it up; or being limited in what one can get so it is a question of using or including Deca or having a really lame cycle without it. Those would be practical reasons for it.)
Dynamo Hum wrote:
Juice: Thanks for your understanding.

Bill: Thanks for sharing the knowledge gleaned from much research and real life practice.

I am a little confused in what makes Deca “very inhibitory due to progestagenic effect”, while you don’t feel Tren has the same tendancy (at least not to a degree as to warrant special treatment like running testosterone longer in a Deca cycle).

They are both progestins right?

No, trenbolone is not. Authors that have stated that it is have confused binding with being active.

Both 19-Nors.

Again, authors that are not medicinal chemists (not all of them but some) are confused on this point. While it sounds scientific, actually there is no more validity to that structural fact being applied the way that they do then there would be to arguing that they have the same number of letters in the name, or both have names ending with “olone.”

Both bind to the progesterone receptor (Tren 60% as much as progesterone itself and Deca 20% as much as Progesterone itself). On paper tren looks more inhibitory.

By this reasoning tamoxifen and clomiphene must cause gyno then: they bind to the estrogen receptor. But no, they bind but are not agonists, in breast tissue.

When actual activity has been studied in the veterinary literature, trenbolone has been found non-progestagenic.

Me: Please excuse my ignorance, but can Tren cause elevated prolactin issues for which many suggest taking cabergoline?

Bill Roberts: Absolutely zero reason to think so (other than from reading authors who claim it but had zero legitimate reason to think so.)

There is no published human data on this but the veterinary literature shows no increase in prolactin from trenbolone usage.

In practice, those injecting no-doubt-about-it trenbolone acetate, made themselves from Fina, and taking no other steroid that might cause the problem, see no issues that would be expected from increased prolactin.

Bill Roberts: And trenbolone does not increase estrogen. So if an AI is needed it will not be on account of the trenbolone.

Error in this area, if it occurs, tends to be in the opposite direction: using trenbolone without an aromatizing steroid and without HCG, and thus driving estrogen too low.

Bill Roberts on Tren concentration: That said, I don’t care for 100 mg/mL trenbolone acetate myself. The most concentrated preparation I’ve liked was 75 mg/mL. However some seem happy with 100 mg/mL formulations. Personally, it seems to me that higher concentration formulations are much more prone to “tren cough” than 50 mg/mL formulations are.
2nd post in this thread 7:35 pm: http://www.T-Nation.com/free_online_forum/sports_training_performance_bodybuilding_gear/special_brew_question_to_bill_r?pageNo=0

Bill Roberts on Progerterone/prolactin sides with Tren: March 6 2009 - http://www.T-Nation.com/free_online_forum/sports_training_performance_bodybuilding_gear/the_trenprogesteroneprolactin_thread?id=2854761&pageNo=1
More precisely, I don’t know that it was NPP. But rather expect it was some non-trenbolone substance.

I do know that various places and persons that claim that references exist showing trenbolone is a progestin and/or that trenbolone increases prolactin are misinterprations, or are assertions that don’t seem to have anything behind them, and are contradictory to studies that do exist.

I know that no one who has consulted with me on their steroid cycles and was definitely using genuine trenbolone ever suffered this problem. That doesn’t prove it could never happen to anyone but is reason for me to doubt it, and certainly reason to be sure it is at least not common.

Particularly given that black market trenbolone is absolutely notorious for frequently being counterfeit.

And for all I know, third-hand “bro knowledge” about someone who definitely used pellets and got gyno may be missing the information of what else was taken, or maybe the pellets were Finaplix-S. (Considering all the mistakes that are made by steroid users, including many long time users, it seems very unlikely to me that no one has ever mistakenly bought S instead of H.)

A final minor point: Trenbolone has been around a long time, in the form of Parabolan and Finaject prior to the days of common counterfeiting. Why is this problem new to the age of frequent counterfeiting and non-pharmaceutical/non-veterinary sources of trenbolone, then?

Should have been happening all along if trenbolone were the culprit. Not the major point, but a minor one that may connect for someone.

The above is the best I can summarize it, I think.

Bill Roberts: March 6 2009 9:28 pm
http://www.T-Nation.com/free_online_forum/sports_training_performance_bodybuilding_gear/special_brew_question_to_bill_r?pageNo=0#2855988
I would make the tren-E at say 100 mg/mL. (TA I prefer less concentrated, and I have not made tren-E, but it would be more readily soluble.

Also from same thread a few posts later: No, I’d cut on test and tren as well, just keeping estrogen under control with an AI.

For that more moderate doses would be fine, even as little as the equivalent of 50 mg/day TA and a minimum of 200 but more preferably 500 mg/week testosterone.

(Not that that isn’t also decent for the typical user for a gaining cycle, it is.)

Bill again later in thread: Yes, side effects of for example testosterone can be controlled with ancillaries.

On the other hand, if happening to have night sweats from tren (btw, just because it happened to an individual before doesn’t mean it will next time, or vice versa) I don’t know of anything to take that avoids that.

Or feeling feverish from too much Equipoise: don’t know anything to avoid that.

Or depression from Deca: There’s sonme support for my thoughts that Winstrol plus pregnenolone, but not nearly enough of an experience base to say it with confidence.

On risk of hepatic cholestasis from alkylated steroids: No known method of avoidance except limited periods of use.

Anyway, saving some for oral use could be a nice option, but as expensive as methenolone enanthate is, and being much more bioavailable by injection, absolutely I’d use at least the great bulk of it for injection.

For example an experiment you might really like is when your natural T is at good levels, try taking Primo at different levels and test the results. For example with 100 mg/week your T may remain unchanged yet you’ll have a benefit. This may be true at 200 mg/week. I knew of one person who found this true at 400 mg/week though while using Clomid at the same time (comparing that state to T levels with no Primo and no Clomid.)

Thanks! That was great that you did that! :slight_smile:

Unfortunately the thread where I specified the veterinary literature reference showing no progestagenic activity seems completely gone though.

Bill

After reading that thread again (good job DH) I have a question. Is it possible that the veterinary literature stating that trenbolone is non-progestagenic does not carry over to humans? My line of thinking is coming from study about clen being anti-catabolic (or anabolic, I forget) in rats but not showing the same effects anecdotally in humans?

Completely objective question. I’ve never used tren before.

Bill -

Is there any chance that while tren has an affinity for the prog receptor but no activity - that this could be different in each with some more sensitive to any potential (i assume as it has affinity there is potential for activity?) activity than others.

Brook