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Trenbolone: PR agonization or ER agonization?

Andy13

Andy13

Elite Mentor
Platinum
Any thoughts on this? The first ring on the trenbolone molecule is planar, like estrogens. This compound does not aromatise however somewhat resembles an estrogen. THis leads me to think that perhaps tren may not be a PR agonizer but a weak ER agonizer.

Anyone use trenbolone by itself and expirience itchy nips that went away with winstrol use (that's winstrol use NOT decreased tren use)?

How about TA and tamoxofin? If TA is a weak agonizer of the ER, I wonder if it would function almost as an estrogen blocker in a cycle with dbol or test....

lets hear your open minded thoughts. I realize everyone "knows" that TA is a PR agonist... But then again, everyone used to "know" that anadrol and deca aromatise, that methandriol dipropionate opens up receptors and that (my favorite) sustanon binds 4 different androgen receptors.

Andy
 
Sound iteresting, but the fact that Trenbolone has slightly higher affinity to progesteron receptor then progesteron itself, makes me think, that i'm close minded:D
 
Andy13

Is there a possible secondary effect once the acetate breaks down that can effect the planar bonding to the receptor site?

Great idea though will see what I can come up with since I never even noticed the itchy nips reaction so have never had to mediate with winny.
 
in any case it must be quite weak as I have never seen or heard of any one getting progesterone or estrogen gyno from fina use alone.
 
Scotsman said:
Andy13

Is there a possible secondary effect once the acetate breaks down that can effect the planar bonding to the receptor site?

Great idea though will see what I can come up with since I never even noticed the itchy nips reaction so have never had to mediate with winny.
Click to expand...

Actually, until the ester is removed, the steroid doesnt bind any receptor at all. And the ester is attached waaaaaay out on carbon #17... The planar ring is the first ring, the opposite end of the molecule.

Andy
 
Interesting question, but I'd have to ommit ER
agonization based on its effects on people
that use it.

Fact is: Tren burns fat very well.

Estrogenic based steroids aren't as efficient
as progestenic-based at burning fat, due to the
fact that progesterone increases glucose
oxidation, and ultimately more fat is used
for fuel.
Estrogen on the other hand decreases glucose oxidation.
Estrogen is VERY LIPOGENIC, while progesterone
is VERY LYPOLITIC.

Just compare: Tren vs Test/EQ/Dball

Test is probably the premier ER agonist, yet you lose
WAY more fat on Tren.
Also, Tren is more androgenic than Test. If tren were
truly an ERagonist A LOT of people would get gyno
from it. Which is just not the case. With test however,
A LOT of people do.

My own little theory regarding Tren is the following:

I think Tren somehow cross-reacts with the progesterone
receptor and the end result is an increase in
blood levels of simple progestins.
This is exactly what happens with EQ. It only aromatizes
to a simple estrogen.(If you where to use
an analogy)
Nandrolone and test however, aromatize into
estrogen and progesterone.

This is just a comparison.(Please assume they
are used by themselves)

1. Test-aromatizes into estrogen.
Lipogenic NOT lypolytic.
No increase in vascularity

#EQ aromatizes into a simple estrogen.
No real impact on fat loss/gain
Increases vascularity

2. Nandrolone converts to progesterone.
Lypolitic
No real increase in vascularity either.

#Trenbolone converts to a simple progestin.
VERY lypolytic
Increases vascularity

Do you see a resemblance?

Godspeed
 
Fonz- I respectfully see numerous flaws in your reasoning


Interesting question, but I'd have to ommit ER
agonization based on its effects on people
that use it.

Fact is: Tren burns fat very well.

Estrogenic based steroids aren't as efficient
as progestenic-based at burning fat, due to the
fact that progesterone increases glucose
oxidation, and ultimately more fat is used
for fuel.
Estrogen on the other hand decreases glucose oxidation.
Estrogen is VERY LIPOGENIC, while progesterone
is VERY LYPOLITIC.

Just compare: Tren vs Test/EQ/Dball

Test is probably the premier ER agonist, yet you lose
WAY more fat on Tren. I assume you mean testosterone, once converted to estrogen is an ER agonist; test has little affinity for the ER unless aromatized.

Also, Tren is more androgenic than Test. If tren were
truly an ERagonist A LOT of people would get gyno
from it. Which is just not the case. With test however,
A LOT of people do.I didn't say that tren was an outstanding ER agonist, I simply said it has a planar first ring. All estrogens have this. When testosterone is aromatized, it's first ring becomes planar since all the carbon atoms are now Sp2 hybridized.

My own little theory regarding Tren is the following:

I think Tren somehow cross-reacts with the progesterone
receptor and the end result is an increase in
blood levels of simple progestins.
This is exactly what happens with EQ. It only aromatizes
to a simple estrogen.(If you where to use
an analogy)
Nandrolone and test however, aromatize into
estrogen and progesterone.
Dont take this the wrong way, but what you just said is an example of chemical illiteracy. Do you know what aromatise means? It means (chemically) that the ring becomes aromatic, with alternating double bonds. Estrogen has an aromatic first ring. Progesterone does not. To say that something "aromatises into progesterone" is an erronious statement since progesterone does not have an aromatic first ring.

This is just a comparison.(Please assume they
are used by themselves)

1. Test-aromatizes into estrogen.
Lipogenic NOT lypolytic.
No increase in vascularity

#EQ aromatizes into a simple estrogen.
No real impact on fat loss/gain
Increases vascularity

2. Nandrolone converts to progesterone.
Lypolitic
No real increase in vascularity either.Here we go again. Nandrolone DOES NOT CONVERT to progesterone. Do you know anything about steroid synthesis? It is mostly one way... progesterone is hydroxylated and then it's 20 and 21 carbon atoms are cleaved to yield androstendione. To say that an androgen can convert back to a progestin is preposterous.

#Trenbolone converts to a simple progestin.
VERY lypolytic
Increases vascularity
ONce again, an androgen CANNOT convert into a progestin. Besides, I think comparing bodyfat loss (especially when you measure it with a mirror) and whether or not a steroid agonizes certain receptors is an irrational comparison......

next?

Andy
 
ahhhhh........ Andy13 - my nominee for the Elite "how to win friends and influence people" award. - but all for the beter understanding of the game! :p :D ;)
 
I love everone on this board... Even the one's that attack my postulates with the most incoherant and rediculous reasoning.

Have you got your oil yet, CYCLEON?
 
Why the hell arent you chemists responding to my post up top i got some questions on the caveman science of trebolone acetate, and without the ester. Read my post above haha. thanks.
 
I'm just going to throw this out there and hope not to be intellectually raped for my efforts. Perhaps even if one reported itchy nips from tren alone it might result (and this would be a minor effect I suspect) at least partially (again not sure about Andy13's theory but I'm not personally convinced - sorry Andy) from the tren binding slightly more readily to progesterone receptors than progesterone does leaving more free progesterone. In individuals with already high levels this could perhaps be the straw that breaks the camel's back.

One thing I would like answered that I'm embarrased to say I don't know is the fate (chemically) of progesterone in the body.
 
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.

APMIS 2000 Dec;108(12):838-46 (ISSN: 0903-4641)

Bauer ER; Daxenberger A; Petri T; Sauerwein H; Meyer HH [Find other articles with these Authors]
Institut fur Physiologie, Research Center for Milk and Food Weihenstephan, Technical University Munich, Germany.

For the steroidal growth promoters trenbolone acetate (TBA) and melengestrol acetate (MGA) neither the complete spectrum of biological activities nor the potential endocrine disrupting activity of their excreted metabolites in the environment is fully understood. The potency of these substances in [3H]dihydrotestosterone ([3H]-DHT) displacement from the recombinant human androgen receptor (rhAR) and from human sex-hormone binding globulin (hSHBG) was evaluated. In addition, the potency for [3H]-ORG2058 displacement from the bovine uterine progestin receptor (bPR) was tested. For comparison, different anabolics and synthetic hormones were also tested for their binding affinities. For 17beta-trenbolone (17beta-TbOH), the active compound after TBA administration, an affinity the rhAR similar to dihydrotestosterone (DHT) and a slightly higher affinity to the bPR than progesterone were demonstrated. The affinity of the two major metabolites, 17alpha-trenbolone and trendione, was reduced to less than 5% of the 17beta-TbOH-value. The affinity of these three compounds and of MGA to the hSHBG was much lower compared with DHT. MGA showed a 5.3-fold higher affinity than progesterone to the bPR but only a weak affinity to the rhAR. The major MGA metabolites have an affinity to the bPR between 85% and 28% of the affinity of progesterone. In consequence, MGA and TBA metabolites may be hormonally active substances, which will be present in edible tissues and in manure. We conclude that detailed investigations on biodegradation, distribution and bio-efficacy of these substances are necessary.
-----------------------------------------------------------------------------------------------------------------------------------------------

I think, it's enough, isn't it?
:o
 
oh yes andy - please check my response :D

Now while andy might be our favorite butthead ;) , I confess that I have not heard of anyone progesterone prone getting gyno from tren only or on tren stacked with other AS and Anti-e's. so I cant see that it actually has a PR effect - but andy, I havent seen any caases of ES effects either so based on empirical evidence ( alimited sample i admit) I just dont know- but in either case it must be rather weak. :p
 
Nathan said:
I'm just going to throw this out there and hope not to be intellectually raped for my efforts. Perhaps even if one reported itchy nips from tren alone it might result (and this would be a minor effect I suspect) at least partially (again not sure about Andy13's theory but I'm not personally convinced - sorry Andy) from the tren binding slightly more readily to progesterone receptors than progesterone does leaving more free progesterone. In individuals with already high levels this could perhaps be the straw that breaks the camel's back.

One thing I would like answered that I'm embarrased to say I don't know is the fate (chemically) of progesterone in the body.
Click to expand...

Intelectually raped... LOL!!

Progesterone can be converted to cortisol or it can be converted into androgen, androstendione.
 
Twisted_Steel said:
So thats what it feels like to get a verbal steel bore brush stuch up ones ass. Point, set, and match. :D
Click to expand...

Great. TS is back <sarcasm> j/k :)

I should have bee more precise in my wording....LOL
I swear Andy is like a coiled cobra waiting to spring......
But no problem, I like being kept on my toes.

Befor I answer Andy's post, Andy13 please look at Panerai's
study. Your little ER theory is now SHOT.

(I had been trying to locate the same study Panerai.)

I should have said that Tren has a lower affinity to
the PR receptors than Deca does.

Same goes with Test and EQ in relation to the ER
receptor.

This would explain why some people get gyno off Deca
while on Tren its pretty rare.

Godspeed
 
Andy,
When you said the carbon ring becomes SP3 hybridized it becomes "aromatic", meaning the double bond(s) occuring switch between the three bonds in the trigonal planar structure. I thought this was called ressonance?
This would mean that it sometimes would be an estrogen and somtimes not because it is shifting form isomer to isomer?
Im in first year college chem, so forgive me if im wrong!
 
Sp3 means tetrahedral. We're talking sp2 here. Yes, this is ressonance, which also means aromatic if we're talking rings. Estrogens have this property. Most Androgens and progestins do not since their first rings are not planar and do not have alternating double bonds.
 
Fonz said:


Great. TS is back <sarcasm> j/k :)

I should have bee more precise in my wording....LOL
I swear Andy is like a coiled cobra waiting to spring......
But no problem, I like being kept on my toes.

Befor I answer Andy's post, Andy13 please look at Panerai's
study. Your little ER theory is now SHOT.

(I had been trying to locate the same study Panerai.)

I should have said that Tren has a lower affinity to
the PR receptors than Deca does.

Same goes with Test and EQ in relation to the ER
receptor.

This would explain why some people get gyno off Deca
while on Tren its pretty rare.

Godspeed
Click to expand...

Sheesh.. I really didn't have a "theory." Just wanted to run some thoughts by... Are you sure that deca has a higher affinity for the PR than tren? Tren has a higher affinity for the AR than deca, right? I imagine it would take either a mighty sensitive person or a person using insane amounts of tren to get gyno from it.. But that wasn't really want I was asking...

So you think the idea that tren could be a weak ER agonizer (also) is ludicrous?


What do you mean test has weaker/stronger affinity for the ER than EQ? Are you talking about the parent steroids or after aromatization?
 
Last edited:
"Estrogenic based steroids aren't as efficient
as progestenic-based at burning fat, due to the
fact that progesterone increases glucose
oxidation, and ultimately more fat is used
for fuel."

FONZ, progesterone DOES not increase glucose utilization, in fact it does the opposite, it decreases glucose tolerance and increases fatty acid levels. This is the reason why women have to be monitored when using progestins.

"Estrogen on the other hand decreases glucose oxidation."

The studies on this are inconclusive, but looks favorably towards having no effect on glucose tolerance.

"Estrogen is VERY LIPOGENIC, while progesterone
is VERY LYPOLITIC."

This is somewhat untrue. Estrogen is lipogenic TOWARDS some tissue types, especially lower body fat depots, but prevents fat accrual in the abdominal areas. Estrogen decreases hormone sensitive lipoprotein lipase in this area. Progesterone is lipolytic, but lipogenic in certain tissues. Women tend to gain weight on progestins. The hormone is redistributing fat stores. In fact, all the major sex hormones have this effect on gender-specific fat stores. Beer-guts for men and dump-truck asses for women.

"Test is probably the premier ER agonist, yet you lose
WAY more fat on Tren.
Also, Tren is more androgenic than Test. If tren were
truly an ERagonist A LOT of people would get gyno
from it. Which is just not the case. With test however,
A LOT of people do."

FONZ, genistein, daidzein, and other isoflavones are estrogenic, but do not cause gyno, because they are weak ER agonists.

"This is just a comparison.(Please assume they
are used by themselves)"

"1. Test-aromatizes into estrogen.
Lipogenic NOT lypolytic.
No increase in vascularity"

"#EQ aromatizes into a simple estrogen.
No real impact on fat loss/gain
Increases vascularity"

"2. Nandrolone converts to progesterone.
Lypolitic
No real increase in vascularity either."

"#Trenbolone converts to a simple progestin.
VERY lypolytic
Increases vascularity"

"Do you see a resemblance?"

You set yourself up for this one.
 
Cockdezl-

So what do you think about the planar ring 1 on trenbolone? Possible ER binder?
 
"Cockdezl-

So what do you think about the planar ring 1 on trenbolone? Possible ER binder?"

Who knows, nothing is impossible.

By the way, love your spiraling helix.
 
Thanks guys... How do you like my floating molucule pic?


ANd Cycle- sorry, bro, about your oil question. To be honest, besides allergic reactions, I really cannot fathom why one oil would be better/worse than another...

The MCT's may not be able to dissolve as much AAS though.... They are not as hydrophobic as long chain esters.
 
Yeah, I guess I did set myself up for the slaughter.........LOL

Anyways,

Interesting concept, dual-agonism.
Then, how on earth do we measure the probablility
of tren agonizing the ER or the PR????

Godspeed
 
I like your sig and avatar buddy! I only wish I could add some knowledge to this thread as well, there is some incredible knowledge here.

M18
 
I'm hoping that tren may be somewhat of an ER blocker! I am in no way stating a theory.. Just a hypothesis.. I'd like to hear from some gyno sensitive guys who have taken tren, test, and both together..
 
I think the only way we are going to find this stuff out is to poll the guys... That's the same way they found winstrol to be an anti-pr, isnt it?

Imagine if tren worked like an anti-ER.. It might take a lot of it though.. Most of it will find it's way to an AR>....

NOw-- If I can just get my damn shins to heal.... I could do legs again.. arghhh
 
Ok here's what I found out...while tren does bind to the PR receptor, it DOES NOT mediate activity. Similarly, while nolvadex and clomid have a strong affinity estrogen receptors, neither do they mediate estrogenic activity. Another example is nestorone is a strong progestin that has a very strong affinity to glucocorticoid receptors, yet it does not mediate any glucocorticoid activity. Cyproterone acetate (experimental BPH drug) is an anti-androgen that has just as strong an affinity for the AR as test, yet it does not mediate any AR activity. Tren does not cause ANY hypertrophy in uterine rat tissue-which is pretty much the gold standard method of assessing progestinic properties.

Bottom line is that just because a molecule will bind to a specific receptor, it doesn't necessarily mean it will mediate activity in that receptor. Show me a study that indicates tren mediates PR activity and hypertrophy in progestinic tissues and I'll change my contention =) Until then, I'm in agreement with Bill.
 
Last edited:
Well i had to chime in on this one, nice to see a little discussion going on


Pharmacological and endocrinological studies on anabolic agents.

Neumann F

When used in connection with animal production the term "anabolic agents" covers a wide range. Ther steroidal male and female sex hormones are included in this list, as are the nonsteroidal estrogens. For the clinician and for the endocrinologist, anabolics are only steroids chemically related to testosterone and 19-nortestosterone. Estrogens, though possessing anabolic properties, too, do not belong to this class. This paper will deal with anabolic agents in in the stricter sense of which mainly trenbolone acetate combined with hexestrol has been recommended for bull and heifer fattening. To consider possible consumer injury from ingestion of meat from anabolic agent treated animals, it is necessary to know the pharmacological properties of the agents, the doses producing certain effects or might produce, and the levels of residues in the meat. Trenbolone acetate will be compared with the following anabolic agents: methenolone acetate, methandrostenolone, nandrone, androstanazole, and 19-nortestosterone. The activity spectrum of trenbolone acetate is similar to that of 19-nortestosterone or those anabolics that are derived from 19-nortestosterone. The compound has about three times stronger androgenic effect than testosterone propionate. Its index of dissociation between anabolic/androgenic activity is 2--3. This index is 3--10 for the other anabolic agents. As regards the virilizing potency, trenbolone acetate is also on the top of the list. It seems that androgenicity and degree of virilization run paralle. The antigonadotropic activity (inhibition of ovulation and testicular growth) of trenbolone acetate exceeds that of testosterone propionate by the factor 3. The compound is not estrogenic and seemingly not or only weakly progestationally active. In principle, the androgenic activity (symptoms of virilization) as well as the antigonadotropic effect (disturbances of the menstrual cycle in women, inhibition of spermiogenesis in men) of trenbolone acetate might be noted. This risk, however, can be excluded by mere calculation. In rats, 0.1 mg/kg trenbolone acetate have an antigonadotropic effect. This corresponds to a daily dose of 5--7 mg in humans. By the same extrapolation, a daily human dose of 100 mg can be calculated for androgenic activity. Such factors of conversion are, of course, not precise because rats are much less sensitive to androgens and anabolics than humans. Thus, testosterone propionate is active only in daily doses of 10--20 mg. If in humans trenbolone acetate also has three times the activity of testosterone propionate, effects in man had to be counted with not less than a daily intake of 3--5 mg trenbolone acetate. The dose which is recommended for livestock fattening is 300 mg. IT can, therefore, be excluded almost with certainty that the meat would contain such large amounts of hormone residues.


And yes i do have two friends who have developed gyno from fina , however we can't directly attribute their gyno to the trenbolone as they both were taking large amounts of XTC at the same time which we've found out causes high levels of prolactin!!!
 
E2 said:
xtc is extacy

prolactin is a female hormone whick enables lactation.
Click to expand...

Which can be blocked using Bromocriptine at 2.5mgs/day.

Godspeed
 
Bigrand - reading your posts and thinking back to first year chem you've now got me picturing the most stable configuration of the ring, i.e. the "chair" configuration - did you guys cover that stuff? :D All that stereochemistry and the nomenclature was really huge pain in the ass. LOL
 
Nathan said:
Bigrand - reading your posts and thinking back to first year chem you've now got me picturing the most stable configuration of the ring, i.e. the "chair" configuration - did you guys cover that stuff? :D All that stereochemistry and the nomenclature was really huge pain in the ass. LOL
Click to expand...

he he.. chair conformation....
 
Last edited:
My Dad's an organic chemist and so I really had no desire to take more courses. I should have though as I never asked him for much help/advice on homework problems and such so could take advantage of that better in future courses. Oh, well.:D
 
Nathan said:
My Dad's an organic chemist and so I really had no desire to take more courses. I should have though as I never asked him for much help/advice on homework problems and such so could take advantage of that better in future courses. Oh, well.:D
Click to expand...

Is he a synthetics chemist? MS, PhD??? $$$???

I know.. it's a lot of questions.. It must be nice to have someone raise you with whom you can have intellegant conversations.
 
I believe that test is test, right? Now that is settled, how do you believe that sus has four receptor sites, and
how so?

I would like to be informed about this. Also, what is the difference between a anabolic receptor/androgenic receptor? I think that they are one and the same.

Please enlignten me about this difference of research
opinions.
 
Laserdude said:
I believe that test is test, right? Now that is settled, how do you believe that sus has four receptor sites, and
how so?

I would like to be informed about this. Also, what is the difference between a anabolic receptor/androgenic receptor? I think that they are one and the same.

Please enlignten me about this difference of research
opinions.
Click to expand...

um... who said there are 4 AR's? There is one (that we know of)
 
Sust dont act on 4 receptors, sust is a combo of 4 test esters of various lengths. This allows test to be released at different times.
There is no anabolic receptor, just an androgen receptor. there are no "anabolics" in the blood like there are androgens, estrogens, progestins and other hormones that need a recepter to attatch to. the term anabolic is in reference to a substance that increases anabolism. Its an act not an actuall substance. I guess...
 
It must be nice to have someone raise you with whom you can have intellegant conversations

You've got to appreciate the irony of this statement and the spelling of "intellegant"


Panerai, where in the hell do ou find these studies????im impressed. The only thing I question. Maybe the PR receptor in the bovine uterus is different then in male humans? Otherwise I think tren would produce instant gyno. Just a guess. the study was following recpetors in the bovine uterus. This does prove that there is however, progesterone binding of tren to some degree anyways. i have been looking for proof of this, thanks.


BigAndy, I think the whole entire trenbolone molecule is planar. except to a small degree the 4th , 5membered ring. There are double bonds on the first 3 rings. I wouldnt know the physiological consequence of this with reguard to ER binding however.....
 
Nitotech acts on all the AR receptors.

[size=-111] That's my intelligent contribution this time...hehe[/size]
 
I have read every study on medline with trenbolone mentioned and that study was the only one that mentions trenbolone and its affinity to the bpr. My problem here I guess is that we are jumping to the conclusion that just because tren binds slightly better than P in a cow's uterus that it also binds in a similar way in humans at other sites in the body. This really seems like a stretch. Help me out here.




Fonz said:


Great. TS is back <sarcasm> j/k :)

I should have bee more precise in my wording....LOL
I swear Andy is like a coiled cobra waiting to spring......
But no problem, I like being kept on my toes.

Befor I answer Andy's post, Andy13 please look at Panerai's
study. Your little ER theory is now SHOT.

(I had been trying to locate the same study Panerai.)

I should have said that Tren has a lower affinity to
the PR receptors than Deca does.

Same goes with Test and EQ in relation to the ER
receptor.

This would explain why some people get gyno off Deca
while on Tren its pretty rare.

Godspeed
Click to expand...
 
Fonz said:

Interesting concept, dual-agonism.
Then, how on earth do we measure the probablility
of tren agonizing the ER or the PR????
Click to expand...

I guess we are talking here about ER and PR CLINICALLY evident action.

In this regards, if Tren were both a ER and PR agonist we should expect a huge amount og gyno from tren alone use, which is not what I have heard and seen so far.

On top of that, if tren was also a ER agonist there would be no need to have it always with estrogen in cattle implants, when an clinically evident estrogen action is required.
 
justwannagetsum said:
It must be nice to have someone raise you with whom you can have intellegant conversations

You've got to appreciate the irony of this statement and the spelling of "intellegant"



.....
Click to expand...

(tee-hee!) I can't spell worth a shit.. I'm always asking my girlfriend how to spell the most rediculous words...
 
macrophage69alpha said:


it is likely that there is more than one... there are at least 2 ER receptors..
Click to expand...

I know there are at least two DNA binding domains on the ER.. There are studies with mutant ERs where the DNA binding domain has been deleted... It still had biological activity.
 
im not all in the chimical breakdown of the tren. i can only speak as the lab rat. i never got itchy nips or any signs of gyno even on very high levels of tren with no anti-e's. i even took high doses of tren and after stopping it for only 2 weeks, i was tested for steroids under suspision in the navy and it came back negative. that was from UCLA. i thought i was fucked. but after only 2 weeks off i get tested negative, i even saw the paperwork that came back from UCLA that showed the results. weird, i thought AAS stays in your body for quite some time. the only problem i had was when i went in for a physical i was on tren only and they said my ketones and protien in my urine was high. i told them i took a lot of protien shakes and they said to lay off for a couple days and come back to retest. i waited 5 days, stayed off the tren and the test came back way normal. the tren goes away from the body rather quickly. hope this helps.
 
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