tren and gyno just don't mix!!!

[panerai]

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.
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What do you mean "not enough evidence"?
The study is clear about binding affinity of Tren to PR. Now, by being not sure about how it activates PR, you, probably meant if it is agonist of PR or antagoinst.
Well, it's not that complecated to prove that Tren is agonist.
As you can see from the same study, Tren's affinity to AR is the same as DHT, which means that all the users should experience "hard on" effect from Tren alone cycles, and it has to be much stronger then from Test or even Test+high dosage of Proviron combo. What do we get in real life? With few exceptions, most users experience Fina dick, or close to it, and definately nothing even close to pure DHT effect.
Why? Same as with Deca - binding to PR. That's the only possible explanation.

Now, you started that thread, saying that Tren when viewed from 3-D can't fit in PR, so how come it does?
Get your facts together.

Trenbolone and Nandrolone, both are progestogens, both derivated from 19-nortestosteron.
Tren - 4,9,11-Estratrien-17beta-ol-3-one
Nandrolone - 4-Estren-17beta-ol-3-one

Don't you see striking similarities? So, comparing these two compouds make a lot of sense.

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Yes, Big Cat, I know what you are going to say...- Study done on a cow and PR was located in uterus-... But, so what?
Study still beats your assumption that TBA has no PR-activity.

 

[Big Cat HH]

ok we are going around in circles now. Lets go at it from another angle.

Say I follow you on this one, and you do have your facts straight, tren is derived from 19Nortest. Say it therefor activates the progestin receptor. Progesterone itself does not cause bitch tits. The reason it does in nandrolone is because progesterone is an estrogen agonist and nandrolone converts to a powerful estrogen as well. As an agonist of the E2 it does indeed cause gyno. But since tren causes no aromatisation of its own, we agree on that much right ? , then what on earth would a progestin stimulation accomplish in these terms ? Had you said it was stacked with an aromatizing compound, then yes, of course. But then again tren wouldn't be the sole cause.

Since tren actually inhibits aromatase when not competing with circulating estradiol, I fail to see how a progestin activation would cause such side-effects. Do you ?

This is not to say I've stepped away from my original idea, just trying to see if this makes sense to you on another level ...

 

[panerai]

Following your logic, Oxymetholone should not cause gyno neither...
Are you denying the fact of Ox gyno, also?

 

[milkbone]

I took finasol made from finaplix-h and nandrosol / androsol. I started developing gyno at the end of the first week. After I started getting symptoms, I stopped the finasol and started taking vitex because that's all I could get my hands on at the time. Although my symptoms are mild, the left nip is definitely larger than the right. Is there any way the prohormones mentioned above could aromatise to cause the gyno instead of the fina causing it? I have a good bit of finasol left and want to finish it, but I know I'm going to have to take something with it to prevent the same thing from happening.

I do remember seeing one post about a guy that was taking fina with winny and was still developing gyno. I later wondered if there was any possibility that his winny could've been fake ... just a thought since this is the only fina/winny cycle I've personally heard of causing gyno.

I'd be willing to sacrafice some of the benefits of the tren in order to prevent the gyno. The question is what works? Everyone says RU-486 which for me is about as helpful as saying don't take the fina because I can't get it. Winny comes in second according to everyone, although I'm worried it might be too hard on my hair (just paranoid). I have also heard a few say arimidex and / or nolva will not help at all. The whole thing just sucks for me either way!

 

[panerai]

There're ER-positive tumors in breast cancer, also there're PR-positive tumors. For either of those, higher level of another sex hormone is not nessecery to promote growth of cancer cells, just IGF-1 increased level is requied.
Anyway, they have some correlation, no matter, if androgen is present or not.

What makes you think, that Tren is aromatise inhibitor, BTW?

 

[Big Cat HH]

There're ER-positive tumors in breast cancer, also there're PR-positive tumors. For either of those, higher level of another sex hormone is not nessecery to promote growth of cancer cells, just IGF-1 increased level is requied.
Anyway, they have some correlation, no matter, if androgen is present or not.

What makes you think, that Tren is aromatise inhibitor, BTW?

Indeed, increased IGF-1. And how does PR increase IGF-1 ? Through agonizing E2. Same story here as we discussed before. if no E2 was present, the IGF-1 levels would not be an issue and your PR-mediated tumor would be a non issue.

As to why I think Tren inhibits aromatase :

StJohn LC, Ekeren PA, Crouse JD, Schanbacher BD, Smith SB, lipogenesis in adipose tissue from ovariectomized and intact heifers immunized against estradiol and/or implanted with trenbolone acetate, J Anim Sci 1987 May, 64 (5) : 1428-33

 

[Big Cat HH]

I took finasol made from finaplix-h and nandrosol / androsol. I started developing gyno at the end of the first week. After I started getting symptoms, I stopped the finasol and started taking vitex because that's all I could get my hands on at the time. Although my symptoms are mild, the left nip is definitely larger than the right. Is there any way the prohormones mentioned above could aromatise to cause the gyno instead of the fina causing it? I have a good bit of finasol left and want to finish it, but I know I'm going to have to take something with it to prevent the same thing from happening.

Well provide you take my evidence into account, a simple aromatase inhibitor would be ample, since PR doesn't cause gyno directly but through E2 agonizing. Eliminate estradiol buildup and you eliminate the mediating effect of PR in this matter. Although I must say Nor-diol was a poor choice for a stack in this matter as it too acts as a progestin and it converts to an estrogen that is quite strong in itself. Neither fina or Nor-diol readily causes gyno, but the fina enhancing the effect of the Nor-diol certainly could.

 

[panerai]

Please, go back and read abstracts that clearly show, that Trenolone by itself is very effective in increasing IGF-1 level. Add activation of PR and you have perfect conditions for PR-positive gyno.

I didn't see your answer to my question about Oxymetholone...

As for study on Tren being aromatise inhibitor, can you, please copy and paste the abstract. Looking for it will take long time for me. As you can see, I, as well as others in this thread, paste the whole abstracts, so it's easier for us to discuss.
Unless, you expect me to take your word for...hehe..

As for your advice to use simple aromatise inhibitor with Fina, well, what for? Fina is aromatise inhibitor, according to you....right?

 

[Big Cat HH]

Please, go back and read abstracts that clearly show, that Trenolone by itself is very effective in increasing IGF-1 level. Add activation of PR and you have perfect conditions for PR-positive gyno.

I did, nowhere did it explain the way in which PR raised IGF-1 levels. I'm sure if someone could provide us with the full study, you'd see that the idea was proferred that the effects were most likely mediated by E2. I'm not saying PR can't raise IGF-1, I'm saying it can't do so without the presence of an estrogen.

I didn't see your answer to my question about Oxymetholone...

To tell you the truth, I wouldn't know, haven't done much research into oxy.

As for study on Tren being aromatise inhibitor, can you, please copy and paste the abstract. Looking for it will take long time for me. As you can see, I, as well as others in this thread, paste the whole abstracts, so it's easier for us to discuss.
Unless, you expect me to take your word for...hehe..

I'll look for it and post it below, but I fail to see how it takes you longer than me. You wanted to know, so I don't see why I have to look for it. But for this once, ok.

As for your advice to use simple aromatise inhibitor with Fina, well, what for? Fina is aromatise inhibitor, according to you....right?

Fina, as you will not from the abstract I will post shortly, but even better if you read the full study (abstracts only say so much), only acts as an aromatase inhibitor when there is no circulating E2. I believe stacking it with Nor-diol does not meet these requirements, so another aromatase inhibitor must be used.

 

[panerai]

Never mind....

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Lipogenesis in adipose tissue from ovariectomized and intact heifers immunized against estradiol and (or) implanted with trenbolone acetate.

J Anim Sci 1987 May;64(5):1428-33 (ISSN: 0021-8812)

St John LC; Ekeren PA; Crouse JD; Schanbacher BD; Smith SB [Find other articles with these Authors]

Forty-two heifers were allotted randomly to six treatment groups: intact controls, intact heifers implanted with trenbolone acetate, ovariectomized heifers, ovariectomized heifers implanted with trenbolone acetate, intact heifers immunized against estradiol and intact heifers immunized against estradiol and implanted with trenbolone acetate. Blood titers of estradiol-17 beta were increased over 100-fold in heifers immunized against estradiol in Freund's complete adjuvant or saline:squalene/arlacel containing Mycobacterium. Lipogenic enzyme activities and acetate incorporation into fatty acids were increased in subcutaneous adipose tissue obtained at slaughter from heifers receiving immunization or the combination of immunization and trenbolone acetate. The increased lipogenic capacity was not reflected in either cell diameter or cells per gram adipose tissue. Ovariectomy in combination with trenbolone acetate caused the lowest activities for all enzymes measured. This treatments also caused the greatest decrease in cell diameter, which resulted in the largest number of cells per gram of adipose tissue. Trenbolone acetate alone had no detectable effect on lipogenesis in the intact heifer, but the combination of ovariectomy and trenbolone acetate caused substantial decreases in enzyme activities, in most cases a significant decrease as compared with ovariectomized heifers. The data suggest that trenbolone acetate is able to depress lipogenesis only when not competing with the effects of circulating estradiol.
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Aromatise inhibition? You are confusing me.