Why does a tren-only cycle not reduce gyno?

Re: Why does a tren-only cycle not reduce gyno?

Posted by: Andy13

[B]We've seen clinical (thank's JB) as well as anecdotal evidence describing a reduction in gyno from nolva treatment.

Nolva blocks estrogen from binding its receptor... But why not eliminate the -production- of estrogen? In the case of gyno reduction, certainly that seems more logical to eliminate estrogen rather than allow its production via aromatase then block it from the ER.

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Trenbolone does not convert to estrogen. It does however decrease natural production of testosterone, which, in turn, decreases the amount of estrogen produced. One would anticipate ultra low estrogen levels upon tren treatment.

So here's the question- why doesn't a tren-only (or any AAS which does not convert to estrogen) work to reduce gyno?

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Couple possibilities-- tren, itself, has modest affinity for the ER, activating it.

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Although tren does not convert to estrogen, it may have metabolites that have ER affinity.

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Gyno symptoms don't decrease bc of activation of the PR by tren.

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Nope (Ojasoo and Raynaud)

I actually have a very mild case of gyno from puberty. I have done tren-only for months. Yet, my gyno did not improve.

Would you agree there is minimal ER activation under these circumstances?

If so, then nolva probably will not work to reduce gyno, no?

Anecdotal evidence has informed us that nolva is only good at reducing hard lumps under the nipples, not the fat or puffiness that often accompanies gyno also. Thus, you have to be more specific about your gyno.

Furthermore, you make the assumption that nolva reduces gyno via preferentially binding to the ER. There is a possibility that this may not be the case whatsoever.

Posted by: Andy13

I actually have a very mild case of gyno from puberty. I have done tren-only for months. Yet, my gyno did not improve.

Would you agree there is minimal ER activation under these circumstances?

If so, then nolva probably will not work to reduce gyno, no?

Indeed. if prolonged tren only cycles do not help, it is quite likely that Nolva or an AI will not help much either.

but, as in many things, there are exceptions to the rules and clearly there is more knowledge to be gained. if you apply a risk/benefit ratio analysis to the situation, you have little to lose and quite a bit to gain with this experiment.

jb

Posted by: Big Cat

Indeed. if prolonged tren only cycles do not help, it is quite likely that Nolva or an AI will not help much either.

You made a comment about an androgen (I believe)/receptor complex being able to activate the ER response element. I've heard about this once before (some steroid + its receptor able to block GR response element site), but it was a while ago in some class. It was a real eye opener to consider genes can be transcribed from ER-RE in the absence of both E2 and ER activation.

Posted by: Andy13

You made a comment about an androgen (I believe)/receptor complex being able to activate the ER response element. I've heard about this once before (some steroid + its receptor able to block GR response element site), but it was a while ago in some class. It was a real eye opener to consider genes can be transcribed from ER-RE in the absence of both E2 and ER activation.

Its very unlikely, but (honesty bids me to admit) not entirely excluded, that tren has such actions because the molecular shape and distance between key activation sites are quite different for 4,9,11-trienes. Its really not fair in any way to compare tren to deca because they are both 19-nor, since the extra double bonds affect its action much more than the absence of 19-CH3. In fact, one study showed that compared to other androgens tested (only a handful), methyltrienolone (structurally more like trenbolone) cause a quite unique conformation of the AR, where the 12th helix (which folds back over the LBD to stabilize the ligand) was bent differently. This can cause an entirely different co-activator binding surface.

Posted by: Big Cat

Its very unlikely, but (honesty bids me to admit) not entirely excluded, that tren has such actions because the molecular shape and distance between key activation sites are quite different for 4,9,11-trienes. Its really not fair in any way to compare tren to deca because they are both 19-nor, since the extra double bonds affect its action much more than the absence of 19-CH3. In fact, one study showed that compared to other androgens tested (only a handful), methyltrienolone (structurally more like trenbolone) cause a quite unique conformation of the AR, where the 12th helix (which folds back over the LBD to stabilize the ligand) was bent differently. This can cause an entirely different co-activator binding surface.

Gotta believe there is an appreciable amount of homology between different steroid receptors. Do you happen to know if they diverge at the ligand binding domain as well as the DNA binding domain?

Posted by: Andy13

Gotta believe there is an appreciable amount of homology between different steroid receptors. Do you happen to know if they diverge at the ligand binding domain as well as the DNA binding domain?

Not sure I understand the question. The DBD seems to play no mentionable role in the differential effects of steroids. In fact, a truncated receptor containing only DBD and AF-1 is a constitutionally active receptor. The rest serves to quench it in the absence of ligand. When the LBD is properly activated LBD causes the AR to fold and create an interaction between LBD and the N-Terminal domain whereby AF-2 folds back over the ligand, which stabilized the ligand-bound receptor and creates the co-regulator binding pocket.