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Low E2 Low Prolactin Still Gyno WTF

I would just like to note that "affinity" does not imply the specific action of binding. There are antagonists that have a high affinity.

And for Tren, it has about one metabolite because all those conjugated bonds limit it's metabolism. The one metabolite of Tren is the greater agonist of the progesterone receptor, regardless of affinity.

I did use the term binding very loosely, given the information within this abstract.

Binding is the sequential action/activation of said ligand upon the receptor, Correct?
 
Would micro pregnenolone be a good way to counter tren gyno. as tren lowers progesterone
 
if you want to lower progesterone naturely without medicine you need to eat less soy-rich food and keep the stress of excerise, the fat can also cause estrogen so wight loss is also a good way

You post utter nonsense a lot of the time.
 
Progesterone and prolactin can be manipulated by using AI's and lowering circulating estrogen (long feedback mechanism).
 
I would just like to note that "affinity" does not imply the specific action of binding. There are antagonists that have a high affinity.

And for Tren, it has about one metabolite because all those conjugated bonds limit it's metabolism. The one metabolite of Tren is the greater agonist of the progesterone receptor, regardless of affinity.

Affinity is generally used for agonists, although antogonists also have affinity, but in almost every case I have seen, when the term affinity is used without specifying antogonist, it is an agonist.

There is massive amounts cross activation in hormones, testosterone even has an affinity for the estrogen receptor, can activate it, may or may not change the subsequent transcription that takes place, unknown, but generally thought that it does not. Vice versa with estrogen having a weak affinity for the androgen receptor as well. Basically all hormones have at least some chance of jamming themselves into the key hole, some as agonists some as antogonists.

Another interesting one is testosterone's affinity for the glucocorticoid receptor, but this time it is an antogonist, blocking it but not activating it.
 
I did use the term binding very loosely, given the information within this abstract.

Binding is the sequential action/activation of said ligand upon the receptor, Correct?

Yah, well binding can bind rather loosely. Affinity does not even mean that a ligand binds strongly to it's receptor. Sometimes it's the opposite, as some 17-methyl steroids have a low affinity, but they actually bind rather strongly once they are able to get in there.

and it's not like a binary switch or anything. Ligand contacts the receptor according to it's particular shape, and the receptor makes a conformational change according to the particular shape. However the receptor changes particularly in response to this particular shape, thus begins that particular chain reaction called activation.

and Affinity is more of a probability and "attractiveness" Affinity is also relative and varies with concentration. It has all the contingencies of probability.
 
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Lol. So what's the verdict on how one goes about reducing tren side effects when AI's and caber aren't doing anything for them? I also struggle with this. I have taken Letro, adex, caber, prami, Nolva. Large doses of AI combined/daily caber and still can get lactating or puffy nips on Tren.
 
finnaly see a girl!!
there are full of boys aboard!

I have been supplementing with test and tren.

Been taking .5 caberet 2x week, adex .5 EOD

Just got bloods e2= 5.4 prolactin =1.0

Still getting gyno symptoms.... What gives???
 

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