Got a feeling something is in the works to answer all this..

Only cause i love you guys..

go here first best pic i can find for now.. Dont worry im going to write up a long response to this in a new post..
http://www.rise.duke.edu/phr150/Performance/images/steroid_response.jpg

now if your looking at the pic you can see the steroid hormone on the outside and than coming in--than in the inside you see the steroid receptor that the steriod hormone connects too..
Now how that works wich i will write up longer for everyone since this is a hot topic.. is the higher the anabolic-androgenic effect the more Steriod hormone there is--it acts like a crowd.. So what i mean by that--is outside where the Steriod Hormone is, lets say your taking test p and tren a... On the outside you have 500 Tren a Sterriod Hromones, and 100 Test p Hormones.. Well guess you is going to shove through faster and more of the one with more out side.. However, you only bind so fast and produce proteon synthesis so fast(yes everyone is diffrent)--but it leaves test p Steriod Hormone on the outside not doing anything but convertining into estor.. sure it makes its way in.. But not as often and usally after the Tren has all been used.. However, not all the test p is avalible because some of it has already converted to estor. The way diffrent compunds work..is how long the live. their Anabolic-adrogenic effect, and how they afeect the DNA process

go here http://www.thepepproject.net/Load/
Choose student
Than hit no for the read me first crap
Go to Moudle 6 up top..
Than on the botom right you can click on the pics read.. Dont worry i'll post more links so you can understand the Higher the anabolic-androgenic effect--Attachets faster more frequent and better to a receptor. But like i said before some do it faster some do it slower.. Wich all benifits because they all tell your DNA to initiate protein synthesis.

This what I understand it to be from the pathophysiology standpoint.... It's about the ligand binding....Tren is a PgR ligand with mixed agonist/antagonist activity... it also highly suppresses natural progesterone as well as alters its metabolism. Antagonist action at the PgR can be just as much an issue as agonist action....It's obvious that they have a similar structure and can travel the same metabolic pathways....understand that the Tren has affinity to bind stronger to the receptor...no fight just a stronger bind and no room for test...leaving the free test floating around to convert which gives the unwanted sides.....as u can see below

The androgen receptor (AR), also known as NR3C4 (nuclear receptor subfamily 3, group C, member 4), is a type of nuclear receptor [6] that is activated by binding of either of the androgenic hormones testosterone or dihydrotestosterone [7] in the cytoplasm and then translocating into the nucleus. The androgen receptor is most closely related to the progesterone receptor, and progestins in higher dosages can block the androgen receptor. [8][9]

The main function of the androgen receptor is as a DNA-binding transcription factor that regulates gene expression; [10] however, the androgen receptor has other functions as well. [11] Androgen regulated genes are critical for the development and maintenance of the male sexual phenotype.

But now of course ur not going to find clinical or medical studies on Tren bc this AAS was never approved for humans ....this is bc there is no medical value for such a powerful hormone....Tren has been used solely in the vet world esp in the bovine class for improving muscularity on cattle to produce quality meat at much faster rate and It's ability to cause food to be utilized to its maximum potential