Exactly what pathway-signal does the aromatase enzyme come from? Hmmm.. Let's find out..

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Let's jump right into it - People will possess different amounts of enzymes as we know, genetics and so on. Basically there's precursors throughout the body and these can be found in all sorts of tissue including adipose tissue.. When a hormone simulates the effects of T it can awaken "storage like cells" or even receptors that will react as if the presence of a specific hormone is about.. Now some agents like Drol doesn't aromatize nor can it activate estro metabolites but how does one get estro like sides?!?! In principle it's said that some AAS won't convert however it's been proven that in some instances "mostly rare" that this can in fact take place outside of what we know as "normal aromatization", there's a vast amount of transformations in the body.. Some aas have been transformed within their positions to avoid this, and others by delivery method (attempting to avoid the stomach by way of enzymes, and gastro tracks or even directly with the liver)..
Yet we still see this effect of estro like sides.. alot has to do with it's loitering time for a good amount of compounds but not all, it's detailed expression with clearance mechanisms, the longer a certain drug is present the greater the chances for metabolites to be activated despite "some" ring positions and its group, here lies the problem for some, regardless if a drug is said that it can be transformed or even if an enzyme is blocked or occupied, estrogen can be produced in small amounts via other tissue like the liver and fat cells as an example.. This can take way merely by a molecule that resembles an other and there hosting receptor sites may react and in fact sensitize and or other tissue my secrete and produce, ER's are now activated and now they initiate PR's and so on.. It's a chain of events with enzymatic reactions regardless of the most parenting hormone, there's a host of tissue that can synthesize and secrete into the blood, unbeknownst to any AI and still have reactions at REC's.. The greatest question in biochemistry has always been "is there a way to prevent unwanted metabolic conversions"? They've done this by the modulation of chemical structures or/and there positions, with that said it's a testament in its own that even science can't fully manipulate or dictate biosynthesis.. Bear in mind depending on the integrity of the bond and how easy aromatization reaction catalyzes by way of aromatase enzyme may be, some bonds are simply impossible to see aromatization for geometrical reasons or even display activities that may resemble estrogenic like proprieties (masteron, proviron and even stenbolone would be great examples).. Does this make any sense? It's truly an individual case to case basis with most AAS..

Also, believe it or not some Food and drugs/AAS can act as estrogen mimickers.

So many different mechanisms of actions can create a cascade of events that can transpire, especially with some genetics, thus it doesn't necessarily have to be by course of action that came directly from the parenting hormone/drug but in fact through other channels and signaling that can take place there after.. once the metabolization is done as we understand it should be excreted through the urine or the kidneys or whatever else and it's done, but that's not the case there's all sorts of other activities that can happen there after just by a small initiation an activation of a sleeping cell so to speak - and blamo now you have some sort of activity.. and like like I stated prior - this could be through diet and all sorts of other actions..
I'm a firm believer that body mass has a lot to do with it depending on the ratio of lean mass versus fat.. because statistically - proven through science and medical journals people who possess a higher fat ratio tend to have more of estrogenic like side effects through a variety of reasons.. when body fat is reduced the symptoms and side effects dissipate or are almost non occurring..

Now I'm not suggesting that someone who is in single digits won't experience estrogenic like side effects by a certain compound, but in my opinion the odds of experiencing them are greatly reduced especially in the environment when ancillaries are employed..

What if E2 is in check during cycle, yet you still get gyno flare-ups or estro sides?
Endogenous estrogenic biosynthesis and promoters of different transcription factors is vast with it's diversity of actions, some people and these people may possess secondary messengers and promoters and this can be expressed through different skeletal tissue, and even by way of stomach enzymes and other non reproductive tissue with E2 synthesis... Genetics is a huge contributor!

Think of a forest fire and all hoses aimed down on one spot attempting to occupy and inhibit that fire from spreading, it just takes one random amber to fly out unbeknownst to anyone and create an entirely differ set of issues behind the backs of the fire-fighters, flanking them so to speak..

Having a keen understanding of the biological actions in which E2 and how it is mediated between the basic formality is very important, this is what we know as the "normal aromatization" by way of hormones and enzyme presence, but in all actuality with the manner in which E2 can be transcribed, it can be hosted by a variety of factors.. It's a complex interplay with multiple identities made up of various interconnected signaling and cross-talk!

KNOW YOUR SENSITIVITIES AND LISTEN TO THEM, AND GET BLOODS!

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