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A look at the biology that's behind aromatase/estro conversion "AI's by EP at PSL"


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A look at the biology that's behind aromatase/estro conversion "AI's by EP at PSL"

What pathway signal does the aromatase enzyme come from and why do some people aromatize more than others?:hmm:

Let's have a quantitative look at the biology that's behind this and what separates individuals from the herd.
People will possess different amounts of enzymes as we know, genetics and so on, so lets pass that winded rant.
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..A lot 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 aromatisation reaction catalyses by way of aromatase enzyme may be, some bonds are simply impossible to see aromatisation 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..

Can other things be estrogen mimickers?

Yes, it doesn't necessarily have to be by course of action that came directly from the parenting hormone 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 blammo now you have some sort of activity.. and like you said it 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 and 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..

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..

Bear in mind that some hormones can be mimickers due to the structures appearing very similar causing cross-reactivity within the system or even at the ER sites and even on blood work.
At the ER sites Drol "can" exhibit similar chit chat with E1/E2 estrogen receptors (ERα, ERβ, mERs (e.g., GPER, others), although that's NOT its intended target, biologically it can initiate similar chitter chat that E1/E2 naturally is instructed to do..When people experience prolactin (gyno, glandular duct inflammation) it's plausible to the PR activation by way of ER's being fooled into a mimicking response..
This is rare, but when there is issues this is suspected to be a potential of the cause and effect.. Hormones can be weird with their unintentional mimicking or simulating the hormonal structures or even activation's of other hormones, much like cross-reactivity with Trenbolone being recognized as estradiol on blood work.. all those lab testing doesn't always possess the abilities to see and recognize the difference is like our body does, sometimes the body just as well can be dictated and manipulated..

This is why Nandrolone, Drol, EQ and even Tren can give false positives with either cellular chit chat or even lab work..

Cross reactivity with tren to estrogen example with blood work there's always going to be draw-backs and the potentials of contamination and report problems, one limitation of steroid hormone immunoassays is interference caused by compounds with structural similarity to the target steroid of the assay.(In my case Tren to Estrogen) Interfering molecules include structurally related endogenous compounds and their metabolites as well as drugs such as anabolic steroids..

Running multi 19-nors:
To my understanding on what I've gathered over the years with running one of MORE 19-nors especially when Trenbolone is in the mix with Nandrolone ~All the drugs above can be a bit sassy and act in multi-functional fashions (2 faced, or more).. Much like a wolf dressed in sheep's clothing, going down pathways that they're not normally intended too (example - why some drugs are used as off labeling treatment drugs, because of actions that are not intended but are known to happen)
As we know 19's are basically synthetic progestins and on a therapeutic level/treatment they have been known to bind at around 20-22% to the PgR's, now with these having multi-functions and possibly initiating/activate sleeper enzymes by way of cross-reactivity, basically a false positive cellular transcription now we're using them at dosages far exceeding "therapeutic", increasing our chances for a larger receptor domination.. Now, when some "sensitive" users employ ancillaries hoping to combat these symptoms that the drugs may have a tendency to display on some individuals they fail to target the specific metabolites/enzymes because they don't appear on the "radar" as a bogie, no tone on the target..

Yet, the receptors see and recognize the false impression of a mimicking hormone now initiating a response directly at the Er or even PgR's (this is rare but it does happen).. Think of the receptors/enzymes like a parking space and the ancillaries are a Road Cones; You place the road cone in the parking spot so no parking can happen (you hope, basic rules of order)..Although that small road cone really ain't doing much, you still can't park there because that little cone is occupying the space, right? This is true for for most AAS, but with compounds that possess the potential to show lack of order to regulatory rules with chemical messengers they can be a bit mutinying. Basically bullying their way through by false representation, deception!

For myself, Finding what agent has the best modulatory effects is pivotal (aside from just not using the drugs in questions period).. I find Masteron to be almost superior in this application with 19's.. Please don't mistake me here, I'm not saying in any fashion that it's and AI.. However, with my ratio of flare-ups and gyno instances Mast works as a antagonist hindering the biological response of the "slutty" drugs attempting to bind to the R's.. I do very well with Masteron as an addition to almost every compound especially Nandrolone, and Drol...
With hormones it will never be a one size fits all, metabolites and enzymes/sleeper cells and other chemical messengers can always instigate chit chat and drugs can go down many pathways adding a whole other layer to the situation, all the while we're accustomed to what we know as "set rules" in a narrow range of the pathways unbeknownst sub-pathways and addition layers..

Why do some people always have sensitive nipples?

Endogenous estrogenic biosythesis and promoters of different transcription factors is vast with it's diversity of actions, some people such as your self 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..

I see and recognize that most of us have a keen understanding of the biological actions in which E2 is mediated between with the basic formality of 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 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!

Examining nipples to often:
Do yourself a favor and stop touching them, every-time you touch it you're stimulating the glandular duct tissue, the more stimulation you're giving greater the chance of you inducing further inflammation to the ducts.. it's very similar to the process with females when milking for babies, it's called supply and demand.. the more you touch it and the more you stimulate it the more potential you have of growth..

This is true...

In fact there was a study conducted on a unit in the German Army honor guard, they would drill repeatedly and their replica rifles would continuously hit a specific side of their pecs, I forget offhand what side it was but we're going to say the left side just for topic sake.. a majority of the soldiers in the honor guard unit were developing gynecomastia on the same exact side.. after a thorough investigation and a study was conducted it was found that the repetitiveness and continuous contact and stimulation to the nipple and the surrounding glandular duct tissue it was inducing gynecomastia.. only on that one side..

This is why I tell people do not continuously investigate, by habitually feeling around and playing with bumps/lumps.. if you can feel tenderness there's no need to investigate further take the appropriate protocols to Target the symptoms, Target first then Implement long-term treatment.. targeting would include tamoxifen as a first strike inhibitor, at the same time I would include or continue the same protocol that you have with your anti estrogen, that will slow down the overall circulation of estrogen as the tamoxifen binds aggressively to The receptors within the ducts blocking the present circulating estrogen from binding to The receptors..


Aromatization (basics)

let's talk about the basic universal principles of Aromatization

Aromatization is the process by which the body converts anabolic steroids and/or testosterone into what?
That's right, estro..
By now this is something that either most of us know,or some are just learning about..But whats not being explained is the reason why?

It's crucial that we understand exactly what is going on...

First and foremost, the principles that govern our body,The human body loves balance. Have you ever heard of the term "homeostasis"?
The term homeostasis represents the dynamics within the body and it's will to regulate the systems within the body.
The body/system/endocrine likes to dictate and micromanage everything: From fat levels, to hormones,muscle mass, your neurotransmitters, and basically your overall body-weight, and keep these in a narrow range.

Fact of the matter is, There's many,many systems of checks and balances within the body. If/when one fails, there is usually another one that will intervene and assist...

Let's take the instance that aromatization is in the process due to AAS, now the body will begin to convert some of the exogenous (whether the introduction comes in the form of injection/IM/Sub-Q,or an oral administration) hormone that come from an outside source, into estrogen to try and keep a balance between male and female hormone/sex hormones in the system/endo. With this being said, even the male body contains natural amounts of the female hormones estrogen and progesterone. However, what the male body does NOT posses (( In most cases )) is enormous amounts of hundreds and in some cases thousands of milligrams of testosterone floating around. The average healthy male who does not have carry a set of bull-Nuts between his legs can/may produces on/around 4-7mg per day..
That's merely around 40-50 milligrams per week. So, with this being said, what exactly do YOU think happens when we inject 250,500+ milligrams of test into our system???
I hope you guessed right..Your estrogen (E2) goes up...Why? Because It has to, back to the term "Homeostasis" the universal principles on how the body likes balance and narrow ranges..What's crucial here is getting bloods (lab work) done,pre,mid,and post-cycle.. This way you have a good indicator of where you are and what's going on with your hormonal levels..This is key to knowing how to treat/combat your E1/E2 "estrogen and progesterone"
Now,What to do about this excess estrogen? Here's the thing, if/when estrogen goes up but yet stays in "proportion" to the increased amount of testosterone, you don't have to worry too much here. However If for some reason,your the unlucky and your genetics produce an enzyme called aromatase, you could have a potential issue on hand.. (By now you should get the idea on where I'm going with this).
Aromatase is an enzyme that will manipulate test,by converting testosterone into estrogen as its primary function,yielding it as it's pivotal roll. The more aromatase you posses in your system, the more testosterone to estrogen conversion you will have as well.
Many people have asked me the following- "How do I know if I'm genetically prone or posses high aromatase levels naturally? Unfortunately,You don't know. You can't,there is no real indicator/test to check for this,and at most cases it's a bit to late by the time you find out (side effects,itchy sore nipples,or worst,lactating ducts)..Unless you have a precondition known as (AES or AEXS) Aromatase excess syndrome..If that was the case,you would be familiarized with everything that I'm discussing here!

where are we going with all of this?

Gyno (gynocomastia),one of the most dreaded words in all of the Anabolic communities/gyms!
What's a key factor here is,knowing your compounds and what drugs are most commonly affiliated with gynocomastia (bitch tits)..To name a few-Methandrostenolone (dianabol) (both liquid and pill), Oxymetholone (anadrol)..And all testosterone esters (yes, even prop), test suspension..And for some users -Nandrolone (Deca)..

With this being said,the most important thing here is what pertains to the aromatization of testosterone/or other compounds into estrogen. The ratio of testosterone to estrogen is what determines how severe your chances are for developing serious estrogenic affects such as gyno/bloat ext... So what do you do to combat this if you are susceptible to gyno/estrogenic effects? Your answer lies in proper use and understanding of anti-estrogen and anti-aromatase drugs,getting BLOOD WORK DONE,and timing your compounds and being proactive and prepared!


:Visions Take home notes:

When an individual has gyno signs,lumps or even worse - lactating you have to Target The receptors and the glandular tissue, when taking a suicide anti-estrogen it takes a long time for them to actually begin working and lowering estro circulation.. when an individual is in this type of situation it's a little bit too far and Beyond to make an inhibitor a priority because now the damage has been done..

In this instance you want to treat the symptoms, thus Tamoxifien would be the best first hand targeting drug of choice.... Target Target Target!!!!!

Below is some basic info pasted to add to the information above (The below author is unknown)


Anti-estrogens can be crucial to safe and effective anabolic steroid usage. There are a few key purposes to use them, and a few nontraditional yet valuable alternative usages as well. We will go over both. Most of the uses vary due to the different mechanism of action for each drug; the way they work. Depending on the mechanism of action, a given anti-estrogen drug may be more or less suited to your unique need.
As a side note, in some of these explanations, the chemical and medical literature will not be the same as you will find in genuine text books on the dry topics. We are using these terms with strict purpose of understanding the physiology and biochemistry of anabolic steroids for our purposes. Please keep this in mind.

Anti-estrogens work in a few basic ways. The first is to block the estrogen receptor itself. This is known as a second line inhibitor because estrogen is allowed to be produced, it is just blocked at the receptor. This occurs by the anti-estrogenic drug fitting into the estrogen receptor, and “taking its parking space”. When the original estrogen comes along, it can no longer fit into the receptor. Examples of second line inhibitor drugs would be clomid or nolvadex. Both of these drugs are actually estrogens, they are just so weak that they do not elicit any of the negative effects of the true estrogen, and thereby, block the negative estrogenic effects. These are also two of the most known drugs since the athletic usage of anabolic steroids began.

First line inhibitors are drugs such as arimidex and proviron. Although these two drugs are from different chemical classes, they are both first line inhibitors. Proviron is actually a steroid with zero direct anabolic activity. As we will soon describe, proviron has other benefits aside from its anti-estrogenic activity. It is used clinically to replace androgens in the male for the purpose of sex drive and virility. Arimidex is a drug which is a chemical antagonist. For the purpose of estrogen talk, we can consider first line inhibitors and chemical antagonists to be the same. What is meant by this, is, the estrogen is inhibited at site of production, not at the receptor. Both arimidex and proviron will bind to the aromatase enzyme and render it inactive. Without the aromatase enzyme the body cannot convert various anabolics into estrogen. Estrogen is essentially blocked at its root, where it is originally produced.
First line inhibitors are usually a more effective and potent method of estrogen control. The disadvantage is that the first line inhibitors will usually not do much for whatever estrogen is already present in the system. It will only work on preventing further amounts of excess estrogen from being produced. In practical terms, this will result in a delay from days’ to weeks’ time before a significant anti-estrognic affect is seen. This is fine if you are just using it as precaution, but if you need immediate anti-estrogen activity due to excessive bloat or, you will want to take a second line inhibitor such as clomid or nolvadex immediately. Once the immediate estrogen is under control, you can add in the first line inhibitors to prevent further accumulation of estrogen metabolites in your system.
Here is a little more detail about these most popular anti-estrogens in order to help you choose how and when to use which:

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Nolvadex is one of the most well known anti-estrogens. It is also one of the oldest and most popular medications for breast cancer victims, which is the text book clinical use for this drug. Nolvadex is actually a weak estrogen and will bind to the estrogen receptor. The receptor is then occupied and when the normal and stronger estrogen floats by the receptor, it has no where to “park”. This is what we have defined as the classic second line inhibitor. Second line, because we are allowing estrogen to be produced, we are just blocking it at the receptor. For male usage, nolvadex is a good drug of choice to use for ant-bloating and to control gyno if you are not particularly susceptible to these estrogenic side effects. If you are not and just need minor control, 20mg per day is probably enough to keep the majority of water off and your nips from being sensitive. If you are susceptible, you may need a stronger ant-estrogen, or may need to combine nolvadex with another anti-estrogenic drug, or may need a much higher dosage of nolvadex (probably closer to 40mg/day).
There is some literature out there that states nolvadex having better leutinizing (testosterone stimulating) properties than clomid. This is with respect to post cycle recovery and jump starting your natural testosterone. Personally, amongst all my friends and colleagues, I have not found this to be true. With respect to post cycle recovery of natural testosterone production clomid is definitely more effective.

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As we’ve stated above, clomid is more effective at restoring natural testosterone production. Everything you read about these two drugs seems to offer the same info. I will afford you with something different. For anti-estrogen protection, nolvadex is probably a little stronger. Its chemical structure makes for a slightly more potent anti-estrogen. I have yet to see any quality literature which describes the affinity for either drug at the estrogen receptor. Clomid after all, is also a weak estrogen. Another term used to classify clomid and nolvadex is “competitive inhibitor”. They are so called due to the fact that they are weak estrogens and actually bind to the receptor. By doing this they are competing for the “parking spot” in the receptor, thereby occupying the space when the truer, stronger estrogen comes along. Its like being at the local mall and having someone pull around the isle, cut you off and take your spot. In a sense they just “competed” with you for your spot and “inhibited” you from taking it. Got it? Good. See this stuff is simple, my fellow friends and athletes.
The literature also fails to describe exactly why clomid works more efficiently as a leutinizer. Even in the medical literature, the drug is primarily used for fertility purposes for both males and females. This means clomid has value in stimulating the pituitary in both men and women. Clomid is used on a five day course in order to stimulate ovulation in the female in order to enable fertilization. There is not a fertility doctor in the world that doesn’t know what clomid is. It is a drug that has always been in their toolbox. Part of the reason is, it works. The literature is less extensive for fertility cases in the male but know that it is indeed used for this purpose. Now, as much as I am all for underground self taught knowledge, we have to hand it to the medical professionals for specific cases. For example, if nolvadex were a better leutinizer, it would be the drug of choice in fertility clinics for stimulating ovulation in the female and for aiding fertility and motility of sperm in the male. Simple fact is that this is not the case. Save your self time and frustration by using a medically time tested drug for your post cycle recovery of testosterone. For recovery of your natural test, use clomid.

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Arimidex is called a chemical inhibitor of estrogen. Actually, it is a chemical inhibitor of the enzyme aromatase. Arimidex has a high affinity (liking for) for the aromatase enzyme. As we’ve said before, it is aromatase that converts various drugs into their estrogenic metabolite that can bind to the estrogen receptor and bring about side effects. Arimidex is an effective anti-estrogen and had a great deal of popularity when physique athletes began to get a hold of it. The only problem was the cost. The pills came in 1mg tabs and were over $10/pill. To top it off, not many underground companies were making legitimate arimidex so you didn’t have much choice as a buyer. Now the price has dropped considerably with the availability of other anti-estrogens such as femara (a much stronger and often unnecessary anti-estrogen). Personally, companies like IP (international pharmaceuticals) have excellent products, you just need to trust your source-but that is your deal.

Okay, assuming you have access to a legit arimidex product, you do not need the full 1mg tab per day. Even if you encounter an estrogenic problem your best bet is to add a second anti-estrogen, rather than simply increasing the dosage of arimidex. No matter how cheap you can currently find arimidex, this will be a cheaper (on your wallet) and more effective technique with respect to killing the side effects. You can find cheap nolvadex and clomid almost anywhere. Just add in 20mg or so of the nolvadex or 50mg per day of the clomid (if you have a cheap connection, sometimes clomid pricing can be outrageous too). If you have an immediate estrogen issue, pick nolvadex over clomid and start your dose closer to the 40mg per day mark. This should wipe out any estrogen currently floating around in your system and causing problems.
As for the arimidex, I (and many friends) have found .5mg every other day (eod) to be perfect. Then again, I do not particularly fall vulnerable to estrogenic side effects. If you are like me and don’t tend to get much estrogen build up, this dose will probably work fine. I have read literature (by gurus) that describes arimidex having a short half life on the accord of 4-8 hours. This is incorrect. If you consult any medical pharmaceutical book you will find the half life is much longer, in the area of 24-36 hours. Now, in my opinion I do not fully trust that the half life is quite that long either. However, I do know that the activity of the drug will last at least that long. The “free” drug in the bloodstream has hours that can be debatable. However, for our purposes we only care about how long the drug can be active binding up that estrogen bad guy. Typically drugs which bind enzymes do not dissociate from them over the course of just a couple hours. The most important thing to consider here is the duration of drug action, which is on par with the half life listed in the medical and pharmaceutical texts, 24-36 hours. Due to the long half life, you could take 1mg of arimidex eod when wishing to increase the dosage. There really is no need to take it every single day unless you are using very small amounts per dose. For example, I like to be consistent every single day with what I do. I’ve tried the eod schedule as I explained above, but often would forget to take the dose on dose day. Instead, I found myself some .25mg tabs and then just took one tab every evening before bed. This worked great. If you are using another anti-estrogen, use it equal time spaces from you arimidex. The theory here is to maximize blood levels of one drug while the other is falling so you have round the clock protection.

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