Get Some
MuscleHead
- Sep 9, 2010
- 3,442
- 649
I've been meaning to post this write up for awhile now. I wrote it a few years back, but this info is timeless. Hope this helps a few peeps understand the "other" hormones on a deeper level.
In my opinion, most people do not pay enough attention to estrogen levels because they are more concerned with testosterone. Even more concerning is the people who don't pay much attention to estrogen while running a nandrolone or trenbolone because of the "prolactin" or porgesterone receptor related sides. Well, I'm here to hopefully clarify these things for some of you. This shouldn't take too long to read and it could save you some real trouble and hassle in the future. I tried to divide it up into basic sections if you are looking for something specific but don't want to read it all (please at least read the portion toward the end about Progesterone interaction).
Estrogen is commonly referred to as "E2" in many threads you will see and is actually a reading of one's "estradiol" levels. Estrogens are made up of Estrone (E1), Estradiol (E2), and Estriol (E3) (though the one we're concerned with is E2 specifically). It is ok to simply refer to these as estrogen, but it's more important that you know how to control your own through a basic understanding of the topic.
Complexity and Sexual Makeup
The mechanisms through which E2 interacts with sexual reproductive organs and other hormones in the male body is actually much more complex than in a woman's body. This is mainly because we have so little E2 compared to our counterparts. The same can be said of testosterone in women; a slight change in levels can trigger huge changes. A lot of people know the term "aromatase" or "aromatization" when it comes to testosterone vs estrogen levels. But, many don't know that the leydig cells in your testicles are responsible for the aromatase process which creates E2. Natural E2 in this instance is responsible for the prevention of sperm cell apoptosis (basically the death of that sperm cell through mutation). So, E2 plays an important role in maintaining healthy sexual function in your life.
What is Normal?
The average human male E2 level will sit somewhere in-between 15 - 60 pg/mL. The middle of this range is obviously ideal for several reasons, but both end of the spectrum need to be examined to better understand the effects it can have on your body. First of all, let's point out that these "normal" male levels are about the same as a post-menopausal female. So, it makes sense that the higher your levels go past that top number, the more female characteristics start to take shape (much like some post-menopausal women may lose some female characteristics and may even develop some testosterone related attributes such as hair on their face). But what about the low end? Is that a graveyard for both sexes?
What is Low and What are the Symptoms?
Low can be described as anything lower than that 15 pg/mL benchmark. However, it is possible for your levels to drop dangerously close to ZERO. It's funny when we as a society think so much about testosterone as the driving force of sexual thought and action in males, but actually E2 levels are just as important in maintaining that sexual desire. And to go even further, it's a desire for life and the feelings and emotions that will propel you through life. With low E2 levels, much of this is lost and most individuals feel like "hope is lost" and experience a very downtrodden feeling. I have been there myself (confirmed labs of less than 10 pg/mL) and I can tell you it's no fun at all.
How to Avoid Dropping Into the Danger Zone
For awhile now in bodybuilding community we have been using SERMs and AIs to control our "estrogen" levels for fear of "bitch tits" or gynecomastia. Well, that is one of the side effects if you let the aromatase process get out of control. On the other end of the spectrum is the loss of sex drive and the previously discussed downtrodden feeling. The main way you find yourself on the low end of the spectrum is by overdoing it in the prevention department. Many men who have had any gyno symptoms at all are so afraid of getting it again that they will consistently use far too high of an AI or SERM dose far too often in an effort to keep it at bay. Knowing the function of these items you are using to combat additional aromatase production is crucial in controlling and stabilizing levels. Since I have found a nice routine, I am able to keep my levels between 20-25 pg/mL with little problem.
Aromatase Inhibitors (AIs) - Dosage and Effective Action
The most common aromatase inhibitor you will hear of people using is Arimidex, which is actually just the name brand for the drug anastrozole. The other two you commonly hear about are Aromasin (exemestane) and Femara (letrozole).
Arimidex (anastrozole) - Has a half life of about 3 days and a common dosage of 1mg per day or 1mg every other day. A more advisable dose is 1mg E3D or 0.5mg EOD. Being that arimidex has a longer half life, it's harder to see what does will be right for you unless you guess right from the outset. Anastrozole works through competitive inhibition. Basically, this means it blocks androgens from finding the necessary enzymes to bond with and go through the aromatase process (see chart below for basic explanation).
Femara (letrozole) - Has a half life of about 2 days and a common dosage of 2.5mg per day or EOD. A more advisable dose would be 1.25mg EOD if you are looking to use Letrozole throughout cycle. However, because Letro acts through BOTH competitive inhibition AND reversible binding, it's much better to just keep this one on hand for flare ups. What's reversible binding you may say? Well take a look back at that chart and imagine the "round-headed" peg has already found it's enzyme. While anastrozole will seek out open slots, letrozole rips out cells from their occupied slots and stops the conversion process. This sounds like the answer right? Well, it's still harder to control this mechanism of action because of the conversion rate of double action going on. Like I said, it is best to start use when you have a gyno flare up and then discontinue use a day or two after the symptoms subside (and go back to using either arimidex or aromasin).
Aromasin (exemestane) - has a half life of about 23-27 hours or roughly one day, and a common dosage is 25mg EOD. A more suitable dosage would be 6.25 mg ED or 12.5mg EOD. Aromasin is a definitive Suicide Inhibitor, meaning it permanently and irreversibly binds to enzymes looking to convert androgens to aromatase. This sounds great on paper, like you would only need a few doses.... but the reality is that our bodies are constantly up-regulating the supply of available enzymes as others die. So, continued use throughout cycle is needed. This is the one drug IMO that if you can find the sweet spot, you are in the money! 12.5mg EOD will be enough for most to keep a steady level going, or you can use 6.25 mg ED to keep levels steady because of the shorter half life (although either method will produce very similar levels in most). Aromasin also binds to SHBG, lowering the available amount to bind with free test, thus increasing free test levels (It's a much more complicated process than that and I'm sure I'll write in more detail about it soon).
Adex vs Asin
The fundamental difference you need to understand about Arimidex and Aromasin (other than half-life) is the actual chemical structure itself. Aromasin is very similar in structure to Androstenedione (I'm sure you all know what that is) and actually fools the enzymes into thinking it is match and they are supposed to attach. By the time the aromasin latches on, it's too late for that enzyme....there is no going back. Arimidex can also occupy that slot, but at some point will be kicked out because of competition and a low cellular structure match (almost like a human body sometimes rejects donor organs). In vitro studies suggest a 90+% protein binding rate for Aromasin, while it makes sense based on the previous comment that Arimidex only has a protein binding rate of about 40%. In addition, the reason that a much smaller dose of arimidex is needed is because the bioavailability is very high at 85-90%, while the bioavailability of Aromasin is near 60%. So, Arimidex is more efficient in doing it's job, but Aromasin appears to be more effective (especially on paper if you go by the numbers).
What about SERMs?
SERMs or Selective Estrogen Receptor Modulators are basically estrogen receptor antagonists. The two most common that we talk about are tamoxifen (Nolvadex) and clomifene (Clomid). Clomifene directs it actions only at the hypothalamus, not directly on breast tissue... so, this indirect approach is not nearly as effective as Tamoxifen. Tamoxifen does act directly on breast tissue but in a different way than the AIs we discussed earlier. While tamox also competitively binds to estrogen receptors/enzymes, it cannot remove or reverse any binding that has already occurred. In addition, it is incapable of causing the "cell death" that AIs can create. This would make tamoxifen a poor choice for those who have experienced gynecomastia in the past or are currently experiencing symptoms. However, if a regimen of 10-20mg EOD is started JUST PRIOR to a cycle it can be effective in limiting the amount of conversion. The reason I use the words "just prior" is because the half life of Tamox is about 5-7 days; much longer than any AI. You want to start using the tamox a few days before your first injection in order to prep your receptors for the onslaught of androgens.
How about Progesterone?
Progesterone and Estrogen are interrelated in the way that they are both byproducts of exogenous hormone administration. 19-nor compounds such as trenbolone and nandrolone will have a pronounced effect on progestenic activity and can stimulate prolactin over-production in breast tissue. It is a very common mistake that people use "prolactin receptor" and "progesterone receptor" interchangeably. They are very different receptors found in different locations in the body. They can have pronounced effects on each other, but only through the key "bridge" that makes it happen.... estrogen. Look at the chart below to get a basic idea of how progesterone can convert to estradiol and other estrogens.
So What's the Estrogen to Progesterone Connection Mean?
As you can see in the chart, all roads lead to estrogen. However, the road also starts much the same. It is very hard for progesterone to do it's job without estrogen present. So, if you keep your estrogen levels under control, then there shouldn't be much of an issue. This is the basic reason why the method of running testosterone higher than a nandrolone WILL NOT minimize any side effects. Those who swear by this method are really just controlling their estrogen levels and giving credit to the higher dose of test. In reality, some people do not run an AI when they run lower levels of test, but they do run an AI or increase the dose with higher levels of test. This may account for the method working better even though the increase in testosterone is not directly attributable.
BOTTOM LINE SUMMARY
1. Get regular blood tests done to check your levels and make sure you are doing a good job of stabilizing them
2. make sure you always have the necessary prevention items in place BEFORE you start your cycle
3. before you resort to using a prolactin antagonist, make sure your estrogen levels are under control first (in fact, many people believe that letrozole is in fact an effective prolactin antagonist, however, it's just really effective at lowering high E2 levels quickly)
4. Experiment until you find what is right for you... don't just aim blindly, but dose based on what I've set forth in this article combined with what works well for others you know. Once you find the sweet spot, this is one less thing you need to worry about.
5. If you actually read this far, pat yourself on the back
- Get Some
In my opinion, most people do not pay enough attention to estrogen levels because they are more concerned with testosterone. Even more concerning is the people who don't pay much attention to estrogen while running a nandrolone or trenbolone because of the "prolactin" or porgesterone receptor related sides. Well, I'm here to hopefully clarify these things for some of you. This shouldn't take too long to read and it could save you some real trouble and hassle in the future. I tried to divide it up into basic sections if you are looking for something specific but don't want to read it all (please at least read the portion toward the end about Progesterone interaction).
Estrogen is commonly referred to as "E2" in many threads you will see and is actually a reading of one's "estradiol" levels. Estrogens are made up of Estrone (E1), Estradiol (E2), and Estriol (E3) (though the one we're concerned with is E2 specifically). It is ok to simply refer to these as estrogen, but it's more important that you know how to control your own through a basic understanding of the topic.
Complexity and Sexual Makeup
The mechanisms through which E2 interacts with sexual reproductive organs and other hormones in the male body is actually much more complex than in a woman's body. This is mainly because we have so little E2 compared to our counterparts. The same can be said of testosterone in women; a slight change in levels can trigger huge changes. A lot of people know the term "aromatase" or "aromatization" when it comes to testosterone vs estrogen levels. But, many don't know that the leydig cells in your testicles are responsible for the aromatase process which creates E2. Natural E2 in this instance is responsible for the prevention of sperm cell apoptosis (basically the death of that sperm cell through mutation). So, E2 plays an important role in maintaining healthy sexual function in your life.
What is Normal?
The average human male E2 level will sit somewhere in-between 15 - 60 pg/mL. The middle of this range is obviously ideal for several reasons, but both end of the spectrum need to be examined to better understand the effects it can have on your body. First of all, let's point out that these "normal" male levels are about the same as a post-menopausal female. So, it makes sense that the higher your levels go past that top number, the more female characteristics start to take shape (much like some post-menopausal women may lose some female characteristics and may even develop some testosterone related attributes such as hair on their face). But what about the low end? Is that a graveyard for both sexes?
What is Low and What are the Symptoms?
Low can be described as anything lower than that 15 pg/mL benchmark. However, it is possible for your levels to drop dangerously close to ZERO. It's funny when we as a society think so much about testosterone as the driving force of sexual thought and action in males, but actually E2 levels are just as important in maintaining that sexual desire. And to go even further, it's a desire for life and the feelings and emotions that will propel you through life. With low E2 levels, much of this is lost and most individuals feel like "hope is lost" and experience a very downtrodden feeling. I have been there myself (confirmed labs of less than 10 pg/mL) and I can tell you it's no fun at all.
How to Avoid Dropping Into the Danger Zone
For awhile now in bodybuilding community we have been using SERMs and AIs to control our "estrogen" levels for fear of "bitch tits" or gynecomastia. Well, that is one of the side effects if you let the aromatase process get out of control. On the other end of the spectrum is the loss of sex drive and the previously discussed downtrodden feeling. The main way you find yourself on the low end of the spectrum is by overdoing it in the prevention department. Many men who have had any gyno symptoms at all are so afraid of getting it again that they will consistently use far too high of an AI or SERM dose far too often in an effort to keep it at bay. Knowing the function of these items you are using to combat additional aromatase production is crucial in controlling and stabilizing levels. Since I have found a nice routine, I am able to keep my levels between 20-25 pg/mL with little problem.
Aromatase Inhibitors (AIs) - Dosage and Effective Action
The most common aromatase inhibitor you will hear of people using is Arimidex, which is actually just the name brand for the drug anastrozole. The other two you commonly hear about are Aromasin (exemestane) and Femara (letrozole).
Arimidex (anastrozole) - Has a half life of about 3 days and a common dosage of 1mg per day or 1mg every other day. A more advisable dose is 1mg E3D or 0.5mg EOD. Being that arimidex has a longer half life, it's harder to see what does will be right for you unless you guess right from the outset. Anastrozole works through competitive inhibition. Basically, this means it blocks androgens from finding the necessary enzymes to bond with and go through the aromatase process (see chart below for basic explanation).
Femara (letrozole) - Has a half life of about 2 days and a common dosage of 2.5mg per day or EOD. A more advisable dose would be 1.25mg EOD if you are looking to use Letrozole throughout cycle. However, because Letro acts through BOTH competitive inhibition AND reversible binding, it's much better to just keep this one on hand for flare ups. What's reversible binding you may say? Well take a look back at that chart and imagine the "round-headed" peg has already found it's enzyme. While anastrozole will seek out open slots, letrozole rips out cells from their occupied slots and stops the conversion process. This sounds like the answer right? Well, it's still harder to control this mechanism of action because of the conversion rate of double action going on. Like I said, it is best to start use when you have a gyno flare up and then discontinue use a day or two after the symptoms subside (and go back to using either arimidex or aromasin).
Aromasin (exemestane) - has a half life of about 23-27 hours or roughly one day, and a common dosage is 25mg EOD. A more suitable dosage would be 6.25 mg ED or 12.5mg EOD. Aromasin is a definitive Suicide Inhibitor, meaning it permanently and irreversibly binds to enzymes looking to convert androgens to aromatase. This sounds great on paper, like you would only need a few doses.... but the reality is that our bodies are constantly up-regulating the supply of available enzymes as others die. So, continued use throughout cycle is needed. This is the one drug IMO that if you can find the sweet spot, you are in the money! 12.5mg EOD will be enough for most to keep a steady level going, or you can use 6.25 mg ED to keep levels steady because of the shorter half life (although either method will produce very similar levels in most). Aromasin also binds to SHBG, lowering the available amount to bind with free test, thus increasing free test levels (It's a much more complicated process than that and I'm sure I'll write in more detail about it soon).
Adex vs Asin
The fundamental difference you need to understand about Arimidex and Aromasin (other than half-life) is the actual chemical structure itself. Aromasin is very similar in structure to Androstenedione (I'm sure you all know what that is) and actually fools the enzymes into thinking it is match and they are supposed to attach. By the time the aromasin latches on, it's too late for that enzyme....there is no going back. Arimidex can also occupy that slot, but at some point will be kicked out because of competition and a low cellular structure match (almost like a human body sometimes rejects donor organs). In vitro studies suggest a 90+% protein binding rate for Aromasin, while it makes sense based on the previous comment that Arimidex only has a protein binding rate of about 40%. In addition, the reason that a much smaller dose of arimidex is needed is because the bioavailability is very high at 85-90%, while the bioavailability of Aromasin is near 60%. So, Arimidex is more efficient in doing it's job, but Aromasin appears to be more effective (especially on paper if you go by the numbers).
What about SERMs?
SERMs or Selective Estrogen Receptor Modulators are basically estrogen receptor antagonists. The two most common that we talk about are tamoxifen (Nolvadex) and clomifene (Clomid). Clomifene directs it actions only at the hypothalamus, not directly on breast tissue... so, this indirect approach is not nearly as effective as Tamoxifen. Tamoxifen does act directly on breast tissue but in a different way than the AIs we discussed earlier. While tamox also competitively binds to estrogen receptors/enzymes, it cannot remove or reverse any binding that has already occurred. In addition, it is incapable of causing the "cell death" that AIs can create. This would make tamoxifen a poor choice for those who have experienced gynecomastia in the past or are currently experiencing symptoms. However, if a regimen of 10-20mg EOD is started JUST PRIOR to a cycle it can be effective in limiting the amount of conversion. The reason I use the words "just prior" is because the half life of Tamox is about 5-7 days; much longer than any AI. You want to start using the tamox a few days before your first injection in order to prep your receptors for the onslaught of androgens.
How about Progesterone?
Progesterone and Estrogen are interrelated in the way that they are both byproducts of exogenous hormone administration. 19-nor compounds such as trenbolone and nandrolone will have a pronounced effect on progestenic activity and can stimulate prolactin over-production in breast tissue. It is a very common mistake that people use "prolactin receptor" and "progesterone receptor" interchangeably. They are very different receptors found in different locations in the body. They can have pronounced effects on each other, but only through the key "bridge" that makes it happen.... estrogen. Look at the chart below to get a basic idea of how progesterone can convert to estradiol and other estrogens.
So What's the Estrogen to Progesterone Connection Mean?
As you can see in the chart, all roads lead to estrogen. However, the road also starts much the same. It is very hard for progesterone to do it's job without estrogen present. So, if you keep your estrogen levels under control, then there shouldn't be much of an issue. This is the basic reason why the method of running testosterone higher than a nandrolone WILL NOT minimize any side effects. Those who swear by this method are really just controlling their estrogen levels and giving credit to the higher dose of test. In reality, some people do not run an AI when they run lower levels of test, but they do run an AI or increase the dose with higher levels of test. This may account for the method working better even though the increase in testosterone is not directly attributable.
BOTTOM LINE SUMMARY
1. Get regular blood tests done to check your levels and make sure you are doing a good job of stabilizing them
2. make sure you always have the necessary prevention items in place BEFORE you start your cycle
3. before you resort to using a prolactin antagonist, make sure your estrogen levels are under control first (in fact, many people believe that letrozole is in fact an effective prolactin antagonist, however, it's just really effective at lowering high E2 levels quickly)
4. Experiment until you find what is right for you... don't just aim blindly, but dose based on what I've set forth in this article combined with what works well for others you know. Once you find the sweet spot, this is one less thing you need to worry about.
5. If you actually read this far, pat yourself on the back
- Get Some
