matt88
Member
Let`s talk about Estrogen. I will call it Estrogen 101. The information below is a combination of things I have learned and things I have researched recently in preparation to write this. I am not a doctor and this is not intended to be medical advice. I intend for this to be public use information so please feel free to share it in any manner you see fit. This is not all inclusive information and many of the things contained here will vary person to person.
There is more than one form of estrogen but for the intent and purpose of this writeup we will stick with E2 (Estradiol). I want this to benefit everyone so I have included the basics and I have also included some cool stuff that perhaps the more experienced person is not aware of as well
I don`t count myself as more experienced per say in comparison to many of you but I definitely learned a lot here. Let`s get into it!
Testosterone can be converted into estrogen through a process called aromatization. The enzyme responsible for this conversion is called Aromatase. This enzyme is predominantly found in various tissues throughout the body, including the testes, adipose tissue (fat cells), and the brain.
When testosterone interacts with aromatase, it undergoes a chemical reaction where the aromatase enzyme converts testosterone into estradiol (e2). This conversion occurs via the aromatization process, resulting in the production of estrogen from testosterone.
The amount of aromatase enzyme present in the body can vary greatly among individuals. Factors such as genetics, body fat percentage, age, etc can influence the expression and activity of aromatase. I want to elaborate on estrogen and fat tissue. You may start your anabolic journey at say 20% body fat, At that time you convert a lot of test into estrogen. Overtime you add lean muscle and/or lose body fat and now you are at 12% body fat. You very well may discover that you no longer convert test into estrogen at the same rate. In fact, in many people this can be a drastic difference. I know for me personally when I first started TRT and anabolics I was pretty fat. I had been a pizza loving functional alcoholic for many years. Overtime as I lost fat tissue I started converting less and less test into estrogen. Fast forward to the present and I am now a very low converter.
Let`s discuss an area where a lot of confusion can be had due to conflicting reports and information. The fact is that most people who are giving said information are not wrong per say bc they are speaking from their own personal experience. It is just that we are all SO different in how much aromatase our bodies have and how our bodies respond to these different compounds.
Let`s look at how DHT derivatives can have an estrogen lowering effect in the body. An example of a DHT derivative is Anavar, Proviron, Primo, Masteron, Winstrol, etc. The indirect effect of certain DHT derivatives on estrogen levels is related to their potential interaction with the estrogen receptor. While these compounds primarily bind to androgen receptors, they can also bind to estrogen receptors to some extent. By occupying the estrogen receptors, they may compete with estrogen molecules for these receptor binding sites.
This competition for estrogen receptor binding can lead to a decrease in the overall estrogenic activity in the body. However, it's important to note that the affinity of DHT derivatives for the estrogen receptor is typically lower compared to their affinity for androgen receptors. As a result, their impact on estrogen receptor binding and subsequent estrogen levels may not be as potent as other compounds specifically designed for anti-estrogenic effects such as aromatase inhibitors. The extent of estrogen reduction and the specific effects can vary depending on the compound and individual. It is for that reason that an individual should not ever 100% rely on DHT derivatives for anti estrogen purposes. Always have an Aromatase inhibitor in your tool box bc the last thing you want to happen is needing it right away and not having it.
We know DHT derivatives can have an estrogen lowering effect and now we know why, so how does this transition into how one goes about planning the first time using one of these compounds? We will use Masteron as our example. For most people I would suggest starting out with running your testosterone and Masteron at a 1:1 ratio. A perfect example of this is Euro Pharmacies TRT plus which is a blend of 200mg/200mg of Test/Mast. I would not suggest using an aromatase inhibitor going into running this because you want to see what your estrogen level is at this 1:1 ratio. I will use myself as an example. I am personally abnormal when it comes to this. I am now a very low converter of test to estrogen and I have discovered that I need my testosterone dosage an entire 200mg higher than my masteron dosage. I feel that this is not normal per say when comparing it to others on the forums. A lot of guys can run their DHT derivative higher than their testosterone dosage. This could be due to the fact that they convert much higher than I do or they could simply just not respond the way I do in regards to their estrogen receptors and how the DHT derivative binds to (or the lack thereof) to their estrogen receptors. Some people can also have their estrogen much lower than others without any negative side effects. I believe the majority of this is simply due to genetic disposition.
Aromatase inhibitors, such as Anastrozole (Armidex)), Letrozole (Letro) and Exemestane (Aromasin) are commonly used to block the activity of aromatase. By inhibiting the aromatase enzyme, these drugs can reduce the conversion of testosterone to estrogen and effectively lower estrogen levels in the body. These are the "gold standard" for estrogen management.
Letrozole is a much more potent aromatase inhibitor compared to anastrozole or Exemestane. It effectively reduces estrogen levels by inhibiting a higher percentage of aromatase activity. For that reason, I suggest anyone new to anabolics should avoid Letro entirely until they gain experience and obtain lab work. Its use should only be considered if you are having to take multiple tablets of Exemestane or Anastrozole a week to maintain a normal estrogen range visualized on lab work. If Letro was utilized in place of a typical Anastrozole or Exemestane dosage it would very likely completely crash your estrogen levels for an extended period of time.
Selective estrogen receptor modulators (SERMs) such as Tamoxifen (Nolvadex), Raloxifene,Clomiphene citrate (Clomid), etc.
SERMS can be used to help mitigate the effects of estrogen.
Estrogen Receptor Blockade: SERMs can compete with estrogen for binding to estrogen receptors in various tissues, including breast tissue and the hypothalamus. By blocking the estrogen receptor, SERMs can help reduce the estrogenic effects in these tissues. In terms of how these work, an example would be a parking lot of empty parking spots and you place a traffic cone in a parking spot to block a car from being able to pull into the parking spot.
Negative Feedback on Hypothalamus: In the hypothalamus, SERMs can potentially inhibit the negative feedback loop that estrogen exerts on the hypothalamic-pituitary-gonadal (HPG) axis. This can result in increased release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which can stimulate testosterone production and potentially reduce estrogen levels which is why they drugs are used during a PCT (Post Cycle Therapy)
Gynecomastia Management: Gynecomastia, the enlargement of breast tissue in males, can occur due to very high estrogen. The SERM would block estrogen receptors in breast tissue to prevent the gyno from growing and possibly even shrinking it till it`s essentially gone.
It is important to note that different SERMs have different usages and they don`t all behave in the same way.
**CONTINUED BELOW**
There is more than one form of estrogen but for the intent and purpose of this writeup we will stick with E2 (Estradiol). I want this to benefit everyone so I have included the basics and I have also included some cool stuff that perhaps the more experienced person is not aware of as well
I don`t count myself as more experienced per say in comparison to many of you but I definitely learned a lot here. Let`s get into it!Testosterone can be converted into estrogen through a process called aromatization. The enzyme responsible for this conversion is called Aromatase. This enzyme is predominantly found in various tissues throughout the body, including the testes, adipose tissue (fat cells), and the brain.
When testosterone interacts with aromatase, it undergoes a chemical reaction where the aromatase enzyme converts testosterone into estradiol (e2). This conversion occurs via the aromatization process, resulting in the production of estrogen from testosterone.
The amount of aromatase enzyme present in the body can vary greatly among individuals. Factors such as genetics, body fat percentage, age, etc can influence the expression and activity of aromatase. I want to elaborate on estrogen and fat tissue. You may start your anabolic journey at say 20% body fat, At that time you convert a lot of test into estrogen. Overtime you add lean muscle and/or lose body fat and now you are at 12% body fat. You very well may discover that you no longer convert test into estrogen at the same rate. In fact, in many people this can be a drastic difference. I know for me personally when I first started TRT and anabolics I was pretty fat. I had been a pizza loving functional alcoholic for many years. Overtime as I lost fat tissue I started converting less and less test into estrogen. Fast forward to the present and I am now a very low converter.
Let`s discuss an area where a lot of confusion can be had due to conflicting reports and information. The fact is that most people who are giving said information are not wrong per say bc they are speaking from their own personal experience. It is just that we are all SO different in how much aromatase our bodies have and how our bodies respond to these different compounds.
Let`s look at how DHT derivatives can have an estrogen lowering effect in the body. An example of a DHT derivative is Anavar, Proviron, Primo, Masteron, Winstrol, etc. The indirect effect of certain DHT derivatives on estrogen levels is related to their potential interaction with the estrogen receptor. While these compounds primarily bind to androgen receptors, they can also bind to estrogen receptors to some extent. By occupying the estrogen receptors, they may compete with estrogen molecules for these receptor binding sites.
This competition for estrogen receptor binding can lead to a decrease in the overall estrogenic activity in the body. However, it's important to note that the affinity of DHT derivatives for the estrogen receptor is typically lower compared to their affinity for androgen receptors. As a result, their impact on estrogen receptor binding and subsequent estrogen levels may not be as potent as other compounds specifically designed for anti-estrogenic effects such as aromatase inhibitors. The extent of estrogen reduction and the specific effects can vary depending on the compound and individual. It is for that reason that an individual should not ever 100% rely on DHT derivatives for anti estrogen purposes. Always have an Aromatase inhibitor in your tool box bc the last thing you want to happen is needing it right away and not having it.
We know DHT derivatives can have an estrogen lowering effect and now we know why, so how does this transition into how one goes about planning the first time using one of these compounds? We will use Masteron as our example. For most people I would suggest starting out with running your testosterone and Masteron at a 1:1 ratio. A perfect example of this is Euro Pharmacies TRT plus which is a blend of 200mg/200mg of Test/Mast. I would not suggest using an aromatase inhibitor going into running this because you want to see what your estrogen level is at this 1:1 ratio. I will use myself as an example. I am personally abnormal when it comes to this. I am now a very low converter of test to estrogen and I have discovered that I need my testosterone dosage an entire 200mg higher than my masteron dosage. I feel that this is not normal per say when comparing it to others on the forums. A lot of guys can run their DHT derivative higher than their testosterone dosage. This could be due to the fact that they convert much higher than I do or they could simply just not respond the way I do in regards to their estrogen receptors and how the DHT derivative binds to (or the lack thereof) to their estrogen receptors. Some people can also have their estrogen much lower than others without any negative side effects. I believe the majority of this is simply due to genetic disposition.
Aromatase inhibitors, such as Anastrozole (Armidex)), Letrozole (Letro) and Exemestane (Aromasin) are commonly used to block the activity of aromatase. By inhibiting the aromatase enzyme, these drugs can reduce the conversion of testosterone to estrogen and effectively lower estrogen levels in the body. These are the "gold standard" for estrogen management.
Letrozole is a much more potent aromatase inhibitor compared to anastrozole or Exemestane. It effectively reduces estrogen levels by inhibiting a higher percentage of aromatase activity. For that reason, I suggest anyone new to anabolics should avoid Letro entirely until they gain experience and obtain lab work. Its use should only be considered if you are having to take multiple tablets of Exemestane or Anastrozole a week to maintain a normal estrogen range visualized on lab work. If Letro was utilized in place of a typical Anastrozole or Exemestane dosage it would very likely completely crash your estrogen levels for an extended period of time.
Selective estrogen receptor modulators (SERMs) such as Tamoxifen (Nolvadex), Raloxifene,Clomiphene citrate (Clomid), etc.
SERMS can be used to help mitigate the effects of estrogen.
Estrogen Receptor Blockade: SERMs can compete with estrogen for binding to estrogen receptors in various tissues, including breast tissue and the hypothalamus. By blocking the estrogen receptor, SERMs can help reduce the estrogenic effects in these tissues. In terms of how these work, an example would be a parking lot of empty parking spots and you place a traffic cone in a parking spot to block a car from being able to pull into the parking spot.
Negative Feedback on Hypothalamus: In the hypothalamus, SERMs can potentially inhibit the negative feedback loop that estrogen exerts on the hypothalamic-pituitary-gonadal (HPG) axis. This can result in increased release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which can stimulate testosterone production and potentially reduce estrogen levels which is why they drugs are used during a PCT (Post Cycle Therapy)
Gynecomastia Management: Gynecomastia, the enlargement of breast tissue in males, can occur due to very high estrogen. The SERM would block estrogen receptors in breast tissue to prevent the gyno from growing and possibly even shrinking it till it`s essentially gone.
It is important to note that different SERMs have different usages and they don`t all behave in the same way.
**CONTINUED BELOW**
