Gynecomastia (Gyno)
Gynecomastia is colloquially referred to as 'gynecomastia', gyno, lesbian scissors, and the presence of abnormal breast tissue in certain areas.
Gynecomastia is most often characterized by the possession of breast tissue.
Gynecomastia is a medical entity that can be caused by a variety of causes, but estrogen, estrogen bodies, or estrogen and/or substances (excluding estrogens from plastics, plants, food, etc.) in the breast tissue, especially in the glandular and nipple areas, are likely causes. There are foods that occur.
It is usually caused by an unbalanced environment where the breakdown of estrogen is mitigated or unbalanced.
Gynecomastia is basically an asset of additional glandular tissue, and in the case of anabolic steroid use, it is usually the result of increased estrogenic activity in the relationship, mostly due to aromatization (conversion of androgens to estrogens), or an estrogenic favorable anabolic steroid in itself (e.g. Nandrol-50).
Gynecomastia tends to occur when a very estrogenic component is added, although it can also occur when an estrogenic component is fixed, which we will discuss more in the case of combining.
It's important to understand that gynecomastia is usually a result of estrogen.
These various causes include puberty, demonology, individual sensitivity, and other behavioral activities in the same subset as progesterone.
We will discuss gynecomastia in more detail later in this article using anabolic stability. It is also very important to note that not all anabolic steroids have the ability to convert to estrogen, but they can contain or reduce gynecomastia, and in fact most anabolic steroids have the ability to produce gynecomastia.
However, some of the most effective and popular anabolic steroid analogs tend to have moderate to high levels of conversion to estrogen.
For example, Dianabol (Mildrostanolone), Testosterone, or Equipoise (Boldenone) will convert to estrogen to a degree that allows for a base building or athletic handle.
However, the unreliable thing about gynecomastia is that it can be taken to a rather extreme, as gynecomastia often uses the same stability as anabolic, but is actually most easily tolerated.
A general description of the three-dimensional structure of gynecomastia cells is as follows
:Estrogen is the mastermind behind the breast and its support in the form of activating and contributing fibroblasts, growth of ductal tissue (called the mammary epithelial response), ductal lengthening and branching, and activation of fibroblasts through signaling to supply and take up matching estrogen within the breast tissue [i].
In other words, estrogen signals to the ducts, and to the growth and lobules of breast tissue through the presence of estrogen in the breast tissue.
It is very important to relate that estrogen acts to promote the growth of breast tissue, whereas androgens act to inhibit the growth of breast tissue [ii].
Considering the fact that dihydrotestosterone (DHT) is one of the few natural and very safe anti-estrogens, this means that it is possible.
To summarize this explanation, it tells us that these details can only be formulated in the right consumer environment, which is necessary in favor of gynecology, where gynecomastia has developed.
Gyno's internals are specific to anabolic steroids used by base stations or athletes and can occur as a result of puberty not previously mentioned.
A minority of puberty gynecomastia is loved as the second most common cause of disorder in men, but it is actually experienced by more men than anabolic steroid-induced gynecomastia.
Puberty gynecomastia (or puberty-scale gynecomastia) is the result of a change in resolution as a result of force of personnel during puberty, and in many young males, estrogen regulation can be high or excessive enough to initiate and activate a handful of gynecomastia.
Puberty-related gynecomastia is very present, affecting approximately 50% or more of all males in families. [iii] [iv].
However, 75% of gynecomastia cases resolve spontaneously without logical puberty treatment within two years of intervention [v].
The structural description of testosterone (composed of androgens) in the environmental board of directors over the age of 45, gynecomastia may also be a futuristic apartment in the future, Sony's male resistance environment is structured in favor of parts to harmonize with estrogen parts. They tend to be more active[vi].
Higher body fat percentages in male soldiers and women also contribute to gynecomastia, as clinical studies have certified that higher body fat percentages are a risk for estrogen[vii].
This is because the aromatase enzyme is very abundant in adipose tissue, so the higher the body fat percentage, the higher the rate at which androgens are aromatized into estrogen.
Gynecomastia is often ridiculed among the uneducated general public as a side effect of anabolic steroid use, but most people and individuals know relatively nothing about the complexities and various factors involved.
In most cases, it is considered a cosmetic side effect, unattractive and unattractive, but not life-threatening.
The unsightly nature of this side effect has led to ridicule over its association with anabolic steroids, and the degree to which the development of gynecomastia appears and manifests on an individual can vary greatly, from minor and barely noticeable to larger and more noticeable, and can appear very feminine, all of which are very difficult to hide.
Gynecomastia is usually the result of ignorance, neglect, or impatience on the part of the anabolic steroid user.
The majority of gynecomastia caused by anabolic steroid use is usually the result of individuals who are not educated about the general use of anabolic steroids and the proper prevention/management of the various side effects.
Today, with easy access to tons of medical and scientific information as well as the proper compounds, supplements, and medications to help prevent/treat issues like gynecomastia, there is no excuse for anabolic steroid users to succumb to the full development of gynecomastia.
Unlike 40 years ago, ignorance of the proper and responsible use of anabolic steroids is not an excuse.
For those who are interested in learning about the complexities of gynecomastia development on a cellular level and the proper preventative measures (and even intended actions to reverse it), this article will efficiently and thoroughly explain and educate the reader on these topics.
After reading this article, the reader can expect to be thoroughly educated and prepared for the prevention and/or treatment of possible breast growth.
Gynecomastia Caused by Anabolic Steroids
As mentioned earlier, we are almost exclusively interested in anabolic steroid-induced gynecomastia rather than other specific forms.
However, whatever the origin or cause of gynecomastia, the end result of gynecomastia formation is the same and is ultimately caused by the same hormonal dysfunction/disruption, usually at the cellular level.
In the case of anabolic steroid-induced gynecomastia, the initial cause must first be identified and explained.
So far, we have mentioned that most anabolic steroid analogs do not actually have the ability to cause gynecomastia, but only a small number of steroids can.
While there are compounds that can directly contribute to and worsen gynecomastia (where the hormone is thought to interact directly with estrogen receptors in breast tissue), most compounds can worsen gynecomastia through aromatization to estrogen, and there are also compounds that can contribute to gynecomastia indirectly (through other pathways that do not involve aromatization).
It is important to understand which anabolic steroids are of concern when it comes to gynecomastia issues, and how these compounds relate to the development of gynecomastia.
As we emphasized earlier in this article, some of the most effective and popular anabolic steroids tend to aromatize into estrogen in varying rates and degrees.
Below is a breakdown of the various compounds of concern when it comes to gynecomastia.
An aromatizing anabolic steroid (high percentage of aromatization):
- Mibolerone.
- Methyltestosterone
Aromatizable anabolic steroids (moderate rate of aromatization):
- Testosterone Testosterone (all esters and mixtures).
- Methandrostenolone Dianabol (Methandrostenolone)
Aromatizable anabolic steroids (low rate of aromatization):
- Deca Durabolin Nandrolone Decanoate (Nandrolone Decanoate)
- Equipoise Boldenone Undecylenate
- Nandrolone Phenylpropionate
A direct estrogenic anabolic steroid:
- Anadrol 50 Oxymetholone (Oxymetholone)
Gestational anabolic steroid:
- Deca Durabolin Nandrolone Decanoate
- Nandrolone Phenylpropionate Nandrolone Phenylpropionate
- Trenbolone Trenbolone
It stands to reason that a higher rate of aromatization creates a hormonal environment that favors an excess of estrogen, increasing the likelihood of gynecomastia.
This is caused by their affinity for the aromatase enzyme (the enzyme that aromatizes androgens to estrogen), with some androgens exhibiting low, medium, or high affinity for interacting with the aromatase enzyme.
Anabolic steroids with direct estrogenic action, such as Anadrol 50 (oxymetholone), are anabolic steroids that do not aromatize to estrogen at any dose, but exhibit estrogenic activity by themselves (or as a result of their metabolites) at estrogen receptors in breast tissue.
Gynecomastia anabolic steroids, also known as progestins, may not convert to estrogen at all (such as trenbolone), but can cause or exacerbate gynecomastia through the interaction of progestins with estrogen receptors, even in the presence of normal physiologic estrogen levels.
All other anabolic steroids not listed above, such as Anavar (Oxandrolone), Winstrol (Stanozolol), Primobolan (Methenolone), or Masteron (Drostanolone), are dihydrotestosterone derivatives and therefore do not convert to estrogen at any dose, and therefore pose no risk of causing or worsening gynecomastia on their own.
The issue of progesterone and progestogenic anabolic steroids and their effects on gynecomastia is a very misunderstood issue in the bodybuilding and anabolic steroid use community.
It's important to correct these misconceptions and shed light on the proper understanding of this hormonal component, as people are often baffled by the development of gynecomastia despite using anabolic steroids that have no estrogenic effects, such as trenbolone.
While estrogen is the main culprit and key component of gynecomastia, progesterone and progestogenic anabolic steroids and hormones are also known to play a role in the development of gynecomastia in that they potentiate the effects of estrogen on breast tissue growth [viii].
Both estrogen receptors and progesterone receptors are present in breast tissue, and it is understood that the activity of estrogen receptors increases/amplifies the sensitivity/responsiveness of progesterone receptors.
The opposite effect can also occur, where progestins can and do increase the affinity/sensitivity of the estrogen receptor to estrogen.
That is, anabolic steroids with high levels of progesterone (aka progestogenic) activity, such as Nandrolone (Deca Durabolin) or Trenbolone, can potentially 'stimulate' estrogen receptors through interaction with progesterone receptors, increasing their affinity and receptivity to any estrogen circulating in the bloodstream.
The result can be an increased sensitivity to estrogenic effects in breast tissue, which can lead to the development or increased likelihood of gynecomastia.
Because pregnancy activity increases the sensitivity of estrogen receptors, gynecomastia can occur even at normal physiologic plasma estrogen levels.
The complex matrix of estrogen, estrogen receptors, progesterone, and progesterone receptors form a network in which gynecomastia can be a significant problem and not just due to excessive estrogen levels.
In these situations, the use of selective estrogen receptor modulators (SERMs) or aromatase inhibitors (AIs) is usually appropriate to alleviate gynecomastia induced by progestogenic anabolic steroids through their action on estrogenic components, but we will discuss in more detail shortly how to properly and efficiently use AIs and SERMs to treat or prevent gynecomastia.
The final relevant component/issue associated with gynecomastia is a hormone known as prolactin, which can be increased through the use of a variety of anabolic steroids, but is most commonly known to be increased through the use of 19-nor progestins such as trenbolone and/or nandrolone (Deca Durabolin).
Prolactin is a hormone that does not contribute to the formation of breast tissue and is not associated with gynecomastia per se, but can and does trigger lactation in the nipple when plasma levels rise to excessive levels.
In men, the nipple area is usually swollen and clear liquid discharge (lactation) may occur.
Sometimes these symptoms can occur in conjunction with true gynecomastia, and are sometimes mistakenly referred to as "prolactin-induced gynecomastia" in reference to the effects on the nipple area, but this is a misnomer and is commonly associated with gynecomastia.
Excessive prolactin levels can be effectively reduced by using prolactin antagonists (also known as dopamine agonists) such as cabergoline, bromocriptine, or pramipexole.
Vitamin B6 has also been proven to have significant efficacy in reducing prolactin levels in the body[ix] [x] [xi].
Overall, gynecomastia and the mechanisms by which it develops at the hormonal and cellular levels are very complex, with many different pathways of development.
The causative factors are very complex and the specifics are largely unknown even to the medical community.
Several causative agents may be involved, including estrogen, progestins, growth hormone, IGF-1, and prolactin.
However, the bottom line is that most medical experts on the condition believe that a decrease in the androgen:estrogen ratio (favoring high estrogen) is a determining factor in the development of gynecomastia, and that blocking the activity of estrogen to lower total serum estrogen levels or increasing testosterone and DHT levels is the main key to addressing gynecomastia.
While prolactin is not the core cause of gynecomastia, it is one of the factors that contribute to it.
Progesterone and progestins are equally influential.
Gynecomastia is a complex condition made up of many gears that make a machine run, and if one or more of the gears can be effectively removed or stopped, the entire machine that is gynecomastia can be disrupted.
Diagnosis, prevention, and treatment of gynecomastia
Once you understand how gynecomastia works and develops at the cellular level (including its hormonal causes and interactions), it becomes much easier to understand how to treat and prevent the condition (including the drugs and compounds used for this purpose).
Initially, however, an accurate diagnosis of the actual gynecologic condition must first be made.
Many people tend to think that they are experiencing gynecomastia symptoms when they are not, and misconceptions about gynecomastia are caused by undue concern and fear, as well as a lack of understanding of the proper symptoms of the condition.
However, one thing that is clear about gynecomastia is the fact that while it may be considered a frequent or common side effect of anabolic steroid use, it is actually the most easily avoidable side effect.
Diagnosis
The diagnosis of gynecomastia is fairly straightforward and simple.
This is because the prominent and distinct signs and symptoms of gynecomastia are unmistakable to the untrained eye, or even to someone who is not a medical professional.
There is very little guesswork or uncertainty involved in the identification and diagnosis of gynecomastia.
The rate or rate at which gynecomastia develops can vary depending on the stage of development.
This also includes the intensity and severity of the growth, which all depend on a number of factors, such as the type of anabolic steroid used, the dosage, the duration of use, and perhaps the single most important factor, the individual's sensitivity to gynecomastia.
Some people may not develop gynecomastia at all, even with an excessive increase in estrogen, while others may suddenly develop gynecomastia at the slightest increase in circulating estrogen levels.
The development of gynecomastia can occur bilaterally or unilaterally[xii] [xiii].
This means that gynecomastia does not necessarily have to occur on both sides of the chest at the same time, and it can (and often does) occur on only one side of the chest.
Gynecomastia can also appear as if there is little development on one side of the breast while there is significant development on the other.
A significant increase in the diameter of the areola (the circular area around the nipple) or asymmetrical development of chest tissue similar to that described above are also signs of gynecomastia[xiv].
In consultation with a healthcare professional, radiologic evaluation of breast tissue to diagnose gynecomastia typically involves ultrasonography[xv].
Breast tissue extracted by fine-needle aspiration may also be examined for periareolar fibrosis, increased subareolar adipose tissue, and dilated ducts indicative of stromal hyalinization[xvi].
Gynecomastia is also categorized into several developmental stages
1. Sensitivity and pain in the nipple area and/or slightly below (medically known as gynecomastia).
2. marked swelling (also known as "puffiness") in the nipple area (medically referred to as fatty mastopathy). This is when the glandular tissue has not yet developed and is generally considered to be the reversible point of gynecomastia development.
3. full gynecomastia development (at this point, full glandular growth and development and full fatty tissue development have occurred, at which point gynecomastia is irreversible without surgery).
The speed at which these stages progress from one to the other depends on many variables (including your hormonal environment, triggers, and other contributing factors). The aforementioned stages can progress as quickly as two or three days, or as slowly as several weeks.
Some cases of gynecomastia may remain in one of the three stages for weeks or months before progressing (or regressing) to the next stage of development.
The severity of breast growth is sometimes categorized by medical organizations into a grading system[xvii]:
Grade 1: Mild enlargement without skin excess.
Grade 2: Moderate enlargement without skin excess.
Grade 3: Moderate enlargement with skin excess.
Grade 4: Marked enlargement with skin excess.
Prevention and treatment
Prevention and treatment of gynecomastia are very closely related, especially in terms of the drugs and compounds used to alleviate or avoid gynecomastia.
Prevention requires techniques other than the use of additional compounds, substances, or supplements, which we will discuss in more detail shortly.
However, it is important to have a good understanding of the different tools available for the prevention or treatment of gynecomastia, which will be covered and explained in detail first.
This will be followed by a brief discussion of the general appropriate use of these compounds.
Selective estrogen receptor modulators (SERMs)
SERMs are perhaps the best example of a first line of attack (defense) against gynecomastia.
In fact, SERMs were developed for a complication associated with breast tissue growth, namely estrogen-responsive breast cancer.
Because estrogen-responsive breast cancer acts through the same hormonal pathways as gynecomastia, the use of SERMs to prevent, suppress, or halt the development of gynecomastia has proven to be very effective[xviii].
However, the formal use of SERMs as a treatment for gynecomastia has not been approved by the FDA[xix].
At the cellular level, SERMs work to specifically block the activity of estrogen in breast tissue by occupying estrogen receptor sites, preventing estrogen itself from binding to these receptors.
This is also known as estrogen antagonism. SERMs have effects in other parts of the body as well, but are particularly relevant to the prevention and/or treatment of breast cancer.
It is important to note that SERMs do not lower total circulating estrogen levels in the body, but rather block the effects of estrogen in various tissues.
The various SERMs include Nolvadex (tamoxifen), Clomid (clomiphene), Fareston (toremifene), and Evista (raloxifene).
Aromatase Inhibitors (AIs)
Unlike SERMs, AIs work by actually lowering the total circulating plasma levels of estrogen in the body, reducing estrogen levels to normal physiological levels (or much lower levels) when estrogen levels have risen to the very high levels that are typically responsible for the development of gynecomastia.
Estrogen is produced through the conversion of aromatizable androgens (such as testosterone) into estrogen, a process known as aromatization.
The enzyme responsible for this aromatization is called aromatase.
AIs work by binding to aromatase, effectively inhibiting its activity so that it cannot exert its effects on circulating testosterone (or other aromatizable androgens).
When the aromatase enzyme is neutralized, no estrogen is produced, resulting in a decrease in total estrogen levels in the body. Some AIs, such as Arimidex and Letrozole, only temporarily inhibit the enzyme, while others, such as Aromasin, permanently neutralize the enzyme.
AIs that permanently disable the aromatase enzyme are known as suicidal inhibitors, and while the existing enzyme may be permanently inhibited at the time of administration, the body will eventually produce more aromatase to restore normal physiological amounts.
Aromatase inhibitors vary in strength and potency, from very mild (e.g., Proviron) to very strong (e.g., Letrozole), depending on how efficiently they inhibit aromatase.
They include a variety of AIs: Aromasin (Exemestane), Arimidex (Anastrozole), Femara (Letrozole), Proviron (Mesterolone), and others.
Dihydrotestosterone (DHT) Cream
There is anecdotal evidence that dihydrotestosterone creams, when applied specifically to the nipples and area (by rubbing the cream directly into the area), can reverse gynecomastia.
While there is no clinical data to support these claims, the general consensus within and outside of the bodybuilding/anabolic steroid use community is to use DHT cream as a tool in the herbal arsenal to block or suppress the development of gynecomastia after all other medications and treatments have been tried. There are those who claim success.
I believe that our understanding of the role of dihydrotestosterone and testosterone (and androgenic testosterone specifically) as important naturally occurring endogenous anti-estrogens[xx], and the practical application of this understanding to the use of DHT creams in gynecomastia, may be possible.
While there are forms of these drugs and substances that may include a small percentage of female breasts (or even reverse gynecomastia in a small percentage of women), it is important for everyone to carefully read and remember that the medical community generally considers surgical removal to be necessary to completely remove breast growth that has been treated for more than a year (or that has grown beyond the point of no return)[xxi].
Specific uses in gynecomastia
The most commonly used, and by far the most potent SERM, is Nolvadex (tamoxifen), which is used to characterize and treat gynecomastia.
The defensinase cluster will be further exemplified by the fact that Arimidex (Anastrozole) and Aromasin (Exemestane) are two properties that tend to be used almost exclusively in the treatment and activity of gynecomastia.
When it comes to adopting any gynecomastia response method during anabolic steroid recovery, it is initially up to the user.
In general, there are three effective methods.
1. dose adjustment and/or moderate dosing
The most cost-effective way to prevent gynecomastia is simple dose moderation and/or anabolic steroid selection that does not interfere with weight gain or health.
Generally speaking, less is more when it comes to compounds.
Choosing a reasonable dosage or anabolic steroid will eliminate the need to add a daily SERM or AI to your cycle.
For example, running a cycle using TRT doses of testosterone (100mg per week or less) while emphasizing the use of a non-aromatizing anabolic steroid such as Winstrol or Anavar at a slightly increased dose will allow the user to keep the dose of testosterone low enough so that little or no aromatization occurs.
2. Use of SERMs during the cycle -
Simply put, this involves the use of a SERM such as Nolvadex daily during an anabolic steroid cycle, typically at a dose of 20mg per day.
This effectively blocks the estrogen receptors within the breast tissue, preventing excess estrogen from binding to these receptors and stimulating the development of gynecomastia.
However, chronic use of SERMs like Nolvadex has been shown to reduce IGF-1 levels in the body by around 30%[xxii], which can have a significant impact on potential gains.
3. AI Use During a Cycle
Using an AI such as Arimidex or Aromasin daily (or every other day) during an anabolic steroid cycle at doses of 0.5mg and 12.5mg respectively is a common practice in the bodybuilding and anabolic steroid use community.
The key in this case is to control estrogen levels.
Medical Reference:
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