Estrogen is Essential for Muscle Growth in Bodybuilders

madman

Member
William Llewellyn’s, ANABOLICS


Estrogen Aromatization

Testosterone is the primary substrate used in the male body for the synthesis of estrogen (estradiol), the principal female sex hormone. Although the presence of estrogen may seem quite unusual in men, it is structurally very similar to testosterone. With a slight alteration by the enzyme aromatase, estrogen is produced in the male body. Aromatase activity occurs in various regions of the male body, including adipose,22 liver,23 gonadal,24 central nervous system,25, and skeletal muscle 26 tissues. In the context of the average healthy male, the amount of estrogen produced is generally not very significant to one's body disposition, and may even be beneficial in terms of cholesterol values (See Side Effects: Cardiovascular System). However, in larger amounts, it does have the potential to cause many unwanted effects including water retention, female breast tissue development (gynecomastia), and body fat accumulation. For these reasons, many focus on minimizing the build-up or activity of estrogen in the body with aromatase inhibitors such as Arimidex and Cytadren, or antiestrogens such as Clomid or Nolvadex, particularly at times when gynecomastia is a worry or the athlete is attempting to increase muscle definition.

We must, however, not be led into thinking that estrogen serves no benefit. It is actually a desirable hormone in many regards. Athletes have known for years that estrogenic steroids are the best mass builders, but it is only recently that we are finally coming to understand the underlying mechanisms why. It appears that reasons go beyond the simple size, weight, and strength increases that one would attribute to estrogen-related water retention, with this hormone actually having a direct effect on the process of anabolism. This is manifest through increases in glucose utilization, growth hormone secretion, and androgen receptor proliferation.

Glucose Utilization and Estrogen

Estrogen may play a very important role in the promotion of an anabolic state by affecting glucose utilization in muscle tissue. This occurs via altering of the level of available glucose 6-phosphate dehydrogenase, an enzyme directly tied to the use of glucose for muscle tissue growth and recuperation.27 28 More specifically, G6PD is a vital part of the pentose phosphate pathway, which is integral in determining the rate nucleic acids and lipids are to be synthesized in cells for tissue repair. During the period of regeneration after skeletal muscle damage, levels of G6PD are shown to rise dramatically, which is believed to represent a mechanism for the body to enhance recovery when needed. Surprisingly, we find that estrogen is directly tied to the level of G6PD that is to be made available to cells in this recovery window.

The link between estrogen and G6PD was established in a study demonstrating levels of this dehydrogenase enzyme to rise after the administration of testosterone propionate. The investigation further showed that the aromatization of testosterone to estradiol was directly responsible for this increase, and not the androgenic action of this steroid.29 The non-aromatizable steroids dihydrotestosterone and fluoxymesterone were tested alongside testosterone propionate but failed to duplicate the effect of testosterone. Furthermore, the positive effect of testosterone propionate was blocked when the aromatase inhibitor 4- hydroxyandrostenedione (formestane) was added, while 17-beta estradiol administration alone caused a similar increase in G6PD to testosterone propionate. The inactive estrogen isomer alpha estradiol, which is unable to bind the estrogen receptor, failed to do anything. Further tests using testosterone propionate and the anti-androgen flutamide showed that this drug also did nothing to block the positive action of testosterone, establishing it as an effect independent of the androgen receptor.


Estrogen and GH/IGF-1

Estrogen may also play an important role in the production of growth hormone and IGF-1. IGF-1 (insulin-like growth factor) is an anabolic hormone released in the liver and various peripheral tissues via the stimulus of growth hormone (See Drug Profiles: Growth Hormone). IGF-1 is responsible for the anabolic activity of growth hormones such as increased nitrogen retention/protein synthesis and cell hyperplasia (proliferation). One of the first studies to bring this issue to our attention looked at the effects of the anti-estrogen tamoxifen on IGF-1 levels, demonstrating it to have a suppressive effect.30 A second, perhaps more noteworthy, the study took place in 1993, which looked at the effects of testosterone replacement therapy on GH and IGF-1 levels alone, and compared them to the effects of testosterone combined again with tamoxifen.31 When tamoxifen was given, GH and IGF-1 levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone. Another study has shown 300 mg of testosterone enanthate weekly to cause a slight IGF-1 increase in normal men. Here the 300 mg of testosterone ester caused an elevation of estradiol levels, which would be expected at such a dose. This was compared to the effect of the same dosage of nandrolone decanoate; however, this steroid failed to produce the same increase. This result is quite interesting, especially when we note that estrogen levels were actually lowered 32 when this steroid was given. Yet another demonstrated that GH and IGF-1 secretion is increased with testosterone administration on males with delayed puberty, while dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-1 secretion.


Estrogen and the Androgen Receptor

It has also been demonstrated that estrogen can increase the concentration of androgen receptors in certain tissues. This was shown in studies with rats, which looked at the effects of estrogen on cellular androgen receptors in animals that underwent orchiectomy (removal of testes, often done to diminish endogenous androgen production). According to the study, administration of estrogen resulted in a striking 480% increase in methyltrienolone (a potent oral androgen often used to reference receptor binding in studies) binding in the levator ani muscle.34 The suggested explanation is that estrogen must either be directly stimulating androgen receptor production or perhaps diminishing the rate of receptor breakdown. Although the growth of the levator ani muscle is commonly used as a reference for the anabolic activity of steroid compounds, it is admittedly a sex organ muscle, and different from skeletal muscle tissue in that it possesses a much higher concentration of androgen receptors. This study, however, did look at the effect of estrogen in fast-twitch skeletal muscle tissues (tibialis anterior and extensor digitorum longus) as well but did not note the same increase as the levator ani. Although discouraging at first glance, the fact that estrogen can increase androgen receptor binding in any tissue remains an extremely significant finding, especially in light of the fact that we now know androgens to have some positive effects on muscle growth that are mediated outside of muscle tissue.


Estrogen and Fatigue

“Steroid Fatigue” is a common catchphrase these days, and refers to another important function of estrogen in both the male and female body, namely its ability to promote wakefulness and a mentally alert state. Given the common availability of potent third-generation aromatase inhibitors, bodybuilders today are (at times) noticing more extreme estrogen suppression than they had in the past. Often associated with this suppression is fatigue. Under such conditions, the athlete, though on a productive cycle of drugs, may not be able to maximize his or her gains due to an inability to train at full vigor. This effect is sometimes also dubbed “steroid lethargy.” The reason is that estrogen plays an important supporting role in the activity of serotonin. Serotonin is one of the body's principal neurotransmitters, vital to mental alertness and the sleep/wake cycle.35 36 Interference with this neurotransmitter is also associated with chronic fatigue syndrome,37 38 so we can see how vital it is to fatigue specifically. Estrogen suppression in menopause has also been associated with fatigue,39 as has the clinical use of newer (more potent) aromatase inhibitors like anastrozole,40 letrozoles,41 exemestane,42 and fadrozole 43 in some patients. These things may be important to consider when planning your next cycle. Although not everyone notices this problem when estrogen is low, for those that do, a little testosterone or estrogen can go a long way in correcting this. It is also of note that the use of strictly non-aromatizable steroids sometimes causes this effect as well, likely due to the suppression of natural testosterone production (cutting off the main substrate used by the male body to make estrogen).

Anti-Estrogens and the Athlete

So what does this all mean to the bodybuilder looking to gain optimal size? Basically I think it calls for a cautious approach to the use of estrogen maintenance drugs if mass is the key objective (things change, of course, if we are talking about cutting). Obviously, antiestrogens should be used if there is a clear need for them due to the onset of estrogenic side effects, or at the very least, the drugs being administered should be substituted for non-estrogenic compounds. Gynecomastia is certainly an unwanted problem for the steroid user, as are noticeable fat mass gains. But if these problems have not presented themselves, the added estrogen due to a cycle of testosterone or Dianabol, for example, might indeed be aiding in the buildup of muscle mass or keeping you energetic. An individual confident they will notice or are not prone to getting, estrogenic side effects, may, therefore, want to hold off using estrogen maintenance drugs so as to achieve the maximum possible gains in tissue mass.



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Nelson Vergel

Founder, ExcelMale.com

 

BuzzSaw

Member
Thank you for this. I'm confused as it mentions estogenic and non estrogenic steriods. Is there a list of what's what? I've been on Sus 250, and also Cypionate. Which group do they fall into?
 

Sides

Member
Thank you for this. I'm confused as it mentions estogenic and non estrogenic steriods. Is there a list of what's what? I've been on Sus 250, and also Cypionate. Which group do they fall into?
Testosterone is an estrogenic steroid, as it partially aromatizes into estrogen. Sustanon 250 and Testosterone Cypionate (assuming you meant Test Cyp, and not some other steroid like Boldenone Cypionate, etc) are both forms of testosterone, and so by nature they are estrogenic. Cypionate is just the ester attached to the testosterone to make it last longer. Sustanon has a mix of four esters, from short-acting to long-acting, so that it has a long duration of activity.

But yes, they are both estrogenic.
 

DS3

Active Member
Thank you for this. I'm confused as it mentions estogenic and non estrogenic steriods. Is there a list of what's what? I've been on Sus 250, and also Cypionate. Which group do they fall into?
Anabolic steroids are going to fall into 1 of three categories: 19-nors, testosterone and testosterone derivatives, and DHT derivatives. There used to be an incredible anabolic steroid chart floating around out there. I can no longer find it.

The breakdown of whether or not a steroid is estrogenic is below. I do not get into the details of how estrogenic a steroid is in comparison to testosterone, but if others want to chime in on this then please do so. Bear in mind, this is not an anabolic steroid forum, and this forum does not condone the use of anabolic steroids outside of HRT. The only hormones you will find with an active use in HRT (despite contention on their ethicality outside of sole-T usage) are oxandrolone (Anavar), nandrolone (Deca), more recently, stanozolol (winstrol).

19-nors :
1. Nandrolone- slightly estrogenic. More progestonic.
2. Trenbolone- Progestonic

Testosterone/Testosterone Derived
1. Testostorone (suspension, propionate, phenylpropionate, cypionate, enanthate, decanoate, undecanoate, all blends (e.g. sustanon)- Estrogenic.
2. Boldenone- Estrogenic. Less than testosterone (about 30% as estrogenic), but still estrogenic.
3. Testosterone Undecanoate (oral)- estrogenic
4. Methyltestosterone- estrogenic
5. Halotestin (derived from methyltestosterone)- not estrogenic
6. Dianabol- estrogenic (highly)

DHT-derivatives
1. Anadrol- estrogenic (highly)
3. Winstrol- non-estrogenic
4. Anavar- non-estrogenic
5. Masteron- anti-estrogenic
6. Proviron- anti-estrogenic
7. Primobolan- non-estrogenic
 
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benaoao

Member
Another study has shown 300 mg of testosterone enanthate weekly to cause a slight IGF-1 increase in normal men. Here the 300 mg of testosterone ester caused an elevation of estradiol levels, which would be expected at such a dose. This was compared to the effect of the same dosage of nandrolone decanoate; however, this steroid failed to produce the same increase. This result is quite interesting, especially when we note that estrogen levels were actually lowered 32 when this steroid was given.
this part is confusing. We know (From AIDS wasting patients and bodybuilders alike) that nandrolone builds more muscle than testosterone yet E2 is much less on nandrolone.

I guess the question is: yes E2 is essential. But how much is actually needed? I highly doubt that more is always better.
 

Gman86

Member
this part is confusing. We know (From AIDS wasting patients and bodybuilders alike) that nandrolone builds more muscle than testosterone yet E2 is much less on nandrolone.

I guess the question is: yes E2 is essential. But how much is actually needed? I highly doubt that more is always better.
Here’s a video along the lines of this topic

 

madman

Member
this part is confusing. We know (From AIDS wasting patients and bodybuilders alike) that nandrolone builds more muscle than testosterone yet E2 is much less on nandrolone.

I guess the question is: yes E2 is essential. But how much is actually needed? I highly doubt that more is always better.

Estradiol being essential is a given and ND only could never provide such.

No one is saying more is better but healthy amounts of estradiol are needed in men.

You will always be bigger/stronger on Test!

Again T and high e2 any day.

Would never waste my time on low dose test with ND let alone ND only.

Much more going on than simply estradiol and water retention.





It appears that reasons go beyond the simple size, weight, and strength increases that one would attribute to estrogen-related water retention, with this hormone actually having a direct effect on the process of anabolism. This is manifest through increases in glucose utilization, growth hormone secretion, and androgen receptor proliferation.
 

madman

Member
Estradiol being essential is a given and ND only could never provide such.

No one is saying more is better but healthy amounts of estradiol are needed in men.

You will always be bigger/stronger on Test!

Again T and high e2 any day.

Would never waste my time on low dose test with ND let alone ND only.

Much more going on than simply estradiol and water retention.





It appears that reasons go beyond the simple size, weight, and strength increases that one would attribute to estrogen-related water retention, with this hormone actually having a direct effect on the process of anabolism. This is manifest through increases in glucose utilization, growth hormone secretion, and androgen receptor proliferation.
 

madman

Member
this part is confusing. We know (From AIDS wasting patients and bodybuilders alike) that nandrolone builds more muscle than testosterone yet E2 is much less on nandrolone.

I guess the question is: yes E2 is essential. But how much is actually needed? I highly doubt that more is always better.

Thought I already made myself clear to you in the other thread when I stated:

think I'll pass seeing as you stated ND is more ANDROGENIC than T clearly confused you are

Go push your ND and MENT only protocols on the other forums with the rest of the herd!
 

DS3

Active Member
Here’s a video along the lines of this topic

I've broken down the results of this study in another thread, demonstrating the following:

Screen Shot 2020-08-09 at 9.30.45 PM.png


From the results of this study, the hypothesis that nandrolone causes greater increases in LBM is not supported. @benaoao posted a couple of studies on another thread discussing their results. One of the studies had highly problematic methods rendering it ineffective at comparing nandrolone and testosterone.

Study link.
 
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DS3

Active Member
this part is confusing. We know (From AIDS wasting patients and bodybuilders alike) that nandrolone builds more muscle than testosterone yet E2 is much less on nandrolone.

I guess the question is: yes E2 is essential. But how much is actually needed? I highly doubt that more is always better.
We actually do not KNOW that nandrolone creates greater increases in LBM than nandrolone.

This study demonstrates the opposite.

Screen Shot 2020-08-09 at 9.30.45 PM.png


This study that you posted has highly problematic methods and is ill-equipped to compare nandrolone and testosterone with regard to lean body mass. The integral issue with the this study you present. The dosing frequency of Testosterone (blend of propionate, phenylpropionate, and decanoate) and Nandrolone was every two weeks. Of the dosage of T that was administered, 150 mg was either propionate or phenylpropionte and 100 mg was decanoate. What does that mean. That means that by the end of week one, the only T left in the participants system was the 100 mg of T decanoate. Due to the suboptimal administration of a blended testosterone preparation, the methods used are ill-equipped to compare the efficacy of 250 mg testosterone to 150 mg of nandrolone.

The other study you posted does not offer the full article, but I would be skeptical that suboptimal methods were used similar to your second study.
 

benaoao

Member
Thought I already made myself clear to you in the other thread when I stated:

think I'll pass seeing as you stated ND is more ANDROGENIC than T clearly confused you are

Go push your ND and MENT only protocols on the other forums with the rest of the herd!
you’re a weirdo dude. Typical me myself and I type. Not sure who the herd is and what my push is about. I’m only here to discuss data. When challenged you go back to making things personal “I will stick to my testosterone”. Good. Idgaf what you do, and idgaf what I do. I only discuss studies and data. If you can’t get to that level then keep jerking off to your balding androgenic reflection in the mirror. Careful with that prostate tho.
 

benaoao

Member
We actually do not KNOW that nandrolone creates greater increases in LBM than nandrolone.

This study demonstrates the opposite.

View attachment 10343

This study that you posted has highly problematic methods and is ill-equipped to compare nandrolone and testosterone with regard to lean body mass. The integral issue with the this study you present. The dosing frequency of Testosterone (blend of propionate, phenylpropionate, and decanoate) and Nandrolone was every two weeks. Of the dosage of T that was administered, 150 mg was either propionate or phenylpropionte and 100 mg was decanoate. What does that mean. That means that by the end of week one, the only T left in the participants system was the 100 mg of T decanoate. Due to the suboptimal administration of a blended testosterone preparation, the methods used are ill-equipped to compare the efficacy of 250 mg testosterone to 150 mg of nandrolone.

The other study you posted does not offer the full article, but I would be skeptical that suboptimal methods were used similar to your second study.
Yes every study that disagrees with the bias is poorly designed and every study that doesn’t is the gold standard. Clearly a 6 weeker of Deca is ideal, groups of 7-8 subjects is ideal, but let’s take their work at face value. I will remind you both that I jumped in saying Nandrolone increases glucose transport and insulin sensitivity. High E2 isn’t needed for that. That high E2 propaganda comes from Neal Rouzier being incapable of converting pmol/L into pg/mL, it is actually embarrassing for him when watching his TOT videos again.

from the same Authors:(PDF) The Administration of Pharmacological Doses of Testosterone or 19-Nortestosterone to Normal Men is Not Associated with Increased Insulin Secretion or Impaired Glucose Tolerance*

In spite of the demonstrated biological effects of the doses of steroid administered, androgen administration for 6 weeks did not increase fasting serum glucose or insulin concentrations. There was also no increase in peak serum insulin levels and areas under the insulin and glucose response curves after a 100-g oral glucose load. However, the mean serum insulin area under the curve decreased significantly in the men given 300 mg ND/week.
So, science speaks for itself. This isn’t about me, contrary to what simple minds would think. I’m solely being objective about a drug that is dissed a lot among “test is best” bros. I thought this forum is to discuss “clinical use of anabolics”? I’m not talking nandrolone anywhere else on excel male.


Further, what I think is interesting is how Deca 100 obliterates T 100. This would be in line with Taeian Clarke’s views that past a certain point (which is reached on as little as 100 mg/wk of nandrolone seemingly) you don’t really get that much more anabolism (muscle androgen receptors saturated) but you’d get more fat burning (and water bloating from all that E2). So in that sense DHT is superior to DHN.

So it comes down to being marginally bigger and stronger at the cost of all the side effects. But that is NOT “clinical use of anabolics” anymore and I don’t care about body dysmorphic individuals.
 

DS3

Active Member
Yes every study that disagrees with the bias is poorly designed and every study that doesn’t is the gold standard. Clearly a 6 weeker of Deca is ideal, groups of 7-8 subjects is ideal, but let’s take their work at face value. I will remind you both that I jumped in saying Nandrolone increases glucose transport and insulin sensitivity. High E2 isn’t needed for that. That high E2 propaganda comes from Neal Rouzier being incapable of converting pmol/L into pg/mL, it is actually embarrassing for him when watching his TOT videos again.

from the same Authors:(PDF) The Administration of Pharmacological Doses of Testosterone or 19-Nortestosterone to Normal Men is Not Associated with Increased Insulin Secretion or Impaired Glucose Tolerance*



So, science speaks for itself. This isn’t about me, contrary to what simple minds would think. I’m solely being objective about a drug that is dissed a lot among “test is best” bros. I thought this forum is to discuss “clinical use of anabolics”? I’m not talking nandrolone anywhere else on excel male.


Further, what I think is interesting is how Deca 100 obliterates T 100. This would be in line with Taeian Clarke’s views that past a certain point (which is reached on as little as 100 mg/wk of nandrolone seemingly) you don’t really get that much more anabolism (muscle androgen receptors saturated) but you’d get more fat burning (and water bloating from all that E2). So in that sense DHT is superior to DHN.

So it comes down to being marginally bigger and stronger at the cost of all the side effects. But that is NOT “clinical use of anabolics” anymore and I don’t care about body dysmorphic individuals.
Unfortunately @benaoao , a study's methods are the key element in any study when determining the validity, reliability, and generalizability of its results. A critical assessment of each study is essential in arguing results, and the study you presented has some blatant flaws. Science does speak for itself, and the results you are discussing are not definitively supported.

"Clearly a 6 weeker of Deca is ideal, groups of 7-8 subjects is ideal, but let’s take their work at face value." The short duration of the study I posted is certainly a weakness of the study, and I wish they would have completed at least 12 weeks.
 
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benaoao

Member
I’ll quickly add that this TE v ND study said the following in the abstract:

Of 15 circumferences, significant increases were observed only for men receiving TE-300 mg/wk (shoulders) and ND-300 mg/wk (shoulders and chest).
So what do we make out of this? Chest gains not interesting?
 

DS3

Active Member
I’ll quickly add that this TE v ND study said the following in the abstract:



So what do we make out of this? Chest gains not interesting?
Abstract is less important than reading the methods. It's the same difference between reading cliff notes and an actual book.

Post the study.
 

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