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@Jimboslice117 all EVO family love here man
but gyno ED BP etc are all facts of high E2 its not a debate to be honestevidence like 10,000,000 steroid users
no joke
but gyno ED BP etc are all facts of high E2 its not a debate to be honestevidence like 10,000,000 steroid users
no joke
Great questions shall we dig into it? Starting with gyno as that is probably the most common thing high estrogen is blamed on. Then we can go into ED.
@Jimboslice117 all EVO family love here man
evidence like 10,000,000 steroid users
Let's dig into the mechanism of action on this one shall. Promise it'll be interesting.
@Jimboslice117 I think @AE1079 said it best here and I cant really dig into something that's fact
I mean you dont agree that testosterone eventually turns into estrogen? via a complex hormonal process called aromatization
You can't dig into what you don't yet know though. Yes estrogen comes testosterone via aromatase. Now let's try this, how would we induce gyno in a man without lifting estrogen? Is it possible? If so, how and if not, why not?
Go ahead you tell us, please share with the EVO family, we are open to your expertise @Jimboslice117
Yes please explain ahead
Gyno is formed when then mammary gland is stimulated via hormonal inputs, disrupting a homeostasis, when the ER is stimulated. When it is, it produces ductal development. For this to happen you need Estrogen to increase. Where does this come from? Testosterone, in this case being steroid users. Sure prolactin can play an effect and yes IGF and is needed. But the initial stimulation is Estrogen. So please tell me how we can get gyno in absence of estrogen?
We can induce gyno without ever raising estrogen. We can induce ED without raising esteogen also. To do this, we apply an Anti Androgen drug like Flutamide or a 5 alpha reductase blocker like Finasteride. Both these class of drug have a gyno and ED as a side effect, yet estrogen was never touched. So what's going on then?
The Androgen to estrogen ratio has become unbalanced. The stimulatory input (in this case estrogen) is now dominate, while the inhibitory imput, Androgens, are not. So the cause of gyno and ED is the unbalancing of the androgen to estrogen ratio or the inhibitory vs stimulatory imput. This is why Masteron was patented and used clinically for gyno treatment, because it would raise the androgen load or inhibitory imput. This is why we cannot blame estrogen for the cause of these issues but rather they're a side effect of an unbalanced ratio which is unique to every individual.
When we raise testosterone, there comes a point where the ratio will become unbalanced. It's at this point we have to options to rebalance the ratio. We can use an AI thereby lowering estorgen by blocking aromatase which will restore the balance OR the healthier way is to simply raise the Androgens with a non Aromatisable compound like DHT derivative, thereby eliminating the use of an AI or SERM and this will prevent the side effect we see from these compounds like lipid skewing, plaque build up in Arteries, collagen infiltration of the myocardium and purkinje fibers and heart enlargement as esteogen is a key player in keeping the heart close to normal size when Androgens increase. When estrogen dominates rather than Androgens the reverse happens, the heart begins to shrink.
I can upload some cross-section scans of a penis under the influence of different ratios for better reference.
From the cross section done here we can see the best outcome an election High E and High T.
Attachments
Gyno is the result of an imbalance between
the stimulatory and inhibitory inputs on
Breast Tissue the evidence here is
overwhelming
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Semantics.
You have literally agreed it is caused by imbalances, when do imbalances occur in steroid users ?
@Jimboslice117 of course there are other types of gyno, prolactin induced and progesterone induced, but for the most part, majority of the gynecomastia we see is related to E2 estrogen issues.
Imbalances involve at least 2 things corresponding to each other and means a state of being out of equilibrium, in this case the "state" is the Androgen to Estrogen ratio. If we induce gynecomastia or ED by artificially lowering DHT with finasteride, it's the Androgens which are the variable, not estrogen. Would it make sense to blame estrogen? It's the imbalance of the androgen to estrogen ratio which is the cause of the side effect, not a singular thing. I've treated clients, along with the medical field with early onset of gyno and ED by simply lifting the androgen load and leaving estrogen as it is. Again, if estrogen was causative, why doesn't gyno or ED persist AFTER androgens are brought up and e2 level are left the same? Because it's a balancing act and not reliant on just estrogen.
I don't think it's semantics or interpretation as this is what the medical field says the cause is including the endocrine society and the world's leading expert in androgen toxicity, Dr Howell. Accuracy on such subjects is very important because our community responds to these side effects with drugs like AI and SERM which have no place in safer practice of PEDs except for planned pregnancy.
I don't think it's semantics or interpretation as this is what the medical field says the cause is including the endocrine society and the world's leading expert in androgen toxicity, Dr Howell. Accuracy on such subjects is very important because our community responds to these side effects with drugs like AI and SERM which have no place in safer practice of PEDs except for planned pregnancy.
You’re missing the initial point.
It’s super simple.
Steroid users are prone to gyno yeah? Why?
The use of Testosterone causing the imbalance, in which genetic dispositions will dictate the body’s reaction to higher androgens, and in most cases, a increase of estradiol primarily due to higher aromatase activity CAUSED - being the key word here, by use of supraphysiological doses of the hormone, the body is extremely efficient - as you said there’s a homeostatic point in males that must be maintained. Some imbalances occur in certain individuals that may have more aromatase enzymes, higher body fat levels, or lower T levels to contribute to a higher E2 level, as part of an equilibrium as you mentioned. Hence why we see variance in E2 related symptoms. In which does not occur with everyone right? I have clients who run 100mg of T, and already will have gland flare ups, others can run 4-500mg, bigger bodies can run more depending on body composition. Again it is extremely subjective.
Back to your original point of state of equilibrium, androgen to Estrogen ratios, basic pharmacology.
As said above, more androgen activity and in this being Testosterone, will cause an imbalance. You literally said it yourself. We are talking Testosterone, not Dianabol, Deca, Tren or Ment.
“If we induce gynecomastia or ED by artificially lowering DHT with finasteride, it's the Androgens which are the variable, not estrogen“
This statement above is not practical, who in the hell would want to induce Gyno or ED Artificially via lowering DHT through Finasteride? This statement is not applicable nor does it makes sense? We aren’t out here on purpose trying to get gyno, but it is a side effect of taking testosterone with different variable tolerances between individuals. And is 99% the causation of Gyno. To treat it you need pharmacological intervention through either a Type 1 or Type 2 or a SERM. Or maybe just lowering the test dose, do you see what the common theme is here? Like you said it’s the imbalance - completely agree with you, but again what is the cause of an Imbalance? Fair, if someone has an imbalance as stated above then your argument is valid, this argument is based of Testosterone Induced Gyno, not Finasteride induced Gyno?
“I've treated clients, along with the medical field with early onset of gyno and ED by simply lifting the androgen load and leaving estrogen as it is. Again, if estrogen was causative, why doesn't gyno or ED persist AFTER androgens are brought up and e2 level are left the same? Because it's a balancing act and not reliant on just estrogen”
This doesn’t make sense either? Tell me how you get someone with early onset gyno, treat them with testosterone, and E2 stays the same? Tell me how often these people jab their testosterone? Pharmacologically this does not make sense.. Basic Pharmacology shows that Testosterone is undergoes aromatisation in higher levels as the body senses excess, again which where tolerances vary, due to this excess, we have a biochemical process called Aromatisation, which is a basic fundamental pathway of the body dealing with excess androgens. Now tell me how you are treating these people with MORE androgens without the use of an AI, SERM or any other intervention?
I think we're missing one another here because I agree with all of that but I'm not just talking about the use is testosterone in the treatment of symptoms
I'm using the dht blocker example of how the ratio of A:E makes the difference between gyno or ED.
As far as treatment goes for me and in historical medical practice, I don't raise testosterone but rather leave it alone and introduce a pure androgen. One that doesn't convert to DHT or estrogen. Masteron for example. Let's say the client gets the symptoms at 300mg of T (split 4 times a week) but he needs 600mg total load to grow. I bring in masteron at 300mg weekly. Now the imbalnce has been removed. E2 stays the same because testosterone is not tirated downwards (a range that previously led to gyno) but androgens have increased and symptoms will stop as the inhibitory imput has been restored. No AI use or SERM use required. Now the individual can enjoy the health benefits of higher e2 like brain, heart and kidney protection without gyno or ED.
That's what I meant by that.
I'm using the dht blocker example of how the ratio of A:E makes the difference between gyno or ED.
As far as treatment goes for me and in historical medical practice, I don't raise testosterone but rather leave it alone and introduce a pure androgen. One that doesn't convert to DHT or estrogen. Masteron for example. Let's say the client gets the symptoms at 300mg of T (split 4 times a week) but he needs 600mg total load to grow. I bring in masteron at 300mg weekly. Now the imbalnce has been removed. E2 stays the same because testosterone is not tirated downwards (a range that previously led to gyno) but androgens have increased and symptoms will stop as the inhibitory imput has been restored. No AI use or SERM use required. Now the individual can enjoy the health benefits of higher e2 like brain, heart and kidney protection without gyno or ED.
That's what I meant by that.
So we dug into it…
Cause of gyno is escalating of androgens, E2 in response increases, prolactin to follow. Causing aromatase enzyme to be activated converting test into estrodiol, then attaching to both E2BR (specifically this receptor responsible for breast tissue stimulation) And E2AR to create stimuli for gyno in this scenario.
This is what we are talking about, onset of gyno in steroid users. And I assume with this comment made by you and quote -
“I would have to respectfully disagree on there being such a thing as high estrogen side effects such gynecomastia, erectile dysfunction etc based on the evidence at hand”
Given publicly available information, pharmacology, biology and anecdotal evidence shows and I have explained it simply above, that High E2 causes these issues
Now your explaining treatment of it, but you haven’t explained to us how high e2 does not cause side effects such as Gyno or ED ect.. we aren’t talking about treatment, we are talking about initial causation of testosterone causing androgen levels, as you said swaying the balance.
In practise, testosterone goes up, e2 follows as I said before as the body’s mechanism to deal with extra androgens, we are not made to have excess testosterone. Hence the increase of converted androgens.
So when this happens and when gyno occurs in someone using test only and NO SERM or AI, gyno can be a side effect of the inputs above.
Which then you into how to treat it. Your intial argument of respectfully disagreeing that high e2 side effects has no merit. Because your treating the issue as you have stated above, and if you were correct in your statement, there would be no treatment in the first place. You mentioned and imbalance being removed via Masteron as a SERM, again.. if E2 didn’t cause these side effects, users would not deploy these therapies for gyno. But E2 does. Doctors prescribe arimidex in TRT patients for a reason, due to the imbalance high e2 can cause and its side effects, such as the inhibition of the aromatase enzyme acting on testosterone or androstenedione creating estrone or estrodiol.
Just like you, swaying the balance with masteron.
Masteron is a steroidal SERM by definition. selective Estrogen receptor modulator, acting as a negative agonist at the EB2R with its metabolites being responsible for this effect,with its prolific effects on breast tissue as its original treatment when it was made. So you have used a SERM in practise of mitigation of estrogen side effects in males. It is not classed as a pure androgen, it’s a DHT Derivative. Hence its effects on vasodilation, effect on serotonin and dopamine in the brain and effects on breast tissue, DHT Derivatives cannot be converted into E2. An Androgen by nature is male sex hormone and is crucial for maintaining and developing male characteristics, and is not a bio-identical hormone in literature. It is classed as an anabolic androgenic steroid, but does not act like a “pure androgen”.
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Ok I need to point out that Drostanolone is not a SERM class drug as its unable to bind to estrogen sites which is what the literature says and ive never seen anything regarding its metabolites in the literature being of a SERM class. If there is literature on please post it as ive never seen it. It was through its mechanism of action via gene transcription and effect on certain proteins that it was used as treatment along with its ability to slow or even prevent the estrogen receptor growth in estrogen-mediated breast cancer. But there's certainly no binding to the ER.
Im assuming the definition high estradiol is above reference range. So 10-50 picograms. Let's take just testosterone first. The aromatase pool is finite. Once saturated, there can be no more conversion of T to E. This is why men can experience gyno or ED at 400mg T but don't suffer from it at 1500mg T. How high would estrogen be at 1500mg T? Probably maxed out as the literature shows 600mg of T yeilding 2-3 times normal estrogen range. Yet there will be no high estrogen side effects as the A:E ratio is sorted. We can do this with any AAS.
The point is that we can have high estrogen on paper, have an imbalance of A:E and symptoms there of, introduce non ARO androgens like anavar or masteron or jack T through the roof and see symptoms leave while blood serum estrogen is in the high range.
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