Although it has been more than three years since I stopped taking finasteride(1mg) and two since saw palmetto and revivogen, I still mantain a very muscular figure. The maximum gain was when I was taking propecia,i had put on very easily alot of muscle on all the upper body and enhanced my overall strength. Since stopping i have never lost my gains but put on a lot of weight which is distributed in a typical female pattern.My estradiol levels are still very high so I was wondering if this could be why I have never lost any muscular mass? I have never used anything else a part from fin.Estrogen is known to have anabolic activity. Could bringing down my estradiol make return to my former self?
I know this kind of contradictory because in many it has caused quite the opposite.All I want is to get rid of the extra fat that does’nt seem to want to come off…if i coul mantain the extra muscle that wouldn’t be bad
In answer to your initial question;
No estrogen is not anabolic.
Estrogen or estradiol as that is the significant and potent estrogen we are by and large talking about is indirectly catabolic or at least it when it is in excess and is dominent.
Estradiol acts against the actions of testosterone in the body and it does so via two principle mechanisms.
First of all excess estradiol tricks the hypothalamus into thinking that the body has too much testosterone when it does not. The hypothalamus is a little stupid to say the least and it cannot properly distinguish the differing sex hormone and so it view the total steroid load.
Increased estradiol results in the hypothalamus downregulating GnRH and then the pituitary downregulates LH which consequently reduces the amount of testosterone that your body produces.
A little and harmless experiment that you can do is to take 50mgs of zinc a day. If you have excess estradiol you might notice that you sleep a little better, feel a little better iun yourself (just a little) and you might even notice a tiny increase in testicle size. Of course this only happens in some men and the level of estradiol is improtant, but it does happen in enough men to be of note. This occurs because zinc is a weak natural aromatase inhibitor that ever so slightly reduces estradiol (in fact there is even a place for zinc encoded into your androgen receptors) and a lack of zinc has been know to cause HPTA problems.
Back to the main point;
So excess estradiol can actually lower your own testosterone production by tricking the HPTA into supressing itself.
The second mechanism of action is by way of the androgen receptor sites. Excess estradiol can actually block the receptor sites and prevent some of your testosterone from being able to do its job, it literally renders some of your testosterone useless to the body, just as SHBG can- though the mechanism is different.
The above is shown unfortunately all to well in men that have overtly high estradiol levels. Often what is seen is a normal total testosterone level but a low free testosterone level thaks to that estrogen blockade of the receptor sites. The Cuban missiles never reached Cuba because of the US naval blocade and in this case the testosterone never reaches the safe harbour of the androgen receptor sites and so floats aimlessly in the blood.
With a lower level of testosterone, particularly free tstosterone, we usually see a somewhat or overtly reduced level of the potent andorgen dihydrotestosterone DHT). Why?
Because DHT is a metabolite of testosterone and with less testosterone we tend to have less DHT, just like you have less of a fire when you burn less coal (I won’t say wood- mixed connotations).
So excess estradiol adversely impacts upon testosterone levels and testosterone is THE key anabolic.
Some people are fortunate enough in that they have had a good androgen status to begin with. People in this boat tend to be less adversely affected by medications that lower androgen status/lower the andorgen to estrogen ratio. But people are still affected one way or another.
Even if I had not seen the original posters pathology I would suspect a reasonable level of testosterone based of musculature (I would have expected muscular atrophy had testosterone been very low). But I would also suspect excess estradiol.
Why?
Well, excess weight is one thing, but what is being described is eunechoid/female weight distribution and that is a hallmark of excess estrogen. I wouldn’t be suprised if there was some gynecomastia, the hips would be a place for excess weight and there may be a little more water retention than prior to propecia use. This of cousre could fit with other pointers such as lowered libido or ED.
The above is shown unfortunately all to well in men that have overtly high estradiol levels. Often what is seen is a normal total testosterone level but a low free testosterone level thaks to that estrogen blockade of the receptor sites. The Cuban missiles never reached Cuba because of the US naval blocade and in this case the testosterone never reaches the safe harbour of the androgen receptor sites and so floats aimlessly in the blood.
I could be and prolly am off here, or maybe i am missing some information to draw conclusions, but i have to say that dont seem very logical.
If total T is normal range and estrogen is high but bound to receptor sites. wouldent Free T be higher if blood was drawn at this point rather than if estrogen was free and testosterone was bound to the receptor? If so isent that contradictive of what u state above? I do however understand that what u are saying is that bioavailable T must have access to receptor sites that it can bind to and that it will be rendered useless if E has bound to most receptors allrdy.
Might seem like im playing word games but im mearly trying to understand how hormone works and this phrase caught my attention.
Cheers.
I never said that estradiol was bound. You are confused between two differing mechanisms of endocrine action and referring to one which relates to SHBG and Albumin- that of being bound by a carrier protein.
I am not referring to the issue of bound hormones in this instance, I am talking about elevated estradiol blocking the Androgen Receptor sites.
This is not theory by the way- I am talking unequivical fact here.
Elevated estradiol blocks androgen recepetor sites and in doing so it prevents your testosterone or at least a certain amount of it from working in the body. It lowers the level of free testosterone. If it doesn’t get intto the recpetor sites it cannot be bioavailable or free.
Again this is categorically true and a factual statement.
I have seen hundreds of pathology reports and when estradiol goes up very often free testosterone comes down, at least it does unless there are other alterations that free more testostreone up such as reductions in SHBG.
So in what why do this estrogen blockade (this i thought u meant was bound) take place if its not by actually binding to the receptor site? In what other way is it causing the testosterone not to bind to the receptor? I understand thats what u explain in the original post but since my enlish isent native i dont understand the explanation? could u try to simplify it even further?
The language is something we can get around sooner or later- no big deal.
I’m not sure what it is that you do not understand?
Maybe you could explain what you want me to detail?
I think he thinks blocking the receptor is the same as binding to it. I dont know enough about this either to comment, but i think its kind of like how clomid blocks the E receptor instead of binding to it. Im out of my league with this topic…lol. Hypo can you elaborate on the difference between binding and blocking?
That post you did Hypo on how E takes out T is well written and very informative. Its very interesting stuff and confirms some of my suspicions about E dominance.
I’ll explain it using Dr Eugene Shippen’s words verbatim from his book The Testosterone Syndrome;
Quote
When it comes to estrogen, the window of optimum effectiveness in the male body is small. Estrogen converted by aromatase can actually lock or displace testosterone at its various receptor sites. Consequently, too much estrogen will switch off activities.
Unquote
So we are talking about blocking or displacing androgens and principally testosterone from its receptor sites. If these androgens, if testosterone doesn’t enter the receptor site then you have no androgenic effect, so when estrogen is too high, we see a progressively higher amount of testosterone prevented from doing its job- a similar effect when considering SHBG.
This is well shown in men that have Androgen Insensitivity Syndrome or an altered genetic androgen receptor make-up, too many CAG receptor repeats etc. What you can sometimes see is a lack of response to androgens. The androgens are present in the body but not reflected in typical male development or reduced androgen action. Androgens not able to do their job, because they cannot enter fully functioning androgen receptors.
Androgens are nothing without the ability to enter fully or adequately functioning AR receptors.
Important to think androgen or testosterone receptor sites and not get confused with estrogen receptor sites and what Clomid or other Selective Estrogen Receptor Modulator (SERM) medications do. That said the effect is in principle the same at a differing receptor site. Estradiol blocks the actions of testosterone but this is not reflected in total testosterone, just as Clomid blocks the actions of estradiol while this is not reflected in estradiol levels in the blood (it would be if you had a free estradiol test- which you can’t get).
The reason this is different from binding is because that term is used for binding globulin and albumin that bind strongly and weakly respectively in the blood. I am talking about effects at the receptor level not simply at the blood level- that is what separates the two terms.
The difference in layman’s terms is not so important.
You just need to know that SHBG binds testosterone in the blood and as a result total testosterone can be high but it is of no use if it isn’t free. Whereas estradiol/estrogens are not binding testosterone in the blood but getting in the way of testosterone at the receptor level…the end result is the same in terms of reducing free testosterone.
Estradiol and SHBG can both cause real and significant problems if present in inappropriate levels. SHBG tends to be a more significant modifier, but that does not mean that the effects of estradiol should be discounted. The levels can be related and they can both cause a series of differing adverse effects.
If I have waffled and not detailed things properly then just ask again and I’ll try and re-explain.
This is the direct translation of a document I found on an Italian site:
Translated:
In the last few years we have assisted to a decisive revalution of estrogen’s role in muscle development. It seems that estrogens favour anabolism by highering GH secretion, IGF-1 and of the the number of receptor sites for testosterone, this decreasing tiredness/exhaustion and allowing a better metabolism of glucose.
This could mean that estrogen although naturally suppressing testosterone by negative feedback on the Hypothalamus, could though favour anabolism in an indirect way in some. 
Estrogen is NOT anabolic, unless you mean that it is helpful at having an optimum male level.
In excess it is NOT anabolic because of its effect in suppressing the actions of testosterone in the male.
This is an unequivical fact.
Anabolic agents are abused in order to increase muscle mass and performance in the world of sport and many things are taken, estrogen isn’t one of them.
If you doubt what I am saying about estrogen take a look at women!
Notice the lack of muscular build in general in comparison to men, then think of the fact that they have much higher levels of estrogen and much lower levels of testosterone.