[quote]Bill Roberts wrote:
Bill Roberts wrote:
So far it has shown to increase muscle mass in men and women, increase bone density in women, slow the growth of prostates in men and reduce the occurrence of breast cancer in women.
DHT will do all these too (seriously.) So can other synthetic anabolic steroids. They show tissue selectivity to. In fact they were developed on precisely that basis.
You are correct, anything that will bind the androgen receptor will stimulate the same gene expression. After all, its the androgen receptor protein itself that actually stimulates the gene expression required for increased muscle mass. Molecules with steroidal structures will bind the androgen receptor, but they also have many unwanted and dangerous side effects.
The #1 reason for developing this drug was to eliminate the side effects of steroids while still being able to bind the androgen receptor. Once the androgen receptor is bound, assuming binding affinities are similar, the receptor will just do its job. I have not seen any papers on the binding properties of Ostarine, but I would assume they are very similar to steroids since there are only so many amino acid residues capable of being bound in the androgen receptor.
So, like you said yes DHT will do all these things, but its the pros vs cons of side effects that will attract many physicians to this drug.
But I can point you to a trial with DHT not showing adverse side effects either. Including not only no adverse side effects on the prostate, but improving BPH.
Many times the existing anabolic steroids at correctly chosen doses can show therapeutic benefits without side effects.
I am not saying it doesn’t exist, but as yet I have not seen the evidence-based reason that anything different is going on here at all. Nor a scientific reason why it would even be expected to be different.
Now in the case of the SERMs, it’s not just buzzword talk. The estrogen receptor actually is selectively modulated: it responds differently according to what is binding it.
If they had shown this true for the androgen receptor then it would not be just a buzzword. But I hadn’t seen that they or anyone had. So far as I know you are correct that any ligand that activates the AR yields the same gene expression. If that is in fact correct then the “selective modulator” phrase is just finding a buzzword and is misusing words. It might be smart marketing – in fact it undoubtedly is – but that there is any practical signifance to the ligand not happening to have a steroid ring structure, perhaps so but I have not any demonstration of it or even logical possible explanation. It would be interesting if there was one, though.
I think I understand what you are trying to say. The SERMs elict different responses b/c they have been developed enough to where they are highly tissue specific. Therefore they only act on estrogen receptors in the tissue desired therefore they will only cause the effects that activating estrogen receptors in that tissue can cause.
In other words, since the SERMs are so selective now, they won’t activate all estrogen receptors in the body. So its not the actual drug that is the difference b/w SERMs and SARMs; its where the estrogen receptor is located combined with the drug being designed to only concentrate in certain tissues.
At this point SARMs aren’t as selective for certain tissues as SERMs, so their effects are seen anywhere androgen receptors are found as long as the drug can access those receptors. Eventually, I think SARMs will be just as specific as SERMs. So this will give you the “specific” effect you are currently seeing in the SERMs