Gain .5 inch/month with no excersizes

I dont want to argue so I will quit posting here.

“Bro, test and DHT are different hormones that exhibit different methods of action. Period. End of story. This is basic first year stuff. “

Bro, DHT and T act on the same receptor. This is a fact.

Nice article by Pat. He created 4ad by the way.

Why don’t you write him and ask him his opinion regarding DHT ability to promote anabolism.

I’d love to see a guy like that chime in….

SO? What’s your point?

So do Oxymetholone, Oxandrolone, Nandrolone, Trenbolone, Methenolone and a whole slew of other hormones.

Do you think that all of them have the same method of action or have the same metabolic pathways once they reach the AR???

Dude, I’m just trying to show you that using a DHT precursor SHOULD be a lot more effective than using a Testosterone precursor that you then have to content with conversion to DHT.

DO you want to argue that it’s test and not DHT that could potentially trigger growth?

I’m not sure why you’re even arguing about this.

“Bro, test and DHT are different hormones that exhibit different methods of action. Period. End of story. This is basic first year stuff. “

…

“Dihydrotestosterone binds the androgen receptor much more strongly than does testosterone at the same concentration, yielding a higher degree of ligand-receptor stability. When the concentration of testosterone is increased however, the receptor stability increases to a level similar to that seen with dihydrotestosterone (10)”

nearlythere has posted both of these. I find it interesting that he denies they T and DHT have the same mechanism, but posts literature stating they share the same receptor and simply have different affinities. I find this very interesting.

They don’t contradict one another.

DHT binds to the AR, as does Test. With a very high concentration of test, the bond becomes as stable as DHT.

Don’t confuse AR stability with methods of action.

Simple as that. Yeah, when you introduce huge doses of Test it will bind as strongly to the AR as does DHT. They still do completely different things though…

Apples and oranges kid.

DHT was more successful in treating micropenis. We use a test precursor because there is so much 5AR in the penis that it gets converted almost immediately.

Jones -

Just post a link to ONE medical study that shows test and DHT have the same effect in humans and I’ll let it die.

Just one kid.

ONE!

Sorry. BS.

PROVE IT!

One study that shows how much 5AR in a human penis and ANY info on rate limiting conversion.

ONE!

Why?

Why not use the already proven successful DHT?

(your words, not mine…)

DHT is a controlled substance. Did you know that?

“bond becomes stable as DHT” ??? That makes no sense. Here is an analogy so you can understand ligand specific androgen activation through the electrostatic interactions with an ezyme:

A house is a cell. The lock is the receptor. To get in, you have two keys that randomly poke at the door. T is rusty key. DHT is a well lubed key. With random actions, which key will get in more times? DHT will. They both open the SAME door.

If the were no 5AR in the penis, then how would the penis have developed in the first place? Did we not agree that it is crucial for growth. Sigh.

Ya.

But DHT precursors are not.