docj077
Senior Member
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Bryan said:Now I know for sure that you didn't understand what I was saying all that time!
I'm going to explain it to you in more detail, and hopefully this will clear it up once and for all: DHT is also a player (along with testosterone and estrogen) in the hypothalamic-pituitary-gonadal axis that controls the production of testosterone. When you take finasteride or dutasteride, your levels of DHT sharply drop, which the brain interprets as a sign of decreased androgenic stimulation. Its response to that is to step-up the production of testosterone, to compensate. It does that by sending the chemical signals LH and FSH to the testes to tell them to start working overtime.
THAT is why testosterone increases when you take finasteride: the brain tells the testes to make more of it. It's not the simplistic notion that less T is turned into DHT, so there's more T floating around. In other words, the body's set point for testosterone (that is, the level of testosterone that the brain WANTS to have) is actually increased, and it's MAINTAINED at that new, higher level, for as long as you take the finasteride. Now do you understand what I'm saying?
Bryan
Yes. That' actually what I was saying. All androgens and estrogen negatively inhibit the HPG axis. The DHT will not necessarily be interpreted as a decrease in androgens as I'm pretty sure that testosterone and DHT bind the same receptors and inhibit their perspective targets molecule by molecule, but I'm not sure about the receptor responses for the two molecules in the brain. A drop in DHT to me should mean more testosterone taking it's place and thus simply regulating the system the same, but I don't know if the brain interprets it that way. If it isn't interpreted as molecule for another molecule in the rest of the body, then one (granted it's a big leap) could assume it isn't the same way in the brain.
What I'm saying is the concept of the shifting set point is relative to the person taking the drug. Not everyone will shift their set point for testosterone so efficiently and thus have no side effects.
That's all I'm trying to say.
Also, if testosterone and DHT do have the same effects on the receptors they bind in the brain, then neither of us will be correct as there would be no set point change for either molecule, since they'd be binding the same receptor and having the same effect.
In your opinion, do you think the HPG axis could keep up with this? I really don't know.