GeneticalChallenge said:
Hey fellas,
I´m new to the board! (and it´s my birthday, for those who care)
Did I read the last post correctly? Finasteride increases estrogen levels by 30% and testosterone by 19% and at the same time blocks the DHT from my scalp? I just started taking propecia since I´m prone to hairloss (also for gyno). Planning a cycle on test and dbol. My question is basically, am I f*cked? The test will increase strenght, the estrogen will cause gyno and if I recall correctly, DHT has some muscle building properties which will be blocked by propecia?
Sorry for any bad spelling, I´m Swedish. No flame please, I´m here to learn.
Cheers!
Welcome to the board & happy birthday bro !
Finasteride may cause a sligt increase in test/estradiol but that's not really relevant on cycle since estrogen increase caused by Dbol/test will be much higher...
Just take Tamoxifen or an aromatase inhibitor if you're prone to gyno.
DHT contributes to gains due to its effect on central nervous system.
It doesn't have much effect in muscle because it gets deactivated by 3bHSD.
from:
DHT and the Athlete: Is it the Enemy?
By William Llewellyn
DHT and the neuromuscular system
It has been suggested that inhibiting the reduction of testosterone to DHT may not always be a good thing in terms of performance enhancement. It seems clear that DHT plays a vital role in the organization and functioning of the central nervous system, effects mediated by androgen receptors in neural cells. The specific importance of DHT in this area is evidenced by studies showing this hormone has a profoundly greater impact in neural cells compared to testosterone. In one such study it was demonstrated that both testosterone and DHT would result in increased androgen receptor proliferation in neural cells at 3 hours and 7 hours post administration, however only DHT sustained this increase at 21 hours. This strong difference lends support to suggestions that DHT and testosterone effect neural cells differently, perhaps such that the dihydrotestosterone-receptor complex and testosterone-receptor complex might even activate the transcription of different target genes. Others maintain that such a difference in effect would only be due to DHT forming a more stable and lasting complex with the androgen receptor, but the vital importance of DHT still remains evident.
The strong interaction between the central nervous system and skeletal muscles may be of key importance to the athlete, as these two areas interact to form what is referred to as the neuromuscular system. Clearly the ability of the body to adapt to training and better call upon nerve endings in muscle tissue is reliant on the functioning of the central nervous/neuromuscular system. Inhibiting the formation of DHT during a testosterone cycle may therefore inadvertently cause less to be achieved in terms of strength and muscle mass gains. We might also take note of the fact that while the anabolic steroid nandrolone is a stronger agonist of the androgen receptor than testosterone, it is much less effective at promoting strength and muscle mass increases in comparison. It seems logical that the loss of DHT (nandrolone actually reduces to a weaker steroid upon interaction with the 5-alpha reductase enzyme) may have something to do with this outcome. What is obvious is that were androgen receptor stimulation in muscle tissue solely responsible for strength and muscle growth, nandrolone would be a more potent drug than testosterone. Yet testosterone compounds remain the primary mass and strength agents among bodybuilders.