Just about everything you wrote made me facepalm so I'm not going to waste my time doing a tit-for-tat rebuttal when lives are at stake here. Just pointing out some of the stupid **** you said.
Good move. It's good you can recognize that you don't have a leg to stand on and that it's time you backed out of the conversation. I would have put a thousand dollars on the fact that your next response would have been something along the lines of "i'm not wasting my time blah blah blah" and try to play it off so that you don't look like you are running away with your tail between your legs. Classic move, well played.
I really don't even know wtf you are arguing here, or if you are arguing at all.
You are very observant, good for you! Most of my last post was dedicated pointing out how ridiculous your responses were.
Rat studies serve no purpose? DHT is involved in rat erections, but not human erections?
Please show me where I said any of this. I love how you can't even identify any weaknesses in my responses so you have to resort to putting words in my mouth.
If DHT is critical for rat erections then it's critical for human erections. Do you agree with this or not?
No; the results from animal studies, especially rat studies, are usually never applied to humans except for obvious ones such as toxicology tests and so on. Animal studies such as these are used to formulate hypotheses, but the results can not be applied to humans in a blanket sense.
I'm not going to even discuss this any more, because here is a nice big wrench to gum up your works. You probably know the drug Dutasteride, right? That fun little chemical blocks some 95% of DHT and pretty much eliminates it from circulation. Even so, erectile dysfunction is experienced by less than 5% of users, and around 1% after a year of continued use.
So you actually might be right here. DHT might be crucial for erections, but it's clear that even having less than 5% of normal DHT levels circulating is more than enough in the vast majority of cases. Certainly if people get by so well on dutasteride, finasteride is a cakewalk!
I'm sure you can find a study on humans. Even the finasteride wiki entry explains the role of DHT. "DHT is a more powerful androgen than testosterone (as it has approximately 3-10x the potency at the androgen receptor, the site of action of the androgen hormones), so 5α-reductase can be thought to amplify the androgenic effect of testosterone in the tissues in which it's found."
Actually I haven't come across any studies that conclude DHT is in any way crucial for humans to achieve erection. Please hunt one down for me, because I don't care to spend more than a couple minutes on these responses.
Who cares if DHT is 'powerful'. That doesn't mean it's necessary for erections or even important for anything else in the human body...
Are you still not convinced?
Not even close, but quite entertained at the very least.
Do you still believe Merck's "DHT is a pesky molecule" lie of the 90's?
Oh so it was just a lie in the 90's but in the 2000's its the truth? Damn pharma companies and their shady dealings.
Try to flesh out your arguments so I know what the **** you are saying and don't waste time with "them's some big words you learned there!"
I can't understand what you are trying to say with those little stars, you should try to type more accurately!
Again, my last post was just to poke fun at how ridiculous your responses were. There isn't much to argue with here, trust me. I'm pretty sure the damp sponge sitting next to my kitchen sink would be able to put up a more challenging debate than you are able to. It's way less mean too! sniff... sniff...
The AR has adjusted to low DHT levels, becoming hypersensitive to it. This is well-known molecular behavior. Your body thinks that 35% DHT is the new norm. When you get off, the return of baseline DHT can saturate the receptor, silencing the signal, which will make it unable to exert its effect. Then you will have PFS. Or, it could adjust back to normal DHT levels. That's what it boils down to, 50/50. Not "1 and 30,000"
Well it sounds like you have figured it all out then. If you already know why PFS happens, why have you not published your findings in a medical journal? You've just found the proof everyone is looking for, which directly implicates finasteride in PFS, meaning all these lawsuits immediately pay out!! Go! Run! Tell the world!
Wow, and you actually said I was the one playing the meaningless numbers game? So it's 50/50 as in I have a 50% chance of getting PFS, and a 50% chance of my DHT levels returning to normal, is that how it is?
Oh, maybe you are trying to make it seem like that, but in reality you mean 50/50 as in there are two possible outcomes! One being I go back to normal, and the other being I develop PFS. Of course anyone knows that just because there are two potential outcomes, it doesn't make it a flip-of-the-coin 50/50 chance. Only a complete idiot would even suggest that, right? You are able to make that distinction, right? Right???
The outcome of returning back to normal is by far the most likely. Let's say there is a 29,999 out of 30,000 chance that this happens. I'll give you a few reams of paper, a box of pencils and a solid weekend to try to figure out the math on the other outcome.