Possible co-relation between amount you take and longevity?

[ripple-effect]

I was just thinking at random if there could be a possible link in the amount of finasteride you take and the length of time it would continue to work. So, for example, I was thinking if a person took 0.5 mg everyday, is there a chance that it could keep working longer than someone who is taking 1.0mg? The concept of tolerance makes this a viable idea.

 

[bubka]

this is not a stimulant or a depressant, there is no tolerance factor with the drug

 

[cal]

It's true that there isn't a tolerance ever getting built up to the Finasteride itself.



But . . .

Androgen receptors, when deprived of their rightful androgens for several years, have shown the ability to mutate and begin stimuating themselves with other (not DHT#2) androgens. This has particularly shown up in attempts to treat prostate cancers with DHT inhibition. The ARs are stopped by the lack of DHT for several years and then they begin to abruptly get stimulated by something again.


So I imagine that there could potentially be some validity to being concerned about "over-depriving" the ARs and training them to mutate sooner.

 

[Bryan]

Androgen receptors, when deprived of their rightful androgens for several years, have shown the ability to mutate and begin stimuating themselves with other (not DHT#2) androgens. This has particularly shown up in attempts to treat prostate cancers with DHT inhibition. The ARs are stopped by the lack of DHT for several years and then they begin to abruptly get stimulated by something again.

That happens in prostate cancer, but not in the hair follicles of non-cancerous men. How do we know that? Because Hamilton found examples of castrated men whose hair had been maintained for as long as 20-30 years afterwards. It's very likely a lifetime benefit.

 

[cal]

I would like to be as confident as you sound about that. But I feel that there is WAY too much anecdotal feedback that finasteride's effects can abruptly lose their preventative powers several years into usage.

Of course there are tons of guys that it never happens to, but it seems to happen often enough that I think there must be some specific process at work to cause it.


Poeple have argued that the finasteride "failures" may just be complaining when the continued gradual loss finally ovetakes the starting baseline. I'm sure there is some of that. But I see a number of cases where they're describing the change being way too abrupt and the new loss rate much more severe. The mutation of the ARs to accept other androgens seems to make a lot of sense to me.

Maybe it's more complicated than this. But the whole thing is still enough to concern me about long-term finasteride's protection.

It also occurs to me that something like topical spironolactone's effect of binding to the scalp's ARs might theoretically prevent the ARs from knowing that they're being deprived at all. That would seem like a good pairing along with DHT suppression.

 

[bubka]

It's true that there isn't a tolerance ever getting built up to the Finasteride itself.



But . . .

Androgen receptors, when deprived of their rightful androgens for several years, have shown the ability to mutate and begin stimuating themselves with other (not DHT#2) androgens. This has particularly shown up in attempts to treat prostate cancers with DHT inhibition. The ARs are stopped by the lack of DHT for several years and then they begin to abruptly get stimulated by something again.


So I imagine that there could potentially be some validity to being concerned about "over-depriving" the ARs and training them to mutate sooner.

MUTATE??? I don't think you know what you are talking about or are incorrectly using the word "mutate"

this is not teenage mutant ninja turtles here, hair follicle cells do not mutate

 

[cal]

I'm starting will the known habits of androgen receptors in one area of the body, I'm noting anecdotal evidence of similar behavior in an androgen-stimulated tissue from a different area of the body, and then I'm theorizing that the second area's ARs might be doing the same thing as the first ones. How silly of me.



And if you're gonna be an effective shill then you've gotta be less obvious about it.

 

[bubka]

are you suggesting that the DNA of the cells changes? That is a "mutation"

 

[cal]

Look at the androgen-dependent tumors in some prostate cancer cases. The tumors sometimes abruptly stop being suppressed by the lack of the appropriate androgens and begin growing again anyway. They've somehow "adjusted" to being stimulated by things other than the original androgens they were supposed to be affected by.

I don't understand the specifcs of how everything works between the structures of the ARs and the various hormones. But the general situation sounds very similar to what some Finasteride users are reporting: Several years of very effective androgen-growth reduction and then a somewhat abrupt loss in effectiveness after that.


My suggestion about topical spironolactone is just an idea and I'm not claiming a very informed opinion on this. But it seems to me that since topical spironolactone works by binding to the ARs themselves, then spironolactone-bound ARs would never really know the DHT was gone.

 

[bubka]

can you answer the question?

I will answer it for you, NO, the cells do not "MUTATE"

 

[cal]

I don't have to prove anything mutates. I never declared I had proof that anything did.

I simply brought up a medically known problem when treating certain cases of prostate cancer. Then you began insisting that it can't happen.

If you really disagree so strongly then go tell the cancer doctors that they're wrong. And tell the patients that they're not really dead from it.

 

[bubka]

CANCER = MUTATION

MPH /= MUTATION

BPH /= MUTATION