Yes, as I've said, DHT is produced where it's used, but excessive amounts travel around your body until it finds something to bind to, which are receptors on other parts of the body where a lot of 5AR type 2 enzymes are located. The serum concentration of any hormone declines when the hormones express themselves. Both estrogen and DHT affects the breast tissue. Estrogen activates, DHT deactivates. DHT suppresses the serum concentration of estrogen by countering estrogenic effects, and that's how DHT affects the testosterone/estrogen ratio.Bryan said:Enden said:
It's certainly measurable, because we've developed good laboratory tests whcih are capable of detecting it. But that doesn't mean that the tiny amounts of DHT in the bloodstream actually do very much to the parts of the body where they aren't actually produced!
0.25 mg Finasteride
- Thread starter Townes
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Enden said:
Now I can see some of the confusion here!
Merck isn't claiming with that terminology that finasteride is NOT an irreversible inhibitor. They're just saying that up to the moment that it actually binds with 5a-reductase, testosterone still has a chance to bind with the enzyme first. But the moment the enzyme binds with finasteride, it's GAME OVER! Sorry for the confusion. It's easy to mis-read some of this arcane language that they use in highly technical studies.Nor do they state that it's a suicide inhibitor. It's essential information IMO.Bryan said:Enden said:
Now I can see some of the confusion here!
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Enden said:
Well if you're bound and determined to believe that, despite what doctors and endocrinologists say and despite what I told you about how purely local 5a-reductase inhibitors can suppress the effects of DHT in the bloodstream of both humans and animals, I guess I'm just not going to be able to convince you. I did my best to explain it to you.
0.25 mg twice a day, 12 hours a part, leaves your body with a serum concentration of finasteride which is higher than 0.05 mg before the next dose. The difference between 0.05 mg and 1 mg regarding enzyme suppression after one dose, isn't significant, as I remember. However, 0.5 mg once day, is less effective.Bryan said:
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Even I myself, when asked in previous years what the best possible way to take finasteride would be, have replied that breaking it up into as many small doses as possible (even to the point of a slow, intravenous drip) would be the best possible way! But this is all really theoretical stuff, and not terribly important. The slow regeneration of the 5a-reductase type 2 enzyme makes it all pretty moot.
Yet, when they know so much, they don't understand what's going on with persistent side effects after using finasteride. Hell, most doctors don't even understand the significance of the testosterone/estrogen ratio. Yes, I trust myself, more than I trust educated fools, which has no experience with finasteride.Bryan said:
Btw, a study which shows that DHT gel affects the testosterone/estrogen ratio; http://www.ncbi.nlm.nih.gov/pubmed/6354523
Bryan, let's cut to the chase and end this discussion properly; you may very well be right about finasteride and dutasteride actually being suicide inhibitors. Results from in vitro experiments are solid evidence, I'll give you that. However, what you're suggesting, if I'm not mistaken, is that finasteride a couple of times a week or something like that, should be equal to a dose of finasteride taken every day, in terms of DHT suppression. IF YOU'RE WRONG, this will compromise the result, and I suggest that people see finasteride as a competitive inhibitor and dose according to its half life, which means that 0.25 mg twice a day, 12 hours a part should be equal to 1 mg finasteride a day. The difference between DHT suppression after one dose of 0.05, 0.2, 0.5 and 1 mg finasteride, isn't significant. Speak up if you disagree.
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Enden said:
I've never said such a thing in all the years I've been posting on hairloss sites. Taking finasteride only a couple of times a week won't be exactly as effective as taking a similar amount every day, but it'll provide a relatively reasonable amount of protection.
Enden said:
In a previous post, I said myself that the most optimum way of all to take finasteride would be to divide your daily dose into as many portions as possible, and take a portion as often as possible throughout the day. But that's just theory. Out of all the finasteride studies I've read, I certainly have never seen one in which serum DHT levels (or any other DHT levels, for that matter) were measured after taking 0.25 mg of finasteride twice a day, compared to those same levels after taking 1 mg exactly once a day; therefore, I have no idea how such a test would turn out in Real Life. I haven't said much about any of this lately for the simple reason that I haven't seen any evidence one way or the other for your "twice-a-day" theory!
No, but you've seen that there isn't any significant difference regarding DHT suppression, after a single dose of 0.05, 0.2, 0.5 and 1 mg finasteride. The half life is 6 hours, and though it's just theory, calculation based on the treatment dosage, half life and minimum effective dose, is correct. People should use 1 mg a day, which is tested and approved, but theoretically, 0.25 mg finasteride, 12 hours a part, should give the same result as 1 mg a day.
Btw, I've been wondering about this statement for a long time, and since I've your attention now, what was it?Bryan said:
What I've heard, is that finasteride was used to treat BPH, and they discovered that some of the users regrew hair, which lead to closer investigation and eventually Propecia. If that's not a random observation, or "accidental discovery", I don't know what is.
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Enden said:
Oh, I wouldn't go so far as to say that! I can show you an early finasteride study in which the effects of various small doses of finasteride were tested on human subjects. The lowest dose they tested (other than placebo) was 0.04 mg, which is why I referred to that dose in an earlier post as being the lowest one which had been tested to have real results. Even though that's slightly lower than the dose you specified of 0.05 mg, nevertheless 0.04 mg in a single dose had a noticeably lesser effect than 1 mg. The difference became less and less as they continued to give those doses over a period of two weeks, but even THEN you could see on the graph that 1 mg/day for two weeks did a little better than 0.04 mg/day for two weeks.
Similar effects were noted in that Merck "dose-ranging" study I mentioned in a previous post. In addition to the specific haircount differences that they got with the different finasteride doses, they also listed the serum DHT values from each one. The larger doses did slightly better than the smaller doses, in both regards (haircounts, and serum DHT).
Enden said:
Maybe, but I'd have to see an actual experiment that tried it, before I could fully believe it.
Fair enough. I believe the difference between 0.04 mg and 0.05 mg is much bigger than it seems though, considering that 0.01 mg was ineffective, and 0.05 mg was considered as the smallest effective dose, with no significant difference from higher doses, regarding DHT suppression after a single dose.
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Enden said:Btw, I've been wondering about this statement for a long time, and since I've your attention now, what was it?Bryan said:
It didn't happen that way. The discovery of DHT as an extra-strong metabolite of testosterone happened in the 1960's, I believe. I have in my personal possession copies of a couple of studies from the early 1970's by some hairloss researchers who measured (among numerous other things) levels of DHT in both balding and non-balding human hair follicles! It's perfectly obvious that by the time finasteride was first synthesized in a chemical laboratory by Merck chemists sometime in the 1980's, the role of DHT as a factor in balding was very well-known!
I can also show you an early study by Merck scientists before the development of finasteride. It was for a substance which is commonly referred to in the literature as "4MA". It was an early 5a-reductase inhibitor, much like finasteride. This early study I'm talking about covered Merck's efforts to use 4MA on stumptailed macaques, in an effort to stop them from balding! The experiment worked, but there were also other problems with 4MA, which is why it was eventually abandoned. Merck found and developed something they called "finasteride", which appeared to be an improvement on 4MA. Anyway...on the first page of that early 4MA study, the Merck scientists mentioned that there was a number of potential uses for a good 5a-reductase inhibitor; they specifically mentioned BPH, acne (they found out much later that finasteride didn't really work for acne), and (I'm not making this up!) MALE PATTERN BALDING!!!
It's right there in black and white, LONG before Proscar and Propecia were developed!