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Topic Title: Is dutasteride's superior results compared to finasteride only to do with its more competitive inhibition of Type II alpha-reductase?
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Created On: 02/15/2009 09:44 AM
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 02/15/2009 09:44 AM
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TheCamdenKid
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I've been thinking about this a lot lately....I'm getting more and more convinced that the benefit of taking dutasteride is only due to it's more potent inhibition of the Type II alpha-reductase enzyme and that we DON'T want to be inhibiting type I.

In the past I've taken finasteride and dutasteride and the one thing I notice while on dutasteride is that my hair becomes dry and lusterless probably because sebum production is way down. Considering that humans with a deficiency of 5-alpha-reductase Type II still have normal sebum production, it seems obvious to assume that the Type I enzyme is purely responsible for sebum production. Because of this, I'm not sure that inhibiting type I is too beneficial for MPB at all. I know it could be argued that both Type I and Type II reductase enzymes can still produce the same end product (DHT) which could ultimately be reabsorbed(?) to cause a negative effect, but I'm beginning to be of the opinion that when DHT is produced, it binds to the androgen receptor where it is needed there and then. The benefits of reduced DHT are because there is less DHT around to bind to ARs, but what I'm kind of saying is that the DHT converted by Type I is converted for a particular purpose there and then and as such there would be no 'leftovers' to contribute to the MPB process - obviously this is in the assumption that the DHT converted by Type II (which I assume is more or less immediately bound to its target AR also) is the main androgen contributor to MPB! It's almost like considering there is two different forms of DHT - which is not the case - one created by Type I and one created by Type II.

This would also point to the idea that by taking dutasteride, yes, you will have a more effective treatment, but you will also be inhibiting DHT which is of no use to inhibit - I remember reading that alpha reductase type I is present in the heart and brain for two additional examples alongside normal scalp sebum production! The two reductase enzymes are found in different areas of the body and it might be prudent to assume they are exactly where they are needed.

Obviously dutasteride has been shown in studies to improve hair counts compared to finasteride by 30 or so hairs per inch squared (or something like that?), but can this not be put down to the fact that dustasteride is 3 times a more potent inhibitor of Type II alpha reductase?


Edited: 02/15/2009 at 09:56 AM by TheCamdenKid
 02/15/2009 10:04 AM
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calvinmd
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The common conclusion is that Dut works because of the type#2 inhibition.

The effects of type#1 on hair is probably not a total zero (as with any other androgen including straight Test). But it's a matter of degree - it's type#2 that is really killing our hair in the big picture. We'd probably be better off leaving anything else alone as much as possible.

Type#1 DHT and Test itself are probably not good for our hair either, but the cost/benefits of reducing them are not very likeable at all.

 02/15/2009 12:19 PM
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TheCamdenKid
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Yeah, I'm sure androstenedione is a player in hair loss too as well as testosterone, but I do think the effect of the DHT produced by the type II enzyme may be zero.

I know I looked up before in what tissues Type I and Type II enzyme are present, but I can't seem to find anything on it anymore.....I know I read somewhere that Type I was present in the heart brain, and bone maybe......Can anyone confirm this for me?
 02/15/2009 01:34 PM
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Bryan
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While I agree that the greater inhibition of the type II enzyme of dutasteride over finasteride (about 98%-99% for dutasteride at the approved dosage, versus around 85%-90% or so for finasteride, depending on the dose) would explain _some_ of its somewhat greater effectiveness at fighting MPB (haircounts while using Avodart were about 22% better than haircounts while using Proscar), I don't think it can explain ALL of it. How would one explain the somewhat better performance of the higher dose of dutasteride (2.5 mg/day) over the smaller dose of 0.5 mg/day? Would inhibiting that remaining 1%-2% of type II activity really make any noticeable difference?

Also, I tend to be suspicious of any claims about Avodart's alleged ability to reduce sebum production. I still haven't seen any studies documenting that effect, which I find peculiar. I also doubt that any such alleged effect, even if it really does exist, would make any noticeable difference in the cosmetic quality of scalp hair.
 02/15/2009 02:04 PM
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Bryan
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Something else I forgot to mention: while I agree that DHT has an effect mainly in the tissues where it's actually synthesized (Dr. Proctor talked about that for years on alt.baldspot), nevertheless it _can_ play the role of an endocrine hormone by affecting more remote body tissues, especially when given in large doses. For example, applying an external DHT gel or giving DHT injections definitely can produce noticeable effects across the body.

So what I'm saying is that by partially inhibiting the type 1 enzyme, dutasteride likely does have an additional beneficial effect over finasteride, not only by further reducing serum DHT, but also other nearby sources of type 1-generated DHT like in the sebaceous glands, which are physically very close to the hair follicle. There are also reports of the type 1 enzyme even existing in certain parts of the hair follicle itself, although I still consider that to be a bit controversial.
 02/15/2009 02:10 PM
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TheCamdenKid
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Couldn't the increased effectiveness of Avodart 2.5mg compared to 0.5mg of Avodart be to do with the fact that 0.5mg reduces scalp DHT by 54% and 2.5mg reduces scalp DHT by 82%?

I'm not saying I'm definitely correct about the use of Avodart causing 'dry' hair, but I can notice a difference when I'm on it perhaps more than others might because my hair is down to my shoulders....lol

EDIT: Obviously, I'm thinking that the additional benefit of an increased dose of Avodart might be from the increased reduction of DHT created by Type II alpha-reductase and not Type I.

Edited: 02/15/2009 at 02:24 PM by TheCamdenKid
 02/15/2009 02:30 PM
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JWM
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Bryan, what about the fear being spread about type 1 5ar being present in the brain and that taking Dut may be detrimental to cognitive ability in the long-run?
 02/15/2009 02:36 PM
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Bryan
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Originally posted by: TheCamdenKid

Couldn't the increased effectiveness of Avodart 2.5mg compared to 0.5mg of Avodart be to do with the fact that 0.5mg reduces scalp DHT by 54% and 2.5mg reduces scalp DHT by 82%?


Personally, I never talk about so-called "scalp DHT", because of the uncertainties of dealing with that expression. "Scalp DHT" obviously includes not only follicular DHT, but DHT in the sebaceous glands and sweat glands, and perhaps other sources.

To me, it sounds a little bit like talking about "head DHT". It strikes me as rather odd and pointless!

Originally posted by: TheCamdenKid
EDIT: Obviously, I'm thinking that the additional benefit of an increased dose of Avodart might be from the increased reduction of DHT created by Type II alpha-reductase and not Type I.


Sure, but would there be an additional noticeable benefit just from going from 1% to 2% down to even 0%??
 02/15/2009 02:48 PM
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jack
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Bryan, would two dut pills a week give similar results as propecia everyday?
 02/15/2009 02:48 PM
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TheCamdenKid
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Do you mean the uninhibited 1/2% serum DHT left over from taking Avodart?
 02/15/2009 02:54 PM
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Bryan
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Originally posted by: JWM

Bryan, what about the fear being spread about type 1 5ar being present in the brain and that taking Dut may be detrimental to cognitive ability in the long-run?


I do think that's a legitimate concern, and I do think it's quite interesting that although there's more than just one example of a spontaneous occurrence in Nature of individuals who have inherited 5a-reductase type II deficiencies (it happens not only with the much-discussed pseudohermaphrodites in the Dominican Republic, but also in at least one or two other countries around the world), there is apparently not so much as even a single known case of people who have ever developed type I deficiencies. The implication, of course, is that any occurence of a type I deficiency might be LETHAL.

It's probably not just a coincidence that the FDA-approved dosage of dutasteride only inhibits the type I enzyme by around 50% or so (maybe a bit more). Who knows? Much more than that may increasingly get people into trouble with side effects.
 02/15/2009 03:00 PM
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Bryan
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Originally posted by: jack

Bryan, would two dut pills a week give similar results as propecia everyday?


That sounds about right.
 02/15/2009 03:11 PM
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Bryan
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Originally posted by: TheCamdenKid

Do you mean the uninhibited 1/2% serum DHT left over from taking Avodart?


No, I'm talking about the uninhibited type II enzyme left over from taking Avodart. Take a look at these excellent graphs from the Gisleskog et al studies on dutasteride and finasteride:

http://www.geocities.com/bryan50001/dutasteride2b.htm

They show the reduction not only of serum levels of DHT from various dosing schemes with dutasteride, but also the specific inhibitions of the type I and type II enzymes from various doses. Lots of good stuff in those graphs!
 02/15/2009 03:31 PM
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TheCamdenKid
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Thanks for the link, Bryan. That's interesting stuff......I know you said you don't really pay attention to talk of scalp DHT levels, but I've heard that dutasteride 0.5mg a day increases serum testosterone levels by about 15% or so - which makes sense as testosterone is not being converted to DHT -, and the same dosage (0.5mg) increases scalp testosterone by over 100%. What's your views on that?

I've heard of people on finasteride and dutasteride experiencing diffuse thinning while continuing treatment rather than a continuation of their original classic MPB pattern. Could this be to do with the increase in scalp testosterone (which is higher in females that are balding) resulting in diffuse thinning like FPB?
 02/15/2009 04:52 PM
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jack
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Do you think one pill would be okay, Bryan? Am having trouble getting the stuff to my country.
 02/15/2009 06:34 PM
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Janks16
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I saw no regrowth after a little over a year's usage of Dut. Though it doesn't mean it won't work for you.
 11/13/2012 12:56 PM
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dontcareneedhair
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Maybe you should take more Janks16.
 11/22/2012 10:42 AM
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Science
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Many are now taking Fin with Dut instead of either or on this site. That is really untested territory.

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this is for information purposes I am not a Dr. for hair loss my advice should not be considered medical/expert advice for such. The poster will not be liable for any direct, indirect, consequential, special, exemplary, or other damages arising therefrom.
 11/22/2012 02:23 PM
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Phalacraphobic
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Originally posted by: dontcareneedhair

Maybe you should take more Janks16.


I'm sorry, but I really don't think you should be giving anyone advice on here.
 11/22/2012 02:25 PM
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Phalacraphobic
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Originally posted by: Janks16

I saw no regrowth after a little over a year's usage of Dut. Though it doesn't mean it won't work for you.


Research some growth stimulators.

While I believe DUT can cause regrowth, I believe it's only through allowing the hair to detract from miniaturizing, allowing something else that's causing the re-growth to work effectively. Therefore, if you feel comfortable with taking DUT, I think you should look into strong growth stimulators, and maybe even minox if you're not already taking it. Be aware though, minox can turn out to be garbage.
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