Question for Bryan
- Thread starter Jupiter1
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All we have to go by is Glaxo's own testing. Since they found a dutasteride dose of 0.1 mg/day to be virtually identical with taking a Proscar every day, I would imagine that an Avodart every fourth day would be slightly more effective (and have a similar slightly higher risk of side-effects) than taking a Propecia every day.
Bryan
Bryan
Jupiter1
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wow fast reply: I actually value your commitment to empirical research and fact, I've learnt the hard way about airy-fairy flakes on these hair loss forums.
Just to be clear
are you saying that
A)0.1mg dutasteride = 5mg finasteride?
or did you mean
B)0.1mg dutasteride = 1mg finasteride
If B) then surely every 5th day would be the equivalent dose and this would also be extra effective with regards to 5A type 1 inhibition benefits?
Just to be clear
are you saying that
A)0.1mg dutasteride = 5mg finasteride?
or did you mean
B)0.1mg dutasteride = 1mg finasteride
If B) then surely every 5th day would be the equivalent dose and this would also be extra effective with regards to 5A type 1 inhibition benefits?
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Jupiter1 said:
I know that feeling well!
Jupiter1 said:
At the time Glaxo did that testing, Propecia wasn't yet available, so they just used Proscar (5 mg finasteride). The hair-count improvements from 0.1 dutasteride/day and 5 mg finasteride/day were almost identical.
Jupiter1 said:
It should be the same effectiveness for male pattern baldness, yes. However, dutasteride's ability to inhibit the 5a-reductase type 1 enzyme starts to fall-off rapidly at those lower doses. There's only a small and insignificant inhibition of type 1 at 0.1 mg/day (or the equivalent Avodart every 5th day).
Bryan
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Bryan said:
Jupiter, I'm going to assume that you aren't that familiar with the published material on dutasteride. Take a look at the following set of graphs, which show levels of inhibition from various doses of dutasteride ("GI198745" was Glaxo's code-name for the drug):
http://www.geocities.com/bryan50001/dutasteride2b.htm
Notice the middle graph of Figure 6, in particular. It shows that after taking 0.1 mg/day of dutasteride for 28 days, the calculated inhibition of the 5a-reductase type 1 enzyme was only around 5% or so.
But notice what an AWESOME ability dutasteride has at inhibiting the type 2 enzyme! It's absolutely kick-*** at that!! :freaked2:
Bryan
stax
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Good question! I'd love to hear an answer to this.
If those people in the republic born without 5AR dont go bald ever, why wouldnt a strong drug like dutasteride do the same for us normal people? I beleive there biology is different than ours despite what people say. Taking dutasteride doesnt make us the same as those people, there bodies work differently and were built/designed differently IMO.
If those people in the republic born without 5AR dont go bald ever, why wouldnt a strong drug like dutasteride do the same for us normal people? I beleive there biology is different than ours despite what people say. Taking dutasteride doesnt make us the same as those people, there bodies work differently and were built/designed differently IMO.
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Nah, it's just a timing issue. The reason drugs like finasteride and dutasteride don't necessarily COMPLETELY stop balding (like what the pseudo's have) is because guys start taking them well after they're already balding. If they were to start taking them prior to puberty, I think the results would be the same as the pseudo's.
Bryan
Bryan
stax
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Bryan, what makes you say that exactly? That seems like a pretty wild claim! Please explain why you say its about timing, and the reasons for that. I dont see the difference if one is balding already, because if we biologically make ourselves like those people in the republic, then we should see no more loss at all because they never see hairloss. It makes no sense about the timing issue. Are you saying that once the process of balding has be started nothing can stop it, or other facotrs start to get involved only after the process has started? Why would this be? People say other factors are involved in male pattern baldness but clearly not for those people in the republic. Dont castrated males totally stop from balding any further, even in old age? If so than the answer isnt internal drugs, its topical anti-androgens like RU which block all androgens from the androgen receptors in the scalp. Why doesnt insulin resistance play a role in balding in those people in the republic, when it plays a role in regular people?
I definetly think those people's bodies work different than ours to some degree.
I definetly think those people's bodies work different than ours to some degree.
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stax said:
I certainly don't have any PROOF of that, but it seems obvious enough that I'd put money on it!
stax said:
Sure. I've long said that balding (especially severe balding) seems to set into motion certain degenerative processes like inflammation and fibrosis which aren't entirely dependent on continued androgenic stimulation. That's why copper-peptides and products like Proxiphen (which is relatively skimpy on any antiandrogenic effect, but is loaded with stuff which can have a "healing" effect on the skin/scalp) can be so helpful for balding.
stax said:
Maybe, but just to be absolutely sure, I'd like to see more precise testing of that than what Hamilton was capable of doing at the time he did his seminal work in that area. All he did was compare old pictures of his subjects with their current status. He certainly didn't have access to haircounts or hairweights, obviously.
Furthermore, I consider castration to have a greater total antiandrogenic effect than what you get with finasteride and dutasteride. That _may_ also have something to do with why castration after puberty might stop balding more consistently than using 5a-reductase inhibitors after puberty.
BTW, there's evidently a different kind of timing issue that _is_ associated with castration! One study I was reading said that castration PRIOR to the age of 40 (I hope I'm remembering that age correctly) will prevent the later occurrence of prostate cancer, but not castration AFTER the age of 40. So I don't see why you find it so difficult to believe that starting finasteride as a young boy (for example) might be considerably more effective than waiting until well AFTER those profound changes start to occur during puberty.
stax said:
What makes you think it DOESN'T play a similar role down there? It's just that because they're the way they are from conception onwards, overt balding never gets started in the first place, so relatively minor influences like insulin resistance later in their lives isn't that much of a factor.
Bryan
stax
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Good post Bryan, it definetly can be a possibility. Interesting about the castration before and after 40 years old thing, i didnt know that!. You're theory is making more sense to me now. Looks like thats why finasteride and dutasteride produce poor results for some people, and results go downhill after a while. We wouldnt want to mess with DHT inhibitors before puberty, and obviously waited untill we noticed some hairloss before staring the finasteride or dutasteride. It looks like topical RU is the answer to maintaining because it totally blocks the androgen receptors in the scalp when applied topically, so that means it blocks all androgens from the scalp and one should theoretically have the same results hair wise as a castrated male?
If the balding process has already started, what other chain of events do you think come into play that contribute to hairloss? Are they all DHT and androgen related? For example does high levels of insulin due to diet or what not cause higher levels of DHT? Or does high levels of insulin contribute to hairloss without having anything to do with DHT and androgens? Is inflammation the last step in the chain that causes hairloss? For example DHT binds to the hair shaft thus causing inflammation, thus causing hairloss? Or can DHT bind to the hairshaft not causing any inflammation/silent inflammation, but still cause hairloss? Ive read that we only lose our hair due to inflammation/silent inflammation. Many different things can cause inflammation, but does inflammation only due to androgens cause the hairs to miniturize?
Thx Bryan.
If the balding process has already started, what other chain of events do you think come into play that contribute to hairloss? Are they all DHT and androgen related? For example does high levels of insulin due to diet or what not cause higher levels of DHT? Or does high levels of insulin contribute to hairloss without having anything to do with DHT and androgens? Is inflammation the last step in the chain that causes hairloss? For example DHT binds to the hair shaft thus causing inflammation, thus causing hairloss? Or can DHT bind to the hairshaft not causing any inflammation/silent inflammation, but still cause hairloss? Ive read that we only lose our hair due to inflammation/silent inflammation. Many different things can cause inflammation, but does inflammation only due to androgens cause the hairs to miniturize?
Thx Bryan.