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http://www.ncbi.nlm.nih.gov/pubmed/10495374
i thought propecia only inhibit something like 30 % scalp dht ?
i thought propecia only inhibit something like 30 % scalp dht ?
Is This Important Study About Serum Dht And Finasteride Accurate?
- Thread starter michel sapin
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This professional study is obviously accurate, but what matters when it comes to androgenetic alopecia is 5AR Type II DHT. Finasteride inhibits that by 90% while Dutasteride inhibits it by 99%. These levels of inhibition are enough to stop hair loss and regrow hair indefinitely for most men.
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@jetlife1 - what is your theory for why some people (including myself) experience drastic hair loss and miniaturization on finasteride? even for a period of over a year? Do you personal think that people who are poor responders to finasteride may respond well to dutasteride?
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The numbers and their measurement errors are consistent with other studies.
The measurement error is due to small number statistics.
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so does tis means that finasteride 1 mg and 5 mg inhibits the same amount of serum dht ?
For people who respond like you, I think that it could be a couple things, I'll list them:
- finasteride is causing the miniaturizing hairs to shed, but they will eventually grow back thicker. I've read that this could happen anywhere from 3-12 months. It could take longer for some people to stop shedding depending on how far along their hair loss is. Remember that everyone has different length hair cycles so that could be a factor as well. For me, my hair was in pretty bad shape and far below baseline at 3 months. It eventually started looking better around 6 months and I'd say I was back at baseline 6-12 months. Now my hair is even more abundant/thicker at 2+ years.
- The finasteride shed made you freak out and you played with dosage, stopping and starting, and not taking it every day like you should. Or you changed your regimen and added minoxidil which will most likely increase the duration and exacerbate the initial finasteride shed.
- You're a non-responder to finasteride. Very rare according to the data and all the studies, and if anything finasteride should slow down your hair loss at least.
If finasteride really doesn't work for you after consistent use and you feel that you've given it enough time then maybe dutasteride will work better. But you have to remember even starting dutasteride will most likely give you an initial shed that can last a while. If I knew that dutasteride worked better than finasteride long term then I would probably use it. However, it is not FDA approved and there are no long term studies on blocking the type 1 5AR DHT so I refuse to use it until then. Type 2 is all that matters in male pattern baldness anyway and I don't know if blocking 9% more would do much more if anything more at all cosmetically.
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There is a tiny difference in inhibition between 0.05 mg/day and 5.00 mg/day, as demonstrated by several independent studies.
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exactly man , i don't know which study is real . If even ncbi are wrong
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Finasteride is good up to ~0.05 mg/day, then you get no benefit.
Small doses of dutasteride are probably better, and the effect of dose does depend on dose. It's a different drug.
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i am currently on 5 mg finasteride daily, because my endo told me that would be better .
Do you think there will be no benefits ? It is not better than 1 Mg? Does it cause more sides ?
Do you think there will be no benefits ? It is not better than 1 Mg? Does it cause more sides ?
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thx anty ; but some doctor like berstein says that 5 mg is not better but cause way more sides than 1 mg of finasteride . But if it inhibit slightly more it might cause slightly more sides right ? and not way more sides .
cyrusthegreat@hotmail.com
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This may have already been duscussed in the past. Here's a bit of bro and non-bro science...please poke holes in this. I know I'm making some gross simplifications and assumptions.
women with fpb tend to maintain hairline while thinning elsewhere due to high/higher aromatase expression at the hairline follicles. This reduces exposure of these follicles to dht by aromatising T to E and sparing them androgen damage. Scalp and follicles behind the hairline in those with fpb lack or have much lower aromatase expression. Above that, some women sufferers may have increased expression of 5ar type 2, 5ar type 1, or both in these regions and perhaps in different locations throughout loss regions of the scalp. Thereby local dht production and exposure may be increased behind the hairline (pretty much anywhere between vertex and hairline). This could explain varying severity of loss between cases of fpb while hairline is mostly maintained. Increased AR sensitivity may also be involved, which could modulate severity of loss due to locally and systemically produced dht.
So like women, men may also experience differing expression of androgen related enzymes in different parts of their scalp.
I for one am of the opinion that local dht Production is more damaging than systemic. At least in the case of the scalp. I figure that dht production throughout the body is higher in some tissues than others. Similarly, dht activity is likely higher in some areas than others. That is, by the time dht produced in one part of the system makes its way to another (say scalp), either it has already exerted its activity in other tissues and cells along the way, or majority of binding sites at the distant site (say scalp) have already succumbed to locally produced dht.
One dutasteride study already suggested that the majority of 5ar found in the scalp is type 1 given % scalp dht reduction on finasteride vs dutasteride compared to systemic. I bro science that and extend to guess that between Androgenetic Alopecia sufferers the expression of 5ar type 1 and 2 can differ throughout the scalp in loss regions and differ among men. It's also possible that this variable expression varies over lifetime. This could explain how some while on finasteride see an acceleration of their loss even after months on the drug.
I've been on finasteride 1mg daily for almost 18 months. In that time I went from a slow diffuse thinning over the past 10 yrs with nw1 and no sign of balding to a 0.5 inch bald spot at the vertex and 1 inch recession at right temple with very noticeable thinning throughout the hairline. My guess is i have higher 5ar type 1 in these areas and due to increased T from finasteride I experienced accelerated loss in these areas from reduction to dht by local 5ar type 1.
Concerning finasteride non response i have no idea what that means. Ive never seen any explanation about this. Does this suggest that somehow systemic dht levels weren't affected and/or some people have 5ar type 2 that finasteride just doesn't affect? I've definitely experienced documented finasteride sides, so it's doing something, several things in fact, except helping my hair.
I will soon turn to dutasteride to a see if I'm right, but I'm considering topical application of dutasteride maybe, not to limit systemic absorption, but to test the idea. That's another topic
women with fpb tend to maintain hairline while thinning elsewhere due to high/higher aromatase expression at the hairline follicles. This reduces exposure of these follicles to dht by aromatising T to E and sparing them androgen damage. Scalp and follicles behind the hairline in those with fpb lack or have much lower aromatase expression. Above that, some women sufferers may have increased expression of 5ar type 2, 5ar type 1, or both in these regions and perhaps in different locations throughout loss regions of the scalp. Thereby local dht production and exposure may be increased behind the hairline (pretty much anywhere between vertex and hairline). This could explain varying severity of loss between cases of fpb while hairline is mostly maintained. Increased AR sensitivity may also be involved, which could modulate severity of loss due to locally and systemically produced dht.
So like women, men may also experience differing expression of androgen related enzymes in different parts of their scalp.
I for one am of the opinion that local dht Production is more damaging than systemic. At least in the case of the scalp. I figure that dht production throughout the body is higher in some tissues than others. Similarly, dht activity is likely higher in some areas than others. That is, by the time dht produced in one part of the system makes its way to another (say scalp), either it has already exerted its activity in other tissues and cells along the way, or majority of binding sites at the distant site (say scalp) have already succumbed to locally produced dht.
One dutasteride study already suggested that the majority of 5ar found in the scalp is type 1 given % scalp dht reduction on finasteride vs dutasteride compared to systemic. I bro science that and extend to guess that between Androgenetic Alopecia sufferers the expression of 5ar type 1 and 2 can differ throughout the scalp in loss regions and differ among men. It's also possible that this variable expression varies over lifetime. This could explain how some while on finasteride see an acceleration of their loss even after months on the drug.
I've been on finasteride 1mg daily for almost 18 months. In that time I went from a slow diffuse thinning over the past 10 yrs with nw1 and no sign of balding to a 0.5 inch bald spot at the vertex and 1 inch recession at right temple with very noticeable thinning throughout the hairline. My guess is i have higher 5ar type 1 in these areas and due to increased T from finasteride I experienced accelerated loss in these areas from reduction to dht by local 5ar type 1.
Concerning finasteride non response i have no idea what that means. Ive never seen any explanation about this. Does this suggest that somehow systemic dht levels weren't affected and/or some people have 5ar type 2 that finasteride just doesn't affect? I've definitely experienced documented finasteride sides, so it's doing something, several things in fact, except helping my hair.
I will soon turn to dutasteride to a see if I'm right, but I'm considering topical application of dutasteride maybe, not to limit systemic absorption, but to test the idea. That's another topic
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