Finasteride didn't work for you? So, did DUT?

[mic28]

Hi James,

RU seemed to have an impact on me and reduce shedding for a couple of days about a month ago. Since then I have been back to normal with an itchy scalp and hair loss. I'm not sure why it worked for such a brief period but if I can get the lack of shedding back again then I'm sure I will start to see improvement. I am still trying to play about with concentrations and maybe this is holding me back

[jamesst11]

Hi James,

RU seemed to have an impact on me and reduce shedding for a couple of days about a month ago. Since then I have been back to normal with an itchy scalp and hair loss. I'm not sure why it worked for such a brief period but if I can get the lack of shedding back again then I'm sure I will start to see improvement. I am still trying to play about with concentrations and maybe this is holding me back

yeah... I am just going straight up 10% with dermarolling before. Let's pray!

[pajason]

Don't want to sound pessimistic but the reality is that for the vast majority of us there is no treatment that is going to grow any significant hair. Once it's gone it's gone. There are a few lucky ones which experience lots of regrowth but those cases are atypical. The absolute best likely result is stopping the loss where it is, with in my opinion the most likely result being slowing the hair loss down(especially in the crown area) I really believe most that have success with DUT or FIN are simply delaying the baldness a few years(not a bad thing at all).

[blohan]

Don't want to sound pessimistic but the reality is that for the vast majority of us there is no treatment that is going to grow any significant hair. Once it's gone it's gone. There are a few lucky ones which experience lots of regrowth but those cases are atypical. The absolute best likely result is stopping the loss where it is, with in my opinion the most likely result being slowing the hair loss down(especially in the crown area) I really believe most that have success with DUT or FIN are simply delaying the baldness a few years(not a bad thing at all).

What about the front of the head?

[tedwuji]

Don't want to sound pessimistic but the reality is that for the vast majority of us there is no treatment that is going to grow any significant hair. Once it's gone it's gone. There are a few lucky ones which experience lots of regrowth but those cases are atypical. The absolute best likely result is stopping the loss where it is, with in my opinion the most likely result being slowing the hair loss down(especially in the crown area) I really believe most that have success with DUT or FIN are simply delaying the baldness a few years(not a bad thing at all).

More than a few. Im at 6. Kobren is at like 25 years. These guys are at 10:

http://www.bernsteinmedical.com/research/10-year-finasteride-study-first-to-investigate-long-term-effects-and-safety/

There is hope!

However, what you said about "Once it's gone, it's gone" is true.

-Prevention is key.

[dm90]

Yes, all hair that is still present can be protected by 5ARI. The more I've looked into everything the more i'm realizing why people lose hair on fin, also i'm beginning to believe its nearly impossible to have any significant hair loss on dutasteride. With 0.5mg DUT at a steady state and adequate sulfotransferase activity theres no reason why you wouldnt gain nearly all of your hair back if you caught it at early diffuse thinning. If you are resorting to dut and stick with it, unless you have unbelievable androgen sensitivity, there is no logical reason why you wouldnt keep your hair indefinitely.

[tedwuji]

Yes, all hair that is still present can be protected by 5ARI. The more I've looked into everything the more i'm realizing why people lose hair on fin, also i'm beginning to believe its nearly impossible to have any significant hair loss on dutasteride. With 0.5mg DUT at a steady state and adequate sulfotransferase activity theres no reason why you wouldnt gain nearly all of your hair back if you caught it at early diffuse thinning. If you are resorting to dut and stick with it, unless you have unbelievable androgen sensitivity, there is no logical reason why you wouldnt keep your hair indefinitely.

But DUT messes with type1 and type2. Safety and side effect profile a little less clear for a few diff reasons. Also i heard some guys still lose hair anyways, unfortunately.

[dm90]

Yes, we do not have a model in nature for a type 1 deficiency so long term side effects are unclear, i'm not encouraging anyone to take dutasteride. Yes dutasteride inhibits both isoforms, but type 1 has no PROVEN role in hairloss, dutasterides increased effectiveness over fin is due to its higher affinity for the type II isoform. Also there is much less standard deviation with dutasterside. Fin has a standard deviation of 15-20% meaning some people will get a great response and inhibit up to 90% of type 2 dht in the DP, however some will only get 60% reduction. DHTs effect on follicles is understood to be mostly an autocrine response. This means that the follicle produces DHT and it then attaches to the AR on the cell that produced it. Now if you are an individual who only gets 60% reduction that leaves 40% remaining to bind to the AR. Now knowing this its actually pretty easy to see how AGA can progress even with finasteride. Hell even the best outcome for fin leaves 10% DP DHT left. DUT at a steady state of 0.5mg inhibits DP type 2 DHT by up to 98% with very little variation. The poorest responder will still get at least 92-95 % reduction. Some say that they have lost hair on DUT, but I havent seen any concrete evidence of this through photographs. Its very hard to believe that 2% of baseline DHT can do any damage. Glaxosmithklines phase 3 avodart trial showed only 1 patient have a slight decrease in hair after six month, which resulted in a 99% efficiency rate. Also theres no way of knowing if that one patient actually experienced a progression of AGA or just his follicles transitioning into the telogen phase. AGA is androgen drive and if you remove the androgen stimulus your retard the condition.

[tedwuji]

Yes, we do not have a model in nature for a type 1 deficiency so long term side effects are unclear, i'm not encouraging anyone to take dutasteride. Yes dutasteride inhibits both isoforms, but type 1 has no PROVEN role in hairloss, dutasterides increased effectiveness over fin is due to its higher affinity for the type II isoform. Also there is much less standard deviation with dutasterside. Fin has a standard deviation of 15-20% meaning some people will get a great response and inhibit up to 90% of type 2 dht in the DP, however some will only get 60% reduction. DHTs effect on follicles is understood to be mostly an autocrine response. This means that the follicle produces DHT and it then attaches to the AR on the cell that produced it. Now if you are an individual who only gets 60% reduction that leaves 40% remaining to bind to the AR. Now knowing this its actually pretty easy to see how AGA can progress even with finasteride. Hell even the best outcome for fin leaves 10% DP DHT left. DUT at a steady state of 0.5mg inhibits DP type 2 DHT by up to 98% with very little variation. The poorest responder will still get at least 92-95 % reduction. Some say that they have lost hair on DUT, but I havent seen any concrete evidence of this through photographs. Its very hard to believe that 2% of baseline DHT can do any damage. Glaxosmithklines phase 3 avodart trial showed only 1 patient have a slight decrease in hair after six month, which resulted in a 99% efficiency rate. Also theres no way of knowing if that one patient actually experienced a progression of AGA or just his follicles transitioning into the telogen phase. AGA is androgen drive and if you remove the androgen stimulus your retard the condition.

Serum dht and scalp dht reduction are two separate animals and i am well versed in this data as well. You are refencing serum DHT levels when you quote 98% redux

May also be worth noting that type1 permeates the blood brain barrier while type 2 does not as a side note.

[dm90]

They're different animals, but completely pointless distinctions. They are also are irrelevant to fin/dut effectives in treating hairloss. The 98% figure i stated was dermal papilla type 2 dht, which as far as we know is the only relevant DHT with regards to hairloss, remember its an autocrine response not paracrine. Serum DHT is just the DHT concentration in the entire body, which includes scalp DHT. Yes most are well versed in the reduction percent curve of finasteride, approx 70% serum, and dutasteride approx 90%. But You have to understand what these numbers mean. Why can serum dht be reduced by 90% while scalp dht is only reduced by 50%? Because DHT isnt evenly concentrated throughout the body. Type 2 is heavily concentrated in the prostate and dermal papilla while type 1 is present in the sebaceous glands and brain. Neither have any significant concentration in the skeletal muscle. Sebaceous glands are in the scalp and therefore there is a significant concentration of the type 1 isoform. Finasteride has no affinity for this isoform and dutasteride, while it does reduce it, doesnt have nearly as strong of an affinity for it as it does for the type 2. Secondly and the most important point is the ratio of type 1 to type 2 in the body. The majority of DHT in the body is converted from the type 2 isoenzyme. I approximately 70-80% of total dht actually. Firstly FIN reduces total serum dht by 70%. Secondly FIN has no affinity for the type 1 isoenzyme, therefore that 70% reduction is completely type 2. Well 70 is about 90% of 80. So given the perfect response finasteride reduces type 2 dht by 90%. This means there is only 10% DHT left in the dermal papilla, the only important DHT. DUT has 3x affinity for the type 2 isoenzyme over finasteride, this means significantly more type 2 is reduced leaving next to no traces of the hormone in the follicle. Lastly, yes type 1 is present in the brain tissue, and dutasteride can pass the blood brain barrier. That isnt really relevant to the point im making.

[dm90]

Just a side note. Theres alot of fear mongering about Fin and DUT on here, yet theres a a sizable group of forum users interested in JAK inhibitors. That is pure insanity to me.

[JohnMPB]

I've heard this theory thrown around recently on various forums and Dr. Proctor, who is very well versed in hair loss agrees that it's quite a possibility...

It's likely fin and dut perform almost the same over the long term in regards to mpb. The idea is there is only type 2 5ar in the dermal papilla which Finasteride is a specific inhibitor. Dut inhibits both forms but type 1 is located in other tissues such as the sebaceous gland. So far there are mainly only 6 month studies showing dut outperforms fin in that timeframe but there are no 1+ year studies to show whether or not dut just works faster.

As we see from other studies, fin continues to increase hair counts beyond 1 year. So the question is does dut really outperform fin in regards to hair counts or just work faster over the short term?

Anti androgens can only get you so far with mpb. It's somewhat rare to see people regrow hair just on fin or dut. Even castrates don't regrow much but can halt their mpb. Hair loss is very complex and from my minimal understanding just chasing the idea that decreasing androgens as much as you can will have diminishing returns IMO, fwiw, just sayin.

[dm90]

I believe it all goes back to the original pseudoherms discovery. Type 2 deficiency results in no AGA, therefore one can infer that there is no type 1 in the DP. I agree that if a person has a good response to fin, maximum dht reduction of 90%, DUT wont outperform fin by much of any degree. However, remember that 10% of people who take fin experience a progression of AGA over 5 years. I believe its because these are the individuals that are on the left side of the DHT reduction bell curve. I see alot of posters say that if fin doesnt work dut wont really either, but to me that just cant be the case. This is because DUT pretty much eliminates all type 2 in the DP for everyone. Remember the standard deviation is so small compared to fin. In the long run i'd say DUT will produce better results everytime compared to fin. Yes hairloss is a complex disregulation of several pathways that leads to hair miniaturization, but remember its all started by the initial androgen stimulation. Understanding the pharmacology of the two drugs also supports that DUT is superior at maitenance. FIN reduces DHT to its maximum effectiveness very rapidly, with 24 hours of its first dose. However fin has a halflife of 8 hours and DHT can fluctuate even if you take it daily. DUT takes a long time to reach a steady state, but once it does youre DHT levels will pretty much remain at their lowest levels. However reaching a steady state on DUT takes 3 months of 0.5 mg daily. Now i have read studies that there are people with genotypes that respond better to fin, however this is pretty rare to my understanding. I'm not saying anyone should jump on DUT, i'm merely saying that if you understand the basic facts about AGA and the pharmacology of DUT its not a ridiculous statement to say that AGA cant progress on DUT. Regrowth is another story, I have read numerous studies on the mechanism of action for minoxidil and basically minoxidil works be forcing some of the pathways disregulation by DHT back into regulation. Really its pretty phenominal all the things minoxidil does, its just that damn sulfotransferase enzyme. If we all had it aga would be essentially cured for many sufferers.

[JohnMPB]

I believe it all goes back to the original pseudoherms discovery. Type 2 deficiency results in no AGA, therefore one can infer that there is no type 1 in the DP. I agree that if a person has a good response to fin, maximum dht reduction of 90%, DUT wont outperform fin by much of any degree. However, remember that 10% of people who take fin experience a progression of AGA over 5 years. I believe its because these are the individuals that are on the left side of the DHT reduction bell curve. I see alot of posters say that if fin doesnt work dut wont really either, but to me that just cant be the case. This is because DUT pretty much eliminates all type 2 in the DP for everyone. Remember the standard deviation is so small compared to fin. In the long run i'd say DUT will produce better results everytime compared to fin. Yes hairloss is a complex disregulation of several pathways that leads to hair miniaturization, but remember its all started by the initial androgen stimulation. Understanding the pharmacology of the two drugs also supports that DUT is superior at maitenance. FIN reduces DHT to its maximum effectiveness very rapidly, with 24 hours of its first dose. However fin has a halflife of 8 hours and DHT can fluctuate even if you take it daily. DUT takes a long time to reach a steady state, but once it does youre DHT levels will pretty much remain at their lowest levels. However reaching a steady state on DUT takes 3 months of 0.5 mg daily. Now i have read studies that there are people with genotypes that respond better to fin, however this is pretty rare to my understanding. I'm not saying anyone should jump on DUT, i'm merely saying that if you understand the basic facts about AGA and the pharmacology of DUT its not a ridiculous statement to say that AGA cant progress on DUT. Regrowth is another story, I have read numerous studies on the mechanism of action for minoxidil and basically minoxidil works be forcing some of the pathways disregulation by DHT back into regulation. Really its pretty phenominal all the things minoxidil does, its just that damn sulfotransferase enzyme. If we all had it aga would be essentially cured for many sufferers.

You make some great points. The fluctuation of DHT levels is true, but nobody knows what's going on within the DP which is really what matters. It's easy to get caught up in the DHT reduction numbers but one thing that Dr. Proctor brought up was that with greater DHT reduction, there is a higher chance of reflex hyperandrogenicity- which is potentially very bad for hair. I've seen posts online of people complaining of huge sheds or losing hairline once switching over to dut and this reflex hyperandrogenicity could explain that. His point was that most people with prostate cancer (as we know these drugs were created to address prostate issues) very strong antiandrogens like flutamide are not enough as they too cause reflex h so these patients simultaneously get castrated as well during their treatments. If we could get 1 year and beyond hair count numbers like we have for fin, this would be all we need.

Makes you wonder....was Avodart pulled because it didn't work as well as fin or even possibly worse over the long term? It's also hard for me to believe the sides for Avodart are less than propecia just due to the fact that serum DHT levels are decreased so much by Avodart and type 1 5ar is reduced by 50%.

[dm90]

Damn everytime i type my long message in response to this my laptop freezes >.>. Anyway in response to the upregulation of the AR from androgen deprivation i found this http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4069023/. It examines the AR concentratiosn in the stromal and epithelia cells of men reporting persistent sexual side effects from fin. Consensus is yes upregulation does occur in both the stromal and epithelial tissues. However it is much greater in the stromal, prostatic cells. Theres a 2 fold increase in the prostatic cells and roughly only a 20% increase in the epithelial tissue. Good news for our hair, not so good for our prostates. This upregulation in the epithelial tissue, if it reigns true for the greater population (this was a small study), would not offset the DHT reduction of fin and definitely not for DUT. Interestingly enough nerve density and structure remained unchanged. Ive never been worried about PFS, but upregulated expression in stromal tissue,leading to hyperplasia, seemed a very real and believable concern to me. I will continue to take these medications because my hair is just that important to me, yeah it may be reckless but its my body, but I mean this isnt something that should be ignored