Topical Dutasteride Case Assessment Thread

[corkmeister]

Let me start off by saying that I'm glad topical dutasteride is working for you Mustang. But I myself remain skeptical in terms of its systemic effects.

Dimitri, you're correct in the sense that most topical finasteride dosages tend to result in near-oral levels of DHT-inhibition (although the studies on this sometimes give mixed and confusing results).

Studies do show that even low dosages of oral finasteride (around 0.05mg and up) accumulate and eventually start significantly inhibiting DHT - despite its relatively short half life. Logically speaking, high enough topical dosages should also accumulate and result in the same effect, which is what several studies show and what many users experience. And at least one of the studies that doesn't show this checked DHT-levels after like 10 days, which is too short of a time frame to account for accumulation.

Finding the appropriate topical finasteride dose (that inhibits DHT in the scalp, but not systemically) has been somewhat of a holy grail in itself. I'm quite convinced that the dosage must be very low, or at least much lower than what most topical formulations tend to contain nowadays. With dosages like 0.25% (which is 2.5 mg of finasteride per dose) I can almost guarantee that enough of it will go systemic and start accumulating over time.

Mazzarella supposedly used an appropriate topical dose in a study from 1999 with 0.01% per day (or 0.005% twice-daily, to be more precise). He tested DHT-levels in the blood and found no inhibition after more than a year, but did note a significant improvement in terms of hair growth. However, several people have tried to replicate this in the past and ended up with systemic DHT-inhibition anyway.

Whatever the case may be. My point is that, considering the above, I don't see how this would be any different for dutasteride. It seems to me that finding the appropriate dose is even more difficult (albeit not impossible), in part due to its much longer half life and the lack of studies to go off of. It would take a lot of trial and error. Even when considering liposomal vehicles; I don't believe that liposomal formulations prevent all systemic absorption while delivering dutasteride to where it needs to be. If it penetrates the scalp, I can only assume that some of it will go systemic and starts accumulating over a longer period of time, resulting in systemic DHT-inhibition.

I'm open to counter-arguments, as I hope I'm mistaken and I'm not a professional in this field. But it seems too good to be true.

 

[Mustang]

Let me start off by saying that I'm glad topical dutasteride is working for you Mustang. But I myself remain skeptical in terms of its systemic effects.

Dimitri, you're correct in the sense that most topical finasteride dosages tend to result in near-oral levels of DHT-inhibition (although the studies on this sometimes give mixed and confusing results).

Studies do show that even low dosages of oral finasteride (around 0.05mg and up) accumulate and eventually start significantly inhibiting DHT - despite its relatively short half life. Logically speaking, high enough topical dosages should also accumulate and result in the same effect, which is what several studies show and what many users experience. And at least one of the studies that doesn't show this checked DHT-levels after like 10 days, which is too short of a time frame to account for accumulation.

Finding the appropriate topical finasteride dose (that inhibits DHT in the scalp, but not systemically) has been somewhat of a holy grail in itself. I'm quite convinced that the dosage must be very low, or at least much lower than what most topical formulations tend to contain nowadays. With dosages like 0.25% (which is 2.5 mg of finasteride per dose) I can almost guarantee that enough of it will go systemic and start accumulating over time.

Mazzarella supposedly used an appropriate topical dose in a study from 1999 with 0.01% per day (or 0.005% twice-daily, to be more precise). He tested DHT-levels in the blood and found no inhibition after more than a year, but did note a significant improvement in terms of hair growth. However, several people have tried to replicate this in the past and ended up with systemic DHT-inhibition anyway.

Whatever the case may be. My point is that, considering the above, I don't see how this would be any different for dutasteride. It seems to me that finding the appropriate dose is even more difficult (albeit not impossible), in part due to its much longer half life and the lack of studies to go off of. It would take a lot of trial and error. Even when considering liposomal vehicles; I don't believe that liposomal formulations prevent all systemic absorption while delivering dutasteride to where it needs to be. If it penetrates the scalp, I can only assume that some of it will go systemic and starts accumulating over a longer period of time, resulting in systemic DHT-inhibition.

I'm open to counter-arguments, as I hope I'm mistaken and I'm not a professional in this field. But it seems too good to be true.

Well, I took a dose 100 times as high to test my plasma DHT and it doesn't.

A dose 100 times smaller nuked it orally.

KDA at work.

 

[blub10]

I made the same experience in practice myself as described by corkmeister with topical Fina

@Mustang, since you are on riods and tadafinil 5mg maybe you experience less sides? Which kind of doctor can you recommend for a DHT Scalp Biopsy?

 

[Dimitri001]

Well, I took a dose 100 times as high to test my plasma DHT and it doesn't.

A dose 100 times smaller nuked it orally.

KDA at work.

You're saying you took topical finasteride and it didn't nuke your DHT or it didn't affect it at all?

What's KDA?

 

[blub10]

No Mustang claims this about topical dutasteride

 

[corkmeister]

Well, I took a dose 100 times as high to test my plasma DHT and it doesn't.

A dose 100 times smaller nuked it orally.

KDA at work.

Just to be clear, I'm not trying to disprove your statements or anything, I'm actually very curious and it does sound very promising, but at the same time I'm skeptical. I'd love to get your thoughts on this, but if you're tired of explaining yourself, I totally understand.

If I understand you correctly, you believe that dutasteride's molecular mass is too high to penetrate the scalp, but nevertheless does inhibit scalp-DHT via a liposomal solution?

I agree that if you applied 100 times the normal dose topically, and it had no effect on systemic DHT-levels, that none of it - or at least a negligible percentage of it - is going systemic. But then I would seriously question whether it's getting to the hair follicle at all. But as I said, I'm no expert, I'm not sure if something can get to the hair follicles without invading the rest of the body.

In another post you mentioned the following:

When I took oral dutasteride at 0.5mg I had 0 DHT (Below 30)
With topical dutasteride I take 20mg (2ml at 1%) which is 40 times higher the oral dosage and my DHT stands at 250 ng/ml (range is 250 to 750)
Without topical dutasteride my DHT stands at 450 ng/ml
With oral finasteride my DHT stands at 170 ng/ml

Isn't this in contradiction to the idea that that a negligible part of it goes systemic? You're saying here that topical dutasteride reduced your DHT from 450 ng/ml to 250 ng/ml, correct? Is that your normal dose, or the experimental extremely high dose you were talking about before? Whatever the case may be, it seems that the topical dutasteride reduced your DHT by around 50%. But considering dutasteride's response curve (which is basically binary, i.e. there's only a very small area between 'full inhibition' and 'no inhibition'), wouldn't that be an extremely unlikely outcome?

I definitely don't think it's impossible, but it seems to me like using topical dutasteride without systemic DHT-inhibition is like walking a tightrope. You may be standing on the rope right now, but if your next step (dosage) is not perfectly measured/timed, you're going to fall off. When we add dutasteride's longer halflife (and thus accumulation) to the mix, you're basically walking the tightrope blindfolded. It seems to me that even if you were able to arrive at 50% DHT-reduction at one particular moment in time, it would take only a slight increase in systemic dutasteride to push you over the edge and arrive at complete inhibition. I hope I'm making sense here.

 

[SausageDawg]

Just to be clear, I'm not trying to disprove your statements or anything, I'm actually very curious and it does sound very promising, but at the same time I'm skeptical. I'd love to get your thoughts on this, but if you're tired of explaining yourself, I totally understand.

If I understand you correctly, you believe that dutasteride's molecular mass is too high to penetrate the scalp, but nevertheless does inhibit scalp-DHT via a liposomal solution?

I agree that if you applied 100 times the normal dose topically, and it had no effect on systemic DHT-levels, that none of it - or at least a negligible percentage of it - is going systemic. But then I would seriously question whether it's getting to the hair follicle at all. But as I said, I'm no expert, I'm not sure if something can get to the hair follicles without invading the rest of the body.

In another post you mentioned the following:

When I took oral dutasteride at 0.5mg I had 0 DHT (Below 30)
With topical dutasteride I take 20mg (2ml at 1%) which is 40 times higher the oral dosage and my DHT stands at 250 ng/ml (range is 250 to 750)
Without topical dutasteride my DHT stands at 450 ng/ml
With oral finasteride my DHT stands at 170 ng/ml

Isn't this in contradiction to the idea that that a negligible part of it goes systemic? You're saying here that topical dutasteride reduced your DHT from 450 ng/ml to 250 ng/ml, correct? Is that your normal dose, or the experimental extremely high dose you were talking about before? Whatever the case may be, it seems that the topical dutasteride reduced your DHT by around 50%. But considering dutasteride's response curve (which is basically binary, i.e. there's only a very small area between 'full inhibition' and 'no inhibition'), wouldn't that be an extremely unlikely outcome?

I definitely don't think it's impossible, but it seems to me like using topical dutasteride without systemic DHT-inhibition is like walking a tightrope. You may be standing on the rope right now, but if your next step (dosage) is not perfectly measured/timed, you're going to fall off. When we add dutasteride's longer halflife (and thus accumulation) to the mix, you're basically walking the tightrope blindfolded. It seems to me that even if you were able to arrive at 50% DHT-reduction at one particular moment in time, it would take only a slight increase in systemic dutasteride to push you over the edge and arrive at complete inhibition. I hope I'm making sense here.

No mate that all made perfect sense and I think we all basically have the same level of skepticism and HOPE as you, the only way we find out is through people trying. It's one of them situations where you want the guy sitting next to you to go 1st

 

[Dimitri001]

Just to be clear, I'm not trying to disprove your statements or anything, I'm actually very curious and it does sound very promising, but at the same time I'm skeptical. I'd love to get your thoughts on this, but if you're tired of explaining yourself, I totally understand.

If I understand you correctly, you believe that dutasteride's molecular mass is too high to penetrate the scalp, but nevertheless does inhibit scalp-DHT via a liposomal solution?

I agree that if you applied 100 times the normal dose topically, and it had no effect on systemic DHT-levels, that none of it - or at least a negligible percentage of it - is going systemic. But then I would seriously question whether it's getting to the hair follicle at all. But as I said, I'm no expert, I'm not sure if something can get to the hair follicles without invading the rest of the body.

In another post you mentioned the following:

When I took oral dutasteride at 0.5mg I had 0 DHT (Below 30)
With topical dutasteride I take 20mg (2ml at 1%) which is 40 times higher the oral dosage and my DHT stands at 250 ng/ml (range is 250 to 750)
Without topical dutasteride my DHT stands at 450 ng/ml
With oral finasteride my DHT stands at 170 ng/ml

Isn't this in contradiction to the idea that that a negligible part of it goes systemic? You're saying here that topical dutasteride reduced your DHT from 450 ng/ml to 250 ng/ml, correct? Is that your normal dose, or the experimental extremely high dose you were talking about before? Whatever the case may be, it seems that the topical dutasteride reduced your DHT by around 50%. But considering dutasteride's response curve (which is basically binary, i.e. there's only a very small area between 'full inhibition' and 'no inhibition'), wouldn't that be an extremely unlikely outcome?

I definitely don't think it's impossible, but it seems to me like using topical dutasteride without systemic DHT-inhibition is like walking a tightrope. You may be standing on the rope right now, but if your next step (dosage) is not perfectly measured/timed, you're going to fall off. When we add dutasteride's longer halflife (and thus accumulation) to the mix, you're basically walking the tightrope blindfolded. It seems to me that even if you were able to arrive at 50% DHT-reduction at one particular moment in time, it would take only a slight increase in systemic dutasteride to push you over the edge and arrive at complete inhibition. I hope I'm making sense here.

Does @Mustang know what his scalp DHT levels were when he was taking topical dutasteride? The fact that it had a systemic impact would lead you to believe it wiped out scalp DHT, but it would be nice to have confirmation.

So, if what Mustang is saying is right, then topical duta would have a lesser systemic impact than finasteride (if we take it that the difference between systemic impact of oral and topical finasteride is negligible - I think someone mentioned studies disagree on this, tho).

 

[Mustang]

I had the worst side effects of my life with topical finasteride, even worse than with oral finasteride.
brain fog was non bearable and libido was completely dead

My hair loss was about 20 hairs a day with both

I had ZERO side effects with topical dutasteride and ZERO hair loss.

I used a MASSIVE dose just to see how much it reduced my plasma DHT and I still had DHT. Higher than with oral finasteride, topical finasteride and oral dutasteride.

Just try it guys. I can't tell you if it will work for you or not. It did for me. It might not do for you. I understand your skepticism about it. It sounds to good to be true.

Now, I only applied once every 15 days. You don't need more than that. Maybe if I take oral twice a month I would also have less sides. Who knows.

I had complete crown regrowth with it. It stopped my hair loss flat and it did within days.

 

[CrimsonTide]

Thank you Mustang and various others who have been experimenting with topical dutasteride and sharing their results with everyone. I sincerely appreciate it. I've been wanting to try topical dutasteride for years but have been too afraid to try out of fear of side effects.

Dutasteride has a molecular weight of 528.53 g/mol which is just larger than what is normally considered to be upper limit to allow for the penetration of a substance transdermally. There are a number of techniques that can be employed to allow for larger molecules (up to even 1000 g/mol) to penetrate the skin and liposomal/micelized deliver is one such way.

What many don't realize is that there two main routes that drugs can get through the skin/epidermis: 1) straight through the spaces in the skin if the molecule is small enough, or 2) via the hair shaft into the pilo sebaceous unit which would allow slight larger molecules in vs non pilo sebaceous unit skin. The pilo sebaceous route is the ideal route for a drug targeting acne or androgenetic alopecia as the drug ends up exactly where it needs to go. Dutasteride seems almost perfect for this purpose as it's just large enough to not be able to easily pass through non hair shaft skin while still small enough to pass through and end up in the hair root / sebaceous gland.

Having said that, would it not be better to instead of using liposomal versions of dutasteride (which enhance and improve transdermal delivery of the drug through the skin) to use pure low dosed dutasteride powder dissolved in a standard ethanol/propylene glycol base for something like a 0.05% solution? This would allow the dutasteride to preferentially enter the hair shafts while minimizing/preventing more widespread absorption via liposomal delivery.

Any thoughts?

 

[whatevr]

Thank you Mustang and various others who have been experimenting with topical dutasteride and sharing their results with everyone. I sincerely appreciate it. I've been wanting to try topical dutasteride for years but have been too afraid to try out of fear of side effects.

Dutasteride has a molecular weight of 528.53 g/mol which is just larger than what is normally considered to be upper limit to allow for the penetration of a substance transdermally. There are a number of techniques that can be employed to allow for larger molecules (up to even 1000 g/mol) to penetrate the skin and liposomal/micelized deliver is one such way.

What many don't realize is that there two main routes that drugs can get through the skin/epidermis: 1) straight through the spaces in the skin if the molecule is small enough, or 2) via the hair shaft into the pilo sebaceous unit which would allow slight larger molecules in vs non pilo sebaceous unit skin. The pilo sebaceous route is the ideal route for a drug targeting acne or androgenetic alopecia as the drug ends up exactly where it needs to go. Dutasteride seems almost perfect for this purpose as it's just large enough to not be able to easily pass through non hair shaft skin while still small enough to pass through and end up in the hair root / sebaceous gland.

Having said that, would it not be better to instead of using liposomal versions of dutasteride (which enhance and improve transdermal delivery of the drug through the skin) to use pure low dosed dutasteride powder dissolved in a standard ethanol/propylene glycol base for something like a 0.05% solution? This would allow the dutasteride to preferentially enter the hair shafts while minimizing/preventing more widespread absorption via liposomal delivery.

Any thoughts?

I think all this talk about molecular weight is far less important than what people give it credit for (at least for overall absorption potential). In the lactoferrin study they talk about large molecular weight proteins (10+ kDa) easily making their way to the to the hair follicle via the hair shaft. They pretty much plopped a 80 kDa protein in nothing but water, smeared it onto mice backs and observed increased hair growth. Granted, it was mice, but I believe that large molecules can enter human skin with similar ease. Here it is (check references as well):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6546667/

I think this is even better because rather than entering via the skin, entering via the hair shaft gives it a greater chance of binding to some part of the DP and staying there, rather than cruising around into the bloodstream. In fact it only makes me want to increase the size of other molecules by attaching some protein to them to make them less likely to cause side effects. However given my experience with fina I'm not going to be one trying this, but good luck to whomever does.

 

[Dimitri001]

Have there been no studies on topical duta?

 

[badhabiz]

I think all this talk about molecular weight is far less important than what people give it credit for (at least for overall absorption potential). In the lactoferrin study they talk about large molecular weight proteins (10+ kDa) easily making their way to the to the hair follicle via the hair shaft. They pretty much plopped a 80 kDa protein in nothing but water, smeared it onto mice backs and observed increased hair growth. Granted, it was mice, but I believe that large molecules can enter human skin with similar ease. Here it is (check references as well):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6546667/

I think this is even better because rather than entering via the skin, entering via the hair shaft gives it a greater chance of binding to some part of the DP and staying there, rather than cruising around into the bloodstream. In fact it only makes me want to increase the size of other molecules by attaching some protein to them to make them less likely to cause side effects. However given my experience with fina I'm not going to be one trying this, but good luck to whomever does.

tried to tell this in other 3d.
this molecular weight "limit" at 500 is a myth, doesnt have any clinical evidence

 

[CrimsonTide]

I think all this talk about molecular weight is far less important than what people give it credit for (at least for overall absorption potential). In the lactoferrin study they talk about large molecular weight proteins (10+ kDa) easily making their way to the to the hair follicle via the hair shaft. They pretty much plopped a 80 kDa protein in nothing but water, smeared it onto mice backs and observed increased hair growth. Granted, it was mice, but I believe that large molecules can enter human skin with similar ease. Here it is (check references as well):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6546667/

I think this is even better because rather than entering via the skin, entering via the hair shaft gives it a greater chance of binding to some part of the DP and staying there, rather than cruising around into the bloodstream. In fact it only makes me want to increase the size of other molecules by attaching some protein to them to make them less likely to cause side effects. However given my experience with fina I'm not going to be one trying this, but good luck to whomever does.

Exactly. Finasteride is a smaller molecule that crosses both non-hair shaft skin as well as entering hair shafts therefore it will always get through the skin easily. The lactoferrin was able to enter only via the hair shaft where it was able to stay more localized which is what we would want with dutasteride. Lactoferrin and other large molecules do not readily cross non-hair shaft skin easily otherwise there would be a lot more drugs that could be delivered transdermally that currently aren't.

tried to tell this in other 3d.
this molecular weight "limit" at 500 is a myth, doesnt have any clinical evidence

There are definitely issues with the 500 limit number due to the many factors that affect absorption through the skin. For example, most early studies that defined this limit had been done on areas of the skin other than the scalp. The scalp has a huge number of large, terminal hair shafts versus other less hairy areas of the body. These non-scalp types of studies aren't very applicable to us as the absorption dynamics would be totally different in the two scenarios with a greater number of larger molecules getting into the hair shaft on the scalp.

I used oral finasteride in the past and eventually had sides after many years of use. When everyone started talking about topical finasteride again a few years ago (with many prominent doctors jumping on the bandwagon) I was surprised because topical finasteride had been discussed over a decade ago with most people coming to the same conclusion: the finasteride molecule is just too small to not pass straight through the skin and into systemic circulation. From many people's reports, this has clearly been the case.

I guess for those of us too afraid to try topical dutasteride or any other experimental treatments just yet, all we can really do is look forward to clascoterone being released within the next few months. It doesn't seem great but the studies seem to indicate that it is safe and safety is currently my main priority.

 

[corkmeister]

There are definitely issues with the 500 limit number due to the many factors that affect absorption through the skin. For example, most early studies that defined this limit had been done on areas of the skin other than the scalp. The scalp has a huge number of large, terminal hair shafts versus other less hairy areas of the body. These non-scalp types of studies aren't very applicable to us as the absorption dynamics would be totally different in the two scenarios with a greater number of larger molecules getting into the hair shaft on the scalp.

I used oral finasteride in the past and eventually had sides after many years of use. When everyone started talking about topical finasteride again a few years ago (with many prominent doctors jumping on the bandwagon) I was surprised because topical finasteride had been discussed over a decade ago with most people coming to the same conclusion: the finasteride molecule is just too small to not pass straight through the skin and into systemic circulation. From many people's reports, this has clearly been the case.

I guess for those of us too afraid to try topical dutasteride or any other experimental treatments just yet, all we can really do is look forward to clascoterone being released within the next few months. It doesn't seem great but the studies seem to indicate that it is safe and safety is currently my main priority.

Interesting. Since you obviously know more about absorption dynamics than me: I've always wondered how much (%) of finasteride goes systemic when applied topically in a typical alcohol-based vehicle. Is there any way to make an educated guess about this? I've seen people say 10% in the past, but I've never seen any theory or science to back it up.

 

[sonictemples]

Exactly. Finasteride is a smaller molecule that crosses both non-hair shaft skin as well as entering hair shafts therefore it will always get through the skin easily. The lactoferrin was able to enter only via the hair shaft where it was able to stay more localized which is what we would want with dutasteride. Lactoferrin and other large molecules do not readily cross non-hair shaft skin easily otherwise there would be a lot more drugs that could be delivered transdermally that currently aren't.



There are definitely issues with the 500 limit number due to the many factors that affect absorption through the skin. For example, most early studies that defined this limit had been done on areas of the skin other than the scalp. The scalp has a huge number of large, terminal hair shafts versus other less hairy areas of the body. These non-scalp types of studies aren't very applicable to us as the absorption dynamics would be totally different in the two scenarios with a greater number of larger molecules getting into the hair shaft on the scalp.

I used oral finasteride in the past and eventually had sides after many years of use. When everyone started talking about topical finasteride again a few years ago (with many prominent doctors jumping on the bandwagon) I was surprised because topical finasteride had been discussed over a decade ago with most people coming to the same conclusion: the finasteride molecule is just too small to not pass straight through the skin and into systemic circulation. From many people's reports, this has clearly been the case.

I guess for those of us too afraid to try topical dutasteride or any other experimental treatments just yet, all we can really do is look forward to clascoterone being released within the next few months. It doesn't seem great but the studies seem to indicate that it is safe and safety is currently my main priority.

Wouldn't RU be better? I know that the safety concerns might be holding us back but hopefully we can get more information via contacting the people whom was involved in the human studies.

 

[blub10]

Interesting. Since you obviously know more about absorption dynamics than me: I've always wondered how much (%) of finasteride goes systemic when applied topically in a typical alcohol-based vehicle. Is there any way to make an educated guess about this? I've seen people say 10% in the past, but I've never seen any theory or science to back it up.

I can only you from experience: After 6 weeks of daily use of 1% topical finasteride I have had the same side as on 0.25mg oral Fina

 

[badhabiz]

I can only you from experience: After 6 weeks of daily use of 1% topical finasteride I have had the same side as on 0.25mg oral Fina

where do you get that dosage?
consider that 0.1 its 1mg of fina per 1ml...you take 10 times that dosage

 

[Mustang]

Yes, I had the same sides with finasteride as well (topical)
Even at 0.05%
Not with Dutasteride

 

[Mustang]

I have tried stem cells injections, minoxidil, PRP, mesotherapy, oral minoxidil (loniten), RU, finasteride, dutasteride, topical finasteride and topical dutasteride, dermarolling, saw palmetto, topical saw palmetto, laser cap, dutasteride mesotherapy and probably many other things the past 15 years.

The 4 things that made the greatest difference on my male pattern baldness were:

1) Oral Minoxidil. You grow hair like a Lion. Side effects are bad, it's a powerful med for high blood pressure. I naturally have very low blood pressure, not for me.
2) Dutasteride Mesotherapy. Once every 15 days. 2mm deep. 2ML of Dutasteride. Using a dermapen.
3) Topical Dutasteride. Stopped my hair loss cold. No sides.
4) Dermarolling. It really works.

What did not work or had too many side effects

1) Oral finasteride and dutasteride, side effects were bad
2) Topical finasteride, same sides as oral
3) PRP, did nothing
4) Stem cells did nothing
5) Saw Palmetto, nada
6) Biotin, vitamins, scalp massages

What worked moderately

1) Laser Cap. It did thicken my hair, still use it 3 times a week.
2) RU, hard to tell as I have no hair loss on topical dutasteride and have none since stopping RU.