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The Cure For Hair Loss - The Truth about 5α-Reductase Inhibitors and Topical Anti-Androgens - Part 2
(excuse the shit formatting, I don't normally write threads, so I can't format for shit)
What does this thread include?
In this thread I will be covering the different treatments depending on your age and situation for hair loss, as well as what impact each of these drugs will have on your development.
1) Introduction
2) Why are you balding in the first place?
3) What can we do about DHT at the scalp?
4) Distinguishing between Type 1 isoenzyme and Type 2 isoenzyme
5) Should I be worried about side effects from FInasteride?
6) Hair loss treatment if you are over 18
7) Hair loss treatment if you are under 18
8) What do do if you still experience hair loss on 5α-Reductase inhibitors
9) Is RU58841 safe for use, since it's a research chemical
10) How to make RU58841 solution
11) Drug dosages
1) Introduction
2) Why are you balding in the first place?
3) What can we do about DHT at the scalp?
4) Distinguishing between Type 1 isoenzyme and Type 2 isoenzyme
5) Should I be worried about side effects from FInasteride?
6) Hair loss treatment if you are over 18
7) Hair loss treatment if you are under 18
8) What do do if you still experience hair loss on 5α-Reductase inhibitors
9) Is RU58841 safe for use, since it's a research chemical
10) How to make RU58841 solution
11) Drug dosages
Introduction.
We all know, hair is life, if you have no hair, you have no life.
Once you down the rabbit hole of finding a "cure" for hair loss, you will find that you have only 2 real options in term of halting the actual hair loss itself. Those options would be Finasteride/Dutasteride (5α-Reductase inhibitor) or research produces like ru58841. In this thread I will go into depth about these, and which one people should use depending on their situation, or if they should use one at all.
Once you down the rabbit hole of finding a "cure" for hair loss, you will find that you have only 2 real options in term of halting the actual hair loss itself. Those options would be Finasteride/Dutasteride (5α-Reductase inhibitor) or research produces like ru58841. In this thread I will go into depth about these, and which one people should use depending on their situation, or if they should use one at all.
Why are you balding in the first place?
The vast majority of men go bald because of a hereditary condition called Androgenic Alopecia (AGA). Unfortunately, the number of men that do not have condition are in the minority, so do not assume that you are safe from the norwood reaper, ever. Everyone's hair follicles has a different sensitivity to androgens. The androgens binding to the hair follicles will make the Anagen phase shorter and shorter until a permanent state of anagen phase is present and the hair follicle is deactivated. The strongest hormone that shorten the Anagen phase is DHT (dihydrotestosteron) and Testosterone. Some woman are so sensitive to DHT and Testosterone that the small amount they produce is sufficient enough to cause hair loss.
What can we do about DHT at the scalp?
As I mentioned above, there is a very limited number of things we can do to combat this, however using the protocols I will outline in this thread will leave you having you hair for life. First we have to take care of the main androgen in causing hair loss, which already outlined above, is DHT. There is only one safe way to decrease the amount of DHT in your body, and that is taking a 5α-Reductase inhibitor such as Finasteride or Dutasteride. In taking on of these 5α-Reductase inhibitors, we are systematically decreasing the amount of DHT in out body, and subsequently decreasing the amount of scalp DHT we have, which is what we want to reduce as much as possible. I will outline which is best to take for each individual, since it's dependant on your age, if you use certain compounds to "pubertymaxx" etc.
Will 5α-Reductase inhibitors stunt bone development?
Is taking 5α-Reductase inhibitors going to keep you boneless forever? Lets find out.
Study:
pubmed.ncbi.nlm.nih.gov
Results: Patients with dihydrotestosterone deficiency present normal bone mineral density, suggesting that dihydrotestosterone is not the main androgen acting in bone.
Study:
pmc.ncbi.nlm.nih.gov
Results:
The two guys on the left have 0 DHT (literally) and they still have a normal bone structure and an identical height, bone density and skeletal mass to their healthy siblings, it have a higher binding affinity to the androgen receptor but it doesn't cause the same physiological response.
The pubertal growth spurt (for men) is also induced by testosterone and not DHT.
Also 5AR is not very active in bone tissues and DHT is mainly a paracrine hormone (i.e it acts where it's produced while testosterone acts on the whole body despite being produced in the testes).
So, does that mean we should all just take the strongest 5α-Reductase inhibitor (Dutasteride) and call it a day? Well, no. First we have to distinguish between the two forms of DHT, as these studies to not distinguish between them, so it is not the full picture.
Distinguishing between Type 1 isoenzyme and Type 1 isoenzyme.
Both these studies show that DHT doesn't have an effect on bones, right? So, we should all just take Dutasteride? Wrong.
These studies have not differentiated between type 1 isoenzyme, and type 2 isoenzyme.
So, first we have to see where type 1 DHT and type 2 DHT are expressed in the body.
Type 2 DHT is not expressed in bones at all, it's only expressed in the genitals, prostate gland, epididymides, seminal vesicles, genital skin, facial and chest hair follicles, and liver, while lower expression is observed in certain brain areas, non-genital skin/hair follicles, testes, and kidneys.
However, Type 1 DHT is actually expressed in bones. This matters because the studies I have shown above, are actually only deficient in the type 2 isoenzyme, which is the one that is not present in bones. This is the reason they present with normal bone mineral density, bone structure etc. If they were also deficient in Type 1 DHT, this would likely not be the case at all.
"5α-Reductase type 1 inactivated male mice have reduced bone mass and forelimb muscle grip strength, which has been proposed to be due to lack of 5α-reductase type 1 expression in bone and muscle.[29] In 5 alpha reductase type 2 deficient males, the type 1 isoenzyme is thought to be responsible for their virilization at puberty.[6]"
Bone growth and change will be minimal after 18, I definitely agree, but it still does happen. Facial bones are flat bones. They do not fuse, so they will continue to change forever, obviously to a lesser extent the older you get. Bones development/growth “stops” when resorption becomes greater than formation. As you age, this is more likely to happen, and will happen at a certain age most likely. Taking Dut with inhibits type 1, which is active in bones would likely have a negative impact, and speed up this process. You also won't achieve the slight bone changes that maybe desirable. It's true you don't know if you will have any noticeable change. Even in terms of BMD, doesn't effect aesthetics, it is still somewhat important for health. I would feel more comfortable to take Finasteride over Dutasteride if natural, since enhanced individuals would probably be able to compensate with supraphysiological Test levels and compensate for the lack of Type 1 DHT. The only thing I can really think of that have possibly comparable DHT type 1 levels to men on Dutasteride, would be women, who do actually have lower bone mass and lower BMD than men, and are at a greater risk of developing osteoporosis compared to men. That is not me saying if you take Dut your bones are going to melt and dissolve off your face.
Study:
Normal bone density in male pseudohermaphroditism due to 5alpha- reductase 2 deficiency - PubMed
Patients with dihydrotestosterone deficiency present normal bone mineral density, suggesting that dihydrotestosterone is not the main androgen acting in bone.
pubmed.ncbi.nlm.nih.gov
Study:
5α-reductase-2 Deficiency’s Effect on Human Fertility - PMC
A most interesting and intriguing male disorder of sexual differentiation is due to 5α-reductase-2 isoenzyme deficiency. These males are born with ambiguous external genitalia due to a deficiency in their ability to catalyze the conversion of ...
pmc.ncbi.nlm.nih.gov
The two guys on the left have 0 DHT (literally) and they still have a normal bone structure and an identical height, bone density and skeletal mass to their healthy siblings, it have a higher binding affinity to the androgen receptor but it doesn't cause the same physiological response.
The pubertal growth spurt (for men) is also induced by testosterone and not DHT.
Also 5AR is not very active in bone tissues and DHT is mainly a paracrine hormone (i.e it acts where it's produced while testosterone acts on the whole body despite being produced in the testes).
So, does that mean we should all just take the strongest 5α-Reductase inhibitor (Dutasteride) and call it a day? Well, no. First we have to distinguish between the two forms of DHT, as these studies to not distinguish between them, so it is not the full picture.
Distinguishing between Type 1 isoenzyme and Type 1 isoenzyme.
Both these studies show that DHT doesn't have an effect on bones, right? So, we should all just take Dutasteride? Wrong.
These studies have not differentiated between type 1 isoenzyme, and type 2 isoenzyme.
So, first we have to see where type 1 DHT and type 2 DHT are expressed in the body.
Type 2 DHT is not expressed in bones at all, it's only expressed in the genitals, prostate gland, epididymides, seminal vesicles, genital skin, facial and chest hair follicles, and liver, while lower expression is observed in certain brain areas, non-genital skin/hair follicles, testes, and kidneys.
However, Type 1 DHT is actually expressed in bones. This matters because the studies I have shown above, are actually only deficient in the type 2 isoenzyme, which is the one that is not present in bones. This is the reason they present with normal bone mineral density, bone structure etc. If they were also deficient in Type 1 DHT, this would likely not be the case at all.
"5α-Reductase type 1 inactivated male mice have reduced bone mass and forelimb muscle grip strength, which has been proposed to be due to lack of 5α-reductase type 1 expression in bone and muscle.[29] In 5 alpha reductase type 2 deficient males, the type 1 isoenzyme is thought to be responsible for their virilization at puberty.[6]"
Bone growth and change will be minimal after 18, I definitely agree, but it still does happen. Facial bones are flat bones. They do not fuse, so they will continue to change forever, obviously to a lesser extent the older you get. Bones development/growth “stops” when resorption becomes greater than formation. As you age, this is more likely to happen, and will happen at a certain age most likely. Taking Dut with inhibits type 1, which is active in bones would likely have a negative impact, and speed up this process. You also won't achieve the slight bone changes that maybe desirable. It's true you don't know if you will have any noticeable change. Even in terms of BMD, doesn't effect aesthetics, it is still somewhat important for health. I would feel more comfortable to take Finasteride over Dutasteride if natural, since enhanced individuals would probably be able to compensate with supraphysiological Test levels and compensate for the lack of Type 1 DHT. The only thing I can really think of that have possibly comparable DHT type 1 levels to men on Dutasteride, would be women, who do actually have lower bone mass and lower BMD than men, and are at a greater risk of developing osteoporosis compared to men. That is not me saying if you take Dut your bones are going to melt and dissolve off your face.
Should I be worried about side effects from Finasteride?
I am not going to say that side effects do not exist, there are going to be the very unfortunate minority that may get side effects, but most of the people that are reporting side effects are schizo, especially if you go to places like r/tressless. They are basically all mentally ill. I’m not saying PFS or side effects in general aren't real, but I am saying that side effects, including PFS, are very much exaggerated in 2025.
Even in long-term studies (10 yr +) in Asians, no evidence of PFS symptoms were ever discovered. Only 1-3% get sexual sides, which wasn't even significantly different from the placebo arm in the original trials.
Only after social media started popping off side effect reports started skyrocketing, and no, it’s not because there were fewer users back in the 2000s, millions of men were already on it back then.
There is some evidence for the existence of PFS and I will link a post here:
looksmax.org
Personally, I would take the chance 10/10 times.
Even in long-term studies (10 yr +) in Asians, no evidence of PFS symptoms were ever discovered. Only 1-3% get sexual sides, which wasn't even significantly different from the placebo arm in the original trials.
Only after social media started popping off side effect reports started skyrocketing, and no, it’s not because there were fewer users back in the 2000s, millions of men were already on it back then.
There is some evidence for the existence of PFS and I will link a post here:
The obsession about DHT needs to end
what about sun? does it inhibit both collagen or elastin? Yes also do u think mt2 alonne all years with 20m tanning beds 3x per week can replace spf? No absolutely not you can't replace SPF. Melanin won't stop aging and UV damage
looksmax.org
Hair loss treatment if you're over 18.
If you are above the age of 18, and are natural, which means you DO NOT take exogenous hormones, such as Testosterone to achieve supraphysiological Testosterone levels in the body, I would recommend taking Finasteride at 1mg ever day.
If you are above the age of 18, and are enhanced, which means you DO take exogenous hormones, such as Testosterone to achieve supraphysiological Testosterone levels in the body, I would recommend taking Dutasteride at 2.5mg a day.
If you are above the age of 18, and are enhanced, which means you DO take exogenous hormones, such as Testosterone to achieve supraphysiological Testosterone levels in the body, I would recommend taking Dutasteride at 2.5mg a day.
Hair loss treatment if you're under 18.
If you are younger than, you don't want to reduce your serum DHT levels since you are obliviously still growing, and DHT does play an important role in puberty. This means we are going to have to deal with scalp DH and Testosterone through compounds that will not effect your systematic levels. This can be accomplished through the use to the research chemical RU58841. This is a anti androgen which is applied topically to the scalp. To put it simply, it binds to the androgen receptors instead of DHT and Testosterone. Since hormones like DHT and Testosterone will not be able to bind, your hair will be safe from the norwood reaper, at least until you are old enough to get on approved treatments.
What should I do if you still experience hair loss while taking a 5α-Reductase inhibitor?
So you may have taken a 5α-Reductase inhibitor and are still seeing hair loss after a few months on treatment. You are probably very sensitive to androgens at the scalp, since for a large majority, 5α-Reductase inhibitors will be enough. If you still experience loss, it is because 5α-Reductase inhibitors will not completely remove scalp DHT, there is still some present at the scalp. As well as this, 5α-Reductase inhibitors don't decrease scalp Testosterone. The only way to deal with any residual DHT at the scalp, and the scalp Testosterone is by using ru58841. I already mentioned above that it does. Adding this on top of 5α-Reductase inhibitors will mean that your scalp will have as little androgens present that is currently possible, and will give your hair the best chance of survival.
Is RU58841 safe for use, since it's a research chemical?
This next part is not my words, it's from a post else where.
I found out about a clinical researcher that worked on the compound.
I wrote him two e-mails, but he didn't answer.
Therefore I tried to call him on the phone. It was quite hard to get to him since his secretaries apparently don't speak English. But the third time I was calling, I was lucky enough to get himself on the phone.
When I mentioned PSK-3841 he knew immediately what I was talking about. Apparently he got at least 10 phone calls in the last 3 years about this subject.
I asked him wether he remembers major safety concerns and he said no. He thinks the research was stopped because of financial issues or bad marketability.
He also said he tried to contact Prostrakan about it, but they are not interested in continuing the research.
He said that PSK-3841 was quite effective when he used it in the 6 month trial. He even suggested crowdfunding to make Prostrakan release the data or continue research.
This corresponds with the following statement, that was released by Prostrakan.
Topical anti-androgen
This is an innovative molecule with a unique mechanism of action for the treatment of androgen-dependent conditions, such as alopecia and acne.
In pre-clinical studies, it has shown promising activity in various models of acne, alopecia and hirsutism. The product has good systemic and dermal tolerance.
In human clinical pharmacology, there was no systemic anti-androgenic activity and again good general and dermal tolerance.
The molecule has completed several Phase I studies and a Proof of Concept Phase II study for alopecia.
It has demonstrated similar efficacy after 6 months treatment as that observed with current oral therapy for alopecia after twelve months, based on the increase in net hair count. Again, no systemic anti-androgenic effect was observed (n=90).
This product is available for licensing.
PS: English is not my native language so I may have not understood everything 100% correctly. But I asked him about the safety concerns 2 times, so I'm quite sure about that.
Edit: I don't want the researcher to get into legal trouble. Therefore I have deleted the name from the post. He has not shared confidential Data with me but I want him to be safe.
I wrote him two e-mails, but he didn't answer.
Therefore I tried to call him on the phone. It was quite hard to get to him since his secretaries apparently don't speak English. But the third time I was calling, I was lucky enough to get himself on the phone.
When I mentioned PSK-3841 he knew immediately what I was talking about. Apparently he got at least 10 phone calls in the last 3 years about this subject.
I asked him wether he remembers major safety concerns and he said no. He thinks the research was stopped because of financial issues or bad marketability.
He also said he tried to contact Prostrakan about it, but they are not interested in continuing the research.
He said that PSK-3841 was quite effective when he used it in the 6 month trial. He even suggested crowdfunding to make Prostrakan release the data or continue research.
This corresponds with the following statement, that was released by Prostrakan.
Topical anti-androgen
This is an innovative molecule with a unique mechanism of action for the treatment of androgen-dependent conditions, such as alopecia and acne.
In pre-clinical studies, it has shown promising activity in various models of acne, alopecia and hirsutism. The product has good systemic and dermal tolerance.
In human clinical pharmacology, there was no systemic anti-androgenic activity and again good general and dermal tolerance.
The molecule has completed several Phase I studies and a Proof of Concept Phase II study for alopecia.
It has demonstrated similar efficacy after 6 months treatment as that observed with current oral therapy for alopecia after twelve months, based on the increase in net hair count. Again, no systemic anti-androgenic effect was observed (n=90).
This product is available for licensing.
PS: English is not my native language so I may have not understood everything 100% correctly. But I asked him about the safety concerns 2 times, so I'm quite sure about that.
Edit: I don't want the researcher to get into legal trouble. Therefore I have deleted the name from the post. He has not shared confidential Data with me but I want him to be safe.
How to make an RU58841 solution.
You can either use a premade solution or you can home brew your own, which is much cheaper.
I will outline how to make your own now.
You will need: Precisions measuring scale 0.001g, Propylene Glycol, Ethanol 95%, RU58841 raw powder, glass measuring beakers.
I will outline how to make a 5% solution.
This will contain 50mg RU58841 per mL. And it will be a 50mL solution.
70% Ethanol 30% Propylene Glycol is the best ratio for the solution.
You can use DMSO if you wish instead of Propylene Gylycol, with the same 70% 30% ratio.
Steps
1) Get the precision scale and put a measuring beaker on it, and set the weight to 0
2) Put the RU58841 powder into the beaker, measuring out 2.5g
3) Using the measuring beaker, measure out 35mL of ethanol 95%, and add that to the one with the RU58841 powder in it.
4) Using the measuring beaker and measure out 15mL of Propylene Glycol and add that to the beaker with the RU58841 and ethanol.
5) Stir until the RU dissolves.
Store the ready made solution in the fridge. Store the raw RU58841 powder in the freezer.
Here is a video from Reddit if you wish to follow that instead:
I will outline how to make your own now.
You will need: Precisions measuring scale 0.001g, Propylene Glycol, Ethanol 95%, RU58841 raw powder, glass measuring beakers.
I will outline how to make a 5% solution.
This will contain 50mg RU58841 per mL. And it will be a 50mL solution.
70% Ethanol 30% Propylene Glycol is the best ratio for the solution.
You can use DMSO if you wish instead of Propylene Gylycol, with the same 70% 30% ratio.
Steps
1) Get the precision scale and put a measuring beaker on it, and set the weight to 0
2) Put the RU58841 powder into the beaker, measuring out 2.5g
3) Using the measuring beaker, measure out 35mL of ethanol 95%, and add that to the one with the RU58841 powder in it.
4) Using the measuring beaker and measure out 15mL of Propylene Glycol and add that to the beaker with the RU58841 and ethanol.
5) Stir until the RU dissolves.
Store the ready made solution in the fridge. Store the raw RU58841 powder in the freezer.
Here is a video from Reddit if you wish to follow that instead:
Drug Dosages.
Why 1mg of FInasteride and not 0.1mg or 5mg?
pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov
Why 2.5mg Dutasteride and not the standard dosage of 0.5mg?
Best RU58841 dosage?
If you still lose hair on the stack mentioned in this thread, you are likely not balding due to AGA.
Clinical dose ranging studies with finasteride, a type 2 5alpha-reductase inhibitor, in men with male pattern hair loss - PubMed
Finasteride 1 mg/day is the optimal dose for the treatment of men with male pattern hair loss and was subsequently identified for further clinical development.
pubmed.ncbi.nlm.nih.gov
The effects of finasteride on scalp skin and serum androgen levels in men with androgenetic alopecia - PubMed
In this study, doses of finasteride as low as 0.2 mg per day maximally decreased both scalp skin and serum DHT levels. These data support the rationale used to conduct clinical trials in men with male pattern hair loss at doses of finasteride between 0.2 and 5 mg.
pubmed.ncbi.nlm.nih.gov
You are taking supraphysiological amounts of Testosterone, which as a result means you are going to have high DHT levels, and if you are particularly prone to androgens raping your hair follicles, you need to be as nuclear as you can be.
Serum DHT inhibition is not that different (about 4% more with 2.5mg) but the Scalp DHT inhibition is almost 80% at 2.5mg compared to 50% with 0.5mg.
Serum DHT inhibition is not that different (about 4% more with 2.5mg) but the Scalp DHT inhibition is almost 80% at 2.5mg compared to 50% with 0.5mg.
I will clarify, by dosage I mean the amount of ru58841 that is applied to your scalp. You are not drinking it or taking it orally, you will be a Testosteroneless creature.
Apply between 50-100mg of RU58841 to the scalp. I would recommend not exceeding 100mg as it will increase the chances of systematic absorption.
Apply between 50-100mg of RU58841 to the scalp. I would recommend not exceeding 100mg as it will increase the chances of systematic absorption.
Also go check out @Jonas2k7 thread about Minoxidil:
The truth about Minoxidil - The holy grail or overhyped Looksmin?
The truth about Minoxidil - Part 1 Growing your eyelashes and eyebrows is one of the best and only true softmaxxes. Because of that, many people choose compounds like Minoxidil to grow hairs in their eye area or even on the scalp. This thread will reveal why you should be cautious with...
looksmax.org
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@imontheloose (I will respond on dc to you, I just haven't gotten round to it yet)
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