Propecia picture

If there's any reason to switch to Dutasteride, it might be here in this interview. I would say John's story along with the Dutasteride twins, and of course the clinical trials for Dutasteride are good reasons to consider its use.
0.5mg of dutasteride a day has been shown to reduce scalp DHT by 50+%. And doses as high as 2.5mg reducing scalp DHT by 80%. 0.5mg Dutasteride has a similar side effect profile to 5mg (1mg) Finasteride. 2.5mg Dutasteride however has a slightly higher chance for sexual sides.
The take away here is scalp DHT (more so interfollicular levels of DHT) will determine how stable one's hair will be on treatment. And dutasteride time and time again has demonstrated it's efficacy superiority over finasteride (even at lower doses)
Timestamps
0:00 Preview Snippet
1:35 Introduction to John
2:45 John's Initial Experience with Hair Loss
4:22 Rogaine Commericals
5:20 John Recalls the early Treatments (especially with Rogaine)
6:44 Kevin ( @haircafe ) Minoxidil Method
7:40 John's Familial history of AGA/hair loss
9:13 John describes his hair loss progression speed
10:30 John talks about starting Propecia (Finasteride)
13:23 John talks about RU58841, early days of online hair loss forums, and more...
19:06 Forums of yesterday like alt.baldspot, hairloss help, and hairloss talk mirror today's spaces like Reddit's Tressless
22:13 Side discussion on recent boxing match between Anthony Joshua vs. Francis Ngannou 😂
23:09 Male Brain Development and hair loss: intensity of experiences
24:48 Resources and Knowledge on Early hair loss treatments. Early treatment is important!
25:32 John Talks about his RU-58841 experiment and the culture of the early hair loss forums
33:18 Logistics and Safety of RU-58841
35:30 Why people use RU-58841
36:11 John recalls fellow RU-58841 user and briefly talks about Avodart (Dutasteride)
37:27 John remembere the "RU-58841 smell" by buying it today
39:32 John's hairstack after finishing the RU-58841 experiment. Switch to Dutasteride
40:30 John Switches to Dutasteride
43:00 20+ Years of Dutasteride Use
43:38 Derma rolling from the early 2000s
44:52 John takes Spironolactone for blood pressure (hypertension)
46:14 Have you noticed side effects on Finasteride or Dutasteride?
47:34 Discussions about PFS and psychosocial factors
48:50 Hair loss and dating: today vs yesterday
50:16 The Reality of Modern Dating and Looks
54:07 Treatment fearmongers
55:56 Negative coverage on Finasteride could have prevented new treatment adoption
58:41 Did you notice anyone talk about post finasteride syndrome in the early days of the hair loss forums?
1:02:43 Is PFS an "English" thing?
1:04:29 Too much fear around finasteride
1:07:23 Corrupted audio: Osteopotin, SCUBE3, FOL005, GT20029 (reuploading this segment soon)
1:11:32 AMP203
1:13:56 SCUBE3, hair stimulation
1:15:40 John thinks we will hear updates about Amplifica Summer 2024
1:20:13 CUT OFF AND CORRUPTED. SECTION WILL BE REUPLOADED
1:24:34 Estrogens are more important to Anagen growth for hair (partially corrupted audio)
1:28:07 The steps of hair growth: fuzzy picture
1:28:29 Lack of more modern treatments with in the last 30+ years
1:30:55 Verteporfin
1:35:35 Funny things about the online hairloss forums
1:40:43 Johns advice to people going through hair loss

I've been using fin for a month from Alldaychemist (ADC) because it was super difficult to find a prescription for me. Is the fin legit? Like is it some random snake pill or have people had success with it ? I know that they send medicine, but are they real pills?
​
The Propecia from ADC is labeled Organon instead of MSD like how I usually see in pictures. Will it still work the same and is there any difference?
*I know that generic and brand-name are supposed to be the same but I'd prefer to use brand-name after reading some anecdotes*
Anyone have results from Propecia from adc? Thanks.
https://preview.redd.it/e3tvxtgc21kc1.png?width=697&format=png&auto=webp&s=8d1a72edff821a82c591360d56d5d71e29a7292a
https://preview.redd.it/iudz9hvs21kc1.png?width=900&format=png&auto=webp&s=3f957d24ed5f88b08d6b17400f69487174f39774

Hey guys, as the end of 2023 nears, I thought I'd do a post for those of you on TRT who are losing hair or have noticed some thinning/receding of your hairline.
I posted this to tressless recently, and thought it would be pertinent to post here as well, especially as TRT can speed up your genetic propensity to baldness (MPB).
So if you are struggling, worried or anxious about losing your hair and take TRT (or don't but are still interested in learning more), in this post I’m going to be talking about the science of hair loss and what to do if you are balding and want to stop it.
I’m a medical student and have donated a lot of my personal time to pharmacology, hormones and hair protocols through research and experimentation. There’s a lot going on here on Reddit, and as a beginner it can be very daunting to decide on what to do. Obviously everything should be discussed with your doctor, but below is my best attempt at a guide to explain a little bit about hair loss:
-
I first noticed I was balding around 12 months ago, and rather than get caught up in the genetics of hair loss and trying to figure out whether it was Dad, my Mum’s Dad, my Mum’s Dad’s Dad or the goldfish he owned when he was 10, I thought to myself:

I can’t change my genetics. Whatever my DNA sequencing (genomic regions) has in store for me in regards to balding, that’s pretty much set. The best I can do is fight as long as I can using the highest quality science, products and methodologies to offset it.

And that’s what I’ve been doing, with good success, over the past 12 months.
Let’s get into it, and I’m going to do this in order of most important to least (in my opinion).
Getting to the root cause: DHT
Okay, so if we look at the entire testosterone/HPT axis pathway, cholesterol is converted to testosterone and some people think that’s the end of the line, but it’s actually not; 5-alpha reductase (5A1/2 in the image below) is the enzyme responsible for converting Testosterone (T) to its much more potent form DHT (dihydrotestosterone).
​
5-alpha reductase converts Testosterone to DHT, the hair killer.
​
Now, interestingly, 5-alpha reductase for whatever reason is very high prevalent in skin tissue - including the human scalp. And side note: this is why guys who take testosterone gel or cream often have very high levels of DHT compared to guys who take injections, because the cream is being converted through the skin into DHT at a much higher rate than injectable esters into muscle bellies. But, basically, it is this 5-alpha reductase activity in the scalp that is converting testosterone to DHT, and DHT through a variety of mechanisms leads to follicular miniaturisation (hair thinning, and eventual loss of your hair follicles).
But why? Well, there are hundreds of factors: hormonal (androgen receptor density & sensitivity to said androgens), physical, genetic, environmental. The list goes on.
Note; this study goes into a lot more depth for those of you interested.
But, how do we actually combat balding?
​
​
Most men tend to lose their hair in patterns as described by the famous Norwood Scale.
Slowing Down Male Pattern Baldness
5-alpha Reductase Inhibitors (Finasteride, Dutasteride):
With how much I’ve spoken about 5-alpha reductase and DHT, it seems logical that stopping this conversion of Testosterone to DHT is the absolute first line of defence against hair loss.
To really, truly combat hair loss, the first mechanism is as follows: you absolutely need to reduce your hair follicles’ exposure to DHT.
And how do we do this? Well, finasteride is a drug that acts as a 5-alpha reductase inhibitor. Sold under the name Propecia, the molecule is a strong 5-alpha reductase inhibitor, and has been shown to inhibit around 70% of serum (blood) levels of DHT from peak. The usual starting dose is 1mg daily. Dutasteride (sold under the name Avodart) is an even more potent inhibitor (usual starting daily dose is 0.5mg), and can block up to 98% of conversion from T to DHT: it is a much more potent inhibitor of the enzyme that converts T to DHT. Dutasteride would be an option if you wanted a nuclear option to block almost all DHT. In fact, one of my favourite studies compared the difference between Finasteride vs. Dutasteride, and as you can see below, the suppression of DHT levels from Dutasteride was significantly more than Finasteride. Not only this, but the half life of Dutasteride is significantly longer than Finasteride (~8 hours vs. 5 weeks!), and you can see that in the Dutasteride group after stopping treatment (Follow-up Period), DHT levels remained suppressed for a much longer time.
​
DHT vs. Finasteride - what a study.
​
Side effects from 5-alpha reductase inhibitors are rare, although we should speak about them. Online, through various forums, Reddit posts, YouTube videos and TikTok’s time and time again I see posts about nasty Finasteride side effects, post-Finasteride syndrome and how Rob can’t get his Johnson hard anymore because of Finasteride, so his girlfriend left him.
Now, don’t get me wrong, side effects have been noted, although current research puts the risk of side effects at around 1-3% of people, so even though online there is a lot of noise about finasteride and its side effects, I personally don’t think the research supports this scaremongering. There is also going to be a natural selection bias with the stories online, because the guy for whom Finasteride is working well and who is not experiencing any side effects, he isn’t really going to post. Because why would he? He’s doing fine.
However, I absolutely sympathise with the people who just cannot tolerate 5-alpha reductase inhibitors. Side effects can be very real, and this is why it is vitally important to always consult with a qualified doctor before deciding on any medication: I’m just presenting the science. Everyone reacts slightly differently, and these can be strong medications - so it's important to be well-informed and sensible with whatever path you and your medical practitioner decide to go down.
Topical Minoxidil 5% (Rogaine):
Minoxidil is a compound that has been shown to increase the rate of DNA synthesis in anagen (growth phase) bulbs of hair follicles. Basically minoxidil stimulates hair cells to move from telogen (resting phase) to anagen (growing phase) - so instead of having hair follicles resting, it is telling the body to move them back into a growth phase by shortening the resting phase. The idea here is that you get more ‘regrowth’ of hair follicles.
​
https://preview.redd.it/dmapvsdymy6c1.jpg?width=700&format=pjpg&auto=webp&s=4137d40c166a5dc7c9bb8a697166821713cbb6ef
Minoxidil stimulates hair cells to shorten the resting (telogen) phase and go back into an anagen (growing phase). Often, progress pictures will show significant new regrowth or ‘baby’ hairs growing with minoxidil treatment.
I apply Rogaine, a 5% strength Minoxidil foam twice daily in areas that I feel are receding. The nice thing about the foam is that it isn’t super sticky (unlike some people report with the gel), and it also acts as a nice way to hold my hair throughout the day, like hair product.
As you can see from the photo below, there is a vast difference between telogen (resting phase) and anagen (growing phase), and the idea is that the more hairs you can keep in anagen, the more healthy your hair will be, by limiting the amount of follicles that inevitably go through an anagen restart and die off.
​
Grow baby hairs, grow!
There is also the option of oral minoxidil, which anecdotally at least seems to be very powerful at regenerating ‘baby’ hairs (or, new regrowth). Again, oral minoxidil can have some pretty significant side effects and drug interactions with blood pressure medications, so speaking through with your doctor is key!
Ketoconazole Shampoo:
This shampoo is primarily an anti-dandruff shampoo, but research has shown it may increase the proportion of hairs in anagen phase (growth phase) - resulting in reduced hair shedding. This study showed that 1% ketoconazole shampoo increased hair diameter over baseline after 6 months of use and reduced shedding. Interestingly, participants’ hair diameter also increased over baseline, showing that it may play a role in creating thicker hair.
Nizoral is a common brand here in Australia of 2% strength ketoconazole shampoo.
​
https://preview.redd.it/n0fyicnzmy6c1.jpg?width=800&format=pjpg&auto=webp&s=eadf085e52734c813eb5a0b22bcd06fee2ed3d24
What is good about ketoconazole, is that it’s also a weak androgen receptor antagonist. What does this mean? It means it competes with DHT and Testosterone for binding to the active binding domain on the human AR (androgen receptor). If a compound can bind to a receptor without influencing its usual effects, it is said to be an antagonist. Basically, if ketoconazole can get into an androgen receptor before Testosterone or DHT, it will occupy that site and block T/DHT from binding and starting their usual process of killing off hair follicles (follicular miniaturisation).
Goodbye DHT, nobody wants you here.
Dermarolling
Derma-what?
Dermarolling is the process of creating micro punctures in the scalp skin to induce a wound healing response, with an array of tiny microneedles.
​
https://preview.redd.it/r7ewf560ny6c1.jpg?width=1082&format=pjpg&auto=webp&s=a19ecbfd36996688f94821cafc53150485ff73c8
In this study, the dermarolling + minoxidil treated group was statistically superior to the minoxidil only treated group in promoting hair growth in men with balding patterns, for all primary efficacy measures of hair growth. In fact, the microneedling group outperformed even the minoxidil group in terms of how much hair was regrown after 12 weeks:
​
https://preview.redd.it/53nnwn51ny6c1.jpg?width=741&format=pjpg&auto=webp&s=ca3dc1032c53bf898bd9246584ab01bcf8c72d9a
The mechanism seems to be that continued microtrauma to the scalp skin leads to a release of platelet derived growth factors and other growth factors that are sent to the area of scalp, to aid in the skin wound regeneration. The added benefit is that there seems to be some carry over effect to hair growth, as dermarolling seems to activate stem cells or ‘unspecialised’ cells that are yet to be differentiated, and differentiate them into hair follicle cells, meaning more hair growth. Basically, its a wound healing response that brings growth factors to the area of the scalp to increase hair growth.
I have played around with a few different protocols, but I use a 1.5mm roller and roll horizontally, vertically and diagonally for about 30 seconds in areas where my hairline is thinning or receding. I do this every 10 days. You don’t want to press so hard that you draw blood, but it should also hurt slightly. I mean, putting hundreds of tiny spikes into your scalp isn’t really my idea of Sunday night fun. But hey, if it regrows some hair why not?
There are also derma-stamps and motorised tools, all of which assist with the end goal: creating a wound healing response to bring growth factors to the scalp, and potentially assist the penetration of Minoxidil deeper into the scalp skin tissue.
Natural DHT blocking compounds:
Natural DHT blockers are also options, although obviously the results aren’t going to be nearly as strong as what is mentioned above.
Some people have good results (anecdotally) with rosemary oil applied topically, green tea and saw palmetto are options here. However, the science is very hit and miss, and in any event, I can’t see natural compounds competing against the 'Big 4'.
RU58841:
Now, that’s all good, but what if you need a nuclear chemical. Something that would attack the androgen receptor at a direct level in your scalp? Well, that compound is below. But a quick warning: I do not recommend this compound. A lot of people use it, but that doesn’t mean it’s safe. There is no (yes, zero) long-term safety data on the compound below, and whether you choose to take a completely untested chemical is up to you. But I don’t recommend it - have I said that enough?
Alright so, apart from sounding like a bunch of random letters because your cat ran over your keyboard, RU58841 is a strong DHT blocker (it has been shown to inhibit around 70% of DHT binding to the androgen receptor), but not in the way that Finasteride or Dutasteride work.
​
The molecular structure of RU58841.
​
Instead of finasteride and dutasteride which work on inhibiting the 5-alpha reductase enzyme, RU58841 works on the AR itself - occupying the active site, so that when DHT tries to get in and exert its hair destructive effects in the scalp, it can’t, it’s literally blocked from accessing the active site of the androgen receptor.
​
RU58841 operates like an androgen receptor antagonist (3rd receptor, on the right). It binds to the receptor and stops testosterone and DHT from binding, meaning that those androgens (DHT in particular) cannot then exert their hair miniaturisation effects.
​
And in this study, RU58841 was found to inhibit 70% of DHT binding. Combining something like finasteride or dutasteride which attacks 5-alpha reductase converting T to DHT with RU58841 which stops ~70% of DHT binding to the androgen receptor, and you’d now be attacking hair loss from 2 vectors: T to DHT conversion, as well as at a receptor level. Now you can start to understand why this is a nuclear option for hair loss, and incredibly powerful.
However, despite how good all of that sounds in practice, just remember, RU58841 is completely untested in regards to side effects. There is no long-term safety data on how it may or can impact human health, so what I’m saying (for legal reasons) is don’t use it. Get what I’m saying?
Final Thoughts:
And, there it is guys. Now, just a quick note, this isn’t a super comprehensive list of all supplements for a hair regrowth/hair protection protocol, but is a solid start.
There are certainly more ‘niche’ options, or compounds in development now that may be promising (or not, looking at you Phase 3 of Pyrilutamide trials), but this guide was just the bare basics for a beginner to wrap his head around (no pun intended) the science and how to start combatting AGA.
In particular, if you want to save your hair, it’s going to be the ‘big 4’: finasteride (or Dutasteride), Minoxidil, Ketoconazole shampoo and derma-rolling roughly once a week to every 2 weeks.
This would follow the best possible science that we have at the moment, in terms of targeting as many vectors as possible:

1. T to DHT blockade (5-alpha reductase inhibitors, Fin/Dut)
2. Anagen/telogen manipulation (Minoxidil)
3. Localised scalp tissue androgen receptor antagonism (Keto, RU58841)
4. Wound healing response cascade (physical microneedling/trauma)

Hope you enjoyed and got something out of this guide! My social links are on my profile if interested in more.

Hey guys, as the end of 2023 nears, I thought I'd do a post for those of you on TRT who are losing hair or have noticed some thinning/receding of your hairline.
I posted this to tressless recently, and thought it would be pertinent to post here as well, especially as TRT can speed up your genetic propensity to baldness (MPB).
So if you are struggling, worried or anxious about losing your hair and take TRT (or don't but are still interested in learning more), in this post I’m going to be talking about the science of hair loss and what to do if you are balding and want to stop it.
I’m a medical student and have donated a lot of my personal time to pharmacology, hormones and hair protocols through research and experimentation. There’s a lot going on here on Reddit, and as a beginner it can be very daunting to decide on what to do. Obviously everything should be discussed with your doctor, but below is my best attempt at a guide to explain a little bit about hair loss:
-
I first noticed I was balding around 12 months ago, and rather than get caught up in the genetics of hair loss and trying to figure out whether it was Dad, my Mum’s Dad, my Mum’s Dad’s Dad or the goldfish he owned when he was 10, I thought to myself:

I can’t change my genetics. Whatever my DNA sequencing (genomic regions) has in store for me in regards to balding, that’s pretty much set. The best I can do is fight as long as I can using the highest quality science, products and methodologies to offset it.

And that’s what I’ve been doing, with good success, over the past 12 months.
Let’s get into it, and I’m going to do this in order of most important to least (in my opinion).
Getting to the root cause: DHT
Okay, so if we look at the entire testosterone/HPT axis pathway, cholesterol is converted to testosterone and some people think that’s the end of the line, but it’s actually not; 5-alpha reductase (5A1/2 in the image below) is the enzyme responsible for converting Testosterone (T) to its much more potent form DHT (dihydrotestosterone).
​
5-alpha reductase converts Testosterone to DHT, the hair killer.
​
Now, interestingly, 5-alpha reductase for whatever reason is very high prevalent in skin tissue - including the human scalp. And side note: this is why guys who take testosterone gel or cream often have very high levels of DHT compared to guys who take injections, because the cream is being converted through the skin into DHT at a much higher rate than injectable esters into muscle bellies. But, basically, it is this 5-alpha reductase activity in the scalp that is converting testosterone to DHT, and DHT through a variety of mechanisms leads to follicular miniaturisation (hair thinning, and eventual loss of your hair follicles).
But why? Well, there are hundreds of factors: hormonal (androgen receptor density & sensitivity to said androgens), physical, genetic, environmental. The list goes on.
Note; this study goes into a lot more depth for those of you interested.
But, how do we actually combat balding?
​
Most men tend to lose their hair in patterns as described by the famous Norwood Scale.
​
Slowing Down Male Pattern Baldness
5-alpha Reductase Inhibitors (Finasteride, Dutasteride):
With how much I’ve spoken about 5-alpha reductase and DHT, it seems logical that stopping this conversion of Testosterone to DHT is the absolute first line of defence against hair loss.
To really, truly combat hair loss, the first mechanism is as follows: you absolutely need to reduce your hair follicles’ exposure to DHT.
And how do we do this? Well, finasteride is a drug that acts as a 5-alpha reductase inhibitor. Sold under the name Propecia, the molecule is a strong 5-alpha reductase inhibitor, and has been shown to inhibit around 70% of serum (blood) levels of DHT from peak. The usual starting dose is 1mg daily. Dutasteride (sold under the name Avodart) is an even more potent inhibitor (usual starting daily dose is 0.5mg), and can block up to 98% of conversion from T to DHT: it is a much more potent inhibitor of the enzyme that converts T to DHT. Dutasteride would be an option if you wanted a nuclear option to block almost all DHT. In fact, one of my favourite studies compared the difference between Finasteride vs. Dutasteride, and as you can see below, the suppression of DHT levels from Dutasteride was significantly more than Finasteride. Not only this, but the half life of Dutasteride is significantly longer than Finasteride (~8 hours vs. 5 weeks!), and you can see that in the Dutasteride group after stopping treatment (Follow-up Period), DHT levels remained suppressed for a much longer time.
​
DHT vs. Finasteride - what a study.
​
Side effects from 5-alpha reductase inhibitors are rare, although we should speak about them. Online, through various forums, Reddit posts, YouTube videos and TikTok’s time and time again I see posts about nasty Finasteride side effects, post-Finasteride syndrome and how Rob can’t get his Johnson hard anymore because of Finasteride, so his girlfriend left him.
Now, don’t get me wrong, side effects have been noted, although current research puts the risk of side effects at around 1-3% of people, so even though online there is a lot of noise about finasteride and its side effects, I personally don’t think the research supports this scaremongering. There is also going to be a natural selection bias with the stories online, because the guy for whom Finasteride is working well and who is not experiencing any side effects, he isn’t really going to post. Because why would he? He’s doing fine.
However, I absolutely sympathise with the people who just cannot tolerate 5-alpha reductase inhibitors. Side effects can be very real, and this is why it is vitally important to always consult with a qualified doctor before deciding on any medication: I’m just presenting the science. Everyone reacts slightly differently, and these can be strong medications - so it's important to be well-informed and sensible with whatever path you and your medical practitioner decide to go down.
Topical Minoxidil 5% (Rogaine):
Minoxidil is a compound that has been shown to increase the rate of DNA synthesis in anagen (growth phase) bulbs of hair follicles. Basically minoxidil stimulates hair cells to move from telogen (resting phase) to anagen (growing phase) - so instead of having hair follicles resting, it is telling the body to move them back into a growth phase by shortening the resting phase. The idea here is that you get more ‘regrowth’ of hair follicles.
​
https://preview.redd.it/4t0zoh83my6c1.jpg?width=700&format=pjpg&auto=webp&s=110d9148122b01726df4006833b5318df83120e1
Minoxidil stimulates hair cells to shorten the resting (telogen) phase and go back into an anagen (growing phase). Often, progress pictures will show significant new regrowth or ‘baby’ hairs growing with minoxidil treatment.
I apply Rogaine, a 5% strength Minoxidil foam twice daily in areas that I feel are receding. The nice thing about the foam is that it isn’t super sticky (unlike some people report with the gel), and it also acts as a nice way to hold my hair throughout the day, like hair product.
As you can see from the photo below, there is a vast difference between telogen (resting phase) and anagen (growing phase), and the idea is that the more hairs you can keep in anagen, the more healthy your hair will be, by limiting the amount of follicles that inevitably go through an anagen restart and die off.
​
https://preview.redd.it/3mhw12r3my6c1.jpg?width=400&format=pjpg&auto=webp&s=499bbdaff6b136092ca699349c990991da805981
There is also the option of oral minoxidil, which anecdotally at least seems to be very powerful at regenerating ‘baby’ hairs (or, new regrowth). Again, oral minoxidil can have some pretty significant side effects and drug interactions with blood pressure medications, so speaking through with your doctor is key!
Ketoconazole Shampoo:
This shampoo is primarily an anti-dandruff shampoo, but research has shown it may increase the proportion of hairs in anagen phase (growth phase) - resulting in reduced hair shedding. This study showed that 1% ketoconazole shampoo increased hair diameter over baseline after 6 months of use and reduced shedding. Interestingly, participants’ hair diameter also increased over baseline, showing that it may play a role in creating thicker hair.
Nizoral is a common brand here in Australia of 2% strength ketoconazole shampoo.
​
https://preview.redd.it/vpq4ipc4my6c1.jpg?width=800&format=pjpg&auto=webp&s=0680f94666eff1292b9c876802d5d5c2f8590a77
What is good about ketoconazole, is that it’s also a weak androgen receptor antagonist. What does this mean? It means it competes with DHT and Testosterone for binding to the active binding domain on the human AR (androgen receptor). If a compound can bind to a receptor without influencing its usual effects, it is said to be an antagonist. Basically, if ketoconazole can get into an androgen receptor before Testosterone or DHT, it will occupy that site and block T/DHT from binding and starting their usual process of killing off hair follicles (follicular miniaturisation).
Goodbye DHT, nobody wants you here.
Dermarolling
Derma-what?
Dermarolling is the process of creating micro punctures in the scalp skin to induce a wound healing response, with an array of tiny microneedles.
​
https://preview.redd.it/bxizbo85my6c1.jpg?width=1082&format=pjpg&auto=webp&s=3ce5bab2b3429152c095a6b14d06ec5de440c506
In this study, the dermarolling + minoxidil treated group was statistically superior to the minoxidil only treated group in promoting hair growth in men with balding patterns, for all primary efficacy measures of hair growth. In fact, the microneedling group outperformed even the minoxidil group in terms of how much hair was regrown after 12 weeks:
​
https://preview.redd.it/ngi3ro46my6c1.jpg?width=741&format=pjpg&auto=webp&s=46e13d483e3184186b0c78f47228ffbad46096e8
The mechanism seems to be that continued microtrauma to the scalp skin leads to a release of platelet derived growth factors and other growth factors that are sent to the area of scalp, to aid in the skin wound regeneration. The added benefit is that there seems to be some carry over effect to hair growth, as dermarolling seems to activate stem cells or ‘unspecialised’ cells that are yet to be differentiated, and differentiate them into hair follicle cells, meaning more hair growth. Basically, its a wound healing response that brings growth factors to the area of the scalp to increase hair growth.
I have played around with a few different protocols, but I use a 1.5mm roller and roll horizontally, vertically and diagonally for about 30 seconds in areas where my hairline is thinning or receding. I do this every 10 days. You don’t want to press so hard that you draw blood, but it should also hurt slightly. I mean, putting hundreds of tiny spikes into your scalp isn’t really my idea of Sunday night fun. But hey, if it regrows some hair why not?
There are also derma-stamps and motorised tools, all of which assist with the end goal: creating a wound healing response to bring growth factors to the scalp, and potentially assist the penetration of Minoxidil deeper into the scalp skin tissue.
Natural DHT blocking compounds:
Natural DHT blockers are also options, although obviously the results aren’t going to be nearly as strong as what is mentioned above.
Some people have good results (anecdotally) with rosemary oil applied topically, green tea and saw palmetto are options here. However, the science is very hit and miss, and in any event, I can’t see natural compounds competing against the 'Big 4'.
RU58841:
Now, that’s all good, but what if you need a nuclear chemical. Something that would attack the androgen receptor at a direct level in your scalp? Well, that compound is below. But a quick warning: I do not recommend this compound. A lot of people use it, but that doesn’t mean it’s safe. There is no (yes, zero) long-term safety data on the compound below, and whether you choose to take a completely untested chemical is up to you. But I don’t recommend it - have I said that enough?
Alright so, apart from sounding like a bunch of random letters because your cat ran over your keyboard, RU58841 is a strong DHT blocker (it has been shown to inhibit around 70% of DHT binding to the androgen receptor), but not in the way that Finasteride or Dutasteride work.
​
The chemical structure of RU58841.
​
Instead of finasteride and dutasteride which work on inhibiting the 5-alpha reductase enzyme, RU58841 works on the AR itself - occupying the active site, so that when DHT tries to get in and exert its hair destructive effects in the scalp, it can’t, it’s literally blocked from accessing the active site of the androgen receptor.
​
RU58841 operates like an androgen receptor antagonist (3rd receptor, on the right). It binds to the receptor and stops testosterone and DHT from binding, meaning that DHT cannot then exert its hair miniaturisation effects.
​
And in this study, RU58841 was found to inhibit 70% of DHT binding. Combining something like finasteride or dutasteride which attacks 5-alpha reductase converting T to DHT with RU58841 which stops ~70% of DHT binding to the androgen receptor, and you’d now be attacking hair loss from 2 vectors: T to DHT conversion, as well as at a receptor level. Now you can start to understand why this is a nuclear option for hair loss, and incredibly powerful.
However, despite how good all of that sounds in practice, just remember, RU58841 is completely untested in regards to side effects. There is no long-term safety data on how it may or can impact human health, so what I’m saying (for legal reasons) is don’t use it. Get what I’m saying?
Final Thoughts:
And, there it is guys. Now, just a quick note, this isn’t a super comprehensive list of all supplements for a hair regrowth/hair protection protocol, but is a solid start.
There are certainly more ‘niche’ options, or compounds in development now that may be promising (or not, looking at you Phase 3 of Pyrilutamide trials), but this guide was just the bare basics for a beginner to wrap his head around (no pun intended) the science and how to start combatting AGA.
In particular, if you want to save your hair, it’s going to be the ‘big 4’: finasteride (or Dutasteride), Minoxidil, Ketoconazole shampoo and derma-rolling roughly once a week to every 2 weeks.
This would follow the best possible science that we have at the moment, in terms of targeting as many vectors as possible:

1. T to DHT blockade (5-alpha reductase inhibitors, Fin/Dut)
2. Anagen/telogen manipulation (Minoxidil)
3. Localised scalp tissue androgen receptor antagonism (Keto, RU58841)
4. Wound healing response cascade (physical microneedling/trauma)

Hope you enjoyed and got something out of this guide! My social links are on my profile if interested in more.

I had a hair transplant to deal with a receding hairline 1 year ago. I also have been taking Propecia and Minoxidil for 3-4 years now. However, I have started to notice that I can see the scalp on the sides of my head. But its in an area that doesn’t usually bald. I am hoping that it is because 1) I have very fine hairs and 2) I have very straight hairs. So when the light hits my scalp head on, you can see right through to the scalp. If you look at the first two pictures, you can see that the first is taken directly in front of the light, and the second is taken away from the light but facing a bright wall.
The video specifically shows how the visibility of the scalp appears to move as I tilt my head. I was just hoping to get some input from Reddit here.
https://preview.redd.it/1q7c42z22w6c1.jpg?width=1169&format=pjpg&auto=webp&s=8105f61255b458ed680a11e901a544414d33803c
https://preview.redd.it/cgmpmkh32w6c1.jpg?width=1175&format=pjpg&auto=webp&s=accfc8452de95d0ccff89b536532a54a6896a2c2
​
Video: https://1drv.ms/v/s!Aqu9UKhK8oUTgtg7CHaBKl6B9Pg1pw?e=8c1KzA
​
Does this appear to be balding? Or is it just the angle and size of my hair strands?

I had a hair transplant to deal with a receding hairline 1 year ago. I also have been taking Propecia and Minoxidil for 3-4 years now. However, I have started to notice that I can see the scalp on the sides of my head. But its in an area that doesn’t usually bald. I am hoping that it is because 1) I have very fine hairs and 2) I have very straight hairs. So when the light hits my scalp head on, you can see right through to the scalp. If you look at the first two pictures, you can see that the first is taken directly in front of the light, and the second is taken away from the light but facing a bright wall.
The video specifically shows how the visibility of the scalp appears to move as I tilt my head. I was just hoping to get some input from Reddit here.
https://preview.redd.it/qigpr15b1w6c1.jpg?width=1169&format=pjpg&auto=webp&s=bc5e6d70319ea0ef1b9c166349a925c99fc53923
https://preview.redd.it/ytx68lib1w6c1.jpg?width=1175&format=pjpg&auto=webp&s=e7150eee59998e3794035094fb83ae11f7c78141
​
Video: https://1drv.ms/v/s!Aqu9UKhK8oUTgtg7CHaBKl6B9Pg1pw?e=8c1KzA
​
Does this appear to be balding? Or is it just the angle and size of my hair strands?

Hey guys, as the end of 2023 nears, I thought I'd do a post for those coming to this sub in desperate need of help.
In this post I’m going to be talking about the science of hair loss and what to do if you are balding and want to stop it.
I’m a medical student and have donated a lot of my personal time to pharmacology, hormones and hair protocols through research and experimentation. There’s a lot going on here on Reddit, and as a beginner it can be very daunting to decide on what to do. Obviously everything should be discussed with your doctor, but below is my best attempt at a guide to explain a little bit about hair loss:
-
I first noticed I was balding around 12 months ago, and rather than get caught up in the genetics of hair loss and trying to figure out whether it was Dad, my Mum’s Dad, my Mum’s Dad’s Dad or the goldfish he owned when he was 10, I thought to myself:
​

I can’t change my genetics. Whatever my DNA sequencing (genomic regions) has in store for me in regards to balding, that’s pretty much set. The best I can do is fight as long as I can using the highest quality science, products and methodologies to offset it.

​
And that’s what I’ve been doing, with good success, over the past 12 months.
Let’s get into it, and I’m going to do this in order of most important to least (in my opinion).
​
Getting to the root cause: DHT
Okay, so if we look at the entire testosterone/HPT axis pathway, cholesterol is converted to testosterone and some people think that’s the end of the line, but it’s actually not; 5-alpha reductase (5A1/2 in the image below) is the enzyme responsible for converting Testosterone (T) to its much more potent form DHT (dihydrotestosterone).
​
5-alpha reductase converts Testosterone to DHT, the hair killer.
​
Now, interestingly, 5-alpha reductase for whatever reason is very high prevalent in skin tissue - including the human scalp. And side note: this is why guys who take testosterone gel or cream often have very high levels of DHT compared to guys who take injections, because the cream is being converted through the skin into DHT at a much higher rate than injectable esters into muscle bellies. But, basically, it is this 5-alpha reductase activity in the scalp that is converting testosterone to DHT, and DHT through a variety of mechanisms leads to follicular miniaturisation (hair thinning, and eventual loss of your hair follicles).
But why? Well, there are hundreds of factors: hormonal (androgen receptor density & sensitivity to said androgens), physical, genetic, environmental. The list goes on.
Note; this study goes into a lot more depth for those of you interested.
But, how do we actually combat balding?
​
Most men tend to lose their hair in patterns as described by the famous Norwood Scale.
​
Slowing Down Male Pattern Baldness
5-alpha Reductase Inhibitors (Finasteride, Dutasteride):
With how much I’ve spoken about 5-alpha reductase and DHT, it seems logical that stopping this conversion of Testosterone to DHT is the absolute first line of defence against hair loss.
To really, truly combat hair loss, the first mechanism is as follows: you absolutely need to reduce your hair follicles’ exposure to DHT.
And how do we do this? Well, finasteride is a drug that acts as a 5-alpha reductase inhibitor. Sold under the name Propecia, the molecule is a strong 5-alpha reductase inhibitor, and has been shown to inhibit around 70% of serum (blood) levels of DHT from peak. The usual starting dose is 1mg daily. Dutasteride (sold under the name Avodart) is an even more potent inhibitor (usual starting daily dose is 0.5mg), and can block up to 98% of conversion from T to DHT: it is a much more potent inhibitor of the enzyme that converts T to DHT. Dutasteride would be an option if you wanted a nuclear option to block almost all DHT. In fact, one of my favourite studies compared the difference between Finasteride vs. Dutasteride, and as you can see below, the suppression of DHT levels from Dutasteride was significantly more than Finasteride. Not only this, but the half life of Dutasteride is significantly longer than Finasteride (~8 hours vs. 5 weeks!), and you can see that in the Dutasteride group after stopping treatment (Follow-up Period), DHT levels remained suppressed for a much longer time.
​
DHT vs. Finasteride - what a study.
Side effects from 5-alpha reductase inhibitors are rare, although we should speak about them. Online, through various forums, Reddit posts, YouTube videos and TikTok’s time and time again I see posts about nasty Finasteride side effects, post-Finasteride syndrome and how Rob can’t get his Johnson hard anymore because of Finasteride, so his girlfriend left him.
Now, don’t get me wrong, side effects have been noted, although current research puts the risk of side effects at around 1-3% of people, so even though online there is a lot of noise about finasteride and its side effects, I personally don’t think the research supports this scaremongering. There is also going to be a natural selection bias with the stories online, because the guy for whom Finasteride is working well and who is not experiencing any side effects, he isn’t really going to post. Because why would he? He’s doing fine.
However, I absolutely sympathise with the people who just cannot tolerate 5-alpha reductase inhibitors. Side effects can be very real, and this is why it is vitally important to always consult with a qualified doctor before deciding on any medication: I’m just presenting the science. Everyone reacts slightly differently, and these can be strong medications - so it's important to be well-informed and sensible with whatever path you and your medical practitioner decide to go down.
​
Topical Minoxidil 5% (Rogaine):
Minoxidil is a compound that has been shown to increase the rate of DNA synthesis in anagen (growth phase) bulbs of hair follicles. Basically minoxidil stimulates hair cells to move from telogen (resting phase) to anagen (growing phase) - so instead of having hair follicles resting, it is telling the body to move them back into a growth phase by shortening the resting phase. The idea here is that you get more ‘regrowth’ of hair follicles.
​
https://preview.redd.it/dy63jn3tjd6c1.jpg?width=700&format=pjpg&auto=webp&s=8670dd032a79aadd7c39bd9df62a0cc89baa2202
Minoxidil stimulates hair cells to shorten the resting (telogen) phase and go back into an anagen (growing phase). Often, progress pictures will show significant new regrowth or ‘baby’ hairs growing with minoxidil treatment.
I apply Rogaine, a 5% strength Minoxidil foam twice daily in areas that I feel are receding. The nice thing about the foam is that it isn’t super sticky (unlike some people report with the gel), and it also acts as a nice way to hold my hair throughout the day, like hair product.
As you can see from the photo below, there is a vast difference between telogen (resting phase) and anagen (growing phase), and the idea is that the more hairs you can keep in anagen, the more healthy your hair will be, by limiting the amount of follicles that inevitably go through an anagen restart and die off.
​
https://preview.redd.it/da6m3qh4kd6c1.png?width=400&format=png&auto=webp&s=a818ded76fe7f0da40b073a78427c5ebef169bcf
There is also the option of oral minoxidil, which anecdotally at least seems to be very powerful at regenerating ‘baby’ hairs (or, new regrowth). Again, oral minoxidil can have some pretty significant side effects and drug interactions with blood pressure medications, so speaking through with your doctor is key!
Ketoconazole Shampoo:
This shampoo is primarily an anti-dandruff shampoo, but research has shown it may increase the proportion of hairs in anagen phase (growth phase) - resulting in reduced hair shedding. This study showed that 1% ketoconazole shampoo increased hair diameter over baseline after 6 months of use and reduced shedding. Interestingly, participants’ hair diameter also increased over baseline, showing that it may play a role in creating thicker hair.
Nizoral is a common brand here in Australia of 2% strength ketoconazole shampoo.
​
https://preview.redd.it/22hcla2ckd6c1.jpg?width=800&format=pjpg&auto=webp&s=556a6c320e825bb32c4776c01ec9a9156fcab0b6
What is good about ketoconazole, is that it’s also a weak androgen receptor antagonist. What does this mean? It means it competes with DHT and Testosterone for binding to the active binding domain on the human AR (androgen receptor). If a compound can bind to a receptor without influencing its usual effects, it is said to be an antagonist. Basically, if ketoconazole can get into an androgen receptor before Testosterone or DHT, it will occupy that site and block T/DHT from binding and starting their usual process of killing off hair follicles (follicular miniaturisation).
Goodbye DHT, nobody wants you here.
Dermarolling
Derma-what?
Dermarolling is the process of creating micro punctures in the scalp skin to induce a wound healing response, with an array of tiny microneedles.
​
https://preview.redd.it/6yjwpgfekd6c1.png?width=1082&format=png&auto=webp&s=39e971f4128c1463f139069e8cb1042ae2a82a8c
In this study, the dermarolling + minoxidil treated group was statistically superior to the minoxidil only treated group in promoting hair growth in men with balding patterns, for all primary efficacy measures of hair growth. In fact, the microneedling group outperformed even the minoxidil group in terms of how much hair was regrown after 12 weeks:
​
https://preview.redd.it/pzoc53hgkd6c1.jpg?width=741&format=pjpg&auto=webp&s=c0635770d6ffdbf90ead61f6404ed4405b635fd2
The mechanism seems to be that continued microtrauma to the scalp skin leads to a release of platelet derived growth factors and other growth factors that are sent to the area of scalp, to aid in the skin wound regeneration. The added benefit is that there seems to be some carry over effect to hair growth, as dermarolling seems to activate stem cells or ‘unspecialised’ cells that are yet to be differentiated, and differentiate them into hair follicle cells, meaning more hair growth. Basically, its a wound healing response that brings growth factors to the area of the scalp to increase hair growth.
I have played around with a few different protocols, but I use a 1.5mm roller and roll horizontally, vertically and diagonally for about 30 seconds in areas where my hairline is thinning or receding. I do this every 10 days. You don’t want to press so hard that you draw blood, but it should also hurt slightly. I mean, putting hundreds of tiny spikes into your scalp isn’t really my idea of Sunday night fun. But hey, if it regrows some hair why not?
There are also derma-stamps and motorised tools, all of which assist with the end goal: creating a wound healing response to bring growth factors to the scalp, and potentially assist the penetration of Minoxidil deeper into the scalp skin tissue.
​
Natural DHT blocking compounds:
Natural DHT blockers are also options, although obviously the results aren’t going to be nearly as strong as what is mentioned above.
Some people have good results (anecdotally) with rosemary oil applied topically, green tea and saw palmetto are options here. However, the science is very hit and miss, and in any event, I can’t see natural compounds competing against the 'Big 4'.
​
RU58841:
Now, that’s all good, but what if you need a nuclear chemical. Something that would attack the androgen receptor at a direct level in your scalp? Well, that compound is below. But a quick warning: I do not recommend this compound. A lot of people use it, but that doesn’t mean it’s safe. There is no (yes, zero) long-term safety data on the compound below, and whether you choose to take a completely untested chemical is up to you. But I don’t recommend it - have I said that enough?
Alright so, apart from sounding like a bunch of random letters because your cat ran over your keyboard, RU58841 is a strong DHT blocker (it has been shown to inhibit around 70% of DHT binding to the androgen receptor), but not in the way that Finasteride or Dutasteride work.
​
The chemical structure of RU58841.
Instead of finasteride and dutasteride which work on inhibiting the 5-alpha reductase enzyme, RU58841 works on the AR itself - occupying the active site, so that when DHT tries to get in and exert its hair destructive effects in the scalp, it can’t, it’s literally blocked from accessing the active site of the androgen receptor.
​
RU58841 operates like an androgen receptor antagonist (3rd receptor, on the right). It binds to the receptor and stops testosterone and DHT from binding, meaning that DHT cannot then exert its hair miniaturisation effects.
And in this study, RU58841 was found to inhibit 70% of DHT binding. Combining something like finasteride or dutasteride which attacks 5-alpha reductase converting T to DHT with RU58841 which stops ~70% of DHT binding to the androgen receptor, and you’d now be attacking hair loss from 2 vectors: T to DHT conversion, as well as at a receptor level. Now you can start to understand why this is a nuclear option for hair loss, and incredibly powerful.
However, despite how good all of that sounds in practice, just remember, RU58841 is completely untested in regards to side effects. There is no long-term safety data on how it may or can impact human health, so what I’m saying (for legal reasons) is don’t use it. Get what I’m saying?
​
Final Thoughts:
And, there it is guys. Now, just a quick note, this isn’t a super comprehensive list of all supplements for a hair regrowth/hair protection protocol, but is a solid start.
There are certainly more ‘niche’ options, or compounds in development now that may be promising (or not, looking at you Phase 3 of Pyrilutamide trials), but this guide was just the bare basics for a beginner to wrap his head around (no pun intended) the science and how to start combatting AGA.
In particular, if you want to save your hair, it’s going to be the ‘big 4’: finasteride (or Dutasteride), Minoxidil, Ketoconazole shampoo and derma-rolling roughly once a week to every 2 weeks.
This would follow the best possible science that we have at the moment, in terms of targeting as many vectors as possible:

1. T to DHT blockade (5-alpha reductase inhibitors, Fin/Dut)
2. Anagen/telogen manipulation (Minoxidil)
3. Localised scalp tissue androgen receptor antagonism (Keto, RU58841)
4. Wound healing response cascade (physical microneedling/trauma)

​
Hope you enjoyed and got something out of this guide! My social links are on my profile if interested in more.

I started thinning back in 2011, i was 21 at the time, in college so all i could afford were supplements like Biotin etc. 2014 I finally got a script for Propecia (fin), which at the time was the only Fin on the market..so i was paying a good $100 a month for that medication. Obviously from 2011 to 2014, i did manage to thin out a bit where you could see my scalp under a light and if the wind blew..forget it…u would think i was bald..so from 2014 until 2021 i hid my balding scalp with the hair i had left…which i had to hairspray down to make sure that it didn’t move when the wind blew (see 5th picture, that’s how i hid my balding for 7 years)…took me like 30 minutes in the bathroom just to do my hair..i would avoid getting my hair wet when going to the beach so as to avoid exposing my balding true self to everyone. Anyways, in 2021, i finally decided to go in for my first HT..locally here in the USA..yes it was pricey..$5 per graft..but one it was COVID so even if i wanted to go overseas, travel was restricted, 2) i had the money i budgeted for it, 3) i wanted to stay local because if something went wrong down the line i can always go back and visit my surgeon and we can tackle the problem..compared to booking another flight and going overseas etc. The initial HT was in Feb 2021 for 1,384 grafts..it was FUT..turned out great…after 14 months, I got hair greedy and wanted to do another transplant just to kinda fill in on the spots where the androgen synchronization occurs of the original transplanted hairs…went back to the same surgeon, he told me i didnt really need it..that i can just add minoxidil (oral) to my routine..but I convinced him otherwise..so we did a second transplant in sept of 2022 for a little less than 1k grafts…it turned out amazing. Upon the 1 year mark of the second transplant, i decided to add minoxidil to my battle against hair loss just to try and get ahead in this never ending war. It’s great now not having to worry about the wind blowing or putting so much product in my hair just to disguise my balding.
So here is my journey through multiple pics, i tried to upload them in order….maybe this will give some of you hope that there is light at the end of the tunnel.

Hey tressless. I want to contribute my before/after pictures of 7 months in total.
My protocol hasn't changed a lot in this time. Here's all the details:

• Finasteride (Propecia brand), oral, 1mg ED - from 5th of February to 15th of May, 2023
• Dutasteride (Avodart brand), oral, 0.5mg ED - since 15th of May, 2023
• Oral minoxidil (Loniten brand), oral, 5mg ED - since 16th of March, 2023

I have not experienced any adverse effects except for hypertrichosis from minoxidil, which I actually welcome since it gave me stronger eyebrows and eyelashes.
The pictures could be better, but it's all I have. I had to buzz my hair for a recent transplant, so I can't take better photos at this time. I will make another post in May next year for a full year on dutasteride.
​
https://preview.redd.it/yja166hmlvnb1.jpg?width=2684&format=pjpg&auto=webp&s=21569cddf9f34c8630bedbd60f7c3e5268a5afe1
https://preview.redd.it/z1kcs7hmlvnb1.jpg?width=2576&format=pjpg&auto=webp&s=e061709346c803234930389c353d7c9b20f3443a
https://preview.redd.it/oatlxahmlvnb1.jpg?width=2646&format=pjpg&auto=webp&s=6296531d8da884e9f97499e2591bb2d1c22c2b23
https://preview.redd.it/syl95uxolvnb1.jpg?width=2608&format=pjpg&auto=webp&s=805f40d617b57acd58b9544a940e4bcc0c2e8c28

Hi guys, I’ve been taking Finasteride for 2 months now and my hair is getting worse. I first started taking Finasteride last December and it killed my libido so after 6 months I decided to take a break and a month later got back to it but since then I’m losing a lot of hair. I read here that there is a shading phase but I did not experience it on my first time taking Finasteride. I’m 28yo taking 1mg every other day. This time I experience less sides (libido is low, sperm is waterish but at least I can get hard) compare to my first time what made me think maybe the Fin that I’m taking now (Proscalpin from India) isn’t as strong as Propecia 🤷🏻‍♂️ although both are just Finasteride.
The first 3 pictures were taken 2 months ago and the 3 other pictures were taken today. You can see that my left side is receding.

Basically title. I'm not sure if I'm too far gone for a transplant to help. Hair has been thinning since at least 22. I've tried acceptance for at least fifteen years, but I still don't feel like I look like "me" in the mirror. I see progress pictures on this sub and get a little teary sometimes--I know what it must mean to those of you who have gone through with the procedure. I just don't want to waste my time if there's little hope, and honestly I need a kick in the pants.
Second question is where. I'm in Oregon, so:
- Turkey is a damn long flight, and doing multiple sessions that aren't just a day apart is pretty infeasible. I worry about complications and followups. Plus I'm spending PTO.
- Mexico seems more feasible. I just don't know how to start my research, and frankly thinking about my hair loss just gets me down sometimes, so researching doctors in another country is difficult as a baseline. Less PTO spend here.
- There are a few doctors in the Portland Metro. This feels like the "safest" option, but it's much more costly to get a transplant in the US. We can afford it, and my wife is encouraging this over travel, but I'm having trouble spending so much of our money on myself.
Red in pictures is desired coverage. I understand the crown is often unrecoverable, but I figured I'll put forth the ideal and work backwards. I'm also totally against Propecia/finasteride; I'd rather have sex than hair.
https://preview.redd.it/6qvt40ivxmdb1.png?width=1675&format=png&auto=webp&s=0c5bf6b58efa62af9e1e3c7d0cdf8774e00aa3dc
https://preview.redd.it/cssqb4jvxmdb1.png?width=1914&format=png&auto=webp&s=a336464b7b590f6ec4013de0e12ddf611a66171f
https://preview.redd.it/04y9c6ivxmdb1.png?width=1768&format=png&auto=webp&s=1e7c38c4cf46415a72a3960df1654cd029597961
https://preview.redd.it/0ofkbfivxmdb1.png?width=1864&format=png&auto=webp&s=6e69d52c017ef7d75e77c195da00ce6371d53bec
https://preview.redd.it/yp4ijshvxmdb1.png?width=1465&format=png&auto=webp&s=5b4b702a151c8ae53aab817da320ce25b3db2142
https://preview.redd.it/d8b1grhvxmdb1.png?width=1459&format=png&auto=webp&s=be329afa1214992badff18712013cdeb5a4ad79f
https://preview.redd.it/k7vmzrhvxmdb1.png?width=1301&format=png&auto=webp&s=b20394fd6c20e695e6a4fa3f4e1f836add46e407
https://preview.redd.it/nx91fuhvxmdb1.png?width=1459&format=png&auto=webp&s=387115192ab0840edd938bf970734dac52f9c6f2

I went for a consultation and they said I’m not a good candidate for fue. Though they are willing to do a transplant. They want me to make a decision today as they’re “squeezing me in.” This is a very reputable hospital in Boston. I have a few questions. I got to see a transplant patient about a year after his proceedure. It looked good. Natural. Though he ran his hand through his hair and I could kinda see dimpling in his pores/folicals. Almost looked like permanent damage. Is this normal? Does the donor site grow back? Normally? And I’m already on rogain foam. But would I have to use finasteride as well? Or can I get away without it. I used propecia for a year and it had side effects I wasn’t crazy about. I don’t want to use it again. Also judging by my picture, am I too late to this for it to be effective? Also how long does it take to heal completely?

1970 - The Jackson 5 make their 2nd appearance on the Ed Sullivan Show in NYC. They perform “I Want You Back/ABC/The Love You Save”
https://youtu.be/ZJMi3m8spJA
1979 - On their Destiny Tour, The Jacksons play the first of two non-consecutive nights at the Arena Theater, Houston, Texas.
1985-Michael visits Brandywine River Museum’s exhibit of paintings by N.C Wyeth in Chadds Ford, Pennsylvania
From Artist Peter Ralston's Blog:

Andy Wyeth calls me and asks me to come to his house for a drink at the end of the day. The question of the day was, "So, who is Michael Jackson?"
Jackson had just come out with Thriller and was the hottest celebrity on the planet, but not surprisingly, Andy hadn't heard of him.
It turns out that Jackson had sent, through a long chain of good contacts, a request to Andy to do a portrait of him. Andy was very reluctant to open up one bit to this sort of thing, but the next morning he brought him a VHS tape of Jackson doing his famous moonwalk at an industry ceremony.
Andy was intrigued enough to send his response down the chain of contacts saying that he would like to meet Jackson to see how things were going.
The day Michael arrived was crazy. He was traveling with a large and diverse entourage and it was all "top secret," but he broke the ice very quickly and we went for a walk in the Brandywine River Museum together and looked at three generations of Wyeth paintings.
What I remember most from that day was a young woman who had obviously taken her boyfriend on a typical cultural tour, and when she looked up and realized she was three feet away from Michael Jackson, she instantly went into another state of consciousness and when he looked at her, smiled at her, and said in his high-pitched voice, “Hello,” she burst into tears.
I remember all the big shots begging me to take a picture with Michael so they could show it to their children, grandchildren and put it on the Wall of Fame.
I clearly remember Michael's shyness. And the sweetness. Above all, I remember that he was most attracted to the boys on the farm. Nothing perverted, nothing weird... what I remember was thinking, 'this guy is like a little kid, he's straight up like Peter Pan.'
Andy didn't get to do the portrait. But here I am with Michael.

​
https://preview.redd.it/jfc20gj6qwya1.jpg?width=1470&format=pjpg&auto=webp&s=547227302ab90deff9654cf7f60ff8e0e67e7964
In Wyeth's biography Andrew Wyeth, a Secret Life by Richard Meryman:

Andrew says that the agents & art dealers, when they found out about the possible portrait, began to fantasize about the millions they would get from the painting and its reproductions. He says they were like "the mob" and didn't care about anything but money.
Andy: "I found (MJ) very sweet, sensitive person, very good, very smart."
At one point someone in Jackson's entourage said that Michael only had ten minutes left to be there and he would have to go.
"We had something good on our hands when those shits got in the way. Poor kid was owned by those people. I felt sorry for him. God help any artist who ends up like this."
Although he felt a real connection to Michael, Andrew dismissed the project saying, "Imagine me painting with all those bodyguards standing there."

Andy died in January 2009.
https://imgur.com/a/MmIC7gb
1986-Michael & Emmanuel Lewis attend the Sunday matinee of Broadway’s Big Deal, which had just opened a month earlier. It's by Bob Fosse and is set in 1930s Chicago. It centers around a group of small-time unemployed African-American men who plan to rob a pawn shop
1993 - Michael Jackson dines at Les Folies Russes in the Hotel Loewes with Prince Albert of Monoco. He's in Monoco for the World Music Awards
https://imgur.com/a/bdf6Low
1997 - Michael Jackson's "Blood On The Dance Floor" hits the Billboard Music charts at #42
1999 - Michael attends a private screening of “Matrix” movie in Manhattan
2000 - Michael receives the "Male Artist Of The Millennium" award at the World Music Awards in Monaco, Monte Carlo for being the best-selling male recording artist of all time. He's presented by Prince Albert of Monaco
https://imgur.com/a/hNiYrfu
https://youtu.be/1JHqqukRY4Q
2005 - Trial Day 49
Michael goes to court with Katherine and Joe.
Joseph Marcus, the property manager at Neverland testified, denying claims that Michael Jackson's teenage accuser and his family were ever held against their will.
Marcus testified that he issued an order instructing guards not to let the accuser or his siblings off the property. "I didn't want the guard to lift the arm and let them out," he said.
Marcus went on to explain that the children had displayed reckless behavior, which included driving vehicles around the property and up to the gate.
The judge moved to strike his explanation after the prosecution objected.
Marcus further testified regarding the cancelled trip to Brazil noting that he spoke with the mother in February of 2003, and she had not complained to him regarding the trip.
"There was no objection at that point that I know of." said Marcus, adding that she only wanted to know how to go about getting passport photos.
The captivity claim and kidnapping are at the heart of the prosecution's conspiracy case.
When questioned about phone calls made at the ranch, Joseph Marcus explained that all calls could be monitored by way of two phones, one in the main house, and one in Jackson's office. Each employee is issued a handbook that warns them of this possible monitoring.
Although he received a complaint regarding telephone monitoring Marcus stated that he did not listen in on calls and added, "I don't think (Jackson) monitored, to my knowledge."
Deputy District Attorney Auchincloss suggested that Marcus' testimony was altered to help Mr. Jackson. "Why do you keep looking at Mr. Jackson?" he asked.
Marcus appeared startled and didn't answer. The defense objected, and the objection was sustained by Judge Melville.
"Do you consider yourself a loyal employee of Mr. Jackson?" the prosecutor continued.
"Yes," said Marcus.
Auchincloss then tried to establish if he took orders from anyone else at the ranch, including Jackson associate Dieter Wiesner, in an attempt to link Mr. Jackson to the alleged conspiracy.
"I would take requests from Dieter Wiesner and address them as needed," he said.
"Dieter Wiesner didn't tell you what to do?" asked Auchincloss.
"True," said the witness.
"Mr. Jackson is the only person that can tell you to handle policies and practices at Neverland?" the prosecutor asked.
True," said Marcus.
Auchincloss tried to discredit Marcus and asked, "Do you have any knowledge of children sleeping in Mr. Jackson's room?" asked Auchincloss.
"Yes," said Marcus.
"And at the time of the search warrant you said you had no knowledge of children sleeping in Mr. Jackson's room?," the prosecutor continued.
"Yes," said Marcus, who later added that events of that day were chaotic and "I was overwhelmed."
Auchincloss directed the attention of the questioning to the adult material seized from Jackson’s Neverland Ranch. "Do you know if Mr. Jackson possesses adult erotic materials?" the prosecutor asked.
"I don't know that he does," Marcus said. "I haven't seen them with him."
The prosecutor then showed a picture of Jackson's desk with tiny figurines of women in bondage attire standing upon it.
"Would you consider the figurines I showed you adult materials?" the prosecutor asked.
"A type of artwork of an adult nature," said Marcus.
"Do you think it's appropriate for children to be exposed to these?" Auchincloss asked.
After pausing, Marcus said "No"
The Prosecutor went on, insinuating that Jackson's "special friends" are mostly boys not girls or women. However, Marcus said there were also females who were close to Mr. Jackson.
When asked for names, the only names he could remember were Elizabeth Taylor, Liza Minnelli, a grandchild of Marlon Brando, and Karlee Barnes (the sister of Brett Barnes) but added that other women had passed through the gates
https://imgur.com/a/JCys409
Court Transcript
2013 - Katherine Jackson v AEG Trial Day 9
Katherine Jackson is not at court.
Karen Faye Testimony
Jackson direct
Faye described how Michael's health had changed over 27 years. She said that his legs, once muscular, were thin, and his face was skeletal. She said that hewas not strong enough for the rigorous concert schedule set by AEG
Michael Bush appeared upset after he finished up a June 2009 fitting inside Jackson's bathroom at Staples Center, Karen Faye said.
"He said 'Oh my god, Turkle. I could see Michael's heartbeat through the skin in his chest'", Faye recounted.
Los Angeles Superior Court Judge Yvette Palazuelos then asked Faye about Bush's tone of voice at the time.
"It was like, 'Oh my god'", Faye said, "He was pretty much in shock"
Around the same time, Faye said she tried to warn Michael's manager, Frank DiLeo, about his health.
"[Frank] was saying pretty much, 'I got it under control, don't worry about it'", Faye said.
"I said 'But he's losing weight rapidly. Why don't you ask Michael Bush to verify taking in his pants and how much weight he's actually losing?'"
Faye said DiLeo went to speak to Bush and she overheard the manager say "Get him a bucket of chicken"
"It was such a cold response",Faye said, "I mean, it broke my heart"
It was Kenny Ortega who came to her, hugged her and told her MJ had died. She said she became weak in the knees
Faye said she prepared MJ's body for the family to see him after he died.
She was asked to work on the This is It film touching up MJ in the footage. She refused. She thought that would be a lie and couldn't
Faye felt that Michael did not have enough muscle mass to do a conceras he was prepping for his This Is It comeback tour.She said he realized he didn't look good in a video that was filmed to be used on giant screens during the concert series. At his request, she said, she assisted technicians retouching his image on the footage
But Karen Faye said that although she was asked, she did not help retouch the posthumous This Is Itdocumentary. "Everybody was lying after he died, sir, that Michael was well",Faye said to the Jacksons' attorney, Brian Panish. "And everybody knew he wasn't.I felt retouching Michael was just a part of that lie"
AEG cross
Karen said under cross examination by Marvin Putnam that Michael went into a rehab program in England that was recommended by Elizabeth Taylor.
"I said I was afraid Michael could die", Faye said in recalling different stages of the Dangerous tour. "Personally, there were times when he was OK and times when I was worried"
Under cross, Faye said she was released,not fired, from the HIStory Tour after the first leg.
She said Debbie Rowe who was then Michael's wife had a role in her being removed from the tour. Debbie was pregnant and very in love with him. Faye said Rowe was jealous of their closeness and also added that she (Faye) had problems with his tour manager
"[Debbie] told me that she was jealous of me being there as Michael's makeup artist", Faye said, "She thought that Michael liked me better than her"
When Faye went back to work for Michael after the HIStory tour he made Debbie apologize to Faye for having a role in getting her fired
Faye did the makeup when Michael made the announcement that he was going to rehab. She said she put false eyelashes on him for the video
Faye said she did request two prescriptions in her name for This Is It. One being Latisse, which is used to lengthen eyelashes, and the hair-growth drug Propecia so that she could give them to Jackson. She also inquired about Botox as a way to remedy hiss onstage sweat that often caused problems with his hair extensions, but said she ultimately did not get that drug
Faye said she expressed her drug abuse concerns about Jackson's health with his oldest sister, Rebbie Jackson, after she was contacted requesting information about Michael. Faye said she could not recall the time period when the conversation occurred.
She said she also had more abbreviated discussions about the same topic with two other Jackson siblings, LaToya Jackson and Randy Jackson.
Faye said that in later years Michael's family members unsuccessfully tried to get him to return to rehab.
"I never knew them to be successful, sir", Faye told Putnam."I'm sure they were trying to help him in any way they could"
Faye could not remember when she discussed her fear of MJ's drug use with his sister Rebbie.
During cross-examination, Faye clarified and said she had been torn about working on the documentary: "My initial feeling was that I didn't want to lie, and the second, my other thing that was tugging at my heart, was that if this movie was going out, I wanted him to look good"
Faye recounted multiple incidents that she says alarmed her about Jackson's use of painkillers from the time he was burned during the filming of a Pepsi commercial, to the stress of his criminal trial on molestation charges, to the day at rehearsal before he died.Yet under cross-examination, Faye said she never had a single conversation with him about his drug use, and that there was a period of time after Jackson went through rehab in 1993 that he seemed to be fine
Karen Faye said she never saw Michael use drugs and that there was only one instance when he asked her if she had painkillers
"He asked me one time if I had pain killers",Faye said, "I said no, I didn't"
Karen said that during his 2005 trial she would spend a lot of time with him, arriving at 3 a.m. to help him get ready, and felt it was not appropriate to confront him about his misuse of prescription drugs.
"I just avoided that issue like the plague, sir, the molestation and the drug areas", she told Putnam
"I was a place of safety for him, and peace and I didn't want to bring up the allegations in my time with him. I wanted that to be a really safe place", she testified
Faye said she also became concerned during Michael's trial that he was using drugs again, saying she based her assumptions on his appearance and his demeanor. She said she got up early every morning to get Jackson ready for court. She said he was hospitalized for part of the trial because of the back pain that likely dated from the Munich accident. She said she decided again to avoid confronting him about possible drug abuse.
"It was my job & my duty as a friend to make that time calm and peaceful. I didn't want to confront him with anything. No matter what he was doing, I could never blame him for that because of the pain", Faye said
Putnam brought up Faye's Twitter account and blog and asked her if she had posted unfavorable things about AEG, she stood firm. "I've stated the truth as far as my experience", she said
Court Transcript