I think I've hacked it

I was not aware that there a lot of these forums, however, I previously posted some comments on a blog that explained hastily about my progress. Now, what I am about to write here, is a one person experiment, and may or may not work on other people. It should also be noted that, since, it was EXTREMELY expensive to follow this protocol, I just did the whole experiment on a small area, on my temples. I've started this about a month ago, and have been able, to grow hair, in a size about a bit less than 1cm*1cm. Therefore, if you are financially capable of doing this, you might have a very effective treatment. HOWEVER, I DO NOT SUGGEST DOING ANY OF THIS. Unless, experimental and with full knowledge.

So let me explain a little about what I have been able to find:

This, to my knowledge, (I have done extensive reading on the subject), is the first time that this THEORY is mentioned, and it is completely my own. Although, I have proven that this works, it still is a THEORY, so take it with a grain of salt. I am also a life scientist.

This text is also a bit technical, so maybe a few people, could grasp the idea fully. If you don't UNDERSTAND it, though, please don't say that it's bad things, and just stop reading now, and keep a positive attitude. I have no agenda to gain from this, and I'm only doing this to spread words and knowledge, and may someone can try this in larger scale that I did.

This is mostly related to Common Patterned Baldness, however, it can, potentially treat alopecia areata as well.

I appreciate, however, if you add educated knowledge into this post.

Anyways, Here is what I did and why I did it:

I think many of you already know that hair follicles have a paradoxical appearance in development. We are born with a hair (Lanugo) that is fuzzy and then it falls down and a terminal hair is grown replacing it. At this stage most of the body, do not have hair shafts. Even though, they, have fully formed hair follicles, that are dormant. Eventually, with puberty though, hair follicles and some other cells of the body (for example, Epiphyseal plates) are told to act differently, and change their nature. This happens mostly as a response to hormonal changes.

For example, hormonal changes in women, (Estrogen) cause a second growth of mammary glands. You will be amazed to know that mammary glands are basically VERY VERY similar to hair follicles. In fact, the way they grow, is by invagination of epithelial layer of skin into the fat pad of the mammary gland, and in the process signalling creation of adipocytes, just like, hair follicles and sebaceous glands. Estrogen Receptor by the way is quite similar to Androgen Receptor.

Anyways, in males, Inactive follicles (let’s call them dormant), are activated by a signal (testosterone and DHT) to produce hair shaft and grow (just like mammary glands). It’s very important to know that during development hair follicles are originated from different populations. For example, dermal part of the hair follicles on the head come from a different part in development than in the body. Their nature is so different they can be quite different physiologically than follicles from the body. This is the main reason Body hair transplantation will not work, and never will. Because these follicles are developmentally different.

It’s very important to know that during development hair follicles are originated from different populations. For example, dermal part of the hair follicles on the head come from a different part (neural crest cells) in development than those fibroblast in the body. Their nature is so different they can be quite different physiologically than follicles from the body. This is the main reason Body Hair Transplantation will not work, and never will. Because these follicles are developmentally different.

Now back to hair loss, some males are susceptible to hair loss, this is highly based the person's genetic background and almost environment plays no rule.

It was found out that people who are castrated early on (before puberty hits) will never go bald. Actually I think Hippocrates found this out. Long Long time ago. Basically, sine these people don’t produce testosterone, they can't have DHT and they don't go bald. This however, is not quite right. As testosterone, in small quantities, can be made elsewhere, maybe in adrenal glans (I think!). So they basically CAN go bald, but, since their population has always been so small and they have low testosterone they won't go bald.

There is one other condition, call androgen insensitivity syndrome. Now, these people also don’t go bald, these people, in contrast to castrated people, have usually a mutation (more than 400 known mutations are there) in their Androgen Receptor (AR) gene. Many of these mutations don’t let these Androgen Receptor genes to get into the nucleus and transcribe a set of genes that can cause baldness (or hair pubical or facial hair growth).

So even though they might be prone to baldness, they do not go bald. (imagine introducing a normal AR gene in their nucleus, they will go bald if they have the genetics back ground for it, this experiment would be like the original experiment of injecting testosterone in Castrated People).

Now another population was identified that they also did not go bald, and they were people who did not have 5-alpha reductase gene (or some mutations in it that made this gene not active), and so these people also did not go bald. As you know, 5-alpha reductase converts Testosterone (TT) to Dehydrotestestrone (DHT), these people also had a smaller Prostate (like the other two populations), so Pharma got interested and stepped in to make a product. They basically cultured a basic cell type, and added thousands of different chemicals to these cells, to see which one, inhibits DHT production and boo, finasteride was born. It was easy to get finasteride approved because it was already approved for benign prostate hyperplasia, that's one reason finasteride is there and other anti-androgen are not here. IT WAS EASIER TO GET AN APPROVED DRUG APPROVED FOR ANOTER DISORDER!

With Finasteride, however, androgen receptor is still able to bind other hormones and get into the cells (like testosterone). Interestingly, no matter how much people increased the dose of Finasteride, it never reversed hair loss in significant proportions, in already miniaturized hair follicles.

Even castration of people did not help hair follicles to come back to life. This was very disappointing for big pharma, they jumped around like idiots, and they did not know what to do. SO THEY GAVE UP, and that's why mostly smaller START-UPs are trying to get into the game.

Before propecia, another drug, minoxidil also was approved that no one had any idea how it increased hair numbers and how it made some hairs to go terminal. Some said K changes, some said, more blood, some said nutrition. However, I will get back to Minoxidil.

Anyways, researchers, still did not know what to do, and so they started to look deeper.

They started to look into stem cells, of the hair follicles. Now, these stem cells are adult stem cells, a set of cells that don’t divide often and when they do, they create one cell (progenitor cell) that can divide so fast producing a set of other cells ( Transit amplifying cells) that can differentiate to cells of the hair follicle (for example dermal papillae or matrix cells [which is epithelial]).

Scientists found out that, hey, hair follicles are alive in the bald scalp and they have the stem cells but they are just not activated, and they lack the signal to call them to get activated. This was interesting, and it made the birth for many companies.

There were a set of signals known to activate adult stem cells, of these, WNT signals were the best known. However, the way these signals work needs a decade more research, there dozens of WNT molecules, and each of them gets modified in dozens of ways and each cells have dozens of receptors for these WNT molecules and each of those receptors bind dozens of other receptors (co-receptors) that each can have dozens of different responses, and each of these responses can act synergistically, or separately.

So we are far from understanding these signalling pathways, and secretion molecules.

There are now, a set of different signalling pathways, like BMP, SHH, FGF, an so on. Anyways, however, some companies tried to mimic these pathways but it will never work out for the simple fact that that it is complex, an no constitutive activation of one signalling pathway (as it is a secondary response) will cause complete activation.

Imagine, you want to tell an asian to go buy you a certain flower and come back home with that flower and put it in the right jar next to a window. Now, you know certain words, when you through those words out, you will have some effect on this Chinese girl (who don’t understand english) but you will never be able to exactly tell this girl by saying some words randomly, or even mimicking some words you've head else wear (like walk) in for example by watching TV shows (other adult stem cells, the technology of Samumed or Histogen) to go and do this complex process, this is just too complex. So any technology or company pursuing secondary signals is doomed to fail, because it’s impossible as of now to know the signals.

I don’t get much into details, however, take my word for granted when I say cloning hair follicles is also not possible any time soon. We are FAR FAR from that. Any company claiming that it is near is LYING, through away Replicel, aderans, intercytex, and other companies that say they will do that. They won’t. It’s possible but it takes a long time to learn the signals. To learn when to add BMP, when to add WNT, when to add FBS. When to co-culture with Keratinocytes, when not to. So it needs tons of research, and no single company is capable of doing this.

Anyway, getting back, to research. From time to time, some factors where shown to be involved in hair follicles. Some pathways, some kinases, some proteins, some inhibitors, they made hair follicles grow, they made them shrink.

But these factors were also so confusing, and almost no one knew what was going on. They still don't. It was hard to make sense of these factors. For examples, it was known that TGF-Beta makes hair shrink and go to Catagen, no longer staying long enough in anagen to produce hair shafts.

IL-6 ( a cytokine increased in hairless scalp, like PGD2) is shown to cause hair follicle to shrink.

WNTs caused hair follicles to grow, they activated beta-catenin but how was it making its effect. Why minoxidil had some effect? Why Arthritis drugs were effective? What was the role of immune system? What were cytokines doing in the hair follicle, and how did they affected hair follicles.

So about 5 months ago, I started to read almost every paper and PUBLICATION I could get my hands on. I read about hair follicles, adult stem cells, hair cloning, hair immune system, … and here is how I found all the connections and patterns, and led it me to develop a theory that could potentially grow hair.

Once again, publishing this here, does not mean, it’s not true [It also does not mean it's true], so once again take it with a grain of salt. I am pro open science, so that’s why I am writing it here. Also don’t think just because you’r reading it here, it’s not original. It’s actually original, and if you look into literature and internet you will not see one person or scientist mentioning this finding that I am about to say.

Any ways, back to the story, I sat down and tried to think how all these connect, and here is what I found. Some scientists that you hear their names here all the time, have told me that this is highly probable and I might be right. None, I guess, however, has yet found time to test this, as they have to go through papers and grants and stuff to do experiments, and some experiments they can never do. While I was able to do a thoughtful small experiment, That's why I think, we need to do what has happened in Computer Science and bring it to biology, self-driven motivation to make science progress.
However, ONCE AGAIN, please if you don't know what you are reading, NEVER try this, also this is quite EXPENSIVE and, so you needs lots of money to follow it.

Anyways, It all came to me, when I read about castration-resistant prostate cancer. Thanks to researchers studying Prostate Cancer (PC), the complex biology of Androgen Receptor has been under heavy investigation. This has led to fascinating discoveries regarding AR activation, localization and dynamics. Not only involved in hair loss, AR is also the major deriving force behind malignancy of Prostate Cancer (PC) cells. Among current therapies for PC is the complete inhibition of testosterone production to stop androgen-dependent growth of PC cells. However, in some of the cases, a recurrence of PC will happen by appearance of a set of androgen-independent malignant cells (CRPC). However, these CRPC cells are still AR dependent. This led researchers to further study mechanisms by which AR activation can happen regardless of androgens. Interestingly, it seems some post-translational modification (phosphorylation) of AR is both necessary and sufficient for activation and nuclear localization of AR in an androgen-independent manner. Notably, the role of cytokine receptors (such as IL-6 receptor) is gaining more ground amongst researchers.

Also I told you earlier about the involvement of Androgen Receptor in male pattern baldness or CMB. Androgen Receptor (AR) is conclusively involved in Common Male Baldness (CMB). Upon binding to androgens, notably dehydrotestestrone (DHT), AR translocates into nucleus to transcribe a set of AR-responsive genes. Finasteride, an FDA approved drug for CMB, inhibits production of DHT by blocking the action of 5 alpha-reductase. However, Finasteride is not capable of inducing hair regrowth in the majority of already miniaturized hair follicles (HFs). Given that an increase in AR levels alone is not the causative agent deriving HF miniaturization, it’s quite probable that AR nuclear localization and/or cytoplasmic retention and not its increased levels is the cause of CMB. AR is a very complex transcription factor that undergoes multitude of post-translational modifications which dictate its function and dynamics. Interestingly, androgen receptor nuclear localization can occur in an androgen independent manner. In fact, androgen-independent AR nuclear transport and activation is a common phenotype of castration-resistance prostate cancer (CRPC) cells. Here, I propose a unifying theory for the onset and progression of CMB and will tell you how I hacked a small section of my hair loss.

Recent findings regarding the involvement of cytokines in the progression of CMB, the inability of potent anti-androgens to reverse HF miniaturization, involvement of AR in the malignancy of castration-resistance prostate cancer (CRPC) cells, and paradoxical AR levels observations in facial and scalp hair follicles, led me to develop this unifying theory of CMB. To better understand my theory, I’ll start by explaining these seemingly unrelated factors in the context of AR nuclear localization and will tell you about some key experiments that I did to conclusively test the fidelity of my theory.

Now here is the explanation of my theory: CMB usually beings with observable miniaturization in the vertex and frontal regions of the scalp and progresses forward and backward, respectively. The progression continues until the two miniaturized regions meet one another. Histological studies showed that cytokine levels are increased in the bald scalp of males with advanced CMB compared to haired scalp (occipital regions). This is important as cytokines are involved in AR androgen independent nuclear localization. Cytokines surpassing a threshold level, therefore, can switch miniaturization of HFs from AR-dependent androgen-dependent (ARDAD) to AR-dependent androgen-independent (ARDAI). This, however, has not escaped my mind that ARDAD and ARDAI nuclear localization can synergistically control AR dynamics. This can explain why early administration of Finasteride is extremely more effective. Since, it theoretically can stops ARDAD switch to ARDAI as the dominant AR nuclear localization signal in miniaturized HFs. Once switched, ARDAI HF miniaturization creates an indefinite loop of positive feedback further strengthening its androgen independent nuclear localization. This potential explains pattern formation and progression through involvement of immune cells (cytokine production).

Recently, pharmacologic inhibition of JAK-STAT signalling pathway by Tofacitinib, has been shown to be involved in early activation HF anagen cycle in mice. Interestingly, in mice AR localizes to nucleus during telogen and catagen but not anagen (in hair bulbs). The binding of Interleukin 6 family of cytokines to its receptor cause STAT3 phosphorylation. Notably, STAT3 phosphorylation is involved in ARDAI nuclear localization in CRPC cells through unknown mechanism(s). This further supports that ARDAI nuclear localization might be involved in miniaturization of HFs. Other papers have shown that Beta-catenin and androgen receptor also co-localize in cytoplasm, recent findings of Dr. Watt regarding beta-catenin and androgen receptor nuclear transport in anagen and other HF cycles, basically, proves why Samumed or Histogen are seeing some basic regrowth but not much. Their technology might work, but basically they to keep Beta-catenin constantly in the cell nucleus, and it's almost not possible if AR is constantly active, so they WON'T work. When you activate WNT pathway, what you do is you activate beta-catenin, and this causes beta-catenin to get into nucleus, and in unknown process you keep Androgen Receptor out nucleus, proving that their effect might work from Androgen Receptor axis of signalling.

Basically Setipiprant will not work (or at least I HIGHLY believe so), as there are lots of cytokines that are increased in the hair follicles microenvironment. Like IL-6, TGF-Beta, PGD2, … and so on. An just stopping one, is not going to have an effect. It’s like a domino, you can’t stop the domino, while it’s in the middle you have to stop it from the start. Even if you stop the receptor for PGD2, what you do is that you cause a build up of PGD2 and subsequently 15d-PGJ2, but the problem is 15d-PGJ2 acts intracellularly, and no receptor has yet been found for 15d-PGJ2. But when you read the paper on PGD2, you see that 15d-PGJ2 is way more detrimental to hair follicles than PGD2, and in a course of 3 days completely blocked the growth rather than 7 days for PGD2. So I’m saying the most effective way is to target L-PGD2 synthase (if at all), as well as PGD2 receptor with Seti. Now since the experiments was done ex vivo, they literally did not include 15d-PGJ2 in their experiments to see if it’s effect can be blocked through GPR-44. So it’s a black hole, one should genetically lower levels of PGD2 synthase, add PGE2 periodically and block GPR-44 to see an effective increase in hair growth. However, again, it's acting as a secondary signal, and it will not work, prostaglandin theory is looking at a small picture and forgetting the large picture.

Now knowing this I set out to see if individually I can test, whether my theory is true, or not. And It seems after thousands of years, I can say, we have a treatment effective enough that can reverse hair follicle miniaturization with one single simple intervention with no side effects, Yes, I know it seems like a fairy tale, but it’s true ( at least so far). Now, Why I am publishing this here, and I'm not trying to monetize it. It's because, I believe in open science. Something like a Github of biology. Like an open source code for biology. It's hard knowing that FDA, even though, extremely useful, sometimes is on the way. Also another reason, that, I do not want to monetize this, is because this treatment will never be useful for the majority of people. It will be ridiculously expensive, at least until the next ten years or so. So no seed funding venture or angel investor is (or will) likely be interested.

again, I know this may be a bit hard for lay people to understand, but please read more about it. Okay, so about a month ago, I sat down thinking how can I prove my theory. I had access to most of the inhibitors that I wanted, also I should have paid for it, it was an instant access. (I am lucky). Basically, Androgen receptor inhibitors are three types:

#1 Recently developed pure AR antagonists (non-steroidal), (these include MDV3100, ODM-201, ARN-509 and other safe AR antagonists).

#2 Non-pure non-steroidal AR antagonists such as (such as RH58841 [We know about this], Flutamide, Bicalutamide and many others)

#3 5-alpha reductase inhibitors (finasteride, dutasteride) can cause regrowth. [these are actually not AR antagonists but I brought them here so you know them]

Based on my theory so far, any of Pure AR non-steroidal antagonists, (these include MDV3100, ODM-201, ARN-509 and other safe AR antagonists) should be able to reverse HF miniaturization (to some extent). ODM-201 should probably be the most effective one, as it doesn't cross blood brain barrier (you won't get brain fog, like finasteride or MDV3100), and also it works on all different types of signalling pathways working on AR, and also has a short half life. And also just because pure antagonists are cancer drugs, it doesn’t mean they are more dangerous than other anti-androgens, You have to look at IC50, and other things, site of actions. Any ways, I say they are not dangerous, but still, I did not have the balls, nor the lack of ethics to try it. It's also very new, so expensive.

However, the effectiveness of Androgen Antagonists should be as follow: 1) pure 2) non pure and at the last 3) 5 alpha inhibitors. I sat down, and I thought what could be an alternative, and my eureka moment was when I was looking at the my stella beer. Yes! gene therapy seemed like an alternative alternative. I designed an Antisense Oligonucleotide, and blast the sequence to human genome, to make sure it specifically target AR with no off targets. Antisense Oligonucleotide are much cheaper to make than siRNA, so I chose them as my option. Also, once inside the cell, they can remain active for almost a week, Unlike siRNA's.

There was one big problem though, there was no way to efficiently driver them pass Stratum Corneum. I tried a novel formulae, a cream with the following compositions: glyceryl monostearate (10%), hydroxypropyl methylcellulose (0.5%), isopropyl myristate (10%), methylparaben (0.5%), propylparaben (0.5%), polyoxyl-40-stearate (15%), and water. I stole the formulae from a publication, however, it seemed that this formulae could only deliver Antisense Oligonucleotides, (ASO) into parts with HFs. So It did not seem to be effective at silencing AR gene. I have to say though, to design the AR-ASO, I used a special section of the gene, that seems active in all different splice variants of AR. There are dozens of Splice variants by the way.

Anyways, I saw almost zero effect, now, ASO technology is extremely expensive. Kynamro patients pay like 250,000 for just one year of treatment, so I was not able to waste a lot of money, so I was only testing this, in 1cm*1cm of my skin, it did not work. I however, believe in the technology, and thought of something else, I injected about 100µl of this ASO ****tail Intradermally, much like a TB test. I say a ****tail of ASO, as I had an ASO targeted to Exon-1 and another ASO targeting Intron-1 on AR. Remember, that I was doing this in a very small area, and chances of it getting systemic was absolute zero, so I was taking all the precautions. Also ASO's in small amount are quick to degrade in circulation, and even if they did go to, the quantity was so small that it was like zero effect (much safer than Finasteride). However, since derm has no blood connection, they accumulate in derma layer, so they will enter the cells. Also, I used a chemical modification that gives them negative charge, so they enter the cells regardless of lipolex (it is a common knowledge), any ways, I injected a bout 1mg/100µl of AR-ASO ****tail, every three days, for one month, in an area (1cm*1cm) that had lost its hair ten years ago. After a month, I saw the hairs coming out. However, I had more than 10 injections with a 31 gauge syringe so the skin needed some time to heal. I was sure that ASO was working, however, it was not proving, whether, this effect could be seen by anti androgens also, so I tried to apply RU58841, in the (1cm*1cm) area, and stopped injection of ASO (which by the way costed me more than 2000$, for a month and only ten injection and for an area of 1cm*1cm). Anyways, applying RU58841, was NOT able to keep the hair, and the hair started to miniaturize.

Now, please don't get excited. This has the potential to reverse hair follicle miniaturization in areas that have lost hair for a long time, but it's ridiculously expensive, and hard to do (lack of a proper vehicle). Therefore, it's as of now, (may be not in ten years), will not come to the market. However, as a scientist, my curiosity led me to do this. Also, since it's an experiment, that is translational and (with a proven target) it was possible to publish this, but, I prefer to not publish such a thing in a low impact journal, but I prefer not to, as I have much more challenging academic ideas to follow, and prefer not to publish such articles. Also, I think, the world is changing and less and less people try to publish things that are not academically as rewarding as such I mentioned. Although, the academically rewarding publications, in the big three, is still highly sought after. For example read this new, [http://www.nature.com/news/the-bigge...proof-1.18509]. Anyways, I hope this not only helps people get a better understanding of AGA, also gives them the hope that it is possible to Reverse hair follicle miniaturization sometime in future.

Mark Watney: Every human being has a basic instinct: to help each other out. ... odds, I'm left with only one option, I'm gonna have to science the shit out of this.

I'll come here from time to time, to answer, well formed thoughtful questions that you might have. Good luck everyone, and enjoy your life.

Dude, I'm just going to straight up say what we're all thinking here; You post saying you've found a cure that will regrow hair in a month with no sides, and yet you have no photographical evidence... I want nothing more than all of this to be true, and for you to be some sort of genius finding a miracle cure in your basement, but to convince people you need more than theoretical science jargan, you need evidence.

Thanks for taking the time to give us all this info though bud, you seem very clued up either way.

Thank you Not Giving Up.
I have photographs, but I do not want to publish them for some reasons. Also, I'm not saying I have the cure, or it's the cure with no side effects. I said no side effects, as I tried this in small amounts, it's quite possible to get sides while increasing the oligo concentration. Another thing, I stopped the experiment in one month, so it could have been a small boost to hair growth, and may be it's not a cure. Also, I'm not trying to convince anyone, those who truly understand what I've done, will know that I have no agenda. I just shared what I had done. And also I'm not a genius.

Thank you for appreciating What I wrote here, it might, someday, come handy, to one person, who knows! take care

wow; I need to read it all again; thank you for sharing.
BTW; you dont think finasteride is safe ?

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Originally Posted by FGF11

and enjoy your life.

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For real?

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Originally Posted by FGF11

Mark Watney: Every human being has a basic instinct: to help each other out. ... odds, I'm left with only one option, I'm gonna have to science the shit out of this.

I'll come here from time to time, to answer, well formed thoughtful questions that you might have. Good luck everyone, and enjoy your life. You should sign up for *******.com

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great stuff!

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Originally Posted by FGF11

I have photographs, but I do not want to publish them for some reasons.

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Get the hell out of here. Just like every other mad scientist scammer. You have something to sell.

Just put in one line what we have to do or take. Give us some f-ing cliffs. If you can't, no one should listen to what you have to say.

Just look at how our current treatments work: take finasteride and apply minoxidil twice a day. Why can't you do that? Because you have an agenda.

Hi, please read Dr Cotsarelis patent(the 2011 one)- it would refute the vast majority of your statements.

Having always been an 'out-of-the-box' thinker myself, i tried to keep an open mind about what you've said. But it's difficult to do so when you gave the remark that the receptor for 15d pgj2 has not been found, for the well-informed 1 would had known this is not true at all.

So it's either:

1)you are well-aware of the fact that 15d pgj2 is the primary endogenous ligand for the PPAR gamma receptor for stimulating adipogenesis(and to a lesser extent- PPAR Alpha and Beta) as well as the CRTh2 receptor(as proven by Dr Cotsarelis's PGD2 study) butchose feign ignorance for whatever 'secret agenda' that you might have or;

2)you are genuinely unaware of the receptors that 15d pgj2 binds to, which would have stripped all of the rest of what you've claimed to hypothesise of any credibility.

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Originally Posted by fred970

Get the hell out of here. Just like every other mad scientist scammer. You have something to sell.

Just put in one line what we have to do or take. Give us some f-ing cliffs. If you can't, no one should listen to what you have to say.

Just look at how our current treatments work: take finasteride and apply minoxidil twice a day. Why can't you do that? Because you have an agenda.

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It pains me to say it as we've clashed many-a-time in these threads; but I agree with you, Fred. If he had something real I guess he could just explain it in its simplest form and be done with it.

No photos, a lot of fancy theoretical scientific terminology that impresses without actually giving much away, I don't think he's a scammer, but something is always off when these posts are presented like this.

Please ban this obvious troll.

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Originally Posted by TJT

Please ban this obvious troll.

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For a troll, he put a lot of energy into this. No, he wants to gain something from this at a point. So he's more a scammer than a troll.

Hi fred970, I wrote what needs to be done, an exact protocol, and things I've used in my self-experiment. I gave the concentration that I used, the oligo, and how often I did this. There is nothing to gain from this, the only agenda I have, is to take credit for this. Self-experimentation, is illegal in some countries/states, and JUST because of that I won't publish my pictures. It's also not ethical so journals don't publish results with self-experimentation.

I've given more than "take finasteride, and apply minoxidil twice a week". I've given a complete protocol for it. It's there. It's just that you need to understand it.

There was no way to do it in a simpler way. If it was, I would have done it. I've actually tried to be as simple as possible. you probably haven't/can't completely read what I've written there. Otherwise you wouldn't have said such a thing. And yes, I've hacked it believed it or not and I'm very proud of myself what I've done.

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Originally Posted by FGF11

I've actually tried to be as simple as possible.

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http://gifsec.com/wp-content/uploads...gif_1.gif?gs=a

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Originally Posted by fred970

For a troll, he put a lot of energy into this. No, he wants to gain something from this at a point. So he's more a scammer than a troll.

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You, fred970, are far too harsh and far too fastidious! I guess the balding process turned you into a very cynical person, or is that just an excuse? i.e. is this just your real personality coming out?

Have you ever heard of the saying: "If you can't say something nice, don't say nothing at all?"

https://www.youtube.com/watch?v=I71cY9Ysy5U

I guess not.

Regardless of whether or not the original poster has ulterior motives, I am absolutely shocked by the way you attack him, and there really is no need for it. I have seen you do this on other threads and hair loss forums too.

Good day to you! (or should that be Bad day to you?)

Hi not giving up, I won't reply to posts [such as this].

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Originally Posted by FGF11

There was no way to do it in a simpler way. If it was, I would have done it. I've actually tried to be as simple as possible. you probably haven't/can't completely read what I've written there. Otherwise you wouldn't have said such a thing. And yes, I've hacked it believed it or not and I'm very proud of myself what I've done.

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lol, please sum this up. I read a lot of stupid stuff about hair loss nowadays. If you can not make it simpler, then you probably did not understand the miracle cure yourself.

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Originally Posted by epipapilla

You, fred970, are far too harsh and far too fastidious! I guess the balding process turned you into a very cynical person, or is that just an excuse? i.e. is this just your real personality coming out?

Have you ever heard of the saying: "If you can't say something nice, don't say nothing at all?"

https://www.youtube.com/watch?v=I71cY9Ysy5U

I guess not.

Regardless of whether or not the original poster has ulterior motives, I am absolutely shocked by the way you attack him, and there really is no need for it. I have seen you do this on other threads and hair loss forums too.

Good day to you! (or should that be Bad day to you?)

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Look at my join date, and then look at yours, I've been in this far longer than you've been.

Every other month, some mad scientist comes up with these miracle cures he found in his basement.

Hi Fred970 I was thinking whether I should do this or not, many times when I did a google search, some of these forums showed up. So I just created an account to share what I did. Now, I did what I needed to do, share my knowledge and findings. Hope it shows up in some google search of someone. Please remember this, I said many times that this is not a complete treatment (or cure). It needs injections [you can't do that to your whole temples, all the time], It is ridiculously expensive, and it might have side effects when done in bigger scale. Also, if you call being employed in one of the most scientifically advanced places in the world, basement. I have nothing further to add. This is the last post I have in this forum or any other forum on the web, the only other place I mentioned this was a blog. Sincerely.

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Originally Posted by FGF11

Hi Fred970 I was thinking whether I should do this or not, many times when I did a google search, some of these forums showed up. So I just created an account to share what I did. Now, I did what I needed to do, share my knowledge and findings. Hope it shows up in some google search of someone. Please remember this, I said many times that this is not a complete treatment (or cure). It needs injections [you can't do that to your whole temples, all the time], It is ridiculously expensive, and it might have side effects when done in bigger scale. Also, if you call being employed in one of the most scientifically advanced places in the world, basement. I have nothing further to add. This is the last post I have in this forum or any other forum on the web, the only other place I mentioned this was a blog. Sincerely.

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On the one hand, I want to thank you for your contribution, but on the other hand, I don't believe you without pics and more proofs... sorry dude ;)

i strongly believe that it is possible for a clever scientist with biological talent and understanding to figure out some approaches which were not yet considered by bigger or famous companies or researchers.
all the things this guy wrote down made sense and sounded really interesting, but now that he was scared away, we will never know.
if he tried to sell something or scam us, nobody will ever know.
it was very shortsighted of some members here to critize the guy in that aggressive way. if he were to scam us, we would have found it out soon.
just because he refuses to post pictures at the first moment doesn't mean anything.

so that's it. chance passed by, and we'll continue with histogen, replicel, pilofocus, and the usual waiting games.

even if one day really a smart guy pops up with real and good research which could shed some new light on the MPB mechanism, he will no chance to be heard.
people who are not familiar with forums and just try to help by writing some interesting ideas into a forum, will leave very quickly if they only get attacked by all members.

like i said, if it was a troll or scammer who tries to sell something, we would have found out very soon. but until then, there's no need to attack just everyone who comes up with a new idea.

Dude, why don't you just post your protocol (even though you claim to not want people to try it...)?

Also, as detailed as your posts are, no one is going to take it seriously without photos.

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Originally Posted by joachim

i strongly believe that it is possible for a clever scientist with biological talent and understanding to figure out some approaches which were not yet considered by bigger or famous companies or researchers.
all the things this guy wrote down made sense and sounded really interesting, but now that he was scared away, we will never know.
if he tried to sell something or scam us, nobody will ever know.
it was very shortsighted of some members here to critize the guy in that aggressive way. if he were to scam us, we would have found it out soon.
just because he refuses to post pictures at the first moment doesn't mean anything.

so that's it. chance passed by, and we'll continue with histogen, replicel, pilofocus, and the usual waiting games.

even if one day really a smart guy pops up with real and good research which could shed some new light on the MPB mechanism, he will no chance to be heard.
people who are not familiar with forums and just try to help by writing some interesting ideas into a forum, will leave very quickly if they only get attacked by all members.

like i said, if it was a troll or scammer who tries to sell something, we would have found out very soon. but until then, there's no need to attack just everyone who comes up with a new idea.

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Do not worry yourself too much. If you were a scientist and you found a cure or effective treatment to MPB, would you make a few posts on a message board and leave it at that? Anyone familiar with hair loss forums would know that such claims would be met with skepticism - and rightly so.

I do not know if this guy is a fake or not. He posted the exact same thing on a popular hair loss blog a day or two ago. He claims that his protocol utilizes some chemical that only a few people have access to, so we wouldn't be able to experiment with it even if he is telling the truth.

Quote:

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Originally Posted by fred970

Look at my join date, and then look at yours, I've been in this far longer than you've been.

Every other month, some mad scientist comes up with these miracle cures he found in his basement.

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Because you joined this forum before me or others does not make your posts or points of view any more valid!

Because you have more posts than me or others does also not make your posts any more valid!

Criticism is fine, but you are too far over the top. I can almost feel your misery, cynicism and bitterness through your words of constant pessimism. You certainly are not doing yourself any favours with this mindset.

Honestly - this is fascinating - kind of brilliant - and it makes sense.

Ultimately, the critical component driving hair loss is the androgen receptor. And he nicely highlights that the androgen receptor is activated (to subsequently undergo nuclear translocation and impact gene expression) through androgen-dependent and androgen-independent pathways. This accounts for why DHT is NOT the whole story, but the disease still CENTERS on the androgen receptor.

His story accounts for what is observed from a genetic perspective. The critical genetic variant on the androgen receptor that leaves us vulnerable to male pattern baldness is carried by 85% of the population (at least among Western Europeans). If you don't have a copy of this variant, then you won't go bald. And this accounts for how a male who becomes NW7 at 21 years of age can have a kid that never loses a hair during his whole life (? John Mayer and Orlando Bloom). He inherited a golden X chromosome from his mother that doesn't carry the AR MPB genetic variant - so no matter what genes he inherits from his father and the remaining genes he inherits from his mother, he'll never go bald - he is protected for life. This also accounts for how a father who never lost a hair his whole life can give birth to a son who goes NW7 at 19. The father may have carried a ton of balding genes - but they effectively could never become "active" because he carried the golden X-chromosome - but then his son inherits a regular X-chromosome from his mother and then his balding genes become relevant and destroys the son's life... :) This is how balding can skip a generation.

It's only 15% of the population that get this lucky - so for the other 85%, your propensity to develop MPB is influenced by genes from both your mother and your father. Most of us (well, all of us on this website), carry the genetic variant on the AR that makes us vulnerable to MPB - so we will go bald with time - but the rate and the extent is dependent upon the other MPB disease modifying genes (and there are probably many, many genes involved) that you inherit from both of your parents. And this is consistent with what we observe - most people end up being a blend of your maternal and paternal genes. Periodically some people get screwed and inherit all of the MPB disease modifying genes carried by both parents and end up going bald much earlier - and others get lucky and avoid the majority of the MPB disease modifying genes and go bald much later.

The game changer is the genetic variant on the androgen receptor that can make you immune.

I think he's right - if new drugs are not directly targeting the androgen receptor - they will never be a definitive fix. Anti-DHT drugs will help - but they don't deal with the cytokines. And anti-cytokine drugs don't deal with DHT. And the problem with anti-cytokine drugs is that there are so many different cytokines that can activate the androgen receptor. So it's not like you can take 1 anti-cytokine drug and a DHT drug and be protected (though that may help a lot). You'll need to take 20 or more anti-cytokine drugs to be protected from all of the different cytokines (depending upon which pathways are operative in you).

And his comment about anti-DHT drugs being of minimal help when MPB is more advanced also makes sense. The scalp is full of cytokines that are up-regulating themselves through positive feedback loops - so even if you get rid of DHT, the cytokines will continue to cause AR activation and you'll continue to lose your hair. So none of the drugs/products under current development are going to be a permanent fix. Though they will likely be synergistic - if you take multiple drugs that target multiple pathways that converge on the androgen receptor, then you'll get better results.

Assuming he's telling the truth, it is reassuring that inactivating the androgen receptor resulted in re-growth. I've always worried that, although the stem cells are still there, that fibrosis which developed may prevent complete re-growth. But maybe not - and that goes along with what has been observed with alopecia areata.

We need a drug that directly targets the androgen receptor. Not an anti-androgen that prevents androgen binding to the androgen receptor - that's not enough because cytokines will still be able to activate the androgen receptor. We need a drug that prevents the androgen receptor from being able to translocate into the nucleus. His anti-sense oligonucleotide would do that (it would prevent the androgen receptor from being translated and hence none would be expressed in the scalp).

Imagine combining the Follicept delivery vehicle (not IGF-1, which was useless - not surprisingly...) with a compound that prevented AR expression in the scalp.

You probably don't need complete AR suppression in the scalp, though. The 15% of people that don't carry the AR genetic variant associated with baldness still have functional androgen receptors (unlike people with androgen insensitivity syndrome). There's something about that variant (and who knows if it's that variant - it could be linked to another genetic variant) that allows androgen receptors to work properly in other aspects of development (allowing you to become a male), but fails to activate the balding process. But we probably don't need to be that specific - people with androgen insensitivity syndrome have normal hair, so we could just shut down androgen receptors in the scalp. We are all afraid of side-effects - and there's no way you'd be able to take a drug that shut down androgen receptors systemically. But a topical that localized to the scalp could work.

It's really interesting - it sounds like they are looking into androgen receptor drugs in prostate cancer. It's conceivable that - like finasteride - the holy grail for hair loss could evolve from a prostate cancer drug.

Anyway - I don't know if this guy is telling the truth - re: hair regrowth - but everything he says makes sense. I'm a physician and a scientist and I think he's made some really interesting inferences.

NEWSFLASH: He has nothing to sell.

These drugs are already locked down and patented by pharma companies. There is no money for him to make if he didn't share this protocol. He could never monetize it himself.

You can ask for pictures and more information about his protocol, but you can't demand photos or be overly suspicious of him. There is nothing for him to sell, and thus no real reason he MUST post pictures. That doesn't mean we can't ask nicely, but we should not be treating him like he's histogen who is trying to sell us something.

Hopefully he comes back because his insights were interesting, to say the least

Some people on these message boards are unbelievably autistic

J Allergy Clin Immunol. 2015 Nov 19. pii: S0091-6749(15)01582-1. doi: 10.1016/j.jaci.2015.11.001. [Epub ahead of print]
Extensive alopecia areata is reversed by IL-12/IL-23p40 cytokine antagonism.
Guttman-Yassky E1, Ungar B2, Noda S3, Suprun M4, Shroff A5, Dutt R5, Khattri S5, Min M5, Mansouri Y5, Zheng X3, Estrada YD5, Singer GK5, Suarez-Farinas M6, Krueger JG3, Lebwohl MG5.
Author information
PMID: 26607705 [PubMed - as supplied by publisher]
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