Riporto tale e quale questa teoria da poco pubblicata su tressless sul presunto fattore causale misterioso della patogenesi della calvizie, che sarebbe la riduzione dell'attività di un enzima, il 3 alfa-idrossisteroide reduttasi, il che spiegherebbe il "paradosso del DHT" e legittimerebbe tra le altre cose l'efficacia delle procianidine della mela:
Hi, guys, recently people have asked me to make a post on this theory I have been developing, so here it goes:
Two main paradoxes led me to persuit another explanation for hair loss that is not often talked. DHT concentration and minoxidil efficacy.
First, the efficacy of finasteride is very similar, from 0.25mg to 5 mg, although the total serum and scalp DHT reduction is higher as we increase the dosage, hair regrow does not follow this premise. So people may have great results with 0.25mg daily and increasing the dose will not result in increased regrow.
This caught my eye, because there is not on single explanation of why this happens. Why reducing 70% of DHT will not be more twice more powerfull than a 35% reduction? Why dutasteride reduces almost 90% of DHT and a NW6 will at most return only to a NW5?
Several explanations have occurred with some authors actually attributing this to the death of the hair follicle. We now know that this isn’t true, and the hair follicle is maintained alive, just in a permanent dormant stage, so why doesn’t it start producing hair after DHT is gone? Why castrated men don’t regrow a head full of hair? Why transgender people don’t regrow hair? These questions have remained without a consensual answer for over than 30 years.
Current research is all about DHT, Androgen Receptors, PGE, PDE2, WNT pathways, and the last 10 years our biggest hope is hair cloning and stem cell.
Hair cloning, PRP, stem cell will never work for a simple factor. We are not addressing the cause of hair loss with any of these techniques. In paper, stem cell is amazing and should regrow hair. Exosomes should regrow hair. Hair cloning should be easy! We can clone other organs, we can even clone teeth, even dolly the sheep has been cloned to a perfectly functional animal. So why won’t any of these things work? Because there is not a single evidence that hair follicles or derma papilla cells from the vertex and crown are different from hair on the back and sides of our head. This is a dangerous assumption, that was taken from the lack of other evidence, and has lead the hair loss research to many dead ends, and so will be hair cloning.
Why would I say this? When all I want is my hair back. All I want is to go to a bar and girls look at me (I’m married, but it feels good). I want to look at a random mirror on the street and not see my horseshoe. I want to take a picture not worried if there is too much light in the room.
So, why would I say that the most hoped for treatment , that is not even for my pocket, will not work? Because research is wrong from the first step, the concept and premises are wrong from the start. People have been trying to clone hair for over 15 years, with zero progress. It has been able to make mice grow human hair, but they failed to understand why that even worked. If we do not correct the real cause of hairloss, we won’t be able to clone functional hair follicles. AND WHEN WE DO, HAIR CLONING WON’T BE NECESSARY because we already will have the technique and solution to simply implement in our own scalp and hair will grow in place!!
Gene editing like crisp won’t work either because there is no such thing as genetically programmed hair follicles that start minutirizing at some point in life, in a known pattern and those genetically programmed genes actually can be somehow reverted by simply adding finasteride, dutasteride or even minoxidil? If they were programmed to shut down, nothing would bring them back. Phenotype and lifestyle don’t mean a thing. Two twins, one on fin and another not taking fin have different outcomes, but the only thing that changes gene expression is gene editing, nothing else would save us if that was the case.
Why has this been “true” for so long? Hair surgeons and big pharma need this to be true, otherwise guess who would lose profit? But I’m not against medical doctors or hair surgeons, actually they also were so blind to assume a premise developed in the 1950s, that since then nobody went behind that assumption and tried a different approach.
Yes, there is a genetic component, but not in the hair follicle. The derma papilla is the same in the back or in the front of the head, it just acts different because different things make it work different.
What I believe is genetic, is what leads to the underlaying cause of hairloss, and this I am not sure what it is exacly, because it also has not been enough studied, and it doesn’t even matter too much for my theory. We can find a solution/cure even without knowing the true cause of the hair falling like rain on temples, vertex and crown in a very distinct and similar patter in all human beings predisposed to it.
We all heard about the scalp tension of the galea aponeurotica, that leads to inflammation and corresponds to the exact pattern, but this theory has lots of flaws. Recently in 2019 a dentist found an unnusual connection between dental malocclusion and baldness, where he found that 100% of people with type 2 were bald, and everyone without this malocclusion had a head full of hair, and he studied 150 x-rays to come to this conclusion and this amazes me that only now someone actually found this. Still it is not understood how and why, but this malocclusion causes the artery that feeds our scalp to be constricted, and there may be some truth in this, and I am currently digging this as well. Maybe aligning the jaw would bring our hair back? I don't know neither does the dentist who discovered this, but he is investigating this, I think.
And both of this could be true, and this is where the genetic factor comes in, skull development and jaw line is actually genetic, also why some muscles may be stretched can be also explained by genetics, and this is all we have, unexplained theories on this, and skull expansion and other things that people came up to explain the unexplainable phenomenon of hair loss in a known pattern. In man and women.
From the previous paragraph, the only scientific truth that has been studied and documented very well, is the fact that the thickness of a balding scalp is significantly different from a non balding scalp, and now we start to get to somewhere, why it is thinner or thicker, I don’t know, but there is a difference and that is what I started perceiving as having something to do with the pattern, in spite of the actuall cause (tension, stretched galea, dental malocclusion with low oxygen and nutrients makes the muscle atrophy and gets inflamed, whatever it is I don’t know and nobody else studied to get to a conclusion) it is a fact and I start from that premise to address to my theory. (Guys, remember how botox injections lead to hair regrow, this theory also explains that)
Before jumping in my hypothesis, one last thing should be emphasized, and that is the fact that BALD SCALPS HAVE THE SAME AMOUNT OF DHT AS NON BALD SCALPS. Also, beard and chest hair only grows because of DHT and NEEDS DHT to grow, and this is the known DHT paradox, as why it makes hair grow in some places and in others (our scalp) makes hair die.
My hypothesis is that DHT is the cause but not the culprit. From now on, everything you will read is a theory that so far I could not disproof, and nobody I discussed it has been able to disproof or refute the facts. I have not invented or discovered any of this. I do not hold any credit or want any credit for this. Everything is documented in studies and papers that are found on the internet and I am writing this because some people talked to me and recommended me presenting this to everyone so that we as a community can discuss it, and everyone be informed of this theory and start contributing in this thread, and I hope we, as a community, can grow this theory and ultimately grow our hair.
I do not have a cure, or even a solution, all I have is a theory based on information I have compiled over the last 6 months of research.
Please, I am not a biologist, medical doctor, medical researcher and have absolutely no chemistry or biochemistry education. I am a civil engineer and a quantum physics freak, with OCD, wich makes me very good at my work and also makes me research all I can and makes me count every single hair that falls on the shower. So people with much more knowledge than me, please help us develop or refute this theory, and whatever the outcome might be, we will be closer to finding a solution and cure for us. And if by any means this post ring some bells and actually smart people, big pharma or anyone with a home lab finds a solution or a way to cure us, this should never be monetized and no profit should ever be taken from a research done on a community like this or someone with obsessive compulsive disorder that spent 6 month reading things about something he barely understands.
So, in a recent post here at tressless (/r/tressless/comments/mw6vt0/sulpharaphane_enhances_a_natural_process_of_skin/), OP (u/VelociraptorRedditor) wrote about an article about sulphoraphane. Lately I have been researching about Procyanidin B2 for hair grow and also sulphoraphane, and these two have one thing in common, that can potentially cure us. Actually, both had impressive hair regrow in their studies, although their research is rather slow and for some reason it is still not on the market in an easy and available sotution that replicates the doses used in their studies. Also studies on this have failed to correlate the most important thing of their findings. I was only able to do this correlation while reading about their effects when used by bodybuilders (shame on you hair loss researchers!!).
So I will just copy paste my comments from that post because I don’t have enough time to rewrite everything and I believe it is a good start for this community to start a debate and discuss, develop or even refute my findings, and in commets I can always provide links, citations, studies and everything we need to grow this, so I commented:´
I believe this is the missing link that nobody talks about. Whenever it is discussed somewhere, it becomes obscured by diverting topics, but to me the cure/treatment is 3alpha-hydroxysteroid reductase.
It explains everything, since the why finasteride works, to why minoxidil works, why LLLT works (not much but there is good data behind it), why micronnedling works, even why scalp massage could even work (these last one I do not believe help much but I have not tried them)
So I stumbled upon 3alpha-hydroxysteroid when researching about procyanidin B2, wich I believe is the most powerfull treatment to AGA, but for some obscure reason has not been enough researched or studied (it is natural and not patentable), even though an oral study demonstrated 125% REGROW in AGA patients (the study had 250 people, and there were zero side effects, and Procyanidin B2 is a natural flavonoid that is very good for the heart and arteries as well as liver, lungs and kidneys, skin and hair). They too missed the link between Procyanidin B2 and 3alpha-hydroxysteroid reductase in the study.
Here is the study if anyone wants to dig a bit (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5775114/).
3alpha-hydroxysteroid reductase is the natural DHT killer that exists naturally and abundantly in our bodies, specially in the muscles, where it degrades DHT. It does this everyday, every hour, every minute, every second, and the muscles use the degraded components to stay healthy. Guess who does this as well? Yep, you're right, derma papila cells. Guess what happens when the enzyme is not present? Yep, DHT binds to where it can, and there goes the hair. the reason it decreases or completely vanishes from the scalp is probably due to the stretching of the galiea muscle, where it occurs abundantly. Maybe some other reason leads to the decrease of 3ahr, and some drugs that are known for eliminating 3ahr have as side effect, what? yep, hair loss.
The most important from what I said before is that people are looking at DHT levels, but they are the same as non balding scalps, the thing we should be looking is the enzyme that is supposed to fuck DHT before it harms our hair follicles, this is the missing key, and guess what also elevates 3ahr? Minoxidil, and what minoxidil also needs to be converted to usable form, sulforaphane, and we'll get that in a moment.
We use finasteride wich blocks the enzyme necessary to convert T to DHT, but the thing is, our body does that every second naturally (gets rid of DHT), where it converts it to androstanediol, a weaker androgen derivate that is good for muscle growth and it's used by cells for other good things like promoting tissue regeneration, hair growth and other cool shit.
The thing I can't find is if we could find a way to use topically. It is known that sulpharaphane boosts 3alpha-hydroxysteroid reductase, and there has been a good study on this for AGA with very good results, but then again people don't even mention it. It is found in brocoli sprouts in great abundance. Also procyanidin also increases greatly not only the 3ahr, but also pathways used for signaling hair growth.
So my thoughts is that combined topical melatonin, with oral procyanidin B2 and a way to reestablish the 3alpha-hydroxysteroid reductase on the scalp in a vigourous way (sulpharaphane), would be a cure. Most importantly, this is an extremelly resilient enzyme, so if we had a way to put it where it is needed, we are talking about a cure. AGA develops so slowly, and is more agressive on some, also minoxidil only works to an extent and for a few years, as long as we still have 3alpha-hydroxysteroid reductase. Over the last years several people tried to bring this to the light, but posts are to techincal for anyone to understand and actually it loses interest by most or the topic is diverted. I will keep everything simple and not talk about pathways and complex molecules and shit.
Minoxidil, procyanidin B2, sulphoraphane, and many other things boosts the DHT killer. And I wouldn't call it killer, it converts DHT to smaller components, the good ones. The ones the that make hair grow. Androstenol is a by-product of DHT, converted by the enzyme, and is still an androgen but weaker, and it has the same binding afinity to the androgen receptor. Because we have less enzyme on the scalp to convert DHT to Androstenol, and because it has the same binding afinity, DHT binds to the Androgen receptor instead of the Androstenol, wich is what we need to happen for hair grow.
The problem is that DHT binding to the AR of derma papila blocks the pathways that make hair grow, instead it signals de cell to die (senescence) because in our bodies, when there is inflamation 3alpha-hydroxysteroid reductase is naturally decreased in order to increase binding of DHT wich in turn makes the cell die and a new one come in place. This is important for muscle growth in deed, as muscle fibers need to be replaced for grow.
When DHT is converted to Androstenol, it sucessfully binds to the derma papila, and it is a completely different story, it signals and promotes hair growth by activating the correct pathways. 3alpha-hydroxysteroid reductase exists naturally in our body, and in great abundance in muscles and some organs like prostate.
For some reason, our balding scalps and the muscle that supports the scalp loses is depleted of 3alpha-hydroxysteroid reductase, and I-m not sure why, and don-t actually know why, but I believe it has to do with stretching of the galea and inflamation, that naturally reduces the 3alpha-hydroxysteroid reductase to increase DHT binding and combat the inflamation. Remember I said earlier that the thickness of the scalp is much different on balding scalps than in normal scalps? Also on back and sides, thicness is different, and this is what I believe leads to our hair loss, a reduction of 3alpha-hydroxysteroid reductase first due to inflamation (it lowers to produce less androstenol and allow DHT to take care of inflammation - greta for bodybuilders and the famous plateau effect), and the thinner muscle also has much less 3alpha-hydroxysteroid reductase, but still has some, and still produces some androstenol, but just not enough to outpace the DHT (this DHT amount is the same or even lower than when we were teenagers, the only thing that changed is the amount of androstenol.
Finatseride and dutasteride work by reducing the available DHT that can actually bind to the hair follicles, so less DHT allows some Androstenol to correctly bind, but as hair loss progresses in a known pattern, also Androstenol follows thepattern, because the underlaying muscle just stops producing 3alpha-hydroxysteroid reductase, and that is why finasteride regrows hair close to the existing hairline, and not randomly on the head, A NW6 regrows hair next to the existing hairline, and not on the original teenager hairline or even in front of temples.
Anyways, minoxidil increases 3alpha-hydroxysteroid reductase, also something that greatly increases 3alpha-hydroxysteroid reductase is sulpharaphane .
So, we can regrow hair by reducing DHT with finasteride, dutasteride, etc. but only in places where there is still 3alpha-hydroxysteroid reductase, and that is why we regrow just a small percentage and for some people doesn-t even work because they have very very low 3ahr.
Minoxidil increases 3alpha-hydroxysteroid reductase, and it actually also uses sulpharaphane to be converted to his usable form.
Microneedling leads to growth factors creating new follicles, but then again, witouth 3alpha-hydroxysteroid reductase it doesn-t get very far because all there is to bind is DHT, unless using minoxidil that boosts 3alpha-hydroxysteroid reductase, and then we will have Androstenol to bind to the AR and the miracle of hair grow happens.
Another thing that also helps a lot is ant oxidants, and there is something called procyanidin B2 wich is very good at promoting hair grow, due to the fact that it gets rid of free radicals, and induces a boost in 3alpha-hydroxysteroid reductase.
I could spend a lot of time explaining other things, but you get the point.
So, as a conclusion, it is known that DHT concentraton on bald scalps is the same as in parts with hair, and also in scalps of people with no hair loss. DHT is bad, yes it is, but not in the way 99.99999% of people think it is, he is in the right place, but not in the right form, it should ave been converted to androestadinol, wich happens amazingly well as teenagers, but for some reason 3alpha-hydroxysteroid reductase gets depleted and no androestadinol is created so no signailng for derma papila so it miniturizes and there goes our self esteem.
Just go to any muscle building forum and ask about 3alpha-hydroxysteroid reductase, they all know what it is. In here, a hairloss forum, all you know is 1mg of finasteride, and thats the whole science around here. We must adress 3alpha-hydroxysteroid reductase, and that is why our curent methods work, in a limited manner, but increasing 3alpha-hydroxysteroid reductase is what we need to do.
Ohh and before anyone asks, transplanted hair brings his own 3alpha-hydroxysteroid reductase and binded androstaidol attached, and in the new place it actually starts working again, wich explains some regrow of hairs around a transplanted hair, and if by chance it is badly harvested, due to shock it gets inflamed and the natural response is DHT binding to the AR, and that hair is gone. This is known as quorum sensing, and I also think that the transplanted 3ahr stays there for a long time, or maybe the transplanted hair even with very low androstanidol hangs for a few cycles (each cycle of 5 to 7 years), which is long enough for someone who was submitted to HT to grow older and with age DHT lowers naturally, so in the next anagen cycle 5 or 7 years later the few androstanidol present outpaces the DHT concentration. This is why people without AGA lose hair as they grow older, if someone gets to 60yo with a head full of hair and then start losing hair, it is not AGA, it is just the body shuting down functions, and to prove this even further, mostly old people lose hair as diffuse hair loss, and not with a norwood pattern. And not so much because DHT is lower (DHT lowers but not so much, and that is why above 60yo prostate issues are higher) but what also lowers in a much higher pace is the 3AHR, thus leading to less conversion of DHT to androstadinol, and as a consequence old people start having hair loss and enlarged prostates, solution? 5mg of finasteride. Here we are again, DHT is often atributed as a cause, but the fact is that it only is a problem because what was needed to convert it to androstanidol is depleted.
We shouldn-t be measuring how much DHT we have, but rather how much 3alpha-hydroxysteroid reductase and androestadinol, because the latter one is the one that should be binding to the AR instead of DHT.
Androstadinol promotes correct signaling pathways for hair growth. DHT blocks those pathways, but it only happens because there is no ANDROSTADINOL, and not because there is too much DHT in the first place.
Then a user (u/PulseQ8) commented the following, and it was very pertinent:
“You know a theory is good when it's coherent, generalizable, and is able to correctly predict other phenomena/experiments. I think this theory potentially solves many poorly understood mechanisms such as:
1- How/why minoxidil grows hair on both the scalp and elsewhere on the body. While on the other hand, DHT thickens hair everywhere on the body except the scalp. Your theory is presenting good solutions for this bizarre phenomenon. And as per my understanding, it should also correctly predict that minoxidil would not work if you have no androgens. Which I don't know if that's true or not, but if it is then it would strengthen the hypothesis.
2- Why bald spots coincide with locations of higher scalp tension. I've seen some superficial explanations for this which leave more unanswered questions, and I think this theory does a better job of explaining it.
I believe this theory may be the closest thing we have to "The Theory of Everything" for hair loss, as it tackles hair loss at a more fundamental level than any other theory we have.”
And this just clicked, because in 6 month I have not once thought exploring hair loss in women to strengthen this theory, and he is actually right, and another user (u/fisharute) presented this study, and everythink makes absolute sense:
“https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2291485/
This article looks at DHT in hirsute women's skin and says similar things. Thanks for this!”
English is not my main language and I am sorry I don’t have the time to write this down better, but I hope we can start from here and discuss this. Please anyone is welcome to develop the theory, or refute it, presenting facts, studies, or anything that can actually hep us in our pursuit.
The solution/cure?
As I said before, I don’t have one. But I strongly believe and I would put my money on this, and someone smarter than me and with the means to do this can easily try it:
All we need to do is put some bacteria producing the necessary enzyme 3alpha-hydroxysteroid reductase. With the enzyme we can easily join DHT and we will get Androstenol. It is very easy to make an in-vitro experiment, all we need is some miniaturized hair follicles (anyone of us can find this easily unfortunately) and culture them in a solution containing DHT+the enzyme, or DHT+androstenol or (this one will hold the truth for sure) putting the hair follicle in a cultured environment with androstenol, and if the hair recovers, we have a cure. These are both natural and safe components that exist in our bodie in great abundance, and in normal scalps they are in great concentration and we also had this high concentration in our teen years, so an in vivo study is also simple then we can start experimenting, adding the enzyme to our scalp and see what happens. Maybe add some Androstenol to the scalp and see what happens. Not sure about penetration on skin, but if the in vitro experiment works fine, this won't be a problem.
This has never been done, ever. Why, I don’t know. Someone smarter and with more knowledge might have an answer, but I don’t have it, so guys, let’s make this so big that at least a small and simple experiment can be done in an UNBIASED way. Non of this is patentable and there is no money to be made here, so I wouldn’t bet big pharma will actually enjoy this being a cure (if a solution comes out of this, it is inexpensive as fuck), and maybe that is why it has not been pursued or studied before, but today we can do this on our own. Bodybuilders know more about 3alpha-hydroxysteroid reductase than we, but if we change this, the world will be more hairy.
Sorry for the bad English, and the lack of technical language, but I hope this can be understood by everyone, and using google scholar you can find the same studies and articles I did for the most instructed people here, and if you ask I can cite and provide the articles I have used, and it is nice that other people search the same so that this research can be “peer reviewed”.
Thanks for all your time reading this, and please let’s find a cure for us, this is driving an OCD man insane.
EDIT: There is a post on https://www.hairlosscure2020.com/increasing-3-alpha-hydroxysteroid-dehydrogenase-to-treat-hair-loss/ writen by a Guy named Roman, and that was found by u/thecreed997 that contains very similar findings and conclusions and is much better written with many techical information that I could not adress when writing this. Please everyone make sure to also check the link. The post is from 2016 and a few studies also corrobate his finding since 2016.
Hi, guys, recently people have asked me to make a post on this theory I have been developing, so here it goes:
Two main paradoxes led me to persuit another explanation for hair loss that is not often talked. DHT concentration and minoxidil efficacy.
First, the efficacy of finasteride is very similar, from 0.25mg to 5 mg, although the total serum and scalp DHT reduction is higher as we increase the dosage, hair regrow does not follow this premise. So people may have great results with 0.25mg daily and increasing the dose will not result in increased regrow.
This caught my eye, because there is not on single explanation of why this happens. Why reducing 70% of DHT will not be more twice more powerfull than a 35% reduction? Why dutasteride reduces almost 90% of DHT and a NW6 will at most return only to a NW5?
Several explanations have occurred with some authors actually attributing this to the death of the hair follicle. We now know that this isn’t true, and the hair follicle is maintained alive, just in a permanent dormant stage, so why doesn’t it start producing hair after DHT is gone? Why castrated men don’t regrow a head full of hair? Why transgender people don’t regrow hair? These questions have remained without a consensual answer for over than 30 years.
Current research is all about DHT, Androgen Receptors, PGE, PDE2, WNT pathways, and the last 10 years our biggest hope is hair cloning and stem cell.
Hair cloning, PRP, stem cell will never work for a simple factor. We are not addressing the cause of hair loss with any of these techniques. In paper, stem cell is amazing and should regrow hair. Exosomes should regrow hair. Hair cloning should be easy! We can clone other organs, we can even clone teeth, even dolly the sheep has been cloned to a perfectly functional animal. So why won’t any of these things work? Because there is not a single evidence that hair follicles or derma papilla cells from the vertex and crown are different from hair on the back and sides of our head. This is a dangerous assumption, that was taken from the lack of other evidence, and has lead the hair loss research to many dead ends, and so will be hair cloning.
Why would I say this? When all I want is my hair back. All I want is to go to a bar and girls look at me (I’m married, but it feels good). I want to look at a random mirror on the street and not see my horseshoe. I want to take a picture not worried if there is too much light in the room.
So, why would I say that the most hoped for treatment , that is not even for my pocket, will not work? Because research is wrong from the first step, the concept and premises are wrong from the start. People have been trying to clone hair for over 15 years, with zero progress. It has been able to make mice grow human hair, but they failed to understand why that even worked. If we do not correct the real cause of hairloss, we won’t be able to clone functional hair follicles. AND WHEN WE DO, HAIR CLONING WON’T BE NECESSARY because we already will have the technique and solution to simply implement in our own scalp and hair will grow in place!!
Gene editing like crisp won’t work either because there is no such thing as genetically programmed hair follicles that start minutirizing at some point in life, in a known pattern and those genetically programmed genes actually can be somehow reverted by simply adding finasteride, dutasteride or even minoxidil? If they were programmed to shut down, nothing would bring them back. Phenotype and lifestyle don’t mean a thing. Two twins, one on fin and another not taking fin have different outcomes, but the only thing that changes gene expression is gene editing, nothing else would save us if that was the case.
Why has this been “true” for so long? Hair surgeons and big pharma need this to be true, otherwise guess who would lose profit? But I’m not against medical doctors or hair surgeons, actually they also were so blind to assume a premise developed in the 1950s, that since then nobody went behind that assumption and tried a different approach.
Yes, there is a genetic component, but not in the hair follicle. The derma papilla is the same in the back or in the front of the head, it just acts different because different things make it work different.
What I believe is genetic, is what leads to the underlaying cause of hairloss, and this I am not sure what it is exacly, because it also has not been enough studied, and it doesn’t even matter too much for my theory. We can find a solution/cure even without knowing the true cause of the hair falling like rain on temples, vertex and crown in a very distinct and similar patter in all human beings predisposed to it.
We all heard about the scalp tension of the galea aponeurotica, that leads to inflammation and corresponds to the exact pattern, but this theory has lots of flaws. Recently in 2019 a dentist found an unnusual connection between dental malocclusion and baldness, where he found that 100% of people with type 2 were bald, and everyone without this malocclusion had a head full of hair, and he studied 150 x-rays to come to this conclusion and this amazes me that only now someone actually found this. Still it is not understood how and why, but this malocclusion causes the artery that feeds our scalp to be constricted, and there may be some truth in this, and I am currently digging this as well. Maybe aligning the jaw would bring our hair back? I don't know neither does the dentist who discovered this, but he is investigating this, I think.
And both of this could be true, and this is where the genetic factor comes in, skull development and jaw line is actually genetic, also why some muscles may be stretched can be also explained by genetics, and this is all we have, unexplained theories on this, and skull expansion and other things that people came up to explain the unexplainable phenomenon of hair loss in a known pattern. In man and women.
From the previous paragraph, the only scientific truth that has been studied and documented very well, is the fact that the thickness of a balding scalp is significantly different from a non balding scalp, and now we start to get to somewhere, why it is thinner or thicker, I don’t know, but there is a difference and that is what I started perceiving as having something to do with the pattern, in spite of the actuall cause (tension, stretched galea, dental malocclusion with low oxygen and nutrients makes the muscle atrophy and gets inflamed, whatever it is I don’t know and nobody else studied to get to a conclusion) it is a fact and I start from that premise to address to my theory. (Guys, remember how botox injections lead to hair regrow, this theory also explains that)
Before jumping in my hypothesis, one last thing should be emphasized, and that is the fact that BALD SCALPS HAVE THE SAME AMOUNT OF DHT AS NON BALD SCALPS. Also, beard and chest hair only grows because of DHT and NEEDS DHT to grow, and this is the known DHT paradox, as why it makes hair grow in some places and in others (our scalp) makes hair die.
My hypothesis is that DHT is the cause but not the culprit. From now on, everything you will read is a theory that so far I could not disproof, and nobody I discussed it has been able to disproof or refute the facts. I have not invented or discovered any of this. I do not hold any credit or want any credit for this. Everything is documented in studies and papers that are found on the internet and I am writing this because some people talked to me and recommended me presenting this to everyone so that we as a community can discuss it, and everyone be informed of this theory and start contributing in this thread, and I hope we, as a community, can grow this theory and ultimately grow our hair.
I do not have a cure, or even a solution, all I have is a theory based on information I have compiled over the last 6 months of research.
Please, I am not a biologist, medical doctor, medical researcher and have absolutely no chemistry or biochemistry education. I am a civil engineer and a quantum physics freak, with OCD, wich makes me very good at my work and also makes me research all I can and makes me count every single hair that falls on the shower. So people with much more knowledge than me, please help us develop or refute this theory, and whatever the outcome might be, we will be closer to finding a solution and cure for us. And if by any means this post ring some bells and actually smart people, big pharma or anyone with a home lab finds a solution or a way to cure us, this should never be monetized and no profit should ever be taken from a research done on a community like this or someone with obsessive compulsive disorder that spent 6 month reading things about something he barely understands.
So, in a recent post here at tressless (/r/tressless/comments/mw6vt0/sulpharaphane_enhances_a_natural_process_of_skin/), OP (u/VelociraptorRedditor) wrote about an article about sulphoraphane. Lately I have been researching about Procyanidin B2 for hair grow and also sulphoraphane, and these two have one thing in common, that can potentially cure us. Actually, both had impressive hair regrow in their studies, although their research is rather slow and for some reason it is still not on the market in an easy and available sotution that replicates the doses used in their studies. Also studies on this have failed to correlate the most important thing of their findings. I was only able to do this correlation while reading about their effects when used by bodybuilders (shame on you hair loss researchers!!).
So I will just copy paste my comments from that post because I don’t have enough time to rewrite everything and I believe it is a good start for this community to start a debate and discuss, develop or even refute my findings, and in commets I can always provide links, citations, studies and everything we need to grow this, so I commented:´
I believe this is the missing link that nobody talks about. Whenever it is discussed somewhere, it becomes obscured by diverting topics, but to me the cure/treatment is 3alpha-hydroxysteroid reductase.
It explains everything, since the why finasteride works, to why minoxidil works, why LLLT works (not much but there is good data behind it), why micronnedling works, even why scalp massage could even work (these last one I do not believe help much but I have not tried them)
So I stumbled upon 3alpha-hydroxysteroid when researching about procyanidin B2, wich I believe is the most powerfull treatment to AGA, but for some obscure reason has not been enough researched or studied (it is natural and not patentable), even though an oral study demonstrated 125% REGROW in AGA patients (the study had 250 people, and there were zero side effects, and Procyanidin B2 is a natural flavonoid that is very good for the heart and arteries as well as liver, lungs and kidneys, skin and hair). They too missed the link between Procyanidin B2 and 3alpha-hydroxysteroid reductase in the study.
Here is the study if anyone wants to dig a bit (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5775114/).
3alpha-hydroxysteroid reductase is the natural DHT killer that exists naturally and abundantly in our bodies, specially in the muscles, where it degrades DHT. It does this everyday, every hour, every minute, every second, and the muscles use the degraded components to stay healthy. Guess who does this as well? Yep, you're right, derma papila cells. Guess what happens when the enzyme is not present? Yep, DHT binds to where it can, and there goes the hair. the reason it decreases or completely vanishes from the scalp is probably due to the stretching of the galiea muscle, where it occurs abundantly. Maybe some other reason leads to the decrease of 3ahr, and some drugs that are known for eliminating 3ahr have as side effect, what? yep, hair loss.
The most important from what I said before is that people are looking at DHT levels, but they are the same as non balding scalps, the thing we should be looking is the enzyme that is supposed to fuck DHT before it harms our hair follicles, this is the missing key, and guess what also elevates 3ahr? Minoxidil, and what minoxidil also needs to be converted to usable form, sulforaphane, and we'll get that in a moment.
We use finasteride wich blocks the enzyme necessary to convert T to DHT, but the thing is, our body does that every second naturally (gets rid of DHT), where it converts it to androstanediol, a weaker androgen derivate that is good for muscle growth and it's used by cells for other good things like promoting tissue regeneration, hair growth and other cool shit.
The thing I can't find is if we could find a way to use topically. It is known that sulpharaphane boosts 3alpha-hydroxysteroid reductase, and there has been a good study on this for AGA with very good results, but then again people don't even mention it. It is found in brocoli sprouts in great abundance. Also procyanidin also increases greatly not only the 3ahr, but also pathways used for signaling hair growth.
So my thoughts is that combined topical melatonin, with oral procyanidin B2 and a way to reestablish the 3alpha-hydroxysteroid reductase on the scalp in a vigourous way (sulpharaphane), would be a cure. Most importantly, this is an extremelly resilient enzyme, so if we had a way to put it where it is needed, we are talking about a cure. AGA develops so slowly, and is more agressive on some, also minoxidil only works to an extent and for a few years, as long as we still have 3alpha-hydroxysteroid reductase. Over the last years several people tried to bring this to the light, but posts are to techincal for anyone to understand and actually it loses interest by most or the topic is diverted. I will keep everything simple and not talk about pathways and complex molecules and shit.
Minoxidil, procyanidin B2, sulphoraphane, and many other things boosts the DHT killer. And I wouldn't call it killer, it converts DHT to smaller components, the good ones. The ones the that make hair grow. Androstenol is a by-product of DHT, converted by the enzyme, and is still an androgen but weaker, and it has the same binding afinity to the androgen receptor. Because we have less enzyme on the scalp to convert DHT to Androstenol, and because it has the same binding afinity, DHT binds to the Androgen receptor instead of the Androstenol, wich is what we need to happen for hair grow.
The problem is that DHT binding to the AR of derma papila blocks the pathways that make hair grow, instead it signals de cell to die (senescence) because in our bodies, when there is inflamation 3alpha-hydroxysteroid reductase is naturally decreased in order to increase binding of DHT wich in turn makes the cell die and a new one come in place. This is important for muscle growth in deed, as muscle fibers need to be replaced for grow.
When DHT is converted to Androstenol, it sucessfully binds to the derma papila, and it is a completely different story, it signals and promotes hair growth by activating the correct pathways. 3alpha-hydroxysteroid reductase exists naturally in our body, and in great abundance in muscles and some organs like prostate.
For some reason, our balding scalps and the muscle that supports the scalp loses is depleted of 3alpha-hydroxysteroid reductase, and I-m not sure why, and don-t actually know why, but I believe it has to do with stretching of the galea and inflamation, that naturally reduces the 3alpha-hydroxysteroid reductase to increase DHT binding and combat the inflamation. Remember I said earlier that the thickness of the scalp is much different on balding scalps than in normal scalps? Also on back and sides, thicness is different, and this is what I believe leads to our hair loss, a reduction of 3alpha-hydroxysteroid reductase first due to inflamation (it lowers to produce less androstenol and allow DHT to take care of inflammation - greta for bodybuilders and the famous plateau effect), and the thinner muscle also has much less 3alpha-hydroxysteroid reductase, but still has some, and still produces some androstenol, but just not enough to outpace the DHT (this DHT amount is the same or even lower than when we were teenagers, the only thing that changed is the amount of androstenol.
Finatseride and dutasteride work by reducing the available DHT that can actually bind to the hair follicles, so less DHT allows some Androstenol to correctly bind, but as hair loss progresses in a known pattern, also Androstenol follows thepattern, because the underlaying muscle just stops producing 3alpha-hydroxysteroid reductase, and that is why finasteride regrows hair close to the existing hairline, and not randomly on the head, A NW6 regrows hair next to the existing hairline, and not on the original teenager hairline or even in front of temples.
Anyways, minoxidil increases 3alpha-hydroxysteroid reductase, also something that greatly increases 3alpha-hydroxysteroid reductase is sulpharaphane .
So, we can regrow hair by reducing DHT with finasteride, dutasteride, etc. but only in places where there is still 3alpha-hydroxysteroid reductase, and that is why we regrow just a small percentage and for some people doesn-t even work because they have very very low 3ahr.
Minoxidil increases 3alpha-hydroxysteroid reductase, and it actually also uses sulpharaphane to be converted to his usable form.
Microneedling leads to growth factors creating new follicles, but then again, witouth 3alpha-hydroxysteroid reductase it doesn-t get very far because all there is to bind is DHT, unless using minoxidil that boosts 3alpha-hydroxysteroid reductase, and then we will have Androstenol to bind to the AR and the miracle of hair grow happens.
Another thing that also helps a lot is ant oxidants, and there is something called procyanidin B2 wich is very good at promoting hair grow, due to the fact that it gets rid of free radicals, and induces a boost in 3alpha-hydroxysteroid reductase.
I could spend a lot of time explaining other things, but you get the point.
So, as a conclusion, it is known that DHT concentraton on bald scalps is the same as in parts with hair, and also in scalps of people with no hair loss. DHT is bad, yes it is, but not in the way 99.99999% of people think it is, he is in the right place, but not in the right form, it should ave been converted to androestadinol, wich happens amazingly well as teenagers, but for some reason 3alpha-hydroxysteroid reductase gets depleted and no androestadinol is created so no signailng for derma papila so it miniturizes and there goes our self esteem.
Just go to any muscle building forum and ask about 3alpha-hydroxysteroid reductase, they all know what it is. In here, a hairloss forum, all you know is 1mg of finasteride, and thats the whole science around here. We must adress 3alpha-hydroxysteroid reductase, and that is why our curent methods work, in a limited manner, but increasing 3alpha-hydroxysteroid reductase is what we need to do.
Ohh and before anyone asks, transplanted hair brings his own 3alpha-hydroxysteroid reductase and binded androstaidol attached, and in the new place it actually starts working again, wich explains some regrow of hairs around a transplanted hair, and if by chance it is badly harvested, due to shock it gets inflamed and the natural response is DHT binding to the AR, and that hair is gone. This is known as quorum sensing, and I also think that the transplanted 3ahr stays there for a long time, or maybe the transplanted hair even with very low androstanidol hangs for a few cycles (each cycle of 5 to 7 years), which is long enough for someone who was submitted to HT to grow older and with age DHT lowers naturally, so in the next anagen cycle 5 or 7 years later the few androstanidol present outpaces the DHT concentration. This is why people without AGA lose hair as they grow older, if someone gets to 60yo with a head full of hair and then start losing hair, it is not AGA, it is just the body shuting down functions, and to prove this even further, mostly old people lose hair as diffuse hair loss, and not with a norwood pattern. And not so much because DHT is lower (DHT lowers but not so much, and that is why above 60yo prostate issues are higher) but what also lowers in a much higher pace is the 3AHR, thus leading to less conversion of DHT to androstadinol, and as a consequence old people start having hair loss and enlarged prostates, solution? 5mg of finasteride. Here we are again, DHT is often atributed as a cause, but the fact is that it only is a problem because what was needed to convert it to androstanidol is depleted.
We shouldn-t be measuring how much DHT we have, but rather how much 3alpha-hydroxysteroid reductase and androestadinol, because the latter one is the one that should be binding to the AR instead of DHT.
Androstadinol promotes correct signaling pathways for hair growth. DHT blocks those pathways, but it only happens because there is no ANDROSTADINOL, and not because there is too much DHT in the first place.
Then a user (u/PulseQ8) commented the following, and it was very pertinent:
“You know a theory is good when it's coherent, generalizable, and is able to correctly predict other phenomena/experiments. I think this theory potentially solves many poorly understood mechanisms such as:
1- How/why minoxidil grows hair on both the scalp and elsewhere on the body. While on the other hand, DHT thickens hair everywhere on the body except the scalp. Your theory is presenting good solutions for this bizarre phenomenon. And as per my understanding, it should also correctly predict that minoxidil would not work if you have no androgens. Which I don't know if that's true or not, but if it is then it would strengthen the hypothesis.
2- Why bald spots coincide with locations of higher scalp tension. I've seen some superficial explanations for this which leave more unanswered questions, and I think this theory does a better job of explaining it.
I believe this theory may be the closest thing we have to "The Theory of Everything" for hair loss, as it tackles hair loss at a more fundamental level than any other theory we have.”
And this just clicked, because in 6 month I have not once thought exploring hair loss in women to strengthen this theory, and he is actually right, and another user (u/fisharute) presented this study, and everythink makes absolute sense:
“https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2291485/
This article looks at DHT in hirsute women's skin and says similar things. Thanks for this!”
English is not my main language and I am sorry I don’t have the time to write this down better, but I hope we can start from here and discuss this. Please anyone is welcome to develop the theory, or refute it, presenting facts, studies, or anything that can actually hep us in our pursuit.
The solution/cure?
As I said before, I don’t have one. But I strongly believe and I would put my money on this, and someone smarter than me and with the means to do this can easily try it:
All we need to do is put some bacteria producing the necessary enzyme 3alpha-hydroxysteroid reductase. With the enzyme we can easily join DHT and we will get Androstenol. It is very easy to make an in-vitro experiment, all we need is some miniaturized hair follicles (anyone of us can find this easily unfortunately) and culture them in a solution containing DHT+the enzyme, or DHT+androstenol or (this one will hold the truth for sure) putting the hair follicle in a cultured environment with androstenol, and if the hair recovers, we have a cure. These are both natural and safe components that exist in our bodie in great abundance, and in normal scalps they are in great concentration and we also had this high concentration in our teen years, so an in vivo study is also simple then we can start experimenting, adding the enzyme to our scalp and see what happens. Maybe add some Androstenol to the scalp and see what happens. Not sure about penetration on skin, but if the in vitro experiment works fine, this won't be a problem.
This has never been done, ever. Why, I don’t know. Someone smarter and with more knowledge might have an answer, but I don’t have it, so guys, let’s make this so big that at least a small and simple experiment can be done in an UNBIASED way. Non of this is patentable and there is no money to be made here, so I wouldn’t bet big pharma will actually enjoy this being a cure (if a solution comes out of this, it is inexpensive as fuck), and maybe that is why it has not been pursued or studied before, but today we can do this on our own. Bodybuilders know more about 3alpha-hydroxysteroid reductase than we, but if we change this, the world will be more hairy.
Sorry for the bad English, and the lack of technical language, but I hope this can be understood by everyone, and using google scholar you can find the same studies and articles I did for the most instructed people here, and if you ask I can cite and provide the articles I have used, and it is nice that other people search the same so that this research can be “peer reviewed”.
Thanks for all your time reading this, and please let’s find a cure for us, this is driving an OCD man insane.
EDIT: There is a post on https://www.hairlosscure2020.com/increasing-3-alpha-hydroxysteroid-dehydrogenase-to-treat-hair-loss/ writen by a Guy named Roman, and that was found by u/thecreed997 that contains very similar findings and conclusions and is much better written with many techical information that I could not adress when writing this. Please everyone make sure to also check the link. The post is from 2016 and a few studies also corrobate his finding since 2016.
Ultima modifica:
