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  1. #331
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    The OP spouts nonsense. The truth is that the weight of fat and skin below head level, weighs upon and pulls down on the skin going across the top of the head. This results in poor blood circulation which makes your follicles go to sleep--like when your foot goes asleep--and while asleep, they are prone to being clogged with dandruff, dust, and oil. This explains why there are so many fat bald men around, because the more body fat, the more the skin is weighed down. It also explains why so many bald heads shine--it's because the scalp is stretched so tight. This is how minoxidil works--derived from a low blood pressure medication, minoxidil improves blood flow to the scalp.

  2. #332
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    Hello Ahab. Thanks for this valuable information. However i found very useful information on these websites:

    1. https://healthandbeautyinfostore.wor...and-solutions/
    2. https://www.holdthehairline.com/articles/
    3. https://www.everydayhealth.com/skin-...hair-loss.aspx

    Hope this articles will help us more to understand Baldness and find out solutions.

  3. #333
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    Quote Originally Posted by FGF11 View Post
    There are a lot of big problems in this world, that hair loss, sometimes seems actually quite small compared to them. Watch The Boy Whose Skin Fell Off, and My Flesh and Blood just to get an idea of how a disease such as Epidermolysis bullosa can be soooooooooo much worse than hair loss.
    Not worse. Only just as bad.

  4. #334
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    Well, where do I start this. I've been investigating on my own i I've come to exactly the same conclusions as you did, maybe with a different path.

    There are a lot of comunication pathways within and outside the cells, so it becomes really hard to create a distinction between causality and correlation even harder to identify the most important underlying mechanisms in any pathology. You can act on hair loss in a million different ways, and still observe some results because of this, but only a few are truly effective and worth the money, time and side effects.

    Lets start with DHT. DHT is old school known to be the androgenic ligand with most affinity with androgen receptors, which means it can act on AR even in small concentration in comparison with other androgens and maybe produce a bigger expression on the target genes. However, I too believe DHT is not the main mechanism here. DHT mediated AR activation upregulates the TGF beta pathway resulting in the productions of cytokins like the mentioned and a particularly small protein called Dkk1. Dickkopf 1 however is an agonist of the Wnt/B catenin pathway by contributing to the degradation of a transcription coregulator Beta Catenin. Reduced cytoplasmic levels of Beta catenin downregulate the Wnt canonical pathway and thus inhibiting its expression and the production of IGF's. So that means DHT favours TGF pathway which in turn produces an Wnt/B cat antagonist (negative feedback).
    As a result, the anagen phase becomes progressively shorter as a result of the smaller and smaller availability of Beta cat and growth factors, leading to the miniaturization of the hair folicles. Thats pretty much it for the main mechanism, or at least one of them (I doubt there are).

    Why is it the main mechanism? Because of what i said before. There are hundreds of studies regarding hundreds of substances and methods, from natural antioxidants, herbs, teas, to mechanical stimulation. There are a multitude of factors that can impact the hair follicles and pretty much everything in our body, but its important to not lose valuable time and money on treatments that only produce small marginal benefits. As an example, DHT is related to an increase of reactive oxygen substances (free radicals for simplicty) which in turn might cause DNA damage, and as a response when detected DNA damage cells usually respond by producing tumor antigens and even induce apoptose. One of the proteins produced is the p53 that downregulates B catenin and consequently halting the cells growth. Therefore, antiox present in some extracts might benefit the follicles but only to a limited extend. Early onset of AGA is also associated with prediabetes or insuline resistance. Would a low glycemic diet promote hair growth then? Probably not, since insuline hormones are involved in a cascade of interactions regulation the active transport of gluscose into the cell which is partially mediated by the activation of Wnt signalling proving the insuline resistance (the fact cells cant properly uptake the right amounts of glucose) is not the cause but maybe the consequence of a faulty/susceptible Wnt/B catenin signalling. Mechanical stimulation is another example. The signalling from the epidermis to the dermal papillae can affect the composition of the matrix and influence the behavior of the surrounding cells; BMP, JAK-STAT, etc but so far everything I've seen is connected to the wnt pathway or the benefits are supressed when DHT is added (meaning DHT action mechanism is more preponderant for the condition).

    So, and why does DHT has a degrading effect on frontal hair and a positive effect on the development of beard, pubic hair, etc? (the famous androgen paradox)
    Well, thats a though question. I cant say for sure, but if I would have to guess I would say the scalp hair must be of a different nature of have key morphological differences regarding body hair. And the same goes for eyelashes. Informally, we can see babies start to develop hair soon after they are born. Slowly vellus hair develop into intermediate and terminal hairs without the need of DHT, however, body hair follicles are also present since the day we are born but only develop after the adolescence in response to DHT. In my opinion, this paradox is a bit of misconception since were comparing two concepts similar at glance, but with completely different working mechanisms.

    Some other thought i would like to add is that hair loss is probably trigger right after the puberty but because of the genetic predisposition of the androgen receptor density/ affinity, some people bald earlier, some people later; at some extends faster, sometimes slower but the clock starts at puberty for everyone. But why does hair loss not halt/slow down when we get older?
    Thats true we lose 2% of free DHT/year if im not mistaken after 25yo but like ive said its not the only factor at play. As we grow older we start to suffer from other pathologies that indirectly may harm our hair, we start to suffer the consequences from oxidative and replicative senescence, increasing the apoptosis rates amongst cells and white hairs.

    I believe the ultimate cause is a genetic polymorphism in the genes which code the androgen receptor, but I think its pretty much what most people think anyway. However, targeting the AR with inhibitors its the most effective way to address AGA, but its also the worst in terms of side effects AND does not equate to regrowth in late stages. So what i propose is to address the cytoplasmic beta catenin by inhibit among all available targets the Dkk1 in special since its the one upregulated (and the others have other functions and are important tumour suppressors).

    So what about regrowth? I asked myself the same questions. If erasing DHT from the equation wasnt enough to revert hair loss then, I assumed 2 central possibilities: there is a more important mechanism than DHT, which i think its impossible because androgens are a must in AGA OR there are other AR activators which arent androgens but that sounded very unlikely too until i found an article about castration resistent prostate cancers too. It makes total sense. If you look at balding patterns, they are always the same. There is a great variation regarding balding duration (20-80) but not so much regarding patterns (comparing to other alopecias). If all follicles were equally sensitive, then because the scalp DHT levels shouldn't fluctuate so much between regions, the extension of the binding reacting should in theory not be enough to cause a "local" balding but instead the balding spots should be evenly distributed (or definitely more distributed and less centered). Thats why I think the immunological response and macrophage/ cytokins population of the inter cellular tissue is a key aspect in the pattern shape and why inflammation plays such a crucial role in balding.

    So just like previously by activating the Wnt pathway you could stop hair loss, you can also induce hair growth! (theoretically)

    Just an example, lets analyze a popular regimen on hair loss talk hormonal route consisting of Cyproterone Acetate, duta and estradiol gel. The first solely is a potent androgen inhibitor, which would prove effective if the goal was only halting the hairloss (depending on the concentrations ofc), duta (not a anti androgen per se) but the regrowth is only possible thanks to the topical estradiol. Estradiol is a potent androgenic antagonist and within the cell, it acts opposite to DHT and inhibits TGF, Dkk1 and activates Wnt by stabilizing beta catenin.

  5. #335
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    Quote Originally Posted by Ahab View Post
    The OP spouts nonsense. The truth is that the weight of fat and skin below head level, weighs upon and pulls down on the skin going across the top of the head. This results in poor blood circulation which makes your follicles go to sleep--like when your foot goes asleep--and while asleep, they are prone to being clogged with dandruff, dust, and oil. This explains why there are so many fat bald men around, because the more body fat, the more the skin is weighed down. It also explains why so many bald heads shine--it's because the scalp is stretched so tight. This is how minoxidil works--derived from a low blood pressure medication, minoxidil improves blood flow to the scalp.
    So why when people have hair transplants doesn't the fat keep pulling the skin tight and make the transplants go to sleep?

    And why do some fat people have plenty of hair while some skinny people go bald?

    And why don't women go bald on the tops of their heads like men?

  6. #336
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    Im not very well educated in hair transplants.

    Fat people usually have low androgens. I dont know if you know that DHT also binds to AR in adipoctytes and stop the production of "fatness". Why do women are less muscular than men and have more fat tissue? Short answer, because they have a lot less circulating androgens than men also hence then rarely go bald, just get thinner hair most of the times.

    But black or white, fat or skinny it doesnt really matter. You can have normal DHT and still suffer the consequences if you have an abnormal AR expression, which imo is most cases. And even if you reduce but not completely erase DHT from your system, cells can adapt either at receptor level, lowering the treshold of required androgens for activation, or also at transcription level, 1 gene instead of producing 1 protein produces 2 or 3. Its too complex.

    Your follicles dont go to "sleep" because of the lack of blood flow. Most of blood flow acts as a termoregulator anyway, cells could live with a portion of it. For that matter mechanical stimulation/microneedling/hot temperatures would produce amazing results, which they dont. At most it has a minor effect on hair loss, it's not even close the main mechanism. Also and maybe more importantly, the partial pressure of circulating oxygen in scalp is also decreased which might favour the expression of some potential proteins. I haven't ruled out that hypothesis but havent investigated it properly either.

    The thing is, there are a million treatments which produce mild results. You could spend a fortune to get shity results, or you could target directly the adequate mechanisms

  7. #337
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    Quote Originally Posted by Ahab View Post
    The OP spouts nonsense. The truth is that the weight of fat and skin below head level, weighs upon and pulls down on the skin going across the top of the head. This results in poor blood circulation which makes your follicles go to sleep--like when your foot goes asleep--and while asleep, they are prone to being clogged with dandruff, dust, and oil. This explains why there are so many fat bald men around, because the more body fat, the more the skin is weighed down. It also explains why so many bald heads shine--it's because the scalp is stretched so tight. This is how minoxidil works--derived from a low blood pressure medication, minoxidil improves blood flow to the scalp.
    I just realized something: I didn't post #331. WTF?

  8. #338
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    Your theory is exciting but did you tried to test it with a more scientific approach?
    I recommend talking with some professors maybe they can help you to develop your theory and even publish a peer-reviewed article.

  9. #339
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    Quote Originally Posted by Beta Catenin View Post
    Well, where do I start this. I've been investigating on my own i I've come to exactly the same conclusions as you did, maybe with a different path.

    There are a lot of comunication pathways within and outside the cells, so it becomes really hard to create a distinction between causality and correlation even harder to identify the most important underlying mechanisms in any pathology. You can act on hair loss in a million different ways, and still observe some results because of this, but only a few are truly effective and worth the money, time and side effects.

    Lets start with DHT. DHT is old school known to be the androgenic ligand with most affinity with androgen receptors, which means it can act on AR even in small concentration in comparison with other androgens and maybe produce a bigger expression on the target genes. However, I too believe DHT is not the main mechanism here. DHT mediated AR activation upregulates the TGF beta pathway resulting in the productions of cytokins like the mentioned and a particularly small protein called Dkk1. Dickkopf 1 however is an agonist of the Wnt/B catenin pathway by contributing to the degradation of a transcription coregulator Beta Catenin. Reduced cytoplasmic levels of Beta catenin downregulate the Wnt canonical pathway and thus inhibiting its expression and the production of IGF's. So that means DHT favours TGF pathway which in turn produces an Wnt/B cat antagonist (negative feedback).
    As a result, the anagen phase becomes progressively shorter as a result of the smaller and smaller availability of Beta cat and growth factors, leading to the miniaturization of the hair folicles. Thats pretty much it for the main mechanism, or at least one of them (I doubt there are).

    Why is it the main mechanism? Because of what i said before. There are hundreds of studies regarding hundreds of substances and methods, from natural antioxidants, herbs, teas, to mechanical stimulation. There are a multitude of factors that can impact the hair follicles and pretty much everything in our body, but its important to not lose valuable time and money on treatments that only produce small marginal benefits. As an example, DHT is related to an increase of reactive oxygen substances (free radicals for simplicty) which in turn might cause DNA damage, and as a response when detected DNA damage cells usually respond by producing tumor antigens and even induce apoptose. One of the proteins produced is the p53 that downregulates B catenin and consequently halting the cells growth. Therefore, antiox present in some extracts might benefit the follicles but only to a limited extend. Early onset of AGA is also associated with prediabetes or insuline resistance. Would a low glycemic diet promote hair growth then? Probably not, since insuline hormones are involved in a cascade of interactions regulation the active transport of gluscose into the cell which is partially mediated by the activation of Wnt signalling proving the insuline resistance (the fact cells cant properly uptake the right amounts of glucose) is not the cause but maybe the consequence of a faulty/susceptible Wnt/B catenin signalling. Mechanical stimulation is another example. The signalling from the epidermis to the dermal papillae can affect the composition of the matrix and influence the behavior of the surrounding cells; BMP, JAK-STAT, etc but so far everything I've seen is connected to the wnt pathway or the benefits are supressed when DHT is added (meaning DHT action mechanism is more preponderant for the condition).

    So, and why does DHT has a degrading effect on frontal hair and a positive effect on the development of beard, pubic hair, etc? (the famous androgen paradox)
    Well, thats a though question. I cant say for sure, but if I would have to guess I would say the scalp hair must be of a different nature of have key morphological differences regarding body hair. And the same goes for eyelashes. Informally, we can see babies start to develop hair soon after they are born. Slowly vellus hair develop into intermediate and terminal hairs without the need of DHT, however, body hair follicles are also present since the day we are born but only develop after the adolescence in response to DHT. In my opinion, this paradox is a bit of misconception since were comparing two concepts similar at glance, but with completely different working mechanisms.

    Some other thought i would like to add is that hair loss is probably trigger right after the puberty but because of the genetic predisposition of the androgen receptor density/ affinity, some people bald earlier, some people later; at some extends faster, sometimes slower but the clock starts at puberty for everyone. But why does hair loss not halt/slow down when we get older?
    Thats true we lose 2% of free DHT/year if im not mistaken after 25yo but like ive said its not the only factor at play. As we grow older we start to suffer from other pathologies that indirectly may harm our hair, we start to suffer the consequences from oxidative and replicative senescence, increasing the apoptosis rates amongst cells and white hairs.

    I believe the ultimate cause is a genetic polymorphism in the genes which code the androgen receptor, but I think its pretty much what most people think anyway. However, targeting the AR with inhibitors its the most effective way to address AGA, but its also the worst in terms of side effects AND does not equate to regrowth in late stages. So what i propose is to address the cytoplasmic beta catenin by inhibit among all available targets the Dkk1 in special since its the one upregulated (and the others have other functions and are important tumour suppressors).

    So what about regrowth? I asked myself the same questions. If erasing DHT from the equation wasnt enough to revert hair loss then, I assumed 2 central possibilities: there is a more important mechanism than DHT, which i think its impossible because androgens are a must in AGA OR there are other AR activators which arent androgens but that sounded very unlikely too until i found an article about castration resistent prostate cancers too. It makes total sense. If you look at balding patterns, they are always the same. There is a great variation regarding balding duration (20-80) but not so much regarding patterns (comparing to other alopecias). If all follicles were equally sensitive, then because the scalp DHT levels shouldn't fluctuate so much between regions, the extension of the binding reacting should in theory not be enough to cause a "local" balding but instead the balding spots should be evenly distributed (or definitely more distributed and less centered). Thats why I think the immunological response and macrophage/ cytokins population of the inter cellular tissue is a key aspect in the pattern shape and why inflammation plays such a crucial role in balding.

    So just like previously by activating the Wnt pathway you could stop hair loss, you can also induce hair growth! (theoretically)

    Just an example, lets analyze a popular regimen on hair loss talk hormonal route consisting of Cyproterone Acetate, duta and estradiol gel. The first solely is a potent androgen inhibitor, which would prove effective if the goal was only halting the hairloss (depending on the concentrations ofc), duta (not a anti androgen per se) but the regrowth is only possible thanks to the topical estradiol. Estradiol is a potent androgenic antagonist and within the cell, it acts opposite to DHT and inhibits TGF, Dkk1 and activates Wnt by stabilizing beta catenin.
    Absolutely

    IMPRESSIVE

    Everything you wrote here In the last 10 years I researched. I have the same conclusion


    GET this data somehow to Japan to replicel dudes that work for the people, because BIG PHARMA will ignore such info as they push minoxidil propecia finasteride posions that do nothing to the people.

    Come on surely slowly we are finding the cure and fixing this baldness problematic gene once and for all for full hairs ! spread the message

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