supernature
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Hair loss theory
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tallglass13
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yeah, that's him. Although now , his hair is grown out, and his beard is very long and full. His hair was absent mostly on top as you can see in that photo, but he had some hair on very top and of course on the sides. So, it is very surprising isn't it. I wish him the best. But he has never posted about his own hair loss, and hope he would design a product specifically for hair growth, like taurine, histadine, zinc Cu . @Helen, anything that would increase co2 topically??
supernature
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I will look into it. I did not check out immortal hairloss regimens.
mattyb
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Anyone ever see a really veiny bald guy (with horseshoe style MPB)? I haven't. Every MPB bald guy I've seen under the age of 50 doesn't have veiny protrusions on their arms/hands. I've seen a lot of veins at work and have been looking at a lot of people walking around, and I haven't really found an exception yet.
My current theory is that MBP is caused by issues with both angiogenesis (oxygenated blood supply) and vascularization (non-oxygenated blood clearance). Hair follicles require rapid and precise shifting of angiogenesis and vascularization depending on hair follicle expansion and regression that occurs naturally with the hair cycle. If the body can't adequately adapt to these demands, either insufficient blood supply to the hair follicle, or insufficient clearance of waste products from the hair follicle, will cause atrophy of the hair follicles. I think when guys go bald, things like direct UV exposure further damages the scalp, almost guaranteeing that it will never grow back.
I think this requires the upregulation of things like VEGF and HIF-1a, but how to go about doing that - I haven't figured that much out yet. And the downside of upregulating those things systemicaly, is that VEGF/HIF-1a are part of tumor growth - so I think the flipside of curing baldness is increasing the risk of cancer.
My current theory is that MBP is caused by issues with both angiogenesis (oxygenated blood supply) and vascularization (non-oxygenated blood clearance). Hair follicles require rapid and precise shifting of angiogenesis and vascularization depending on hair follicle expansion and regression that occurs naturally with the hair cycle. If the body can't adequately adapt to these demands, either insufficient blood supply to the hair follicle, or insufficient clearance of waste products from the hair follicle, will cause atrophy of the hair follicles. I think when guys go bald, things like direct UV exposure further damages the scalp, almost guaranteeing that it will never grow back.
I think this requires the upregulation of things like VEGF and HIF-1a, but how to go about doing that - I haven't figured that much out yet. And the downside of upregulating those things systemicaly, is that VEGF/HIF-1a are part of tumor growth - so I think the flipside of curing baldness is increasing the risk of cancer.
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I am looking at the cases of hairloss more now, since I see a lot of people are bothered with hair. I will try to outline the regimens more precisely.
You need to understand that Co2 and carbs for some hairloss will be bad. And for other hairloss cases good. I think hairloss is a balance between nitric oxide and Co2. And I am not sure that hairloss is too much of nitric oxide. Since we know tons of cases where people regrew all the hair from nitric oxide boosters.
I think hairloss is from lack of NADPH in one case. And NADPH is what makes your nitric oxide. Without NADPH there is no nitric oxide.
And in another cases, it could be low thyroid low Co2 low protein hairloss, low zinc hairloss.
in any case, I will try to outline more of the exact regimens which I would try for different types of hairloss.
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No not true, I know many people with crazy veins with hairloss, It could be from thick blood thou. A lot of fibrogen in blood. There are gazzillion different hairlosses. the hairloss when the person has great hair everywhere else but the top of the head, I am pretty sure nitric oxide connected. Glutathione recycling is shut and that person gets zero circulation at those areas. Nitric oxide is made with NADPH. NADPH is what recycles glutathione. This is why for the person like that, I would recommend a series of Breuss fasts which will grow hair for them even on the bald head. Especially if combined with the salt scrubbing. Also birch tar.
If you lack glutathione recycling you pretty much get fibrosis, in lungs, everywhere. liver. So hairloss is a lack of circulation and and lack of antioxidation which causes fibrosis.
I have seen one person completely regrow their hair with birch tar. that person was as bald as Haidut, and it worked. but who knows what body chemistry that person was in. I dont know.
Diffuse hairloss people need to slow down so the body does not run on cortisol too much.
This is why Cxx5 which blocks the zinc finger and thus blocks the cortisol basically fixes I would assume the diffuse hairloss cases. But who knows how that will work out for the rest of the body.
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Also nitric oxide can be low because of lack of SOD. Since nitric oxide production causes creation of superoxide. And this superoxide can cause free radicals.
So nitric oxide could be low because of low superoxide dismutase or it can be low since glutathione recycling is low. Since superoxide dismutase will create hydrogen peroxide, and that in turn can creates hydroxyl radicals.
So basically if you have tons of NADPH, SOD, and glutathione peroxidase. and all component for nitric oxide synthase .You should not have hairloss since you will have high nitric oxide which promotes the hair growth.
Glutathione recylcing also will recycle vitamin E and C and those will take care of lipid oxidation and hydrogen peroxide.
If you have low thyroid , this will make too much of nitric oxide available and that could be also bad since that will have too much of free radicals.
So this is a balancing act.
So nitric oxide could be low because of low superoxide dismutase or it can be low since glutathione recycling is low. Since superoxide dismutase will create hydrogen peroxide, and that in turn can creates hydroxyl radicals.
So basically if you have tons of NADPH, SOD, and glutathione peroxidase. and all component for nitric oxide synthase .You should not have hairloss since you will have high nitric oxide which promotes the hair growth.
Glutathione recylcing also will recycle vitamin E and C and those will take care of lipid oxidation and hydrogen peroxide.
If you have low thyroid , this will make too much of nitric oxide available and that could be also bad since that will have too much of free radicals.
So this is a balancing act.
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I will have to dig them up again.
The idea is that it's causing the pituitary gland to secrete TSH, which in turn induces the thyroid to elevate its own as well. Otherwise how else could TSH be high in the case of hyperthyroidism? Albeit Helen previously presented a second explanation for why.
tallglass13
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According to a Dr Lin, he believes adrenaline, prolactin, and cortisol constrict the blood flood flow to the top of the head. Minoxidil is a nitric oxide donor. Some people that are high sexed seem to go bald. Maybe getting all those erections uses all the nitric oxide up , leaving less or borrowing it from the scalp. Maybe that is why people get an itch or inflammation in the scalp during masturbation or sex.
Aleksandr
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supernature
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mattyb
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It is extremely rare that a young person with lots of vascularity is bald. I have taken blood on like 500 people, and have trained another 500 easily - super rare. I have been paying close attention to this for months. Old people it's much more common, but old people are a different story. I think young and old people lose hair for different reasons.
Either way, what we're saying overall is the same. NO is essential in quick adaptations needed to balance vascularization and angiogenesis. I'm sure it's involved too. And I'm sure free radical management is involved as well - because it always is no matter the condition.
Speaking from my own experience - my head has no shortage of blood flow. It gets really hot and it flushes, and during those times my scalp quality diminishes significantly. I think a big issue is blood clearance, or regulation of small vasculature and improper targeted delivery to the hair follicle that does not coincide with proper coordination with the hair cycle. Somewhat like vascular leak/permeable, where blood spills out of the microcirculatory system. I have tons of hair in early anagen, but they never mature to late anagen because if I pull out one of those hairs the bulb is never fully formed. If I could get them to fully mature I would have a full head of thick hair. VEGF is required to build the microvascular network for both arterial supply and venous return, and then once built VEGF diminishes in late anagen. DHT promotes VEGF, so the presence of DHT in the scalp of men with MPB could indicate that DHT is either upregulated to try and rescue VEGF mediated angiogenesis because of poor androgen receptor signalling, or it's a pathological issue where DHT is overexpressed, causing a permanent upregulation of VEGF-mediated angiogenesis and too much oxygen and blood flow is pumped into the area, causing excess oxygen radical formation and subsequent oxidative stress, which doesn't allow for full maturation into late anagen. I honestly think it could be both depending on the person - I think young people are more likely to suffer from that excess blood flow/flushing, while older people are more likely to have issues with improper AR signalling and diminished angiogenesis. I can speak from experience - I have no issues with angiogenesis and blood flow on every other part of my body. I often run hot, with good blood flow to the skin everywhere.
Also UV irradiation causes upregulating of VEGF. I notice that when my scalp gets direct UV exposure the flushing/heat issue becomes much worse. This year I've made a really strong attempt to always wear a hat when I'm outside in the sun, and my scalp quality has improved a lot. But that could also be due to UV-induced oxidative stress.
mattyb
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No, microvasculure circulation on the top of the scalp is different from arterial supply to the brain. The brain is supplied directly by several major arteries that pass through the base of the skull, and is permeated by those major arteries. The top of the scalp is supplied mostly by the superficial temporal artery on the outside of the side of the head.
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Matty, NO activates VEGF. The problem is that eNOS will generate superoxide if BH4 is absent. And this is why you need glutathione, and histidine, since bh4 is recycled by NADPH and tetralfolate. and tetralfolate is made by NADPH and if histidine is low, tetralfolate is prohibited, since tetralfolate will break it down into glutamic acid. This is why hairloss people feel heat on the head. Since histamine receptors H2 are going nuts with low histidine. and without histidine there is no tetrafolate, and without tetralfolate there is no bh4 and without bh4, eNOS does not make NO, but makes superoxide. And boom, you got 2 things going, you got superoxide creation and super sensitivity to histamine.
Also without NO as you said VEGF will not start up. Actually NO itself does many things what you think VEFG does.
eNOS is a dimer containing two identical monomers of 134 kD constituted by a reductase domain, which displays binding sites for nicotinamide adenine dinucleotide phosphate (NADPH), flavin mononucleotide (FMN), and flavin adenine dinucleotide (FAD), and an oxidase domain, which displays binding sites for heme group, zinc, the cofactor tetrahydrobiopterin (BH4), and the substrate L-arginine.[13] The reductase domain is linked to the oxidase domain by a calmodulin-binding sequence.[14] In the vascular endothelium, NO is synthesized by eNOS from L-arginine and molecular oxygen, which binds to the heme group of eNOS, is reduced and finally incorporated into L- arginine to form NO and L-citrulline.[15][16] The binding of the cofactor BH4 is essential for eNOS to efficiently generate NO.[17] In the absence of this cofactor, eNOS shifts from a dimeric to a monomeric form, thus becoming uncoupled.[18] In this conformation, instead of synthesizing NO, eNOS produces superoxide anion, a highly reactive free radical with deleterious consequences to the cardiovascular system.[19][20]
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@mattyb
Tetrahydrobiopterin is biosynthesized from guanosine triphosphate (GTP) by three chemical reactions mediated by the enzymes GTP cyclohydrolase I(GTPCH), 6-pyruvoyltetrahydropterin synthase (PTPS), and sepiapterin reductase (SR).[12]
BH4 can be oxidized by one or two electron reactions, to generate BH4 or BH3 radical and BH2, respectively. Research shows that ascorbic acid (also known as ascorbate or vitamin C) can reduce BH4 radical into BH4,[13] preventing the BH3 radical from reacting with other free radicals (superoxide and peroxynitrite specifically). Without this recycling process, uncoupling of the endothelial nitric oxide synthase (eNOS) enzyme and reduced bioavailability of the vasodilator nitric oxide occur, creating a form of endothelial dysfunction.[14] Ascorbic acid is oxidized to dehydroascorbic acid during this process, although it can be recycled back to ascorbic acid.
And vitamin C is recycled by glutathione in ascorbate cycle. then Vitamin C recycles Bh4 and vitamin E. Which basically increases eNOS and also decrease fibrosis .
Tetrahydrobiopterin is biosynthesized from guanosine triphosphate (GTP) by three chemical reactions mediated by the enzymes GTP cyclohydrolase I(GTPCH), 6-pyruvoyltetrahydropterin synthase (PTPS), and sepiapterin reductase (SR).[12]
BH4 can be oxidized by one or two electron reactions, to generate BH4 or BH3 radical and BH2, respectively. Research shows that ascorbic acid (also known as ascorbate or vitamin C) can reduce BH4 radical into BH4,[13] preventing the BH3 radical from reacting with other free radicals (superoxide and peroxynitrite specifically). Without this recycling process, uncoupling of the endothelial nitric oxide synthase (eNOS) enzyme and reduced bioavailability of the vasodilator nitric oxide occur, creating a form of endothelial dysfunction.[14] Ascorbic acid is oxidized to dehydroascorbic acid during this process, although it can be recycled back to ascorbic acid.
And vitamin C is recycled by glutathione in ascorbate cycle. then Vitamin C recycles Bh4 and vitamin E. Which basically increases eNOS and also decrease fibrosis .
supernature
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mattyb
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@Helen
Yup, I know. I'm not saying VEGF just starts acting on it's own magically. I know its regulated by NO. I'm just saying that I think the issue can be both ways, too much VEGF mediated signalling or not enough. VEGF is also responsive to other hormones like DHT, so although NO is kind of the master-switch other hormones can influence it's activity as well. I'm also interested in the side-effects of increasing this directly, one of which could be more aggressive cancer.
But yes, overall this comes down to restoring an insanely complex metabolic process. Making sure antioxidant enzymes are working fully, making sure citric acid cycle and aerobic metabolism are humming along, minimizing superoxide and hydroxyl radical formation, making sure arginine conversion to NO is working, etc. The problem is this general idea isn't super helpful yet, because the testing to allow people to make right choices in which interventions to apply isn't accessible to most people. So I'm very interested in clinical symptoms that are easily observable to know which type a person is, what their problems actually are, and then with proper identification they can start trying out interventions.
Yup, I know. I'm not saying VEGF just starts acting on it's own magically. I know its regulated by NO. I'm just saying that I think the issue can be both ways, too much VEGF mediated signalling or not enough. VEGF is also responsive to other hormones like DHT, so although NO is kind of the master-switch other hormones can influence it's activity as well. I'm also interested in the side-effects of increasing this directly, one of which could be more aggressive cancer.
But yes, overall this comes down to restoring an insanely complex metabolic process. Making sure antioxidant enzymes are working fully, making sure citric acid cycle and aerobic metabolism are humming along, minimizing superoxide and hydroxyl radical formation, making sure arginine conversion to NO is working, etc. The problem is this general idea isn't super helpful yet, because the testing to allow people to make right choices in which interventions to apply isn't accessible to most people. So I'm very interested in clinical symptoms that are easily observable to know which type a person is, what their problems actually are, and then with proper identification they can start trying out interventions.
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Well people at least should be taking everything for the eNOS to work. and everything to recycle BH4. I think if you can recycle BH4. hairloss will be gone. Since NO will tell your hairs to mature since NO does that.
I think high DHT that they found is scalp is because BH4 is missing and NO is not being produced , so extra NADPH is avaiable for DHT there locally.