Reversing Wrinkled Skin And Hair Loss In Mice By Restoring Mitochondrial Function.

Squeegee 2.0

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Betaine could be another weapon as well to restore mitochondrial function.
Betaine is a positive regulator of mitochondrial respiration
https://www.sciencedirect.com/science/article/abs/pii/S0006291X14021706
Betaine increases mitochondrial content and improves hepatic lipid metabolism.
https://www.ncbi.nlm.nih.gov/pubmed/30534761
Betaine enhances the cellular survival via mitochondrial fusion and fission factors, MFN2 and DRP1
https://www.tandfonline.com/doi/full/10.1080/19768354.2018.1512523
tacs_a_1512523_uf0001_oc.jpg

"These data suggest that betaine could play an important role in remodeling mitochondrial dynamics to enhance mitochondrial function and cell viability"
 
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Xenophon

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the thing is, this is just one issue with male pattern baldness. The problem has always been fibrosis.

the fibrosis surround the hair follicle. Follicular fibrosis is the actual find.

if you look at zoomed in scalp pictures of the condition you can see the development of circular looking lesions around the follicle.

Inflammation causes fibrosis. What causes the inflammation is yet to be determined but i am starting to think toxic metal buildup in the follicle prompts the immune system to attack our hair resulting in fibrosis.

Insofar as male pattern baldness is caused by the inflammation/fibrosis feedback cycle I don't think this aspect is a big mystery. The question is to what degree this is causal. It probably varies a lot from person to person. The primary cause I think has got to be simple genetics: those who inherit hair follicles which are especially vulnerable to DHT's effects. Chronic low grade inflammation however is significantly in our control to the extent that it is a product of a bad diet, one that is low in fat-soluble vitamins and magnesium, and high in PUFAs.

We seem to know that Mg and taurine as well as microneedling help prevent or even undo calcifciation and fibrosis. To what degree and what empirical evidence is there (biopsies etc)? It's quite easy and cheap to apply Mg topically.
 

HairCook

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The role of mitochondria in stem cell fate and aging.
https://dev.biologists.org/content/develop/145/8/dev143420.full.pdf


Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026732/

Resveratrol is an AhR antagonist. A real AhR antagonist did show 50-fold increase in CD34 expression.

Regarding ursolic acid, I saw at least two or three on amazon. (I linked even one and there was no word of it being only 25% or so).
 

Armando Jose

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What causes the inflammation is yet to be determined but i am starting to think toxic metal buildup in the follicle
which metal? ;) why don´t enrancied sebum?

https://ca.bodybuilding.com/store/ast/urso-x.html?skuId=AST980106
Rosemary Extract (Rosmarinus officinalis) (leaf) containing 25% Ursolic Acid
A inexpensibe product, at least in my country

Insofar as male pattern baldness is caused by the inflammation/fibrosis feedback cycle I don't think this aspect is a big mystery
+1
 

polishkickbuttowski

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I'm willing to be a guinea pig for ursolic acid because its mechanism of action seems very promising. Can someone help me make it into a solution? Im thinking I'll make a 10mg ursolic acid/ ml of DMSO solution and I'll use 2 ml a night. I'm welcome to any input. I'm gonna use urso-x from bodybuilding.
 

HairCook

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I'm willing to be a guinea pig for ursolic acid because its mechanism of action seems very promising. Can someone help me make it into a solution? Im thinking I'll make a 10mg ursolic acid/ ml of DMSO solution and I'll use 2 ml a night. I'm welcome to any input. I'm gonna use urso-x from bodybuilding.

Meh, thats then 100% dmso, your scalp will peel. do 30% of the 10mg/ml solution and mix it with castor/borage/olive... oil (after dissolving it in dmso) or whatever usually has issues penetration and is beneficial for hair (or maybe just purified water should be ok as oil will be sticky). Theoretically you could combine it with resveratrol (16mg/ml in dmso according to google), there are even micronized powders around (https://www.amazon.de/gp/product/B007X5WLV6/ref=ask_ql_qh_dp_hza)

If after predissolving in dmso there is something at bottom of the bottle leave it there and transfer it dmso solution to another bottle as those will be unsoluble fillers from the supplement like magnesium stearate.

Also make sure to read about handling dmso (only glass bottles, glass pipettes... wash your hands and scalp before applying etc... it basically almost an injection as it is able to drag anything into your blood).

DMSO kinda sucks, maybe someone with more chemical knowledge can help.
 

polishkickbuttowski

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After reading about DMSO i no longer want to use it as it seems potentially dangerous and not fully understood. I think I'll try just ursolic acid and water and see if anything happens.
 

HairCook

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After reading about DMSO i no longer want to use it as it seems potentially dangerous and not fully understood. I think I'll try just ursolic acid and water and see if anything happens.

dmso is generally safe. I used it for a long time, did few 100% dmso peels as well.

But sure if you dont want to handle it, it might be better to stay off it.
 

hailbrotzu

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I'm willing to be a guinea pig for ursolic acid because its mechanism of action seems very promising. Can someone help me make it into a solution? Im thinking I'll make a 10mg ursolic acid/ ml of DMSO solution and I'll use 2 ml a night. I'm welcome to any input. I'm gonna use urso-x from bodybuilding.

which ursolic acid are you going to try? I would also be willing to try it. I think we could use distilled water or water/ethanol.
 

HairCook

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pegasus2

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Been taking taurine and resveratrol for years. I can't say they help, but they probably do, and there's no good reason not to take them.
 

Squeegee 2.0

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Bump! Androgenic Alopecia is a results of Mitochondria dysfunction motherfuckers!!

Progressive expression of PPARGC1α is associated with hair miniaturization in androgenetic alopecia
Introduction


Male patterned hair loss, or androgenetic alopecia (Androgenetic Alopecia) is the most common form of hair loss, prominent in males and characterized by progressive miniaturization of hair follicles1. Androgen signaling was considered as prominent cause for Androgenetic Alopecia as castrated men do not exhibit baldness. Dihydrotestosterone (DHT) acts on androgen receptor (AR) at the DP and directly induces the expression of growth inhibiting factors such as TGF-β2, DKK1 and IL-62,3,4. Drugs blocking testosterone metabolism including Finasteride have been proven effective against male Androgenetic Alopecia in more than half of patients5,6,7. However, there is increasing evidence that additional causes may be involved in Androgenetic Alopecia pathogenesis, particularly in women8,9.

Recent studies have shown the involvement of oxidative stress and mitochondrial activity in Androgenetic Alopecia. The dermal papilla cells display reduced ability in alleviating oxidative stress despite increased levels of catalase and total glutathione10,11. Moreover, regulators of energy metabolism and inflammation such as the nuclear Peroxisome proliferator-activated receptors (PPARγ, α, β) are also involved in hair loss12. PPARγ is mainly expressed in the epidermis and sebaceous glands in the skin13,14,15. In an anagen human hair follicle PPARγ expression is detected in the mesenchymal DP cells, epithelial cells of the outer root sheath (ORS), inner root sheath and matrix16. It was shown to inhibit keratinocyte proliferation and promotes terminal differentiation17. Total and conditional knock out of PPARγ in hair follicle bulge stem cells showed similar result where scarring alopecia was observed in mice with the loss of pilosebaceous units and inflammatory cells infiltration18,19. Recent studies showed that treatment of hair follicles by agonistic modulators induced entry into catagen with an anti-inflammatory mechanism20.

PPARGC1α (PGC1a) is a transcriptional coactivator which interacts with PPARγ in regulating genes in the energy metabolism pathway induced during exercise21,22,23. However, its role in the skin and hair development is not well characterized.

https://www.nature.com/articles/s41598-019-43998-7
 
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Armando Jose

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Interesting, the paper point to regulators of energy metabolism and inflammation implicated in baldness but,
Are mitochondria different in the pattern of common hair loss?
 

Pigeon

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Bump! Androgenic Alopecia is a results of Mitochondria dysfunction motherfuckers!!

Progressive expression of PPARGC1α is associated with hair miniaturization in androgenetic alopecia
Introduction


Male patterned hair loss, or androgenetic alopecia (Androgenetic Alopecia) is the most common form of hair loss, prominent in males and characterized by progressive miniaturization of hair follicles1. Androgen signaling was considered as prominent cause for Androgenetic Alopecia as castrated men do not exhibit baldness. Dihydrotestosterone (DHT) acts on androgen receptor (AR) at the DP and directly induces the expression of growth inhibiting factors such as TGF-β2, DKK1 and IL-62,3,4. Drugs blocking testosterone metabolism including Finasteride have been proven effective against male Androgenetic Alopecia in more than half of patients5,6,7. However, there is increasing evidence that additional causes may be involved in Androgenetic Alopecia pathogenesis, particularly in women8,9.

Recent studies have shown the involvement of oxidative stress and mitochondrial activity in Androgenetic Alopecia. The dermal papilla cells display reduced ability in alleviating oxidative stress despite increased levels of catalase and total glutathione10,11. Moreover, regulators of energy metabolism and inflammation such as the nuclear Peroxisome proliferator-activated receptors (PPARγ, α, β) are also involved in hair loss12. PPARγ is mainly expressed in the epidermis and sebaceous glands in the skin13,14,15. In an anagen human hair follicle PPARγ expression is detected in the mesenchymal DP cells, epithelial cells of the outer root sheath (ORS), inner root sheath and matrix16. It was shown to inhibit keratinocyte proliferation and promotes terminal differentiation17. Total and conditional knock out of PPARγ in hair follicle bulge stem cells showed similar result where scarring alopecia was observed in mice with the loss of pilosebaceous units and inflammatory cells infiltration18,19. Recent studies showed that treatment of hair follicles by agonistic modulators induced entry into catagen with an anti-inflammatory mechanism20.

PPARGC1α (PGC1a) is a transcriptional coactivator which interacts with PPARγ in regulating genes in the energy metabolism pathway induced during exercise21,22,23. However, its role in the skin and hair development is not well characterized.

https://www.nature.com/articles/s41598-019-43998-7
Interesting, so what can we do about it?
 

whatevr

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Interesting, so what can we do about it?

Nothing. The authors of the study he quotes aren't even sure themselves if this is something that contributes to Androgenetic Alopecia or is simply a reactive mechanism to the damage:

"The fact that PGC1a, as a master regulator for mitochondrial biogenesis and ability to bind to large array of genes such as RXRα, estrogen receptors and androgen receptor adds to the complexity of deciphering its role in hair growth4143. Further work needs to be done to distinguish if PGC1a is involved in Androgenetic Alopecia pathogenesis or plays a protective role against Androgenetic Alopecia."
 
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