Anyone Had Success With Reversal Of Grey Hair?

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The best sources of choline in the diet are egg yolks and beef liver. One large egg contains 113 mg of choline.
You could use eggs to condition the scalp to help reverse gray hair. Or maybe you prefer putting a beef liver on your head, fine too, I say go for it.
 
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Janna

Janna

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General Orange,

thank you very much for the info. It’s all rather confusing irrespective if it’s the egg or liver on my head. What’s on yours today?

I think i’m going to work around the basic blocks first, and save delving into dealing with my Msr enzyme for later. They say it’s the Met’s debris that impair tyrosinase in the first place. So adding more Met to the system should produce more debris, no? If available Met in vivo gets converted to MetO, how adding more Met would prevent its oxidation, I don’t understand. I would thereby get more Met, i’m sure, but it’d also create more debris. The problem is that it doesn’t get recycled. What can block recycling in my case is mercury. But not everyone with grey hair has it.. I’m going through chelation by the way.

Anyone has two cents on this bit of research?
 
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Excessive stress can interrupt the trans sulfuration pathway of Methionine - Glutathione, due to a poor phosphatidylcholine synthesis that in turn cause a poor choline-phosphatidyl ethanolamine synthesis. So supporting the phosphatidylcholine synthesis will help Methionine getting used for Glutathione and help repair the hair by methionine sulfoxide with less "debris"

https://www.hindawi.com/journals/isrn/2013/637897/
Comparison of fluorographic and autoradiographic images indicated that glutathione had incorporated -methionine demonstrating that functional transsulfuration occurs in mammary cells.

Choline and methionine differentially alter methyl carbon metabolism in bovine neonatal hepatocytes
Methionine supply is further challenged by its use for the de novo synthesis of choline when choline is unavailable.
see figure 1
pone.0171080.g001
 
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Janna

Janna

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Thank you, General Orange. In this case I would rather supplement with cysteine directly if we aim to increase glutathione levels. But the question is is my cysteine low? Or is my glutathione low? Why can’t it be low catalase or plain low copper to impair tyrosinase directly?
I think I should just go and do some tests. I can do red cell GPx, plasma SOD and copper. If GPx come low, and I already supplement with Se, then I’d infer that it must be cysteine or glutamine that’s low. Or if GPx is good, but copper is low, i’d infer that it’s low copper affecting tyrosinase or SOD, or that it’s the catalase that needs fixing..
What do you think?
 
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I found this:

What is the biomolecular pathway that causes the graying of hair?
In their 2011 article on the biochemistry of hair pigmentation, Schallreuter et al. suggest that hydrogen peroxide, or H2O2 leads to gray hair through a multitude of pathways. Accumulation of hydrogen peroxide can affect antioxidant machinery, tyrosinase activity in melanogenesis, and cAMP signaling, among other mechanisms.

Under normal conditions, hydrogen peroxide is split to H2O (water) and O2 by catalase. Higher than normal concentrations of hydrogen peroxide and metals lead to hydroxyl radicals which oxidize methionine and tryptophan, deactivating catalase. Low catalase activity is linked to both vitiligo and gray hairs. The decrease in catalase activity causes deleterious effects on tyrosinase, an important enzyme in melanogenesis (the formation of the hair and skin pigment known as melanin). In turn, these effects on tyrosinase also affects tyrosine concentrations, causing a decrease in melanogenesis and hair color.

Hydrogen peroxide also affects levels of POMC-derived peptides, which target skin and hair follicles, by reducing POMC processing. This in turn leads to decreased concentrations of these POMC peptides ACTH, alpha and beta MSH as well as beta-endorphin, which have roles in pigmentation and regulation of cAMP, which upregulates tyrosinase. Due to the low concentrations of the POMC peptides, cAMP synthesis decreases, leading to lower activities of cAMP and tyrosinase leading to graying hair.

As seen, increased hydrogen peroxide concentration overall leads to the decrease of tyrosinase through decreased cAMP levels and catalase activities. These two pathways work separately to inhibit tyrosinase, the enzyme directly linked to melanogenesis. For more information and further details, refer to the Schallreuter et al. paper.

titopic1.png
 
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Janna

Janna

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Thank you, General Orange. In this case I would rather supplement with cysteine directly if we aim to increase glutathione levels. But the question is is my cysteine low? Or is my glutathione low? Why can’t it be low catalase or plain low copper to impair tyrosinase directly?
I’ve been supplementing with Se, a co-factor of
 

mujuro

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Ray wrote in his publication "generative energy" that his eyebrows were restored from white back to dark brown with large amounts of copper. Eyebrows were useful because they grow to full length then fall out and are replaced.

I vaguely recall someone on here said that they or someone they knew got a lot of color back in their hair by donating blood (iron) and supplementing copper.
 

agnostic

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Janna

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I found this:

What is the biomolecular pathway that causes the graying of hair?
In their 2011 article on the biochemistry of hair pigmentation, Schallreuter et al. suggest that hydrogen peroxide, or H2O2 leads to gray hair through a multitude of pathways. Accumulation of hydrogen peroxide can affect antioxidant machinery, tyrosinase activity in melanogenesis, and cAMP signaling, among other mechanisms.

Under normal conditions, hydrogen peroxide is split to H2O (water) and O2 by catalase. Higher than normal concentrations of hydrogen peroxide and metals lead to hydroxyl radicals which oxidize methionine and tryptophan, deactivating catalase. Low catalase activity is linked to both vitiligo and gray hairs. The decrease in catalase activity causes deleterious effects on tyrosinase, an important enzyme in melanogenesis (the formation of the hair and skin pigment known as melanin). In turn, these effects on tyrosinase also affects tyrosine concentrations, causing a decrease in melanogenesis and hair color.

Hydrogen peroxide also affects levels of POMC-derived peptides, which target skin and hair follicles, by reducing POMC processing. This in turn leads to decreased concentrations of these POMC peptides ACTH, alpha and beta MSH as well as beta-endorphin, which have roles in pigmentation and regulation of cAMP, which upregulates tyrosinase. Due to the low concentrations of the POMC peptides, cAMP synthesis decreases, leading to lower activities of cAMP and tyrosinase leading to graying hair.

As seen, increased hydrogen peroxide concentration overall leads to the decrease of tyrosinase through decreased cAMP levels and catalase activities. These two pathways work separately to inhibit tyrosinase, the enzyme directly linked to melanogenesis. For more information and further details, refer to the Schallreuter et al. paper.

titopic1.png

Thanks very much! Now it makes more sense. I saw US patent on grey hair reversal
Involving application on scalp of cAMP based compounds. I’m going to read it.

So what do we do in practical terms, General Orange?

1. Boost catalase. How exactly? One of my earlier queries was can we do it via H2O2 challenge?
2. Enable tyrosinase. Add copper plus lots of folic acid, which is essential for tyrosine metabolism.
3. Add l-methionine??
4. What do we do to upregulate cAMP? Is it step 3?
5. Does it mean that glutathione isnt critically involved in greying?
 

dreamcatcher

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And given the new findings, it fits the vitamin E story. Apparently in the conditions of excess H2O2, a by product of oxidation, the load becomes toxic and destroys terosinaise, an enzyme producing hair pigment. Catalase and glutathione peroxydase are supposed to neutralise H2O2, but are over burdened, and don’t do their job. Then there’s the “doctor” enzyme that is also over loaded.

In theory the solution should include a) anti oxidants such as E to reduce the H2O2 load, b) consumption of amino acids and co-factors responsible for production of those enzymes. Ray says to add copper for this reason; copper is a co factor of tyrosinase, but so are amino acids, hence importance of adequate protein in the diet.

Selenium, cysteine and glutamine are co factors of glutathione peroxydase. Interestingly, catalase has iron as a co factor. But adding iron isn’t a solution, according to Ray. Hmm I read that in yeast cultures H2O2 challenge boosts catalase levels significantly. Anyone tried adding H2O2 drops? I think this is what H2O2 therapy is all about. They start with a few drops and increase it, hence it’s a challenge.
Excellent, thank you for sharing this information!
 

dreamcatcher

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Dear, Janna

About your grey hair and how to treat it:

Cause:
Accumulation of hydrogen peroxide (H2O2) bleaches human hair when methionine sulfoxide is insufficient to repair it.


"Senile graying of human hair has been the subject of intense research since ancient times. Reactive oxygen species have been implicated in hair follicle melanocyte apoptosis and DNA damage. Here we show for the first time by FT-Raman spectroscopy in vivo that human gray/white scalp hair shafts accumulate hydrogen peroxide (H2O2) in millimolar concentrations. Moreover, we demonstrate almost absent catalase and methionine sulfoxide reductase A and B protein expression via immunofluorescence and Western blot in association with a functional loss of methionine sulfoxide (Met-S=O) repair in the entire gray hair follicle. Accordingly, Met-S=O formation of Met residues, including Met 374 in the active site of tyrosinase, the key enzyme in melanogenesis, limits enzyme functionality, as evidenced by FT-Raman spectroscopy, computer simulation, and enzyme kinetics, which leads to gradual loss of hair color. Notably, under in vitro conditions, Met oxidation can be prevented by l-methionine. In summary, our data feed the long-voiced, but insufficiently proven, concept of H2O2-induced oxidative damage in the entire human hair follicle, inclusive of the hair shaft, as a key element in senile hair graying, which does not exclusively affect follicle melanocytes. This new insight could open new strategies for intervention and reversal of the hair graying process.

https://www.fasebj.org/doi/abs/10.1096/fj.08-125435

Possible solution:
Choline-related supplements improve abnormal plasma methionine-homocysteine metabolites and glutathione status in children with cystic fibrosis.

Objective: The objective was to address a possible relation between altered methionine-homocysteine metabolism and choline metabolism in children with CF.

"Supplementation with lecithin, choline, or betaine resulted in a significant increase in plasma methionine, SAM, SAM:SAH, and glutathione:GSSG and a decrease in SAH ..."

Choline-related supplements improve abnormal plasma methionine-homocysteine metabolites and glutathione status in children with cystic fibrosis. - PubMed - NCBI
What kind of lecithin would be beneficial? Sunflower? Thank you.
 
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Yeah, when you are chelating metals the glutathione can deplete quickly and needs support. I think boosting cysteine and choline /phosphatidylcholine /lecithin should help maintain methionin-glutathion to tackle excessive Hydrogen peroxides and restore the catalase and tyrosinase activity. So you dont need to directly supplements methionine.

Little glutathione boosting food listed here: link
list of Choline supplements: link

@Rosie De-oiled Lecithin is the better choice, the source used does not really matter then, be it soy or sunflower.
 

dreamcatcher

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Yeah, when you are chelating metals the glutathione can deplete quickly and needs support. I think boosting cysteine and choline /phosphatidylcholine /lecithin should help maintain methionin-glutathion to tackle excessive Hydrogen peroxides and restore the catalase and tyrosinase activity. So you dont need to directly supplements methionine.

Little glutathione boosting food listed here: link
list of Choline supplements: link

@Rosie De-oiled Lecithin is the better choice, the source used does not really matter then, be it soy or sunflower.
Thank you so much for your efforts to post this! Very informative and helpful! Many thanks!!
 

ejalrp

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Dear, Janna

About your grey hair and how to treat it:


"Supplementation with lecithin, choline, or betaine resulted in a significant increase in plasma methionine, SAM, SAM:SAH, and glutathione:GSSG and a decrease in SAH ..."

Choline-related supplements improve abnormal plasma methionine-homocysteine metabolites and glutathione status in children with cystic fibrosis. - PubMed - NCBI

I have been taking almost daily SAM-E for a couple of years and don't believe it has had any effect on the amount of gray hair I have unfortunately.
 
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Janna

Janna

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Yeah, when you are chelating metals the glutathione can deplete quickly and needs support. I think boosting cysteine and choline /phosphatidylcholine /lecithin should help maintain methionin-glutathion to tackle excessive Hydrogen peroxides and restore the catalase and tyrosinase activity. So you dont need to directly supplements methionine.

Little glutathione boosting food listed here: link
list of Choline supplements: link

@Rosie De-oiled Lecithin is the better choice, the source used does not really matter then, be it soy or sunflower.
Thank you for your views and all the info you’ve shared with us! This is helpful. And I understand things a little better now.
 
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Janna

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I have been taking almost daily SAM-E for a couple of years and don't believe it has had any effect on the amount of gray hair I have unfortunately.
Thank you, Ejalrp. Were you taking it to increase cysteine-glutathione or for something else?
 
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@ejalrp I dont think supplementing SAM-e is enough to support the choline-phosphatidylethanolamin synthesis.

I found something what we can do to support that pathway, next to increasing Choline or PC, is with the Shiitake mushrooms that contain eritadenine that increases the phosphatidylethanolamin in the liver. This should help maintain the PC - Choline synthesis. See figure 1

Dietary Eritadenine and Ethanolamine Depress Fatty Acid Desaturase Activities by Increasing Liver Microsomal Phosphatidylethanolamine in Rats | The Journal of Nutrition | Oxford Academic

"The effects of eritadenine, a constituent of the Lentinus edodes mushroom, and ethanolamine, the base constituent of phosphatidylethanolamine (PE), on fatty acid desaturase activities and lipid profiles were investigated comparatively in rats. Rats were fed a control diet or a diet supplemented with either eritadenine (0.05 g/kg) or ethanolamine (8 g/kg) for 14 d. Eritadenine and ethanolamine had marked hypocholesterolemic effects. The concentration of liver microsomal PE was significantly increased and the ratio of phosphatidylcholine (PC) to PE was significantly decreased by both eritadenine and ethanolamine. ..."

Methionine metabolites in the liver.
The concentration of SAM in the liver was significantly increased by dietary Er and conversely decreased by dietary EA (Table 1). The concentration of SAH was markedly increased by Er and was unaffected by EA. Consequently, the SAM/SAH ratio was markedly decreased by dietary Er and slightly decreased by EA

Phospholipid classes in the liver.
The concentration of PC in the liver microsomes, expressed in terms of microsomal protein, was significantly decreased by Er and was unaffected by EA (Table 2). Conversely, the concentration of PE was markedly increased by both Er and EA. The concentrations of the other phospholipids in the liver microsomes were less affected by these compounds. Neither Er nor EA affected the concentration of cholesterol in the liver microsomes. The effects of Er and EA on the phospholipid class composition in the liver microsomes, mitochondria and plasma membranes were also measured (Table 3).

[EDIT]
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Here we see a study done with rats [oops, with mink] that a diet rich in PE will result in higher Homocysteine and a increased conversion of PE to PC.

A diet rich in phosphatidylethanolamine increases plasma homocysteine in mink: a comparison with a soybean oil diet. - PubMed - NCBI
The effects of high dietary levels of phosphatidylethanolamine (PE) on plasma concentrations of homocysteine (tHcy) have not previously been studied. Eighteen mink (Mustela vison) studied were fed one of three diets during a 25 d period in a parallel-group design. The compared diets had 0, 17 and 67 % extracted lipids from natural gas-utilising bacteria (LNGB), which were rich in PE. The group with 0 % LNGB was fed a diet of 100 % soyabean oil (SB diet). Phospholipids are the main lipid components in LNGB and Methylococcus capsulatus is the main bacteria (90 %). The fasting plasma concentration of tHcy was significantly higher when the mink consumed the diet with 67 % LNGB than when they consumed the SB diet (P=0.039). A significantly lower glutathione peroxidase activity was observed in mink consuming the 17 % LNGB diet or the 67 % LNGB diet than was observed in mink fed the SB diet. The lack of significant differences in the level of plasma PE due to the diets indicates that most of the PE from the 67 % LNGB diet was converted to phosphatidylcholine (PC) in the liver. It has previously been hypothesised that phosphatidylethanolamine N-methyltransferase is an important source of tHcy. The present results indicate that plasma tHcy is at least partly regulated by phospholipid methylation from PE to PC. This methylation reaction is a regulator of physiological importance.

- With the addition of extra Glycine from gelatine rich Peat food, like bone broth, Glycine together with Homocysteine should further support the synthesis of Glutathione.
 

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