I dug deeper into the hair color recovery phenom. Turns out there is more research behind vitamin B12 affecting my hair color. But it also involves Methyl Folate, which I’ve been using as well! Also, links to the two supplements I use below.
The functional info:
Vitamin B12 activates Methyl Folate to make Methionine. Methionine is an essential amino acid. You use methionine for:
- Blood cell formation
- White blood cell formation, for your immune system
- Hair melanocyte preservation, which keeps hair color. Lack of methionine leads to oxidation and malfunction of the color-producing melanocytes. So there it is!
- Vitamin B12 is also needed for the brain and nervous system. Methyl Folate is needed for RNA and DNA building.
Your body does not make Vitamin B12 nor Methyl Folate. You must get them from food. Supplementation is good because it’s hard to get enough of these micronutrients from food.
Important: a lack of one leads to a lack of the other. It’s a chain reaction. If you supplement with one, take the other as well.
B12 is found in eggs, meat, fish, nuts. From Wikipedia:
“Vitamin B12 is found in most animal derived foods, including fish and shellfish, meat (especially liver), poultry, eggs, milk, and milk products. However, the binding capacity of egg yolks and egg whites is markedly diminished after heat treatment.”
Let me add some adjectives to that list: Grass fed or pastured meats, wild fish, and eggs soft boiled or over easy. Keeping the yolks moist or runny preserves the fat and nutrients!
B12 supplement as Methylcobalamin or Cyanocobalamin. From Wikipedia:
“Cyanocobalamin is converted to its active forms, first hydroxocobalamin and then methylcobalamin andadenosylcobalamin in the liver.”
“The metabolic fate and biological distribution of methylcobalamin are expected to be similar to that of other sources of vitamin B12 in the diet.”
“No cyanide is released with methylcobalamin, although the amount of cyanide (2% of the weight, or 20micrograms cyanide in a 1 mg cyanocobalamin tab) is far less than ingested in many natural foods. Although the safety of cyanocobalamin has long been proven, the safety of the other types is also well established.”
But I will soon use:
I’ll explain the switch in a moment.
5000mcg every morning.
Methyl Folate is found in green leafy vegetables, butter and seafood. Go for real food. From Wikipedia:
“Folate naturally occurs in a wide variety of foods, including vegetables (particularly dark green leafy vegetables), fruits and fruit juices, nuts, beans, peas, dairy products, poultry and meat, eggs, seafood, grains, and some beers. Avocado, spinach, liver, yeast, asparagus, and Brussels sprouts are among the foods with the highest levels of folate.”
Use Methyl Folate supplement, not folic acid. Manufactured foods like bread and cereal have the synthetic, inactive form, folic acid. You can see it on food labels, but is not effectively converted by your body. From Wikipedia:
“Folic acid is synthetically produced, and used in fortified foods and supplements on the theory that it is converted into folate. However, folic acid is a synthetic oxidized form, not significantly found in fresh natural foods. To be used it must be converted to tetrahydrofolate (tetrahydrofolic acid) by dihydrofolate reductase (DHFR). Increasing evidence suggests that this process may be slow in humans”
800mcg or two pills every morning.
Other stuff to know
B12 sublingual lozenge:
Easier if you tuck it in after taking the other vitamins. Tastes fruity, which I had to get used to with chocolate butter coffee. With work in the morning, I had to take my vits and drink coffee on the drive. You might want to somehow separate the two. I now drink my coffee first, then take the vits after. This is good because some are fat soluble!
B12 Supplement switch:
I was looking into why I get a sore feeling in my stomach after taking supplements. It’s like a dull, sour tummy. I found that stearic acid or magnesium stearate from vegetable sources can cause this. It’s used commonly in pills as a lubricant for powder, to stick together better. The culprit, I believe, is the larger Jarrow milk thistle pill that contains vegetable stearates. Omitting only this, I noticed a direct absence of the sore feeling.
The supplements listed above also have this ingredient. They’re both made by Jarrow. I’m switching to B12 made by BulkSupplements because they just have it in pure powder form. No other ingredients. Going to try, even though my symptom is gone and I’ve still been using the above pills for the past one week.
Sometimes what works is good enough, and there are times when I want to up the quality. I never paid attention to this particular symptom until recently, so it’s time for me to try something else. I’ll keep you updated!
To powerful living!
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Review of the dirty science:
[Bracketed inserts] and Bolding of text mine.
1. Senile hair graying: H2O2-mediated oxidative stress affects human hair color by blunting methionine sulfoxide repair. https://www.ncbi.nlm.nih.gov/pubmed/19237503
FASEB J. 2009 Jul;23(7):2065-75. doi: 10.1096/fj.08-125435. Epub 2009 Feb 23.
Wood JM1, Decker H, Hartmann H, Chavan B, Rokos H, Spencer JD, Hasse S, Thornton MJ, Shalbaf M, Paus R,Schallreuter KU.
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 (H(2)O(2)) 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 H(2)O(2)-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.
2. Cobalamin dependent methionine synthesis and methyl-folate-trap in human vitamin B12 deficiency. http://www.ncbi.nlm.nih.gov/pubmed/871432
Br J Haematol. 1977 Jun;36(2):189-98.
Sauer H, Wilmanns W.
The activity of methionine synthetase (MS) is important for the rapid growth of human haematopoietic cells [blood cell components] and cultured lymphoblastoid cells [form of lymphocytes that become B cells and T cells]. The MS reaction is the only known metabolic step in which both vitamin B12 and folate are essential in a single enzyme reaction. In vitamin B12 deficiency the MS activity in bone marrow cells is significantly lower than that in normal bone marrow. Free tetrahydrofolic acid (H4PteGlu) is normally liberated from its metabolically inactive storage form, 5-methyl-H4PteGlu (CH3H4PteGlu), in the cobalamin-dependent MS reaction. Thus, in vitamin B12 deficiency H4PteGlu is not available in sufficient concentration to maintain the de novo synthesis of thymidylate and purines, and accords with the methyl-folate-trap hypothesis. After treatment with amethopterin (Methotrexate), the incorporation of 3H-deoxyuridine into cellular DNA is reduced. In proliferating normal cells this effect of methotrexate can be prevented (and the cells rescued) with CH3-H4PteGlu or with CHO-H4PteGlu (5-formyl-H4PteGlu; Leucovorin). On the other hand, in vitamin B12 deficient bone marrow cells this so-called rescue-effect could only be achieved with CHO-H4PteGlu and not with CH3-H4PteGlu. These observations also support the hypothesis of the methyl-folate-trap in vitamin B12 deficiency. Decreased MS activity in vitamin B12 deficiency seems to be the essential metabolic fault, which is responsible for secondary alterations of folate metabolims. Thus, measurement of MS activity may allow direct functional assessment of vitamin B12 deficiency, at least with regard to DNA metabolism.
5. Vitamin B12-folate interrelationships. http://www.ncbi.nlm.nih.gov/pubmed/3927946
Annu Rev Nutr. 1985;5:115-41.
Shane B, Stokstad EL.
The studies discussed in this review support the view that biochemical and clinical symptoms common to both folate and vitamin B12 deficiency are due to the induction of a functional folate deficiency, which in turn is induced by cobalamin deprivation. The interrelationship between these two vitamins is best explained by the methyl trap hypothesis stating that vitamin B12 deficiency can lead to lowered levels of methionine synthetase, which results in a functional folate deficiency by trapping an increased proportion of folate as the 5-methyl derivative. In addition, as 5-methyl-H4PteGlu is a poor substrate for folylpolyglutamate synthetase, there is a decreased synthesis of folylpolyglutamates and consequently a decreased retention of folates by tissues. The real folate deficiency that ensues because of decreased tissue folate levels is probably as important physiologically as the functional deficiency caused by the methyl trap. The sparing effect of methionine can be explained by adenosylmethionine inhibition of methylenetetrahydrofolate reductase, which would prevent the buildup of 5-methyl-H4PteGlun. A deficiency in vitamin B12 would not, in itself, be sufficient to cause a disturbance in folate metabolism. The deficiency would have to result in lowered methyltransferase levels before any such disturbance would be manifest.