World Hair Research

Vitamin B9, Folic Acid (Folate) is a water-soluble B vitamin that takes its name from the Latin word for leaf, folium, because it was first isolated from spinach leaves.

Folic Acid helps maintain healthy hair, nails and skin. It may aid in preventing hair loss.
Along with Pantothenic acid, may delay graying of hair.
It is necessary for DNA & RNA synthesis, which is essential for the growth and reproduction of all body cells
It is essential to the formation of red blood cells by its action on the bone marrow and aids in amino acid metabolism
Folic Acid is crucial for methylation in the body.

Biochemically, folic acid functions as a methyl donor after being enzymatically reduced to tetrahydrofolate by the enzyme dihydrofolate reductase. This biochemical reaction is the target of a number of chemotherapeutic antimetabolites such as methotrexate that bind to the enzyme and prevent the reduction.

Folic acid promotes normal red blood cell formation, helps to maintain the central nervous system, and promotes normal growth and development. Recent investigations show that folic acid deficiency may be responsible for neural tube defects, a type of birth defect that results in severe brain or neurological disorders (see Spina Bifida).

The U.S. Public Health Service recommends that women of child-bearing age take 0.4 mg of folic acid daily. Women should continue to take that dose through the first three months of pregnancy. The RDA for men is 400 mcg and women is 200 mcg.

Folic acid is effective in the treatment of certain anemias and sprue.

Folic acid is found in Brewer’s yeast, liver, fruits, leafy vegetables, oranges, rice, soybeans, and wheat, organ meats, leafy green vegetables, legumes, nuts, whole grains.

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Notes:

• It is good to supplement Betaine HCl, or Betaine anhydrous, (with a meal) because stomach acid will convert it into trimethylglycine (TMG). *
• If you’re not taking real (non-synthetic) forms of B-vitamins, you might be more susceptible to androgenic alopecia (hair loss).
• The most important B vitamins to keep strong methylation going are: Choline, Folate (not folic acid), B6 (natural form is better) and B12.
• Both Folate and vitamin B12 stimulate methylation.
• The occipital hair follicles in male-patterned hair loss are properly methylated, however the vulnerable MPB hair follicles are not.
• For most people, extra methylation will help.

What is Methylation?

Methylation contributing to epigenetic inheritance can occur through either DNA methylation or protein methylation.

DNA methylation in vertebrates typically occurs at CpG sites (cytosine-phosphate-guanine sites, that is, where a cytosine is directly followed by a guanine in the DNA sequence). This methylation results in the conversion of the cytosine to 5-methylcytosine. The formation of Me-CpG is catalyzed by the enzyme DNA methyltransferase. Human DNA has about 80%-90% of CpG sites methylated, but there are certain areas, known as CpG islands, that are GC-rich (made up of about 65% CG residues), wherein none are methylated. These are associated with the promoters of 56% of mammalian genes, including all ubiquitously expressed genes. One to two percent of the human genome are CpG clusters, and there is an inverse relationship between CpG methylation and transcriptional activity.

Protein methylation typically takes place on arginine or lysine amino acid residues in the protein sequence.[1] Arginine can be methylated once (monomethylated arginine) or twice, with either both methyl groups on one terminal nitrogen (asymmetric dimethylated arginine) or one on both nitrogens (symmetric dimethylated arginine) by peptidylarginine methyltransferases (PRMTs). Lysine can be methylated once, twice or three times by lysine methyltransferases. Protein methylation has been most-studied in the histones. The transfer of methyl groups from S-adenosyl methionine to histones is catalyzed by enzymes known as histone methyltransferases. Histones that are methylated on certain residues can act epigenetically to repress or activate gene expression.[2][3] Protein methylation is one type of post-translational modification.

The Methyl group is so important that when a cell is broken down the methyl is saved inside a toxic amino acid called Homocysteine.

Homocysteine is toxic to keep bacteria and parasites away from it during the short trip to the liver where it is unpacked and the methyl gets used up by the various steps of methylation which supply compounds ranging from Tryptophan to SAMe used for DNA methylation and neurotransmitters, hormones and Serotonin.

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Impact of inflammation on epigenetic DNA methylation – a novel risk factor for cardiovascular disease?

Stenvinkel P, Karimi M, Johansson S, Axelsson J, Suliman M, Lindholm B, Heimbürger O, Barany P, Alvestrand A, Nordfors L, Qureshi AR, Ekström TJ, Schalling M.

Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden. peter.stenvinkel@ki.se
Abstract

OBJECTIVE: The lifespan of dialysis patients is as short as in patients with metastatic cancer disease, mainly due to cardiovascular disease (CVD). DNA methylation is an important cellular mechanism modulating gene expression associated with ageing, inflammation and atherosclerotic processes.

DESIGN: DNA methylation was analysed in peripheral blood leucocytes from three different groups of chronic kidney disease (CKD) populations (37 CKD stages 3 and 4 patients, 98 CKD stage 5 patients and 20 prevalent haemodialysis patients). Thirty-six healthy subjects served as controls. Clinical characteristics (diabetes mellitus, nutritional status and presence of clinical CVD), inflammation and oxidative stress biomarkers, homocysteine and global DNA methylation in peripheral blood leucocytes (defined as HpaII/MspI ratio by the Luminometric Methylation Assay method) were evaluated. CKD stage 5 patients (n=98) starting dialysis treatment were followed for a period of 36 +/- 2 months.

RESULTS: Inflamed patients had lower ratios of HpaII/MspI, indicating global DNA hypermethylation. Analysis by the Cox regression model demonstrated that DNA hypermethylation (HpaII/MspI ratio <0.01) and cardiovascular (RR 13.9; 95% CI: 1.8-109.3; P<0.05) mortality, even following the adjustment for age, CVD, diabetes mellitus and inflammation.

CONCLUSION: The present study demonstrates that global DNA hypermethylation is associated with inflammation and increased mortality in CKD

Br J Dermatol. 2011 Mar 24. doi: 10.1111/j.1365-2133.2011.10335.x. [Epub ahead of print]

Evidence of increased DNA methylation of the androgen receptor gene in occipital hair follicles from men with androgenetic alopecia.

Cobb JE, Wong NC, Yip LW, Martinick J, Bosnich R, Sinclair RD, Craig JM, Saffery R, Harrap SB, Ellis JA.

Department of Physiology, University of Melbourne, Victoria Australia 3010 Developmental Epigenetics, Murdoch Childrens Research Institute, Flemington Road, Parkville, Victoria Australia 3052 Department of Dermatology, St Vincent’s Hospital, Victoria Australia 3065 New Hair Clinic, 627 Chapel Street, South Yarra, Victoria Australia 3141 National Hair Institute, 104 Canterbury Road, Middle Park, Victoria Australia 3206 Environmental and Genetic Epidemiology

In order to compare and clarify the underlying hormonal basis, a study was conducted in 12 young women (ages 14-33) and 12 young men (ages 18-30) with AGA (Sawaya and Price, 1997). Androgen receptor, type I and type II 5x-reductase, and cytochrome p-450 aromatase, were measured in hair follicles from scalp biopsies of these young subjects. Both young women and young men had higher levels of type I and type II 5x-reductase and androgen receptors in frontal hair follicles compared to occipital hair follicles; however, the levels in women were approximately half the levels in men (Sawaya and Price, 1997). At the same time, young women had much higher levels of cytochrome p-450 aromatase in frontal follicles than men who had minimal aromatase, and women had even higher aromatase levels in occipital follicles. The differences in aromatase, which is capable of converting testosterone to estradiol, are particularly notable. The findings of this study suggest that the milder expression of AGA in women may in part be the result of lower levels of 5x-reductase and androgen receptors in frontal follicles of women compared to levels in men; additionally, higher levels of aromatase in women may result in increased local formation of estradiol from testosterone, and less formation of 5x-reductase products such as DHT.

Due to the understanding of male pattern baldness as Androgenic Alopecia (i.e. as an androgen-dependent process), many studies have focused on androgen metabolism (AM) in the body and how androgens effect hair.  Studies have shown that “all dermal papilla cells from androgen-sensitive sites contain low capacity, high affinity androgen receptors.” [18]

The dermal papilla (DP), at the base of the hair follicle, has androgen receptors (AR’s) that androgens from the blood bind to. In androgen-sensitive follicles, the androgens are synthesized and diffused over small distances; this induces changes in neighboring cells (like keratinocytes cells) in what is known as “paracrine interactions”. The diffusible proteins are called paracrine factors. [18]

When beard and scalp cells were incubated in androgens, androgens stimulated the cells’ ability to triggered mitosis (cell division) in beard cells but not in scalp cells. The interesting outcome here was that incubation with androgens had the exact opposite effect on scalp cells; these (scalp) cells’ mitogenic capacity was inhibited. [18]

Androgen-sensitive follicles are not simply targeted and affected by androgens; they are actually involved in androgen metabolism (AM) and can convert androgens using steroid-producing (steroidogenic) enzymes, also known as intrafollicular steroidogenic enzymes. [25]

A 2004 study shed more light on specific processes that shorten the hair cycle (that occur within the DP). According to the study, the three processes are as follows: “(1) the conversion of testosterone to DHT by type II 5-alpha-reductase; (2) the synthesis of TGF-beta2 in dermal papilla cells; and (3) the activation of the intrinsic caspase network.” [6]

The research seems to indicate AM activity at the DP of the hair follicle, amongst other interactions is not fully understood yet. Some of the known intrafollicular steroidogenic enzymes found in the DP are: Steroid Sulfatase (STS), 17beta-hydroxysteroid dehydrogenases (17b-HSD), 3beta-hydroxysteroid dehydrogenases (3b-HSD)  and type 1 and 2 5alpha-reductase (type 1 and type 2 5alpha-R). Type 2 5-alpha-reductase has been the target of a number of studies that showed it to accelerate the conversion of free testosterone into DHT. [10] [11] [12] [24] [25] [28] [31]

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