Effects of dietary supplementation of high-dose folic acid on biomarkers of methylating reaction in vitamin B(12)-deficient rats.
"A greater methyl group supply could lead to compensation for vitamin B(12) deficiency. On this basis, the present study was conducted to examine the effects of high-dose folic acid (FA) supplementation on biomarkers involved in the methionine cycle in vitamin B(12)-deficient rats. Sprague-Dawley rats were fed diets containing either 0 or 100 microg (daily dietary requirement) vitamin B(12)/kg diet with either 2 mg (daily dietary requirement) or 100 mg FA/kg diet for six weeks. Vitamin B(12)-deficiency resulted in increased plasma homocysteine [Homocysteine can be recycled into methionine, large plasma levels of homocysteine means the body thinks it is methionine and in turn S-Adenosyl Methionine deficient], which was normalized by dietary supplementation of high-dose FA. However, FA supplementation and vitamin B(12) deficiency did not alter hepatic and brain S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) concentrations and hepatic DNA methylation. Supplementation of high-dose FA improved homocysteinemia in vitamin B(12)-deficiency but did not change SAM and SAH, the main biomarkers of methylating reaction."
Folic Acid also helps in ensuring that growth plate chondrocytes stay methylated. There's no evidence from this article to suggest that Vitamin B12 has an additional effect on top of FA. S-Adenosyl Methionine is best in terms of making sure growth plate chondrocytes stay methylated. However, taking one of Folic Acid, B12, or B6 is probably enough for most normal people. Excepting if you get enough of these in the data. Of course, your body could be resistant to say Folic Acid in which case B12 or B6 would be the only way to ensure proper methylation. You could also rely on your diet for the proper amounts of the chemicals but as more of your cells divide then the more Folic Acid et al. you need.
Change of epigenetic control of cystathionine beta-synthase gene expression through dietary vitamin B12 is not recovered by methionine supplementation.
"Vitamin B12 (B-12) is an essential cofactor for methionine synthase, and methionine is critical for the methylation of various biological molecules including DNA. Whether changes in B-12 levels can alter specific gene expression through DNA methylation and whether dietary methionine has any effect on general DNA methylation status still remains controversial.
We raised severely B-12-deficient rats as well severely-B-12 deficient rats but supplemented with 5% methionine. mRNA levels of methionine cycle-related enzymes were analyzed.
Gene expression patterns changed under B-12-deficient conditions but were recovered by dietary methionine supplementation to B-12-deficient rats. However, cystathionine beta-synthase mRNA levels, which had decreased under B-12-deficient conditions, did not recover with supplementary dietary methionine. The CpG island of the cystathionine beta-synthase promoter was hypomethylated in B-12-deficient rats, and showed no recovery after methionine addition.
Dietary B-12 can affect epigenetic machinery by regulating DNA methylation status and dietary methionine may have small effects on DNA methylation."
Deficiency in Vitamin B12 can produce irreversible damage in the cystathionine beta-synthase promoter. The CBS does have a role in the bone and could cause your height to be reduced. But whether CBS has a role on height is unclear.
The reason that it's called epigenetics is that your methylation status can affect your progeny.
Maternal methyl supplements increase offspring DNA methylation at Axin Fused.
"Transient environmental exposures during mammalian development can permanently alter gene expression and metabolism by influencing the establishment of epigenetic gene regulatory mechanisms. Methyl donor supplementation of female mice before and during pregnancy permanently increases DNA methylation at the viable yellow agouti (A(vy)) metastable epiallele in the offspring. The current study tested whether another murine metastable epiallele, axin fused (Axin(Fu)), similarly exhibits epigenetic plasticity to maternal diet. We found that methyl donor supplementation of female mice before and during pregnancy increased DNA methylation at Axin(Fu) and thereby reduced by half the incidence of tail kinking in Axin(Fu)/+ offspring. The hypermethylation was tail-specific, suggesting a mid-gestation effect. Our results indicate that stochastic establishment of epigenotype at metastable epialleles is, in general, labile to methyl donor nutrition, and such influences are not limited to early embryonic development."
The methylation status of the parents can affect the methylation status of the child. So if you are Vitamin B12 deficient the CBS deficiency could possible carry to the offspring. Make sure you get enough Vitamin B12 in your diet to increase your height and increase your children's heights.
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