@zadig777
There are no methylation agents? LOL what? Methyl groups are methylation agents)) haha
You need both processes to work )) methylation and demethylation.
Redox in the cell controls epigenome)) You need to understand that. All this bs about methylation and demethylation is ignorant stuff.
These processes are controlled by methylation and demethylation enzymes. and Redox in the cell controls it.
Both systemic and local deficiency affects the availability of ascorbate to the cell. Furthermore, the transport of ascorbate to the nucleus is the key for ascorbate to reach to the chromosomes, which then influences the epigenome by participating in the demethylation of DNA and histones. More importantly, ascorbate is merely one component of the redox network in the cell. The degradation and recycling of ascorbate is largely controlled by the redox status. For example, the status of redox couples including GSH/GSSG, NADH/NAD and FADH2/FAD are capable of impacting the ascorbate/DHA redox couple, and thus, the availability of ascorbate to the DNA and histone demethylation machinery. Consequently, redox status in the cell, especially in the nucleus, will have a profound impact on the epigenome via ascorbate. It is well known that redox status changes along with development, aging, health and diseases. Bridging the gap between redox biology and genomics, we suggest an interdisciplinary research field that can be termed “
Redox Genomics” to study the dynamic role of redox in health and diseases. Embryonic development, aging and many diseases such as chronic inflammation, cancer, diabetes, and neurodegenerative disorders, could be reassessed from the perspective of Redox Genomics.
As you see ascorbate/ DHA ratio is controlled by glutathione.( redox) in the cell
it is called glutathione ascorbate cycle. where glutathione keeps vitamin C in form of ascorbate, and not in form of DHA.
Glutathione-ascorbate cycle - Wikipedia
this ascorbate then recycles BH4 which fixes hypomethylation, and also increases TET enzymes which promotes demethylation.
taking drugs cant fix this problem )) since it is not about hypomethylation or hypermethylation. It is about REDOX in the cell
and if you go and check on propecia forum, the tests, you will see that there is simply zero reduced glutathione in the cell of PFS people.
There is no recycling of glutathione, thus the body has to go and make glutathione de novo from cysteine.
And this stops methylation totally, since methionine synthase goes down, and all homocysteine goes to make cysteine)) so there is CBS pathway activation.
Regulation of the Epigenome by Vitamin C
Finasteride binds NADPH, so it directly kills glutathione reductase. Glutathione reductase controls reduced / oxidized glutathione status which then controls ascorbate, which is a cofactor for methylation and demethylation enzymes.