John A. Catanzaro
MTHFR, COMT and many other genes known in DNA methylation are commonly misunderstood.
Mitochondrial crosstalk basically involves what is called histone modifications that regulate mitochondrial metabolism. Often there is misinterpretation of the true nature of methylation and its relationship to certain methylated nutrients.
One of the major concerns is the use of single nutrients in high doses to influence the methylation circuit in one way or another. I have written several articles on mitochondrial energy and related gene adaptive epigenetics.
I would like to simply state that methylation is a self-regulated process in relation to internal and external stress. It is not as simple as taking one single nutrient to address over methylation or under methylation action.
Human biochemistry requires interaction of substrates and catalysts that coordinate homeostasis (mitochondria regulatory balance).
Please do not jump to conclusions that a single nutrient will correct or cause methylation dysfunction. There is a definite difference between sensitivity to a biochemical nutrient verses a direct cause / correction of methylation dysfunction.
The better approach is specific balanced formulation that focuses on mitochondrial regulation. Mitochondrial methylation is complex and requires the availability and cooperation of key nutrients in concert to facilitate protection of overstressed metabolism or under performance.
More research is needed in adaptive mitochondrial epigenetics. We cannot simply conclude that it is faulty genetics being the cause of depletion or excess. Moreover, a single genetic failure (MTHFR or others) should never be isolated as the only standard for resolution.
I believe the more reasonable argument is indeed to be found in adaptation epigenetics and the corrections required to keep healthy ER and mitochondrial crosstalk.