I'm starting to wonder why my post is so absent any replies - I've tried to make viewing my methylation and detox panel's as easy as possible - can everyone see them ok? (if you hover your mouse over them it increases the size)
2nd one is very hard to read. When making a screen shot, it's good to open up "Paint", paste the screen shot in, then select around the part you want and crop it.
http://www.heartfixer.com/AMRI-Nutrigenomics.htm has some good explanations for your results on the first page you posted. Basically it suggests that you can't convert inactive forms of B12 and folic acid into active forms easily, and that you additionally use up any existing methyl-B12 too quickly. Supplementing methyl-B12 and methylfolate are probably a good idea. BH4, tyrosine and tryptophan also might help.
CYP genes affect how you metabolize certain drugs, and the creation of lipids (including steroids and cholesterol). But it looks like its activity is more controlled by food (and drugs) than by genetics.
The
wikipedia page for CYP1A2 has a nice list of "inhibitors" which slow down the ability to metabolize certain "substrates". Whereas the "inducers" can help speed up the metabolism of the "substrates" . I think
So if you take anything on the substrates list, its effects might be longer lasting or more intense than they would be for normal people, and if you take something from the inhibitors list, it also might make things worse. But taking something on the inducers list might help restore normal functioning, which could be beneficial when it comes to producing essential lipids like cholesterol and steroids.
CYP1B1 is somehow involved in aldosterone production, and is inhibited by St John's wort. Can't really find any additional info on that one - sounds like it's a bit more of a recent discovery than some of the other CPY genes.
Wikipedia also has nice pages for
CYP2C19 and
CYP2D6 with a list of their substrates, and the inhibitors and inducers which can affect the metabolism of those substrates.
SOD2 also has a wikipedia page, and "this protein transforms toxic superoxide, a byproduct of the mitochondrial electron transport chain, into hydrogen peroxide and diatomic oxygen". It's also interesting because it's implicated in protecting the heart from arrythmia and heart attack. A 50% deficiency in mice results in a normal life span but increased DNA damage and incidence of cancer. So it might be nice to see if there's a way to get it to work more effectively, or an alternative way to get rid of superoxide.
NAT2 R197Q says you'll be a slow metabolizer of various drugs containing "heterocyclic amines", and possibly exhaust fumes and tobacco smoke.
