Thanks Mastemah and Blossom. One thing I saw on blogs was how little people understand the chemistry of the body, making them so vulnerable to panic and snake oil salesmen.
I have a pretty good handle on this now so I want to share it. This page
has several diagrams and he writes in a style that I can understand.
The whole point of it all is to produce S−Adenosyl Methionine (SAMe), which is the main methyl donor in the body and is used in lots of important pathways. Norepinephrine -> epinephrine uses SAMe, for example.
Methionine is the rate limiting substrate in the production of SAMe. The only other factor is ATP and if you're running low on that you have much bigger problems than this.
When SAMe gives up its methyl group to some other compound it becomes SAH and when an adenosine molecule is taken off the H is homocysteine. If that was the end of it the only way to make more SAMe would be to eat more methionine.
So there are two parallel pathways from homocysteine -> methionine, both of which simply add a methyl group to homocysteine. One uses methylfolate and the other uses betaine (trimethyl glycine). It is easy to speculate that having two ways of doing the same thing shows how important it is to produce more methionine without having to eat it.
The enzyme the 677 gene codes for just changes one form of methylfolate to another form of methylfolate, 5,10 MTHF -> 5 MTHF.
has a bunch of info about names and isomers, and says about 70% of the folate in food is in the final usable form, so the enzyme isn't needed at all.
There are other odds and ends but I'll quit. There is a lot of chatter about high homocysteine and CVD, etc but it seems to me the important issue is low SAMe if the methylation cycle is sub par for any reason.
Edit: my statement that methionine is the rate limiting substrate in the production of SAMe was incomplete. There is an enzyme involved in addition to ATP, which may be rate limiting.