I also just came across these charts in a book. I did not realize that B2 stabilizes (and thus increases the activity of) MTHFR enzymes along with 5MTHF. Unfortunately, I am not sure that I can post the charts, but they can be found on page 261 of
Homocysteine in Health and Disease.
Here is a link to the google book, although you might not get access to the same pages.
I don't entirely understand the experiment (anyone know what a menadione oxidoreductase assay is?) but Here is a table of results extrapolated from the graph. Percents are approximations, and I haven't included indications for standard deviations, which often stretch about 10% in either direction...basically, look at the charts, if you can.
5MTHF in medium

________________________0 (uM)____18.9 (uM)________170 (uM)
% residual activity for wild-type MTHFR

________40%______65%____________95%
% residual activity for MTHFR C677T

__________12%______32%____________65%
FAD in medium

__________________________0 (uM)_____.29 (uM)________1.45 (uM)
% residual activity for wild-type MTHFR

________30%_______75%___________90%
% residual activity for MTHFR C677T

___________5%_______30%___________65%
In any case, I hadn't realized that both B2 and 5MTHF stabilize MTHFR. Perhaps the reason I experienced immediate positive effects from B2 is that I am MTHFR C677T +/+.
@Asklipia,
@Little Bluestem, and anyone else who has had a positive experience with B2, do any of you know your MTHFR SNP status?
I know that the
potential benefits of B2 that have been discussed go far beyond the MTHFR enzyme, and even if I am right about this interaction, all we might be seeing is that C677T +/+ individuals feel good with extra B2, at least until other things are fixed.
PS. When I began high doses of B2, I stopped taking any 5MTHF, and only took one mg of methylcobalamin per day (and no other B12). After two weeks or so, I can say that the lack of 5MTHF has slowly eroded my energy and ability to concentrate, so it seems that decently high B2 does not necessarily negate the need for methylfolate.
PPS: To further clarify, this from
Folate in Health and Disease, Second Edition on page 60 in a chapter by Patrick Stover:
The C677T mutation "enhances the loss of the flavin adenine dinucleotide cofactor (FAD), creating a thermolable protein."
Maybe it is a chicken-or-the-egg thing, but Patrick Stover is saying that C677T is less functional
because it more easily loses hold of B2. Although, again, it seems that having 5MTHF attached to the enzyme also preserves function.