You know what?
I want to take a minute to rant.
I did a post on “MTHFR” in quotes.
It's just a riboflavin deficiency.
If you didn't see this, go check it out.
It has like, I think, like three point something thousand shares on Facebook so far.
It's 100 or 200 comments a day, I think.
There's a lot of people out there who are saying, "Look, I take riboflavin and it doesn't
change the fact that I feel like crap unless I take methylfolate.
It doesn't change the fact that I need to be careful with methylated B's, or it doesn't
change the fact that all these other things."
What I was saying in that post is that there's a compelling argument that the reason the
C677T and probably by extension the A1298C polymorphisms lower the activity of MTHFR
is because they decrease the binding affinity for riboflavin, and the MTHFR enzyme, if it's
not bound to riboflavin, is defective.
If you have mediocre riboflavin concentrations and you have C677T homozygous MTHFR, you have
low MTHFR activity because fewer of the MTHFR enzymes are bound to riboflavin.
You can fix that by increasing riboflavin concentrations, and so you just supplement
extra riboflavin and you can normalize MTHFR activity.
I put MTHFR in quotes because I meant it the way that people mean when they say, "I have
MTHFR."
Everyone has MTHFR.
What people mean by that is they have these MTHFR polymorphisms.
What I meant by that title is that there's a very compelling—It's not totally airtight.
It's not completely proven.
There's a very compelling argument that the low activity of the C677T polymorphism in
MTHFR is exclusively a result of mediocre riboflavin concentrations.
That's what I meant by just your MTHFR in quotes means the polymorphism, the result
of the polymorphism.
Just riboflavin means that the enzyme activity is only lower as a result of that polymorphism
because of the mediocre riboflavin concentrations.
I get a lot of people that come and say, "Well, I'm taking riboflavin and I still have to
do X. I'm taking riboflavin, and I still see-saw.
If I take this or that, I still get negative reactions to this.
Blah, blah, blah, blah, blah."
I very much believe that people have way deeper problems than MTHFR, and they're just sticking
the MTHFR label on it.
I think the testing of MTHFR is, I don't know.
I think it has a proper place, and I promote it.
But I think the way people are using it out there is doing more harm than good.
Because I think the overwhelming proportion of people in these MTHFR groups are taking
a collection of deeper problems, and because they get tested for MTHFR and the MTHFR comes
back in a bad genotype, they use the genotype as a label that they smack on all their problems.
To them, MTHFR doesn't mean the rate of the MTHFR enzyme.
It's a general label for all their health problems that they put Band-Aid solutions
on like these tedious distinctions between these different forms of B vitamins and stuff
like that that in a healthy well-balanced system don't matter.
If people are hypersensitive to little distinctions in the type of B vitamins they’re taking
like this, their problem is not just MTHFR.
Their problem might be related to methylation.
They probably have mineral deficiencies, or other genetic polymorphisms, or other health
problems, thyroid-adrenal stuff that are causing that.
The reason that MTHFR isn't simply about riboflavin for those people versus the well-controlled
studies of showing that riboflavin supplementation specifically lowers homocysteine 40%, specifically
in people with MTHFR C677T homozygous, specifically with poor riboflavin status.
The reason their story isn't clean like the research is is because MTHFR is a catch-all
label for a host of other problems.
I think the protocols out there that are making all these tedious distinctions, like if you're
an overmethylator you can't take this, if you're under methylated you have to take this,
this, this and this, I think those are slapping Band-Aids on problems, and they're preventing
people from finding what the underlying resolution of those problems is.
I think that's a really important rant that I needed to get out there.
With that preface, I'm not saying that there's no one out there who shouldn't take cyanocobalamin
or shouldn't take methylcobalamin.
But I am saying that if by MTHFR you literally mean the problems that are specifically a
result of the polymorphism in the MTHFR enzyme that you have, then I don't think it has any
implication whatsoever for whether you take cyanocobalamin or methylcobalamin.
The one thing that I would say is that some people might have a negative reaction to methylcobalamin.
If they do, that they don't have to other forms of vitamin B12, then they are profoundly
hypersensitive to the supply of methyl groups in a way that absolutely cannot be explained
by MTHFR, unless it's a very poorly managed MTHFR, which would be most cases of MTHFR.
But I say that because, first of all, these methyl groups on the nutrients are not that
significant.
You put one of these molecules into your body, and that methyl group is used up almost instantaneously.
And then your endogenous addition of methyl groups to that molecule takes over thousands
and thousands of times a day for days and days and days and days on end to that same
one molecule.
That one methyl group that came in is a drip in the ocean of methyl groups that will be
added to that molecule in the lifetime of that molecule in your body.
If you are hypersensitive to the methyl group on the methylcobalamin that you took in, you
have an extremely poorly buffered methylation system.
That could be a result of poor glycine levels.
And the way that MTHFR would relate to that is that methylfolate is the off switch for
the glycine buffer system.
If you have low levels of methylfolate chronically, you will have chronic glycine depletion.
If you don't have a strategy to supply the alternative methyl donor choline, if you don't
have a strategy to reduce the use of methylfolate by creatine supplementation, for example,
if you don't have a strategy to chronically replete the methylfolate by getting low doses
of methylfolate spread throughout the day, and if you don't replete the loss of glycine,
then yeah, you might have negative reactions to methylcobalamin.
But when you're out there saying that overmethylators can't tolerate methylcobalamin or they get
terrible reactions to this, you're slapping overmethylator label on someone whose problem
is that they just don't have a rational strategy for dealing with their MTHFR.
Because no one is an overmethylator or an undermethylator, unless it's a collection
of symptoms of a poorly managed methylation system.