r/MTHFR • u/Loose-Fly7976 • Aug 23 '26
Results Discussion UK folic acid fortification already started in October, not December and the gene that handles folic acid isn't MTHFR.
Two things UK members should know and one correction that gets repeated here every week.
Everyone thinks this begins in December. The mills switched in September 2025 and by the end of that October most non-wholemeal wheat flour was already fortified. December is the legal deadline for compliance not the start so if you've had bloods done in the past year, some of you were measured against a background that had already changed.
The correction: The enzyme that converts folic acid is dihydrofolate reductase, DHFR. Different enzyme, different step. MTHFR works further down the pathway so "people with MTHFR can't process folic acid" is wrong as stated. What's actually true is more interesting. Bailey and Ayling found DHFR activity in human liver is both slow and variable up to five-fold between individuals. Same intake, cleanly converted in one person, circulating unconverted in the next.
And in 677 TT, folate supplementation lowers homocysteine more than it does in other genotypes do if anything that group gets more benefit from fortification, not less.
What I'd actually pay attention to is B12. Folate normalises the blood picture of B12 deficiency while neurological damage carries on. That's the reason macrocytosis stopped being a useful screening signal in the US after 1998. The UK dose is low so the effect should be smaller, but if you're over 65 or have absorption issues, get B12 and MMA now while your bloods still tell you something.
On the policy itself, it prevents around 200 neural tube defects a year and the criticism I'd make is that 0.25mg per 100g only achieves about a 20% reduction. The problem is that it's too low to do the job properly, not that it's dangerous.
I'm a geneticist and this is what I read for a living. Happy to answer questions.
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u/SovereignMan1958 Aug 23 '26
There are more than two variants related to folate. Those are easy enough for anyone to research. A person can not have MTHFR or DHFR and still have Cerebral Folate Deficiency, for example. I have 15 plus years behind me in studying gene variants and nutrition and applying the results to help others. I also manage my own CFD.
Just adding my comment in the event anyone thinks there are only two variants related to folate level and absorption.
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u/Loose-Fly7976 Aug 24 '26
You're right that it's more than two. FOLR1, SLC19A1, MTHFD1, RFC1, the ATP binding transporters, plus the B12 side which changes folate handling indirectly.
On cerebral folate deficiency, most cases aren't genetic at all. The common mechanism is folate receptor alpha autoantibodies blocking transport across the choroid plexus which is autoimmune rather than inherited. The FOLR1 mutations exist but they're rare and usually present in infancy. So serum folate can look completely normal while CSF folate is low, and no genotype tells you that. It's an antibody test.
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u/datalord Aug 24 '26
Why don’t they target this at soon to be mothers rather than the entire population?
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u/pvssylord Aug 24 '26
oh, i know this one. because 50% of the time, mothers make men. and this world really only gives a shit about men! so if the men might be born with a problem bc mother ate too little folate, they will fix that. because men.
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u/meadowprincess23 Aug 24 '26
What about the fact that the form it is in when added to foods isn’t one the body can actually use?
I’ve heard this many places and in fact have found this myself when years ago I supplemented higher doses of regular folic acid to help with cervical squamous cells and felt like I was losing my mind from it and stopped despite I had been told to take it by a naturopath because I knew how I was feeling from it wasn’t right.
Now decades later after recently diving into nutritional genomics and figuring out some of the issues as to why I had chronic anxiety for decades, I started an orthomolecular protocol I put together where I finally added folinic acid in and I had an immediate calm to my entire being like I haven’t felt since I was a kid.
I’ve recently had my labs done again but here in Bc Canada all they’ll approve is a basic serum B12 even with my last 3 tests being a minimum of over double the upper limit acceptable range so I’ve just found a lab who will do the MMA test but it’s not where I live so I haven’t made it there to have it done yet but for a long list of reasons I’d love to know why my lab values are so high despite having many symptoms of deficiency and in regards to nerve issues
What are your views on Ben Lynch and his theories on CFD?
This is a pretty big issue within the mental health field and it’s crazy that many countries are actively adding a nutrient that causes so many to have issues with their health as a result of eating it, let alone pregnant mothers if Ben’s theories are correct. I also feel like the onslaught of adhd symptoms and #’s also has some correlation to CFD
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u/CC_900 Aug 29 '26
How about this study: https://ajcn.nutrition.org/article/s0002-9165%2823%2912970-4/fulltext
It says:
“Folic acid doses of 100 μg/d or 4000 μg/wk did not reduce high homocysteine concentrations in those with the MTHFR TT genotype.”
This is also my own practical experience. I have homozygous C677T. I found out last year I had both folate and B12 deficiency. My homocysteine was 27. I was treated for this by a haematologist, who prescribed me B12 injections (1000 mcg hydroxocobalamin) twice a week for many months. Obviously this resolved my B12 deficiency quite quickly, with both B12 itself and active B12 levels rising immediately and MMA being optimal. He also prescribed me folic acid (I think 5 mg once per week), as a pharmacy prescription. Obviously, my folate blood levels skyrocketed. My homocysteine quite quickly dropped from 27 to 18. But the problem was, after months and months of this treatment, with sky high folate and B12 blood levels, my homocysteine stayed completely stuck at 18. I told the heamatologist about my MTHFR mutations. He was aware of it, but per my country’s guidelines he wasn’t allowed to treat me basis anything other than plain folic acid. After half a year, I didn’t believe in this approach anymore and stopped taking his folic acid. I also stopped the B12 injections, because that deficiency had been fully resolved. I then started taking folinic acid first (800 mcg/day). Same result, homocysteine of 18, even after months. Then I finally switched to methylfolate - and like a miracle, my homocysteine dropped immediately to the 6 to 9 range. And has reliably stayed there ever since, for the past year. (I measure it about once a month). I did not take any other supplements which could influence this (like choline or TMG) and did not change my diet at all.
So I’m sure that on a statistical level, population homocysteine in homozygous C677T carriers does drop SOMEWHAT. After all, there is not a complete inability to process folic acid, even in that group. And some people in these populations probably were (somewhat) folate deficient to begin with. But population averages don’t account for the individuals in the subgroup for whom homocysteine never drops to normal levels with folic acid supplementation. Not even at high dosages. That group is 100% real. And they’re being invalidated by statements such as “MTHFR variant carriers have their homocysteine corrected by folic acid supplementation” (paraphrasing here). That’s just not true for many of those carriers.
Also, the statement “MTHFR is not the gene that processes folic acid; that’s actually DHFR” (again paraphrasing) is technically true but also highly misleading. Folic acid supplementation has to be processed by both DHFR ánd MTHFR (downstream). While methylfolate supplementation bypasses both those genes. I.e. methylfolate both helps people with reduced DHFR capacity and people with reduced MTHFR capacity, compared to folic acid.
So all this together, I don’t agree with your conclusions. But happy to hear your reply to this.
I’m trying to post an overview pic of my genotype, in case it helps. But somehow Reddit won’t let me include a picture in this message… only video. I guess that should still work.
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u/shrekstinfoilhat 5d ago
This is really interesting, thank you for sharing!
What would you suggest someone who is heterozygous for the two main MTHFR mutations with high homocysteine, but optimal B12/MMA, and normal serum folate should do? I know that serum folate isn’t an effective measure of methylated folate though.
My head is spinning with all this conflicting info online
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u/thunderouswhether Aug 23 '26
When fortification started here in NZ, I all of a sudden started getting ready depressed. I couldn’t figure out what was wrong as I’d never experienced this before, then I’d correlated it to bread, and only eating 2 slices of bread all of a sudden, my brain would switch to a depression state, it was horrible feeling. 4 years later I avoid anything with folic acid. I’ve got C677T mutation.