Methylfolate vs Folic Acid: Which Is Better?

Folate is the vitamin your body needs for DNA synthesis, cell division, and methylation, and it exists in two very different supplement forms. Folic acid is the synthetic form that has fortified grain products in the United States since 1998 and sits in most prenatal vitamins. Methylfolate (5-MTHF) is the biologically active form that your cells use directly. The difference matters most for a specific group: people with MTHFR gene variants, which impair the conversion of folic acid into its active form, and people using folate therapeutically for depression or elevated homocysteine. The research shows methylfolate raises plasma folate more efficiently than folic acid in a direct pharmacokinetic comparison, while folic acid carries decades of neural tube defect prevention evidence at a fraction of the cost. This guide compares both forms across absorption, genetics, depression, pregnancy, and cost, so you can match the supplement to your situation instead of the marketing.

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Methylfolate vs Folic Acid: What Is the Difference?

Both forms end up as the same active molecule in your blood, but they get there by different routes. Folic acid is a synthetic, oxidized compound that must be reduced by the enzyme dihydrofolate reductase (DHFR) and then methylated by the enzyme MTHFR to become 5-methyltetrahydrofolate, the form that circulates and enters cells. Methylfolate supplements skip both steps because they already contain the final product, typically as a stabilized salt such as calcium L-methylfolate (Metafolin) or the glucosamine salt Quatrefolic.

The practical differences follow from that single fact. Methylfolate works regardless of how efficiently your MTHFR enzyme functions, and it does not leave unmetabolized folic acid (UMFA) in the bloodstream the way high doses of folic acid can. Folic acid is cheaper, vastly more studied for pregnancy outcomes, and stable enough for food fortification. Neither is “toxic” at normal doses, and for a healthy person without gene variants, both raise folate status effectively.

A pharmacokinetic study by Prinz-Langenohl et al. in the British Journal of Pharmacology directly compared single doses of 400 mcg of folic acid and 416 mcg of [6S]-5-MTHF in women with either two copies (TT) or no copies (CC) of the MTHFR C677T variant. The active form produced significantly higher plasma folate levels (area under the curve and peak concentration) and reached them faster than folic acid in both genotypes, and unmetabolized folic acid appeared regularly after folic acid but rarely after 5-MTHF (PubMed). That is the cleanest summary of the difference: methylfolate gets folate into your blood more efficiently, and folic acid leaves more of itself behind unprocessed.

What Is Methylfolate (5-MTHF)?

Methylfolate is the dominant form of folate in your blood and the form your body actually uses. Its chemical name is 5-methyltetrahydrofolate, and it serves as the methyl donor in the reaction that converts homocysteine back to methionine, which then feeds the methylation cycle that produces SAMe, the compound that methylates DNA, proteins, and neurotransmitters.

That one reaction connects methylfolate to three of its main clinical uses. Because it clears homocysteine, it matters for cardiovascular risk in people with elevated levels. Because methylation supports neurotransmitter synthesis, it has been studied as an adjunct in depression. Because the MTHFR enzyme is needed to make it from folic acid, people with MTHFR variants get more benefit from taking the finished product directly.

Typical dosing by use: 400 to 800 mcg daily for general health and food-equivalent intake; 1,000 to 5,000 mcg daily for people with MTHFR variants, especially C677T homozygotes; 7.5 to 15 mg daily for the depression-adjunct indication studied in clinical trials, always under medical supervision. Products at the 7.5 to 15 mg level are high-dose therapeutic tools, not daily vitamins.

What Is Folic Acid?

Folic acid is the synthetic form of the vitamin, developed because natural food folate is fragile and hard to deliver at population scale. It is what fortifies enriched grains in the United States, Canada, and dozens of other countries, and it is the form in most standard prenatal vitamins.

Its strengths are real. The Medical Research Council Vitamin Study, a randomized trial in 1,817 women who had already had a pregnancy affected by a neural tube defect, found that 4 mg of folic acid daily around conception cut the recurrence risk by 72 percent (relative risk 0.28, 95% CI 0.12 to 0.71), while a mixture of other vitamins did not (PubMed). Population fortification that began in the United States in 1998 was followed by a substantial decline in neural tube defect rates, and organizations including the CDC and ACOG continue to recommend 400 to 800 mcg of folic acid daily for all women who could become pregnant.

Its limitation is the conversion bottleneck. Folic acid must be processed by DHFR and MTHFR, and DHFR capacity in the liver is easily saturated at doses above about 400 to 800 mcg. When that happens, unmetabolized folic acid circulates in the blood. A nationally representative survey of American adults aged 60 and older found unmetabolized folic acid in the serum of a large share of supplement users (PubMed), and an earlier study in postmenopausal women detected unmetabolized folic acid in 78 percent of fasting plasma samples, where its presence was associated with roughly 23 percent lower natural killer cell activity (PubMed). No study has shown that unmetabolized folic acid causes disease in humans, and the authors of both papers called for more research rather than alarm, but it is the main theoretical mark against folic acid at higher doses.

Typical dosing: 400 to 800 mcg daily for general prevention and standard prenatal care; 4 mg daily for women with a previous neural tube defect pregnancy (prescription-level, under obstetric care).

How Do MTHFR Gene Variants Change the Equation?

The MTHFR gene codes for the enzyme that converts the intermediate form of folate into methylfolate. Two common variants, C677T and A1298C, reduce that enzyme’s activity. The C677T variant is the one with the clearest clinical impact: people with one copy (heterozygous) have moderately reduced enzyme function, and people with two copies (homozygous, the TT genotype) have substantially reduced function that varies with riboflavin status.

A comprehensive HuGE review by Botto and Yang estimated that about 10 to 15 percent of North Americans of European ancestry are C677T homozygotes, and roughly 40 to 50 percent carry at least one copy of a common MTHFR variant (PubMed). That is why the “30 to 40 percent of people have MTHFR mutations” figure is common in supplement marketing, though the share that actually matters clinically, the homozygotes, is much smaller.

What the variants change in practice: homocysteine levels tend to run higher in TT homozygotes, especially when riboflavin (vitamin B2) status is low. A randomized trial by McNulty et al. in Circulation found that 1.6 mg of riboflavin daily for 12 weeks lowered homocysteine by up to 22 percent in TT homozygotes (and by 40 percent in those with the lowest riboflavin status at baseline) while having no effect in people with normal genotypes (PubMed). Riboflavin is the cofactor that MTHFR needs to hold onto, which is why B2 status matters for this variant.

For folate supplementation, the logic is straightforward: if your MTHFR enzyme is slow, giving you the product it is supposed to make, methylfolate, sidesteps the bottleneck entirely. A meta-analysis of 25 case-control studies found that maternal C677T homozygosity roughly doubled the odds of a neural tube defect pregnancy (odds ratio 2.02, 95% CI 1.51 to 2.71), which is why women with the variant are the group where methylfolate has the clearest rationale (PubMed).

What the data says: Roughly 10-15% of people of European ancestry carry two copies of the MTHFR C677T variant; in that group 1.6 mg of riboflavin daily lowered homocysteine by up to 22% (40% when baseline riboflavin status was low), and maternal C677T homozygosity carried an odds ratio of 2.02 for neural tube defects across 25 case-control studies.

Which Is Better for Depression?

Folate status is relevant to depression for two reasons: low folate levels are overrepresented in depressed patients and blunt antidepressant response, and methylation supports neurotransmitter synthesis. The pivotal trial is by Papakostas et al., published in the American Journal of Psychiatry, which ran two multicenter trials of L-methylfolate added to a stable SSRI in patients with SSRI-resistant major depression. The first trial, with 148 patients, used 7.5 mg daily for 30 days followed by 15 mg for 30 days and did not separate from placebo. The second trial, with 75 patients, used 15 mg daily throughout and found significantly greater response and symptom improvement than placebo, with a number needed to treat of about six (PubMed).

Two details matter for honest interpretation. First, the dose that worked was 15 mg daily, which is the prescription-level amount, far above the 400 mcg to 1 mg doses sold as general supplements. Second, methylfolate was an add-on to antidepressants in patients who had not fully responded, not a standalone mood supplement. The evidence does not support methylfolate as a self-directed treatment for depression; it supports discussing the 15 mg adjunctive approach with a psychiatrist if you have had a partial response to an SSRI.

The marketed claim that methylfolate “improves antidepressant response by 32 percent” is a loose paraphrase of trial results that does not appear as a single figure in the published abstract. The accurate statement is that 15 mg adjunctive L-methylfolate significantly outperformed placebo on response rate and symptom scores in one of two trials, with an NNT near six.

Key takeaway: In the pivotal 2012 American Journal of Psychiatry trial, 15 mg of L-methylfolate added to a stable SSRI significantly improved response in 75 patients with SSRI-resistant depression (number needed to treat about 6), while the 7.5 mg stepped dose in a 148-patient trial did not separate from placebo; methylfolate for depression is an adjunctive, prescription-level strategy, not an over-the-counter mood pill.

Which Is Better in Pregnancy?

Folic acid is the evidence-based standard, and that is not a close call. The MRC trial showing a 72 percent reduction in neural tube defect recurrence (PubMed), the population-level fortification success, and the consistency of the recommendation across the CDC, ACOG, and WHO all rest on folic acid specifically. Standard guidance: 400 to 800 mcg of folic acid daily, starting at least one month before conception, for everyone who could become pregnant, and 4 mg daily for women with a previous NTD pregnancy.

Where does methylfolate fit? For women with known MTHFR C677T homozygosity, taking the active form is biologically sensible, and methylfolate-containing prenatal vitamins are widely available. But no large trial has compared methylfolate to folic acid for neural tube defect prevention head-to-head, and folic acid’s record is unmatched. The practical guidance from most obstetricians: if you have normal MTHFR status, take the folic acid prenatal; if you carry the C677T variant or simply prefer the active form, methylfolate at the equivalent dose is a reasonable choice, discussed with your obstetrician.

The observational evidence for folate in pregnancy extends beyond neural tube defects. In the Norwegian Mother and Child Cohort of 85,176 children, maternal folic acid use around conception was associated with a lower risk of autistic disorder in the children (adjusted odds ratio 0.61, 95% CI 0.41 to 0.90), though the authors noted the finding cannot establish causality and no association was seen for Asperger syndrome or PDD-NOS (PubMed).

Bottom line: For pregnancy, folic acid remains the evidence-backed standard (400-800 mcg daily for everyone planning pregnancy, 4 mg daily after a previous neural tube defect pregnancy), while methylfolate is a reasonable alternative for women with MTHFR variants; no trial has compared the two forms head-to-head for neural tube defect prevention, so the choice should follow your obstetrician’s advice.

Can Methylfolate or Folic Acid Support Brain Health in Aging?

Low folate status and elevated homocysteine track with worse cognitive performance in older adults, which raises the question of whether supplementation can slow age-related decline. The best data come from the FACIT trial, a randomized, double-blind, placebo-controlled study in the Lancet. Durga et al. gave 818 adults aged 50 to 70 with elevated homocysteine either 800 mcg of folic acid or placebo daily for three years. Serum folate rose by 576 percent and homocysteine fell by 26 percent in the supplement group, and those participants showed significantly better three-year outcomes than placebo on memory, information processing speed, and sensorimotor speed, the cognitive domains that tend to decline earliest with age (PubMed).

Two caveats keep this from being a prescription for everyone. The participants were selected for elevated homocysteine and normal B12 status, so the result applies to people with a measurable reason to supplement rather than the general public. And the trial used folic acid, not methylfolate; no comparable long-term cognitive trial has used the active form. What the finding does show is that correcting an actual folate-homocysteine imbalance can move cognitive measures, which supports checking homocysteine and B-vitamin status in older adults with memory concerns rather than guessing.

Do These Supplements Help With Migraines?

Migraine with aura has been linked to the MTHFR C677T variant and higher homocysteine, which led researchers to test B-vitamin supplementation in affected women. The largest trial, by Menon et al. in Pharmacogenetics and Genomics, randomized 206 women with migraine with aura to a daily B-vitamin combination (B6, B9, and B12) or placebo for six months. Supplementation significantly reduced homocysteine, headache severity, and the proportion of participants with high migraine disability compared with placebo, and the response was strongest in women carrying the C allele of the MTHFR C677T variant (PubMed).

This is promising but not definitive. It is a single trial in a specific population, the effect took months to appear, and riboflavin, which some migraine guidelines use at 400 mg daily, is a separate story from folate. For a woman with migraine with aura who also has elevated homocysteine or a known C677T variant, a B-vitamin trial under medical guidance is reasonable; for everyone else, the migraine evidence does not justify high-dose folate on its own.

What About Homocysteine and Heart Health?

High homocysteine is a risk marker for cardiovascular disease, and folate, B12, and B6 are the nutrients that clear it. The largest relevant trial is the China Stroke Primary Prevention Trial: 20,702 adults with hypertension but no prior stroke or heart attack received either enalapril alone or enalapril plus 0.8 mg of folic acid for a median of 4.5 years. The folic acid group had a 21 percent relative reduction in first stroke (2.7 percent versus 3.4 percent; hazard ratio 0.79, 95% CI 0.68 to 0.93), driven by ischemic stroke, in a population with low baseline folate and widespread MTHFR variants (PubMed). Trials in well-nourished Western populations with normal folate status have generally not shown the same benefit, which fits the idea that folic acid helps most where deficiency or impaired conversion exists.

Methylfolate’s role here is mechanistic: it clears homocysteine without needing MTHFR, and it should be paired with vitamin B12, which is the cofactor in the same reaction. A key safety point applies to any high-dose folate: it can mask the megaloblastic anemia of B12 deficiency while the neurological damage continues, so B12 status should be checked before starting high-dose folate, per hematology guidelines (PubMed). A practical stack for elevated homocysteine is methylfolate 800 to 1,000 mcg, methylcobalamin 500 to 1,000 mcg, and B6 25 to 50 mg daily, with a repeat homocysteine test after 8 to 12 weeks.

How Do You Choose Between Methylfolate and Folic Acid?

The decision framework is shorter than the marketing suggests:

Choose methylfolate if: you are homozygous for MTHFR C677T (or compound heterozygous with elevated homocysteine); you have elevated homocysteine that has not responded to folic acid; you are discussing 7.5 to 15 mg adjunctive folate with a psychiatrist for SSRI-resistant depression; or you eat heavily fortified foods, supplement folate, and want to avoid unmetabolized folic acid entirely.

Choose folic acid if: you are planning pregnancy or are pregnant and do not carry MTHFR variants (it is the evidence-backed default with the proven neural tube defect record); cost matters and you just need standard prevention; or you are simply following standard medical guidance for anemia or general health.

Either works if: you are healthy, eat a reasonable diet, have no known variants, and are choosing between a 400 mcg folic acid pill and a 400 mcg methylfolate pill for general maintenance. At those doses the difference is theoretical for you, and the cheapest reliable option is a fine choice.

The practical takeaway: Match the form to the situation, not the marketing: 400-800 mcg of either form covers general needs, methylfolate earns its premium for C677T homozygotes, elevated homocysteine that did not respond to folic acid, and prescription-level depression adjuncts, while folic acid stays the default for pregnancy and budget prevention, and everyone on high-dose folate needs adequate B12.

What Are the Best Methylfolate Supplements?

All four picks below use the active L-methylfolate form (not folic acid) and include the B12 cofactor, matching what the research and the methylation pathway actually need:

Best Overall

THORNE 5-MTHF 1 mg (60 Capsules)

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Best for MTHFR

L-Methylfolate 7.5 mg + Methyl B12 (60 Capsules)

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Best Budget

Organic Methylfolate 1,000 mcg + Methyl B12 (300 Servings)

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Best for High-Dose Therapy

L-Methylfolate 15 mg + Methyl B12 (60 Capsules)

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THORNE 5-MTHF is the top pick because it delivers the standard 1 mg daily dose in a clean, NSF Certified for Sport formula from a brand with a strong third-party testing record, at $24.00 for 60 capsules. That is the dose most people with an MTHFR variant or a desire to avoid folic acid will settle into long-term.

For C677T carriers who want more than maintenance dosing, the 7.5 mg option with methyl B12 at $19.99 is a reasonable middle point below the 15 mg therapeutic level. The organic 1,000 mcg formula at $24.00 for 300 servings is the value leader for the standard 1 mg daily dose. The 15 mg product at $21.99 matches the dose studied in SSRI-resistant depression and should be used under medical supervision rather than self-prescribed.

Prices were checked at the time of writing. If you choose another product, look for L-methylfolate (5-MTHF) stated on the label, a named branded form such as Metafolin or Quatrefolic, the elemental dose in mcg, and third-party testing. Avoid “folate blends” that hide how much is folic acid versus methylfolate.

How Should You Dose and Switch Between Forms?

Matching dose to goal:

• General health or food-equivalent intake: 400 to 800 mcg of either form daily
• MTHFR variant, heterozygous: 1,000 to 2,000 mcg methylfolate daily
• MTHFR variant, homozygous C677T: 2,000 to 5,000 mcg methylfolate daily, with riboflavin 1.6 mg daily (the MTHFR cofactor, per the Circulation trial)
• Elevated homocysteine: 800 to 1,000 mcg methylfolate plus 500 to 1,000 mcg B12, retest after 8-12 weeks
• Depression adjunct: 7.5 to 15 mg methylfolate, only as prescribed alongside an antidepressant

Switching from folic acid to methylfolate: no washout is needed. Stop the folic acid and start the methylfolate at the equivalent dose the next day. If you start at a high dose (5 mg or more), watch the first week for the rare overmethylation symptoms, anxiety, irritability, insomnia, or headache, and drop the dose if they appear; they resolve quickly when the dose is reduced. Taking methylfolate with B12 is non-negotiable for high doses, and taking it in the morning avoids the insomnia some people get from late-day dosing.

What Are the Side Effects and Interactions?

Methylfolate is well tolerated. The clinical trials reported adverse event rates no different from placebo even at 15 mg daily (PubMed). The side effects that do occur, mostly at doses above 5 mg, are overmethylation-type symptoms: anxiety, irritability, insomnia, headache, and nausea, which reverse with dose reduction. True allergic reactions are rare. Folic acid at standard doses is also very well tolerated, with the theoretical concerns being unmetabolized folic acid at higher doses and B12 masking.

Drug interactions to know:

• Methotrexate: blocks DHFR, which is exactly the enzyme folic acid needs; methylfolate can bypass that block, which is why it is sometimes used alongside low-dose methotrexate for rheumatoid arthritis, but this should be coordinated with your doctor.
• Anticonvulsants: folate supplementation can lower levels of phenytoin and phenobarbital in some people; discuss before adding either form.
• 5-fluorouracil and capecitabine: folate can amplify their toxicity; oncology guidance is required.
• Antifolates used for infections (pyrimethamine, trimethoprim): folate may reduce their effectiveness.

Because of the B12 masking issue, anyone starting high-dose folate should have B12 checked first, and anyone with anemia or neurological symptoms should not self-supplement folate at all before a workup.

What About Dietary Folate and Fortification?

Food provides natural folate as a mix of reduced forms, and the word folate refers to the food form while folic acid refers to the synthetic one. Rich sources include cooked lentils (about 180 mcg per cup), spinach and other dark leafy greens, asparagus, broccoli, avocado, beans, and liver. Natural food folate is about 50 to 80 percent as bioavailable as folic acid, which is why dietary folate equivalents adjust for the difference, and cooking losses are real: boiling can destroy a large share of the folate in vegetables, while steaming preserves more.

In the United States and more than 80 other countries, enriched grains are fortified with folic acid, so a person eating a standard diet gets roughly 100 to 200 mcg of folic acid daily from fortification on top of food folate. That matters for people who also take a supplement: at combined intakes above the conversion threshold, unmetabolized folic acid appears in the blood. It is one more argument for methylfolate if you eat a lot of fortified grains and also supplement, though again, no harm from circulating UMFA has been proven.

For most people, the food-first answer is the same as for any nutrient: build the diet around lentils, greens, beans, and vegetables, and use a supplement to fill the specific gap, whether that is a 400 mcg folic acid pill for general prevention or a methylfolate product for a variant or therapeutic need.

Frequently Asked Questions

Why do some people say methylfolate is 7 times more bioavailable?

That specific figure circulates widely but does not come from the published studies. What the pharmacokinetic research actually shows is that a single dose of 5-MTHF produces significantly higher peak plasma folate and total exposure than an equivalent folic acid dose, in both MTHFR genotypes, with unmetabolized folic acid appearing after folic acid but rarely after methylfolate (PubMed). Real but smaller than the marketing version.

I have the MTHFR C677T variant. Do I need methylfolate?

If you are homozygous (TT), methylfolate is a reasonable choice because your MTHFR enzyme runs at reduced efficiency, and a meta-analysis links maternal TT status with roughly double the neural tube defect odds (PubMed). If you are heterozygous, the case is weaker but still sensible, especially with elevated homocysteine. If you are negative, both forms work fine.

Is folic acid dangerous?

At standard doses, no. Folic acid has an extraordinary safety record across fortification and pregnancy use. The open questions concern unmetabolized folic acid at higher doses, where a 2006 study found lower natural killer cell activity in postmenopausal women with detectable UMFA (PubMed), and the B12 masking effect. Both argue for staying at recommended doses and knowing your B12 status, not for avoiding folic acid.

Why is my doctor recommending folic acid when methylfolate seems better?

Because the pregnancy evidence, the fortification data, and the public health recommendations all rest on folic acid, and for a woman without MTHFR variants it works. Doctors also see supplements change brands and doses between pregnancies, and folic acid is the form whose benefit has actually been measured. Methylfolate is a reasonable personal choice; folic acid is the evidence-backed default.

Does methylfolate cause insomnia?

Some people, mainly at higher doses, report trouble sleeping, part of the overmethylation symptom cluster. Taking methylfolate in the morning rather than evening usually solves it. If sleep problems persist, lower the dose.

Can I take methylfolate with other B vitamins?

Yes, and for the methylation pathway you should: methylcobalamin (B12) is the cofactor in the homocysteine reaction, P5P (B6) supports it through a parallel route, and riboflavin (B2) supports MTHFR directly, with 1.6 mg daily shown to lower homocysteine in C677T homozygotes (PubMed). A quality B-complex with active forms covers all of these at once.

Does riboflavin matter for MTHFR?

More than most people realize. The MTHFR enzyme loses its riboflavin-derived cofactor (FAD) more readily in the C677T variant, which is why homozygotes have higher homocysteine specifically when riboflavin status is low. In the Circulation trial, correcting riboflavin status with 1.6 mg daily brought homocysteine down by up to 22 percent in TT homozygotes while doing nothing in other genotypes (PubMed). If you have the variant, take the riboflavin.

Should athletes care about methylfolate?

Only through the same pathways as everyone else: red blood cell production and homocysteine clearance matter for endurance, and some older studies looked at folate and B12 in runners with MTHFR variants. The practical advice is identical, keep B12 and folate status adequate rather than chasing high doses, and if you are drug-tested, choose a supplement with NSF or Informed Choice certification, which the Thorne product in this guide carries.

Is methylfolate safe in pregnancy?

Folic acid remains the standard recommendation because its neural tube defect evidence is unmatched and it costs pennies. Methylfolate is used in many prenatal vitamins and is safe, and it is a reasonable personal choice for women with MTHFR variants, but product and dose should follow your obstetrician’s advice rather than a supplement label.

How long does methylfolate take to work?

It depends on what you are measuring. Homocysteine responds within weeks and is worth retesting at 8 to 12 weeks. Mood, in the depression trials, was measured at 30 and 60 days. Energy and cognition changes, when they occur, typically build over a month or more. There is no legitimate “instant” version of this supplement.

Related Reading

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• Best Supplements for Hormonal Balance in Women

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References and Clinical Studies

1. MRC Vitamin Study Research Group. Prevention of Neural Tube Defects: Results of the Medical Research Council Vitamin Study. The Lancet, 1991. PubMed
2. Botto LD, Yang Q. 5,10-Methylenetetrahydrofolate Reductase Gene Variants and Congenital Anomalies: A HuGE Review. American Journal of Epidemiology, 2000. PubMed
3. Prinz-Langenohl R, Brämswig S, Tobolski O, et al. [6S]-5-Methyltetrahydrofolate Increases Plasma Folate More Effectively Than Folic Acid in Women With the Homozygous or Wild-Type 677C>T Polymorphism of Methylenetetrahydrofolate Reductase. British Journal of Pharmacology, 2009. PubMed | DOI
4. Papakostas GI, Shelton RC, Zajecka JM, et al. L-Methylfolate as Adjunctive Therapy for SSRI-Resistant Major Depression: Results of Two Randomized, Double-Blind, Parallel-Sequential Trials. American Journal of Psychiatry, 2012. PubMed | DOI
5. McNulty H, Dowey LRC, Strain JJ, et al. Riboflavin Lowers Homocysteine in Individuals Homozygous for the MTHFR 677C>T Polymorphism. Circulation, 2006. PubMed
6. Yan L, Zhao L, Long Y, et al. Association of the Maternal MTHFR C677T Polymorphism With Susceptibility to Neural Tube Defects in Offsprings: Evidence From 25 Case-Control Studies. PLOS ONE, 2012. PubMed | DOI
7. Huo Y, Li J, Qin X, et al. Efficacy of Folic Acid Therapy in Primary Prevention of Stroke Among Adults With Hypertension in China: The CSPPT Randomized Clinical Trial. JAMA, 2015. PubMed | DOI
8. Surén P, Roth C, Bresnahan M, et al. Association Between Maternal Use of Folic Acid Supplements and Risk of Autism Spectrum Disorders in Children. JAMA, 2013. PubMed
9. Durga J, van Boxtel MP, Schouten EG, et al. Effect of 3-Year Folic Acid Supplementation on Cognitive Function in Older Adults in the FACIT Trial: A Randomised, Double Blind, Controlled Trial. The Lancet, 2007. PubMed
10. Troen AM, Mitchell B, Sorensen B, et al. Unmetabolized Folic Acid in Plasma Is Associated With Reduced Natural Killer Cell Cytotoxicity Among Postmenopausal Women. The Journal of Nutrition, 2006. PubMed
11. Bailey RL, Mills JL, Yetley EA, et al. Serum Unmetabolized Folic Acid in a Nationally Representative Sample of Adults Aged 60 Years and Older in the United States, 2001-2002. Food and Nutrition Research, 2012. PubMed
12. Devalia V, Hamilton MS, Molloy AM. Guidelines for the Diagnosis and Treatment of Cobalamin and Folate Disorders. British Journal of Haematology, 2014. PubMed
13. Menon S, Lea RA, Roy B, et al. Genotypes of the MTHFR C677T and MTRR A66G Genes Act Independently to Reduce Migraine Disability in Response to Vitamin Supplementation. Pharmacogenetics and Genomics, 2012. PubMed | DOI