Folic Acid
Compiled from published pharmacological and botanical literature. Not independently verified by Herbuno. Spotted an error or have a correction? Flag it below →
| Compound | Folic acid (pteroylmonoglutamic acid, synthetic vitamin B9) |
|---|---|
| Chemical class | Fully oxidised pteroyl monoglutamate — not a naturally occurring folate |
| CAS | 59-30-3 (folic acid) · 6484-89-5 (sodium folate) |
| Molecular weight | 441.40 g/mol |
| DFE conversion | 1 µg folic acid = 1.7 µg DFE in fortified food, 2.0 µg fasted |
| Activation route | Requires DHFR reduction — low, saturable human capacity |
| Claim strength | High for neural tube defect prevention; High for the UMFA and masking issues |
| Buy from Herbuno | Liposomal Vitamin B9 (Folic Acid) Powder · plain folic acid / sodium folate: availability on request |
| Origin | Processed / Sourced from India |
| MOQ | R&D 100 g / 250 g (subject to stock) · Pilot batch 1–5 kg · Bulk 10 kg, 25 kg and above |
| Lead Time | Dispatch within 72 hrs from stock · fresh-batch production (typically 50 kg+): 10 working days |
| Documentation | CoA & MSDS standard with every lot |
Name origin: From the Latin folium, leaf, after the spinach from which Mitchell, Snell and Williams isolated the growth factor in 1941. The name properly belongs to the natural folates; folic acid specifically is the synthetic compound, first made in 1945, and the distinction between the two is the single most important thing to understand about this material.
Folic acid is not a natural folate: Natural food folates are reduced compounds carrying a polyglutamate tail — chiefly 5-methyltetrahydrofolate and 10-formyltetrahydrofolate, with three to eight glutamate residues. Folic acid is fully oxidised and carries a single glutamate. It does not occur in meaningful quantity in unfortified food. To be used it must first be reduced by dihydrofolate reductase to tetrahydrofolate, and human DHFR activity toward folic acid is low and saturable.
The bioavailability inversion: Counter to the usual natural-is-better assumption, folic acid is more bioavailable than food folate, not less. Food folates must be deconjugated at the intestinal brush border before absorption and are labile to heat and oxidation; folic acid is absorbed more completely. This is why dietary folate equivalents convert at 1 microgram of folic acid to 1.7 micrograms DFE in fortified food and 2.0 micrograms taken fasting.
Commercial source: Folic acid is produced by chemical synthesis; there is no commercial fermentation route and no botanical source at any meaningful concentration. The reduced vitamers — calcium L-5-methyltetrahydrofolate and others — are separate and more expensive articles with their own stability profiles.
Evidence for Folic Acid Applications
Neural tube defect prevention is among the strongest findings in all of micronutrient science, and it is specifically folic acid that carries it. Randomised and population-level evidence established that periconceptional folic acid at 400 micrograms daily substantially reduces neural tube defect incidence, which led to mandatory flour fortification in a large number of countries and to a measurable fall in incidence following it. The trials used folic acid, not reduced folates, which is worth noting when a methylfolate product borrows this evidence. Claim strength: High.
Folic acid is more bioavailable than food folate, which inverts the usual assumption and is worth stating to customers who think otherwise. Natural folates require brush-border deconjugation of the polyglutamate tail before absorption and are labile to heat and oxidation; folic acid is absorbed more completely. Hence the dietary folate equivalent conversion of 1 microgram folic acid to 1.7 micrograms DFE in fortified food and 2.0 fasting. A "whole-food folate" positioning implying superior absorption is contradicted by the conversion factors it would have to use. Claim strength: High.
High-percentage botanical folate claims do not survive arithmetic, and this is a sourcing trap worth stating explicitly. Folate occurs in leafy and citrus material at the microgram-per-hundred- gram level — on the order of 0.0001% of dry weight at best. An extract cannot contain more of a constituent than the feedstock holds, so a botanical extract assaying at 1% folate, let alone 5%, is not a concentrated extract: it is either synthetic folic acid on a botanical carrier, or an assay artefact. Where a product is described as plant-source folate at percentage-level assay, ask for the assay method and the reference standard before accepting it. Claim strength: High.
Unmetabolised folic acid in plasma is a real phenomenon whose significance is unresolved. Because DHFR capacity for folic acid is low and saturable, single doses above roughly 200 to 400 micrograms produce measurable unmetabolised folic acid in circulation. Associations have been proposed with reduced natural killer cell cytotoxicity and with other outcomes, and the finding drives much of the commercial interest in reduced folates. The evidence of harm is not established, and the honest position is that UMFA occurs, its clinical significance is debated, and dividing doses reduces it. Claim strength: Emerging.
Folic acid can mask vitamin B12 deficiency, which is a genuine and serious consideration. Both deficiencies produce megaloblastic anaemia; folic acid corrects the haematological abnormality without addressing the B12 deficit, so the anaemia resolves while subacute combined degeneration of the cord progresses. This is the principal argument for pairing folic acid with B12 in any product aimed at populations at risk of B12 deficiency — older adults, vegans, metformin users, those with atrophic gastritis — and it is a formulation decision rather than a label warning. Claim strength: High.
The MTHFR argument for methylfolate is mechanistically real and clinically modest. The C677T polymorphism reduces methylenetetrahydrofolate reductase activity, lowering 5-methyltetrahydrofolate production, and supplying the methylated vitamer bypasses the step. TT homozygotes have higher homocysteine and lower folate status at equivalent intake. What has not been established is that methylfolate produces better clinical outcomes than folic acid for most endpoints in most people, and the neural tube defect evidence base is folic acid's. Riboflavin status also modulates MTHFR activity, which is often omitted from the discussion. Claim strength: Emerging.
Sourcing folic acid from Herbuno. We hold folic acid in a liposomal format; plain folic acid and sodium folate are availability on request.
Two things we will say plainly. Folic acid is the synthetic, fully oxidised vitamer and it is more bioavailable than food folate, not less — it is also the form the neural tube defect evidence used. And a botanical extract assaying at percentage-level folate is not a concentrated extract: folate occurs in plant material at the microgram-per-hundred-gram level, so the arithmetic does not permit it. Ask for the assay method and reference standard. All lots ship with CoA and MSDS; request a quotation for pilot or bulk volumes.
Dosage & Formulator Specification
Dose in micrograms and state whether the declaration is folic acid or dietary folate equivalents, because the two differ by a factor of 1.7 to 2.0. Adult reference intakes are commonly expressed as 400 micrograms DFE; periconceptional recommendations are 400 micrograms of folic acid daily, rising to higher doses where there is a prior affected pregnancy. Upper intake levels for folic acid specifically — typically 1,000 micrograms daily for adults — apply to the synthetic form rather than to food folate, which is an unusual arrangement and a common source of labelling error.
Pair it with B12 wherever the target population might be B12-deficient. Folic acid corrects the megaloblastic anaemia of B12 deficiency without addressing the deficit, so neurological damage can progress while the blood picture normalises. For products aimed at older adults, vegans, metformin users or anyone with absorption compromise, co-formulating B12 is the responsible design rather than a bonus ingredient, and it should be decided at formulation rather than added for marketing reasons.
Low solubility constrains liquid formats. Folic acid as the free acid dissolves very poorly in water, in the region of 0.0016 grams per 100 millilitres at neutral pH, so a liquid product requires the sodium salt, which is freely soluble. Solubility also rises steeply with pH. The free acid is adequate for dry formats — tablets, capsules, powder premixes — where it is the standard and cheaper article.
Stability is good dry and poor in solution under the wrong conditions. Folic acid is reasonably stable as a dry powder but degrades in solution with light exposure, in acidic conditions, and with heat, and the degradation is accelerated by reducing agents and by trace metal ions. In a liquid multivitamin it is one of the less stable components, and a formulation carrying both folic acid and vitamin C needs stability data rather than assumption, since ascorbate's interaction with folate chemistry runs in both directions depending on conditions.
For analytical control, specify identity and assay by HPLC against a folic acid reference standard, with the form stated by CAS number — 59-30-3 for folic acid, 6484-89-5 for sodium folate, and separate numbers for the reduced vitamers, which are not interchangeable. Where a material is presented as a botanical folate, require the assay method and reference standard explicitly: a microbiological assay or an HPLC method calibrated against folic acid will read a folic-acid-on-carrier blend exactly as though it were a botanical concentrate. Standard coverage includes heavy metals, residual solvents, microbiological limits, loss on drying and sulphated ash.
On vitamer selection, the honest framing separates three considerations that marketing usually merges. Evidence: folic acid carries the neural tube defect literature and the fortification record; reduced folates do not, and should not borrow it. Bioavailability: folic acid is more completely absorbed than food folate, so a natural-source positioning cannot rest on absorption. Metabolism: folic acid requires saturable DHFR reduction and produces measurable unmetabolised folic acid above roughly 200 to 400 micrograms per dose, which is the legitimate argument for calcium L-5-methyltetrahydrofolate, alongside the MTHFR C677T polymorphism. That argument is mechanistically real and clinically modest, and riboflavin status modulates MTHFR activity too — a point usually missing from methylfolate positioning.
Frequently Asked Questions — Folic Acid
Is folic acid less bioavailable than natural folate?
No — the opposite. Natural folates carry a polyglutamate tail requiring brush-border deconjugation before absorption and are labile to heat and oxidation; folic acid is absorbed more completely. That is why the conversion is 1 microgram folic acid to 1.7 micrograms DFE in fortified food, 2.0 fasting. A natural-source positioning cannot rest on absorption.
Can a botanical extract really contain 1% or 5% folate?
No. Folate occurs in leafy and citrus material at the microgram-per-hundred-gram level — around 0.0001% of dry weight at best — and an extract cannot contain more of a constituent than the feedstock holds. Percentage-level assay means synthetic folic acid on a botanical carrier, or an assay artefact. Ask for the method and reference standard.
What is unmetabolised folic acid and does it matter?
DHFR capacity for folic acid is low and saturable, so single doses above roughly 200 to 400 micrograms produce measurable unmetabolised folic acid in plasma. Associations have been proposed with reduced natural killer cell cytotoxicity among others, but harm is not established. UMFA occurs, its significance is debated, and dividing doses reduces it.
Why must folic acid be paired with B12?
Because it masks B12 deficiency. Both produce megaloblastic anaemia; folic acid corrects the blood picture without addressing the B12 deficit, so subacute combined degeneration of the cord can progress while the anaemia resolves. For products aimed at older adults, vegans or metformin users, co-formulating B12 is responsible design, not a bonus.
Is methylfolate better than folic acid?
Mechanistically arguable, clinically modest. The MTHFR C677T polymorphism reduces enzyme activity and supplying the methylated vitamer bypasses that step, and TT homozygotes do have higher homocysteine at equivalent intake. What is not established is better clinical outcomes for most endpoints in most people — and the neural tube defect evidence is folic acid's. Riboflavin status also modulates MTHFR, which is usually left out.
Can I use it in a liquid?
Not as the free acid — it dissolves at about 0.0016 g per 100 ml at neutral pH. Use sodium folate, CAS 6484-89-5, which is freely soluble. Note also that folic acid degrades in solution with light, acid, heat, reducing agents and trace metals, so a liquid multivitamin carrying it needs real stability data.