Folate (Vitamin B9)
Folate is the umbrella term for a family of water-soluble B vitamins essential for DNA synthesis, methylation, and red-blood-cell production. Its most publicised role is preventing neural tube defects when supplemented before and during early pregnancy — one of the most successful nutritional public-health interventions in history.
Folate vs folic acid vs methylfolate
- Folate — the natural food form (polyglutamates).
- Folic acid — synthetic, added to fortified grains and most supplements. Highly bioavailable; converted to methylfolate by DHFR and MTHFR.
- 5-methyltetrahydrofolate (5-MTHF, "methylfolate") — the active circulating form. Sold as L-methylfolate supplements for people with MTHFR polymorphisms.
Daily requirements (dietary folate equivalents)
- Adults: 400 µg DFE/day.
- Preconception / early pregnancy: 400 µg (up to 800 µg) folic acid daily starting at least 1 month before conception — prevents ~70% of neural tube defects.
- Pregnancy: 600 µg DFE.
- Lactation: 500 µg DFE.
- Tolerable Upper Intake Level: 1,000 µg folic acid/day from supplements or fortified foods. No limit on food folate.
Neural tube defects — the key intervention
Neural tube closure occurs on days 21–28 after conception — often before pregnancy is recognised. Peri-conceptional folic acid supplementation (400–800 µg/day) prevents spina bifida and anencephaly. Higher doses (4 mg/day) are recommended if a previous pregnancy was affected or in women on antiepileptics. Since the US mandated folic acid fortification of enriched grains in 1998, neural tube defect rates fell ~36%.
MTHFR polymorphisms
Common polymorphisms (C677T, A1298C) reduce MTHFR enzyme activity by 30–70%, producing higher homocysteine and slightly lower serum folate. About 10% of the population is homozygous C677T. Whether MTHFR carriers benefit from taking methylfolate instead of folic acid is debated — most people convert folic acid to methylfolate adequately. For those with documented hyperhomocysteinaemia or recurrent pregnancy loss, methylfolate is a reasonable alternative.
Deficiency
Causes megaloblastic anaemia (indistinguishable from B12 deficiency on peripheral smear). Symptoms: fatigue, glossitis, elevated MCV, low reticulocyte count. Chronic folate deficiency raises homocysteine and modestly increases cardiovascular risk. Alcoholism, malabsorption, and antifolate drugs (methotrexate, sulfasalazine, phenytoin) are the most common causes.
Food sources
- Beef liver (3 oz cooked): 215 µg
- Fortified breakfast cereal (½ cup): 100–400 µg
- Lentils (½ cup cooked): 179 µg
- Spinach (½ cup cooked): 131 µg
- Asparagus (½ cup): 134 µg
- Avocado (½): 82 µg
- Fortified rice, pasta, bread — variable, check label
Caution: masking B12 deficiency
Folic acid supplementation can correct megaloblastic anaemia caused by B12 deficiency without correcting the underlying neurological damage. If you're on high-dose folic acid (> 1,000 µg/day), check B12 too — chronic combined supplementation is standard in pregnancy and older adults.