Folic acid around conception reduces brain and spinal birth defects. First stroke risk falls where baseline folate is low. Folate lowers a blood sulfur-amino-acid marker and corrects folate-deficiency anemia, but does not reliably prevent heart attacks in well-nourished adults. Milligram doses can hide vitamin B12 deficiency while nerve injury continues. Folic acid has birth-defect trials; other forms lack those trials. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Serum folate | Often >15–20 ng/mL (>34–45 nmol/L) | Short-term intake |
| Red-cell folate | ≥906 nmol/L (≈400 ng/mL) if preconception; otherwise rising stores vs baseline | Tissue stores over months |
| Homocysteine | Functional clinics often <8–10 µmol/L | One-carbon throughput |
| Vitamin B12 | Functional often >400–500 pg/mL | Masking risk |
| Methylmalonic acid (MMA) | Typically <0.3–0.4 µmol/L | B12-specific function |
| MCV | Often 80–92 fL | Detects megaloblastic change |
| MTHFR genotype (optional) | No numeric target; 677TT vs CC/CT | Explains high homocysteine |
Cadence: 8–12 weeks after a change, then every 6–12 months if the protocol is stable, or sooner if anemia, neuropathy, or new anticonvulsant or methotrexate therapy appears