Iron helps only those measurably short of it: correcting a shortfall reverses anemia, lowers tiredness, eases restless legs at night, and cuts hospital admission in heart failure. Stores that keep climbing track with liver damage, joint replacement, diabetes and, in genetic studies, a shorter life. The body cannot unload an excess, so measurement, not supplementation, comes first. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Ferritin | 50–100 ng/mL (women), 50–150 ng/mL (men) | Primary estimate of stored iron |
| Transferrin saturation | 25–35% | Share of transport protein carrying iron; flags both deficiency and overload |
| Hemoglobin | 13.5–15.0 g/dL (women), 14.5–16.0 g/dL (men) | Detects anemia and confirms response to repletion |
| C-reactive protein | Below 1.0 mg/L | Determines whether ferritin can be believed |
| Mean corpuscular volume | 85–92 fL | Average red cell size; falls in established iron deficiency |
| Soluble transferrin receptor | Laboratory-specific reference interval | Marks true tissue iron need and is unaffected by inflammation |
| Alanine aminotransferase | Below 25 U/L (men), below 20 U/L (women) | Detects hepatic injury from iron loading |
| HbA1c | Below 5.4% | Screens for the glucose dysregulation associated with iron excess |
| Liver iron by magnetic resonance imaging | Below 36 µmol/g dry weight | Confirms or excludes true hepatic iron loading without a biopsy |
Cadence: Complete blood count at 4 weeks; ferritin and transferrin saturation at 8–12 weeks; then every 6–12 months once the course ends. Annual testing continues indefinitely with long-term supplementation, frequent blood donation, or an HFE variant.