Selenium is a trace mineral the body cannot make. Where intake is genuinely low, the case is strong: severe shortage causes a heart muscle disease that supplementation abolishes, and autoimmune thyroid disease improves. Where intake is already adequate, the picture inverts: more diabetes, more aggressive prostate disease, hair, nail, and skin problems. Body levels, not intake, carry the signal. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Plasma or serum selenium | 110–130 µg/L | Determines whether supplementation can help or will only add risk |
| Selenoprotein P (SELENOP) | 4.0–5.5 mg/L | The functional readout; it plateaus once selenoprotein synthesis is saturated |
| Glutathione peroxidase 3 activity | At or above assay plateau | Confirms enzymatic repletion rather than mere circulating selenium |
| Fasting glucose | 75–90 mg/dL | Detects the principal harm before it becomes diagnosable diabetes |
| Glycated haemoglobin (HbA1c) | <5.4% | Captures glycaemic drift that a single fasting glucose misses |
| Thyroid-stimulating hormone with free thyroxine and free triiodothyronine | TSH 0.5–2.0 mIU/L | Tracks the thyroid effect that motivates most selenium use |
| Thyroid peroxidase antibodies | As low as achievable; no established target | The endpoint that moved in the randomised trials |
| High-sensitivity C-reactive protein | <1.0 mg/L | Contextualises both the inflammation benefit and a falsely low selenium reading |
Cadence: Selenium at baseline, 3 months and 12 months, then every 12 months while supplementation continues; thyroid markers at 3 and 6 months in thyroid indications; glycaemic markers annually