Iodine is a required nutrient with an unusually narrow useful range. Restoring genuinely low intake reliably restores thyroid hormone output and shrinks an enlarged gland. Modest excess tips the thyroid of people carrying thyroid antibodies into underactivity, and glands that have formed nodules into overactivity. Harm evidence is stronger than most benefit evidence; measured intake decides. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Thyroid-stimulating hormone (TSH) | 1.0–2.0 mIU/L | The earliest signal that intake has moved the thyroid in either direction |
| Free thyroxine (free T4) | Upper half of the laboratory reference interval | Confirms whether a shifted pituitary signal has actually changed hormone output |
| Free triiodothyronine (free T3) | Upper half of the laboratory reference interval | Detects impaired conversion, which selenium shortfall and illness both cause |
| Thyroid peroxidase antibodies (TPO antibodies) | Negative, below the assay cut-off | Identifies the autoimmune thyroid in which added iodine causes underactive thyroid |
| Thyroglobulin | 3–15 µg/L | A functional marker of iodine supply over months, rising in both deficiency and excess |
| Spot urinary iodine concentration | 100–199 µg/L for non-pregnant adults; 150–249 µg/L in pregnancy | The direct measure of intake and the only way to know whether a deficiency exists |
| Serum selenium | 120–150 µg/L | Determines whether the conversion and peroxide-clearing enzymes can keep pace with added iodine |
Cadence: Baseline set before any intake above food level. At nutritional intake, pituitary signal and free thyroxine at three months, then every twelve months. At milligram-scale intake, testing at four weeks, twelve weeks, then every three to six months, with antibodies repeated annually.