A sulfur-rich brown-seaweed fibre the gut cannot digest, so it acts mainly inside the digestive tract. The firmest human finding is slowed disease progression when added to cancer treatment. Longevity claims rest on animal work. It lengthens clotting times, and seaweed-derived preparations can carry enough iodine to disturb thyroid function. Product quality varies widely. (Full Review)
| Marker | Target | Why |
|---|---|---|
| TSH | 0.5–2.0 mIU/L | Earliest signal of iodine-driven thyroid drift |
| Free T4 | 1.0–1.5 ng/dL | Confirms whether a TSH change reflects real thyroid output |
| Urinary iodine (spot) | 100–299 µg/L | Quantifies total iodine load from supplement plus diet |
| aPTT | Within the laboratory reference range and unchanged from the individual's own baseline | Detects the heparin-like prolongation fucoidan produces |
| Platelet count | 150–400 × 109/L | Defines clotting reserve before adding an antiplatelet effect |
| hs-CRP | < 1.0 mg/L | Tracks the inflammatory tone fucoidan is proposed to lower |
| Fasting insulin | 2–6 µIU/mL | Identifies the impaired baseline in which metabolic benefit appeared |
| HbA1c | 5.0–5.4% | Medium-term glucose control, the endpoint the metabolic trials targeted |
| ALT | 10–26 U/L (women), 10–33 U/L (men) | Baseline liver status, relevant given liver-protective claims |
| eGFR | > 90 mL/min/1.73 m2 | Absorbed fucoidan is cleared by the kidneys, so kidney function sets exposure |
Cadence: Baseline before the first dose; thyroid and clotting markers repeated at 8–12 weeks and metabolic and inflammatory markers at 12 weeks; the full set every 6–12 months during continued use, and at 6-week intervals once a thyroid or clotting value drifts.