Broccoli seed is the densest store of a compound the body converts into its active form; whether that conversion happens depends on the preparation. Human evidence is strongest for faster clearance of inhaled pollutants. Blood sugar and liver changes are smaller and limited to people whose values started abnormal. Harms are mostly digestive; home sprouting has caused foodborne outbreaks. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Fasting glucose | 75–85 mg/dL | Primary metabolic endpoint with human trial support |
| HbA1c | 4.8–5.2% | Three-month glucose average; the endpoint that moved in the diabetes trial |
| Alanine aminotransferase | 10–19 U/L (women), 10–25 U/L (men) | Liver enzyme that fell in the fatty-liver trial |
| Gamma-glutamyl transferase | <20 U/L (men), <15 U/L (women) | Second liver enzyme that moved, and a glutathione turnover marker |
| Thyroid-stimulating hormone | 0.5–2.0 mIU/L | Detects the one theoretical risk specific to this compound |
| Free thyroxine | 1.0–1.5 ng/dL | Confirms or excludes a real thyroid effect if the stimulating hormone drifts |
| Urinary iodine | 100–200 µg/L | Defines whether the goitrogen concern applies at all |
| High-sensitivity C-reactive protein | <0.5 mg/L | General inflammation marker aligned with the NF-κB mechanism |
| Prostate-specific antigen (men over 40) | <1.0 ng/mL under age 60, <2.0 ng/mL thereafter | Relevant where prostate risk motivates use |
| Urinary sulforaphane metabolites | No established target; track the change from the individual's own baseline after a fixed test dose | The only direct check that a given product actually delivers |
Cadence: Baseline, then metabolic and liver panel at 12 weeks, at 6 months, then annually; thyroid function once at 6 months and thereafter only if symptoms appear or iodine intake changes; drug level at 4 weeks for anyone taking a narrow-margin CYP1A2 substrate and after any change in dose or product.