Formed when broccoli and related vegetables are crushed or chewed, it raises the activity of the body's own protective and waste-removal systems. The best-repeated human effect is faster removal of inhaled and dietary pollutants. Smaller, less certain signals: blood sugar, mental speed and mood in older adults, cell division. Digestive upset is common; much research carries commercial ties. (Full Review)
| Marker | Target | Why |
|---|---|---|
| TSH | 0.5–2.0 mIU/L | Detects the historical goitrogenic concern |
| Free T4 | 1.0–1.5 ng/dL | Confirms thyroid output independent of pituitary signaling |
| TPO antibodies | Negative, below 9 IU/mL | Identifies autoimmune thyroid disease, the subgroup with least safety data |
| Spot urinary iodine | 100–199 µg/L | Determines whether the goitrogenic concern applies at all |
| Fasting glucose | 75–86 mg/dL | Primary metabolic endpoint in the sulforaphane trials |
| HbA1c | 4.8–5.3% | Averages blood sugar over about three months, smoothing daily noise |
| ALT | 10–26 U/L in men, 10–19 U/L in women | The one liver marker moved in a controlled trial |
| GGT | Below 20 U/L in men, below 15 U/L in women | Tracks liver oxidative stress and glutathione turnover, the pathway sulforaphane acts on |
| hs-CRP | Below 0.5 mg/L | General inflammation marker; sulforaphane trials have mostly failed to move it |
| GSTM1/GSTT1 genotype | No established target; genotype is fixed — track the response to a fixed dose instead | Indicates how fast sulforaphane is conjugated and cleared |
Cadence: Baseline, then thyroid and liver panels at 12 weeks, 6 and 12 months, and annually thereafter if stable; metabolic markers at 12 weeks and 6 months. TPO antibodies and genotype once at baseline.