A reactive sulfur compound released from raw watercress. A defined daily amount in divided doses for one to two weeks measurably raises excretion of several harmful inhaled chemicals, far more so in adults lacking two detoxification genes. In rats the same reactivity promotes bladder tumors, never looked for in people. (Full Review)
| Marker | Target | Why |
|---|---|---|
| GSTM1 / GSTT1 genotype | Double-null predicts strongest response | Determines whether the protocol does anything |
| TSH | 0.5–2.0 mIU/L | Thyroid suppression from iodide competition |
| Free T4 | 1.0–1.5 ng/dL | Actual hormone output when TSH drifts |
| Urinary iodine | 100–200 µg/L | Deficiency state in which thyroid risk appears |
| Urinalysis with microscopy | No blood or casts, specific gravity <1.020 | Earliest analog of the rodent bladder injury |
| eGFR and serum creatinine | eGFR >90 mL/min/1.73 m² | Clearance sets urinary metabolite concentration |
| ALT and AST | <25 U/L (men), <20 U/L (women) | Liver signal seen in rodent promotion studies |
| Urinary mercapturic acids of acrolein and benzene | No target; track change from own baseline | Confirms the compound is generated and working |
| INR (if anticoagulated) | Individually prescribed target | Destabilization from vitamin K in watercress |
| hs-CRP | <1.0 mg/L | Systemic inflammation endpoint unmoved in trial |
Cadence: Baseline before starting. TSH, free T4, urinalysis at eight weeks, then each cycle end or six-monthly. Narrow-index drug levels four weeks after starting and stopping. Mercapturic acids before and after two weeks of dosing.