A traditional Southeast Asian tea leaf, sold as a concentrated extract for blood sugar support. Which of its active plant compounds does the work is unsettled. Short trials show lower blood sugar after meals and lower fasting levels where these are already raised, with modest blood fat, insulin and blood pressure changes. Effects are small next to established treatments. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Fasting glucose | 75–86 mg/dL (4.2–4.8 mmol/L) | The primary target of the intervention |
| Hemoglobin A1c | 4.8–5.4% | Three-month average blood sugar; smooths daily noise |
| Fasting insulin | 2–5 µIU/mL | Detects compensation before glucose itself rises |
| HOMA-IR | Below 1.0 | Single number summarizing insulin resistance |
| Triglycerides | Below 80 mg/dL (0.9 mmol/L) | Tracks the secondary lipid effect seen in trials |
| Blood pressure | Below 115/75 mmHg | Small reductions were reported in trial data |
| Creatinine and eGFR | eGFR above 90 mL/min/1.73 m² | Kidney safety, given the acute kidney injury case report |
| ALT and AST | Below 25 U/L (men), below 20 U/L (women) | Liver safety of a concentrated botanical extract |
| Continuous glucose metrics | Mean below 100 mg/dL; over 90% of time in 70–120 mg/dL | Captures the post-meal effect fasting tests miss |
Cadence: Capillary or continuous glucose daily for the first two weeks; fasting glucose and insulin at four weeks; full panel including kidney and liver markers at 12 weeks; every six months thereafter.