A sour fruit with long traditional use and a modest human trial record. The most consistent findings are lower harmful cholesterol and lower low-grade inflammation, with blood sugar pointing the same way. Blood pressure signals are mixed. The clearest concern is reduced platelet stickiness, relevant with blood thinners or surgery. Most retail products fall short of their labels. (Full Review)
| Marker | Target | Why |
|---|---|---|
| LDL cholesterol | Under 70 mg/dL | The endpoint with the strongest amla evidence |
| Apolipoprotein B | Under 80 mg/dL | Counts plaque-forming particles directly, unlike calculated LDL |
| Triglycerides | Under 100 mg/dL | The lipid measure where amla trial results conflict |
| HDL cholesterol | Above 55 mg/dL (men), above 65 mg/dL (women) | Amla raises it modestly; useful for the total-to-HDL ratio |
| Glycated haemoglobin | 4.8–5.3% | Three-month glucose average; a validated amla endpoint |
| Fasting glucose | 75–86 mg/dL | Detects the earliest and largest amla glucose effect |
| Fasting insulin | Under 5 µIU/mL | Reveals insulin resistance before glucose moves |
| High-sensitivity C-reactive protein | Under 0.5 mg/L | The most statistically consistent amla effect |
| Platelet count | 175–250 × 10⁹/L | Bleeding-risk context for amla's antiplatelet effect |
| Platelet aggregation response | No established target for supplement users; track change from the individual's own baseline | The mechanism behind amla's one serious hazard |
| Alanine aminotransferase | 10–26 U/L | Confirms no liver signal, which trials have not found |
| Blood lead | Under 1.0 µg/dL | Contamination check for unverified powders |
Cadence: Full baseline panel before starting; lipid, glucose and inflammation panel repeated at 12 weeks, then every 6–12 months if amla is continued. Platelet count and liver enzymes annually. On glucose-lowering medication, fasting glucose self-monitoring several times weekly for the first 4 weeks.