A Sri Lankan plant extract that blocks the gut enzymes splitting starch and table sugar, flattening the blood sugar and insulin rise after a carbohydrate meal. Continued use produces a small drop in the average blood sugar marker. Gas, bloating and loose stools are the main harm. Product identity is often wrong, and use beyond three months is unstudied. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Fasting glucose | 75–85 mg/dL (4.2–4.7 mmol/L) | Baseline metabolic status; not the main target |
| HbA1c | 4.8–5.4% | The only marker capturing sustained rather than single-meal effect |
| 2-hour post-meal glucose | Peak under 120 mg/dL (6.7 mmol/L) | The direct target of the mechanism |
| Fasting insulin | 2–5 µIU/mL | Detects the compensatory insulin load that precedes glucose rise |
| HOMA-IR | Under 1.0 | Single index of insulin resistance |
| LDL cholesterol | Under 100 mg/dL, lower if other risk is present | Captures the reported lipid effect |
| Triglycerides | Under 80 mg/dL | Most carbohydrate-sensitive lipid marker |
| ALT | Under 20 U/L men, under 17 U/L women | Confirms the absence of liver strain seen in trials |
| eGFR | Above 90 mL/min/1.73 m² | Kidney safety, and a modifier of dosing |
| Body fat mass and lean mass | No established target; track change from own baseline | Detects unintended loss of weight or lean tissue |
Cadence: Capillary or continuous glucose daily for the first two weeks, more often where a sulfonylurea or insulin is in use; full laboratory panel at 12 weeks, then every six months; body composition at 12 weeks and annually thereafter