Monk fruit's sweet molecules pass through the gut mostly unabsorbed. Its value lies in what it removes: replacing sugar avoids the blood sugar and insulin rise and does not feed tooth-damaging bacteria. The benefit is wholly conditional on displacing sugar. Most tabletop products are almost entirely a sugar alcohol bulking agent, the real source of complaints. Evidence is thin. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Fasting glucose | 75–86 mg/dL | Tracks the glycaemic load removed |
| Fasting insulin | 2–5 µIU/mL | Most sensitive early marker of sugar displacement |
| Glycated haemoglobin (HbA1c) | 4.8–5.3% | Three-month average blood sugar |
| Triglycerides | <80 mg/dL | Responds directly to fructose and added-sugar intake |
| Triglyceride to HDL ratio | <1.5 (mg/dL units) | Practical proxy for insulin resistance |
| High-sensitivity C-reactive protein | <0.5 mg/L | General inflammatory load that sugar intake raises |
| Alanine aminotransferase (ALT) | <20 U/L men, <17 U/L women | Fatty liver responds to added-sugar reduction |
| Waist circumference | <half of standing height | Central fat, the depot most responsive to sugar reduction |
| Continuous glucose monitor time in range | >90% of readings between 70–120 mg/dL | Detects excursions a fasting draw misses |
| Body weight | No established target; change from own baseline | Confirms whether displaced energy stays displaced |
Cadence: Baseline before switching, with two weeks of glucose readings first for anyone on insulin or a sulfonylurea; metabolic panel repeated at 12 weeks, then every 6–12 months. Continuous glucose monitor users review the first two weeks daily, then monthly. Bowel symptoms declare themselves within days of a dose change and need no laboratory follow-up.