A bulk sweetener absorbed almost completely and passed out unchanged in urine. It does not raise blood sugar or insulin, is gentler on the gut than other sugar alcohols, and mouth bacteria cannot turn it into tooth-eroding acid. People with more of it in their blood have more heart attacks and strokes; whether eating it causes that harm is unresolved. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Fasting glucose | 75–86 mg/dL | Sets the glycemic exposure that erythritol substitution is meant to lower |
| HbA1c | 4.8–5.4% | Three-month average blood sugar; higher values mean more internally produced erythritol |
| Fasting insulin | 2–5 µIU/mL | Detects the insulin resistance that raises baseline erythritol before any is eaten |
| ApoB | Under 80 mg/dL, under 60 if high risk | Counts atherogenic particles, the background risk against which any clotting signal is judged |
| hs-CRP | Under 1.0 mg/L | Tracks vascular inflammation alongside the platelet activation concern |
| eGFR | Above 90 mL/min/1.73 m² | Erythritol leaves the body only through the kidneys, so filtration sets exposure duration |
| Platelet reactivity | No established target for this purpose; track change from the individual's own baseline if tested | The mechanism behind the cardiovascular concern, but not validated for dietary monitoring |
Cadence: Baseline panel before habitual use begins; repeated after 8 to 12 weeks of steady intake, then every 6 to 12 months thereafter, or within 4 weeks of any change in kidney function or any new cardiovascular diagnosis