A sugar alcohol that tastes like sugar, carries fewer calories, and barely raises blood sugar. Its clearest effect is in the mouth, where it starves the bacteria behind tooth decay and boosts saliva. Larger single amounts cause diarrhea and bloating until the gut adapts. A disputed link to heart attacks and strokes is unresolved. Lethal to dogs in small amounts. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Salivary mutans streptococci | < 10⁵ CFU/mL | Direct target of xylitol’s mechanism; the earliest marker to move |
| Plaque index (Silness–Löe) | < 0.5 | Quantifies the biofilm burden xylitol is meant to reduce |
| New carious lesions (bitewing radiographs) | No new or progressing lesions per 12–24 months | The outcome that actually matters; everything else is a surrogate |
| Unstimulated salivary flow rate | > 0.25 mL/min | Saliva buffers acid and remineralizes enamel; the pathway xylitol stimulates |
| HbA1c | 4.8–5.4% | Confirms that sugar substitution is translating into glycemic gain |
| Fasting insulin | < 6 µIU/mL | Detects whether bulk xylitol use is adding a metabolic load |
| Platelet function (aggregometry) | No established target for xylitol users | The only direct readout of the disputed clotting mechanism |
| Stool consistency (Bristol Stool Scale) | Types 3–4 | Simplest early signal that the dose has exceeded gut tolerance |
Cadence: Salivary bacteria and plaque at 4–6 weeks; metabolic markers at 3–6 months; lesions radiographically at 12 months, then every 12–24 months; digestive tolerance continuously during titration and intermittently thereafter