Raw potato starch mostly escapes digestion and feeds large-bowel bacteria. The firmest human evidence covers blood sugar handling and bowel function; single trials point to less liver fat and modest weight loss. Response varies sharply: the bacteria able to break down the starch are plentiful in some guts and scarce in others. Gas and bloating grow with the amount taken. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Fasting glucose | 75–86 mg/dL | Primary endpoint with meta-analytic support |
| Glycated haemoglobin | 4.8–5.3% | 90-day integrated glucose exposure |
| Fasting insulin | 2–5 µIU/mL | Detects compensated insulin resistance before glucose rises |
| Insulin-resistance index | Below 1.0 | Single number combining fasting glucose and insulin |
| High-sensitivity C-reactive protein | Below 0.5 mg/L | Outcome-validated inflammation marker; did not move in pooled trials |
| Triglycerides | Below 80 mg/dL | Most diet-responsive lipid; the one that moved for granular starch |
| Alanine aminotransferase | 10–26 U/L (men), 8–22 U/L (women) | Accessible proxy for liver fat, the endpoint of the largest trial |
| Fecal short-chain fatty acids | No established range; change from own baseline | Direct readout of whether fermentation is occurring at all |
| Continuous glucose monitor post-meal peak | No consensus target; change from own pre-intervention peaks | Captures the post-meal flattening that is the most reproducible effect |
Cadence: Baseline panel before starting; bowel diary at four weeks; metabolic panel at twelve weeks, once the target dose has been held for eight; then every six to twelve months.