Removing one sweetener from the diet; cheap, needs no product. A real gain arises only for people who cannot clear one of the protein building blocks it releases, plus a small group whose headaches respond. Beyond them the case rests on studies tracking large groups over time. What replaces it decides the outcome: water keeps the balance, sugar reverses it. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Body weight | Within 1 kg of baseline | Detects sugar substitution earliest |
| Waist circumference | <94 cm men, <80 cm women | Central fat tracks the substitution effect |
| Fasting glucose | 70–85 mg/dL | Flags a return to sugar-sweetened drinks |
| Glycated haemoglobin | 4.8–5.4% | Integrates the dietary swap over months |
| Fasting insulin | 2–5 µIU/mL | Detects insulin resistance before glucose moves |
| Triglycerides | <80 mg/dL | Most sugar-responsive lipid marker |
| Alanine aminotransferase | <20 U/L men, <17 U/L women | Tracks liver fat, which rises with sugar |
| High-sensitivity C-reactive protein | <0.8 mg/L | Background inflammatory tone |
| Blood pressure | <120/80 mmHg | Cardiovascular endpoint most affected by the swap |
| Plasma phenylalanine | <12 µmol/dL | Only relevant with phenylketonuria carrier status |
Cadence: Baseline panel, then body weight weekly for three months; full laboratory panel at three months and again at twelve months, then every twelve months while avoidance continues. The three-month panel is brought forward to six weeks where fasting glucose, triglycerides or liver enzymes sat outside range at baseline.