The main building block of cell membranes and the body's chief store of choline; supplementing tops up a nutrient, not a drug. Strongest evidence is liver: purified soy preparations lower liver fat and enzymes in fatty liver disease, and preventing outright choline shortfall protects liver and muscle. Cheap and well tolerated, with an unsettled cardiovascular question at higher doses. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Alanine aminotransferase | <20 U/L (men), <17 U/L (women) | Liver cell injury and the primary trial endpoint |
| Gamma-glutamyl transferase | <20 U/L | Bile-duct stress and oxidative load |
| Controlled attenuation parameter | <248 dB/m | Direct ultrasound measure of liver fat |
| Trimethylamine N-oxide | <6.2 µmol/L | The central safety question, made measurable |
| Apolipoprotein B | <80 mg/dL, or <60 mg/dL if cardiovascular risk is high | Counts atherogenic particles, the outcome the metabolite signal is about |
| Triglycerides | <100 mg/dL fasting | Endpoint that moved most in the liver and lipid trials |
| Hemoglobin A1c | 4.8–5.4% | Three-month glucose control |
| Estimated glomerular filtration rate | >90 mL/min/1.73 m² | Clearance capacity for trimethylamine N-oxide |
| Homocysteine | <9 µmol/L | Whether the methyl-donor pathway phosphatidylcholine feeds is adequately supplied |
| Plasma free choline | No established optimal target; track change from baseline | Confirms the supplement is actually raising choline status |
| PEMT rs12325817 genotype | No range applies; the result is a genotype, tested once | Predicts how much internal phosphatidylcholine synthesis to expect |
Cadence: Liver enzymes and trimethylamine N-oxide at 8–12 weeks; lipid panel and glycemic marker at 3 months; direct liver-fat measurement at 6 months; then every 6–12 months once values are stable