An inexpensive, food-derived compound with one clear job — handing out the small chemical tags called methyl groups — and one clear consequence. It lowers the blood marker homocysteine consistently, and at the same doses raises total and harmful cholesterol. Lower-body strength improves; liver fat shifts in people who already have fatty liver. The longevity claim rests on aged mice. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Homocysteine | 5–8 µmol/L | The target betaine acts on |
| LDL cholesterol | <100 mg/dL; <70 mg/dL with existing cardiovascular disease | The principal adverse effect at 4 g daily or more |
| Total cholesterol and triglycerides | Total <180 mg/dL; triglycerides <100 mg/dL | Both rose in the pooled betaine trials |
| Alanine aminotransferase (ALT) | <25 U/L in men, <20 U/L in women | Marks liver injury |
| Plasma methionine | 15–35 µmol/L | Accumulation precedes brain swelling; needed only above 6 g daily or in inherited metabolic disease |
| eGFR | >90 mL/min/1.73 m² | The kidney is where betaine concentrates most |
| Vitamin B12 and folate | B12 >500 pg/mL; folate >10 ng/mL | Shows whether the folate route is already saturated |
| TMAO | No established target; track the change from the individual's own baseline | Betaine feeds the gut pathway that produces it |
Cadence: Baseline panel before starting; lipid recheck at 6 to 8 weeks; homocysteine repeated at 12 weeks. If both are stable the cadence drops to annual, returning to 8 weeks after any dose change.