A stable salt of a molecule the body makes from food. Strongest human evidence sits away from longevity: lower blood phosphate in kidney failure, slower bone breakdown after menopause. The longevity case rests on animal work a large independent programme did not reproduce, and on uncontrolled seller data. Anyone tracking blood work and capping total calcium faces modest exposure. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Serum calcium (albumin-corrected) | 9.0–10.0 mg/dL | Detects excess from the mineral load |
| 24-hour urinary calcium | Men below 250 mg/day; women below 200 mg/day | Earliest stone signal |
| Intact parathyroid hormone | 15–35 pg/mL | Flags undiagnosed hyperparathyroidism |
| 25-hydroxyvitamin D | 40–60 ng/mL | Governs calcium absorption |
| Serum phosphate | 3.0–4.0 mg/dL | The salt binds dietary phosphate |
| Estimated glomerular filtration rate, creatinine and cystatin C | 90 mL/min/1.73 m² or above; within 10% of baseline | Kidney handling of the calcium load |
| High-sensitivity C-reactive protein | Below 0.5 mg/L | Tracks the inflammation pathway |
| Red-cell magnesium | 5.0–6.5 mg/dL | Calcium competes with magnesium |
| Ferritin with transferrin saturation | Ferritin 50–150 ng/mL; saturation 25–35% | Calcium blunts non-heme iron uptake |
| Epigenetic age (DNA methylation clock) | No target; track own baseline | The human trial's primary endpoint |
Cadence: Calcium panel at six weeks, full panel at six months, annual thereafter; 24-hour urinary calcium every one to two years; epigenetic clock no sooner than twelve months.