Vitamin C certainly cures and prevents its own deficiency, greatly increases how much plant iron a meal delivers, and shortens and softens colds. Blood pressure falls a little and connective tissue repairs better. People with more vitamin C in their blood die later, but supplements do not reproduce this. Higher doses bring bowel upset and, in men, kidney stones. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Plasma vitamin C | 50–80 µmol/L | Direct measure of status; decides whether supplementation adds anything |
| 24-hour urinary oxalate | Below 30 mg/24 h | The route through which vitamin C creates kidney-stone risk |
| Serum creatinine and eGFR | eGFR at or above 90 mL/min/1.73 m² | Detects the reduced kidney reserve that makes oxalate loading dangerous |
| Ferritin and transferrin saturation | Ferritin 30–100 ng/mL; saturation 20–40% | Vitamin C increases iron absorption, which harms the iron-loaded |
| hs-CRP | Below 1.0 mg/L | Tracks the inflammatory burden that low vitamin C status accompanies |
| Blood pressure | Below 120/80 mmHg | Captures the modest reduction seen in supplementation trials |
| Fasting glucose and HbA1c | Glucose 75–90 mg/dL; HbA1c 4.8–5.4% | Baseline for the glycemic changes reported in type 2 diabetes |
| G6PD activity | No numeric target applies; track deficiency status against the assay's own normal range | Screens for the deficiency that makes intravenous vitamin C dangerous |
Cadence: Baseline before starting; recheck plasma vitamin C and blood pressure at 8–12 weeks, then every 6–12 months. Urinary oxalate annually only at sustained gram-level doses.