High-Dose Vitamin C to Treat Cancer - Quick Reference Sheet
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High-Dose Vitamin C to Treat Cancer

Created on 08/11/2026 – Quick Reference based on Evidence Review created using AI4L / Opus 5 – Audit

Only the infused route reaches blood levels where vitamin C damages tumour cells more than healthy ones; tablets do not. Infusions reach those levels and are tolerated, with milder symptoms in small studies. Whether they lengthen life is unsettled. A missing red-cell enzyme, kidney disease, iron overload and one blood-cancer drug make them hazardous. (Full Review)

Protocol

Dose
25–100 g
0.1–1.5 g/kg, escalating from a 15 g test dose; academic protocols fix 75 g, or 87.5 g with radiation
Schedule
2–3× weekly
Whole dose as one infusion, not split; morning or early afternoon
Target concentration
≥20 mmol/L
All academic protocols titrate to plasma concentration mid-infusion rather than to a fixed dose
Time to effect
Millimolar plasma level
Mid-infusion
Half-life roughly two hours; levels return to baseline within about four hours, so exposure is a series of brief spikes
Symptoms and fatigue
2–4 weeks
Where they occur, from the start of a thrice-weekly schedule
Tumour burden
8–12 weeks
Assessed on the oncology imaging schedule, not the infusion schedule

Benefits

Contraindications
  • Glucose-6-phosphate dehydrogenase deficiency of any severity
  • Stage 4–5 chronic kidney disease (eGFR <30 mL/min/1.73 m²) or any dialysis dependence
  • Active oxalate nephropathy, primary hyperoxaluria, or recurrent calcium oxalate stones within 12 months
  • Hereditary haemochromatosis or transfusional iron overload (ferritin above 1,000 ng/mL)
  • Active bortezomib- or ixazomib-based myeloma therapy
  • Decompensated heart failure (New York Heart Association Class IV) or uncontrolled ascites
  • Pregnancy
    •
Key Interactions
  • Platinum and taxane chemotherapy (carboplatin, cisplatin, paclitaxel)
  • Gemcitabine and erlotinib
  • Anticoagulants (warfarin)
  • Deferoxamine and other iron chelators
  • Oral iron and heme-iron-rich meals
  • Dextrose-containing intravenous fluids
  • Additive oxidant or oxalate supplements (alpha-lipoic acid, vitamin K3, green tea extract)
  • Antioxidant supplements (N-acetylcysteine, vitamin E, glutathione, selenium)
  • Over-the-counter analgesics (aspirin, acetaminophen)
  • Aluminium-containing antacids (aluminium hydroxide)
  • Radiation therapy
    •

Risk & Side Effects

  • High: Oxalate nephropathy and acute kidney injury; haemolysis in glucose-6-phosphate dehydrogenase deficiency; falsely elevated point-of-care glucose readings
    •
  • Medium: Infusion-related symptoms and fluid–sodium load; displacement of effective conventional treatment; antagonism of bortezomib-based myeloma therapy
    •
  • Low: Calcium oxalate kidney stones; iron overload aggravation; tumour lysis syndrome
    •
  • Speculative: Antioxidant blunting of radiation or chemotherapy (conflicted); selection for ascorbate-resistant, more metastatic cells
    •

Monitoring

Marker Target Why
G6PD enzyme activity Normal activity, ≥60% of the laboratory's reference mean Absent enzyme means infusion can rupture red cells
Creatinine and eGFR eGFR ≥60 mL/min/1.73 m²; below 30 is a contraindication Kidney capacity to clear the oxalate load
Plasma ascorbate Peak ≥20 mmol/L mid-infusion; trough 50–70 µmol/L Confirms the pharmacological threshold was actually reached
Urinary oxalate, 24-hour <40 mg per 24 hours Detects the oxalate accumulation that precipitates in tubules
Haemoglobin and reticulocytes Stable within 1 g/dL of the individual's own baseline Detects red-cell destruction after infusion
Lactate dehydrogenase Within the laboratory reference range Rises when red cells or tumour cells rupture
Ferritin and transferrin saturation Ferritin 50–100 ng/mL; saturation 25–35% Identifies the iron overload that amplifies oxidative damage
C-reactive protein No established target during active cancer; track the direction of change from the individual's own baseline The inflammation marker that moved in the clinic series
Sodium and potassium Sodium 135–142 mmol/L; potassium 4.0–4.5 mmol/L Tracks the salt load delivered with buffered ascorbate
Uric acid, phosphate, calcium Uric acid 3.5–5.5 mg/dL; phosphate 2.5–4.0 mg/dL; calcium 9.0–10.0 mg/dL Screens for the metabolic release of tumour lysis
Disease-specific tumour markers No universal target; track the trajectory against the individual's own pre-treatment value The only direct read on whether disease burden is moving

Cadence: Kidney function and electrolytes before each cycle; full blood count and red-cell breakdown markers 24–48 hours after each of the first two infusions; then at 2 weeks, 4 weeks, and every 4–8 weeks while treatment continues, with plasma ascorbate measured mid-infusion whenever the dose changes.

Qualitative Assessment

  • Fatigue severity, scored the same way each week rather than recalled
  • Appetite and weight trajectory
  • Pain scores and analgesic requirement
  • Sleep continuity, particularly night-time urination on infusion days
  • Cognitive clarity, including the transient altered mental status reported after infusion
  • Nausea, constipation and mood
  • Tolerability of the infusion itself: vein discomfort, thirst, tremor, post-infusion lethargy
Not medical advice. Educational distillation of a single evidence review. Confirm any decision with a qualified clinician, especially in the presence of prescription drugs or chronic conditions.