Vitamin C and Immune Function
Vitamin C has long been a means for enhancing the immune system and supporting the body during periods of inflammation, infection and disease (Klenner, 1949; Iqbal, Khan, & Khattak, 2004) such as:
- Viral infections (e.g. colds, flu, pneumonia, herpes, shingles, hepatitis, HIV),
- Bacterial infections (e.g. Helicobacter pylori, E. coli),
- Allergies and asthma,
- Chronic fatigue and glandular fever,
Vitamin C deficiency is a common factor in many chronic and acute illnesses (Buffinton, & Doe, 1995; Long, Maull, & Krishnan, 2003). Vitamin C is important for promoting the function of immune cells and protecting them from oxidation, and has an anti-bacterial and anti-viral effect via interaction with metal ions creating a pro-oxidant environment that kills or inactivates pathogens through the production of high levels of hydrogen peroxide (Furuya, et al., 2008; Strohle, Wolters, & Hahn, 2011).
Intravenous Vitamin C (IVC) Therapy
Critical illness involves extreme oxidative stress, especially in the cardiovascular system, and several clinical trials have observed that high doses of vitamin C may lead to more positive outcomes (Nathens, et al., 2002; Biesalski, & McGregor, 2007). Serious acute infections such as pancreatitis may respond rapidly to vitamin C, with blood parameters and biomarkers of oxidative stress returning to normal quickly and a reduction of symptoms, complications and time spent hospitalised (Du, et al., 2003). Likewise, patients that have suffered from sepsis (Wilson, 2009) or significant trauma such as severe burns may also have a better recovery with vitamin C (Tanaka, et al., 2000).
Intravenous doses of up to 1.5g/kg have been given to humans with few adverse events (Hoffer, et al., 2008; Padayatty, et al., 2010). Most adverse events associated with IVC are transient and mild (such as diarrhoea, headache, fatigue), however for people with glucose-6-phosphate dehydrogenase (G6PD) deficiency, high doses of vitamin C could cause hemolysis so should be avoided (Campbell, Steinberg, & Bower, 1975).
There have been concerns that high doses of vitamin C may increase the risk of kidney stones, as one of the byproducts of vitamin C metabolism is oxalic acid which can form calcium oxalate deposits (Massey, Liebman, & Kynast-Gales, 2005). However, some studies may have exaggerated the risk by using analysis methods that cause conversion of vitamin C to oxalate. When people with normal renal function receive IVC and urine samples are processed appropriately, less than 0.5% of the vitamin C is converted (Robitaille, et al., 2009). However, as a precaution, people with impaired renal function or a history of stone formation should be monitored carefully.
The information provided here is only for general reference and cannot replace personalised professional medical advice from a doctor. You are welcome to discuss any points during your consultation with our doctors.
- Biesalski HK, McGregor GP. (2007). Antioxidant therapy in critical care–is the microcirculation the primary target? Crit Care Med. 35:S577-S583.
- Buffinton GD, Doe WF. (1995). Altered ascorbic acid status in the mucosa from inflammatory bowel disease patients. Free Radical Res. 1995;22:131-143.
- Campbell GD, Steinberg MH, Bower JD. (1975). Letter: Ascorbic acid-induced hemolysis in G-6-PD deficiency. Ann Intern Med. 82:810.
- Du WD, Yuan ZR, Sun J, et al. (2003). Therapeutic efficacy of high-dose vitamin C on acute pancreatitis and its potential mechanisms. World J Gastroenterol. 9:2565-2569.
- Furuya A, Uozaki M, Yamasaki H, et al. (2008). Antiviral effects of ascorbic and dehydroascorbic acids in vitro. Int J Mol Med. 22:541-545.
- Hoffer, LJ, Levine M, Assouline S, et al. (2008). Phase I clinical trial of i.v. ascorbic acid in advanced malignancy. Ann Oncol. 19:1969-1974.
- Iqbal K, Khan A, Khattak MMAK. (2004). Biological significance of ascorbic acid (Vitamin C) in human health – a review. Pak J Nutr. 3:5-13.
- Klenner FR. (1949). The treatment of poliomyelitis and other virus diseases with vitamin C. South Med Surg. 111:209-214.
- Long CL, Maull KI, Krishnan RS, et al. (2003). Ascorbic acid dynamics in the seriously ill and injured. J Surg Res. 109:144-148.
- Massey LK, Liebman M, Kynast-Gales SA. (2005). Ascorbate increases human oxaluria and kidney stone risk. J Nutr. 135:1673-1677.
- Nathens AB, Neff MJ, Jurkovich GJ, et al. (2002). Randomized, prospective trial of antioxidant supplementation in critically ill surgical patients. Ann Surg. 236:814-822
- Padayatty SJ, Sun AY, Chen Q, et al. (2010). Vitamin C: intravenous use by complementary and alternative medicine practitioners and adverse effects. PLoS One. 5:e11414.
- Robitaille L, Mamer OA, Miller WH, et al. (2009). Oxalic acid excretion after intravenous ascorbic acid administration. Metabolism. 58:263-269.
- Strohle A, Wolters M, Hahn, A. (2011). Micronutrients at the interface between inflammation and infection–ascorbic acid and calciferol: part 1, general overview with a focus on ascorbic acid. Inflamm Allergy Drug Targets. 10:54-63.
- Tanaka H, Matsuda T, Miyagantani Y, et al. (2000). Reduction of resuscitation fluid volumes in severely burned patients using ascorbic acid administration: a randomized, prospective study. Arch Surg. 135:326-331.
- Wilson JX. (2009). Mechanism of action of vitamin C in sepsis: ascorbate modulates redox signaling in endothelium. Biofactors. 35:5-13.