Vitamin C and Gout
Vitamin C or L-ascorbic acid, or simply ascorbate (the anion of ascorbic acid), is an essential nutrient for humans and certain other animal species. Vitamin C has been advocated for many other therapeutic uses. Vitamin C functions as an antioxidant and is necessary for the treatment and prevention of scurvy, though in nearly all cases dietary intake is adequate to prevent deficiency and supplementation is not necessary. Though vitamin C has been promoted as useful in the treatment of a variety of conditions, most of these uses are poorly supported by the evidence and sometimes contraindicated. Despite previous studies touting its benefit in moderating gout risk, new research reveals that vitamin C does not reduce uric acid (urate) levels to a clinically significant degree in patients with established gout. Vitamin C supplementation, alone or in combination with allopurinol, appears to have a weak effect on lowering uric acid levels in gout patients according to the results published in the American College of Rheumatology (ACR) journal, Arthritis & Rheumatism.
There is continuing debate within the scientific community over the best dose schedule (the amount and frequency of intake) of vitamin C for maintaining optimal health in humans. A balanced diet without supplementation usually contains enough vitamin C to prevent scurvy in an average healthy adult, while those who are pregnant, smoke tobacco, or are under stress require slightly more.
High doses (thousands of milligrams) may result in diarrhea in healthy adults, as a result of the osmotic water-retaining effect of the unabsorbed portion in the gastrointestinal tract (similar to cathartic osmotic laxatives). Proponents of orthomolecular medicine claim the onset of diarrhea to be an indication of where the body's true vitamin C requirement lies, though this has not been clinically verified.
Gout is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis—a red, tender, hot, swollen joint. The metatarsal-phalangeal joint at the base of the big toe is the most commonly affected (approximately 50% of cases). However, it may also present as tophi, kidney stones, or urate nephropathy. It is caused by elevated levels of uric acid in the blood. The uric acid crystallizes, and the crystals deposit in joints, tendons, and surrounding tissues.
"While current treatments are successful in reducing the amount of uric acid in the blood, there are many patients who fail to reach appropriate urate levels and need additional therapies," explains lead author, Prof. Lisa Stamp, from the University of Otago in Christchurch, New Zealand. "Vitamin supplementation is one such alternative therapy and the focus of our current study, which looked at the effects of vitamin C on urate levels in patients with gout."
The study showed that a modest dose of vitamin C (500mg/d) for 8 weeks had no clinically significant urate lowering effect in patients with gout despite increasing plasma ascorbate. These results differ from findings in hyperuricaemic healthy controls. The uricosuric effect of modest dose vitamin C appears less in patients with gout both as monotherapy and in combination with allopurinol.
"Though vitamin C may reduce risk of developing gout, our data does not support using vitamin C as a therapy to lower uric acid levels in patients with established gout," concludes Prof. Stamp.
For further information see Vitamin C and Gout.
Gout image via Wikipedia.