High serum levels of uric acid (hyperuricaemia) are a risk factor for the development of gout. Gout is a medical condition whereby uric acid crystallises out of solution and accumulates in the joints of the body. This causes inflammation in the joint characterised by heat, redness, pain, swelling and loss of function. In this regard, gout can be considered a form of arthritis. Medications to eliminate uric acid are the mainstream medical treatment for gout, and such medications aim to lower uric acid levels either through enhanced elimination or through inhibition of the rate limiting synthesising enzyme, xanthine oxidase. Dietary advice regarding the treatment of gout usually involves the recommendations to reduce intakes of meat and seafood, limitations on alcohol consumption, while increasing the amount of plant foods in the diet. This last recommendation is pivotal, because plant foods are rich in vitamin C, and vitamin C is highly effective at reducing plasma levels of uric acid in humans.
In a meta-analysis of the relevant studies to date1, researchers assessed 13 publications that involved the effects of vitamin C on plasma uric acid levels in human subjects in controlled clinical trials that lasted more than 1 week. The total number of subjects in the 13 trials was 556, and the mean vitamin C intake was 500 mg per day. The serum uric acid levels of the subjects was between 2.9 and 7.0 mg per dL prior to vitamin C consumption, whereas the pre-treatment vitamin C concentrations varied from between 27.0 to 77.7 μmol/L. Consumption of vitamin C reduced serum uric acid levels by 0.35 mg per dL over all trials, and was associated with significant reductions in 8 of the 13 trials. The authors reported significant heterogeneity between the trials suggesting that subject biochemistry and methodological differences may have affected the results. Analysis of the results showed that those trials where subjects had concentrations of uric acid above 4.85 mg per dL had larger positive effects from the vitamin C supplementation, while studies using a placebo showed significant reductions in uric acid levels.
The mechanisms by which vitamin C can lower serum levels of uric acid have been investigated. The most likely explanation is that vitamin C acts as a competitive inhibitor of the anion exchange system in the proximal tubule in the nephrons of the kidneys. In this regard vitamin C may prevent the reabsorption of uric acid through the urate transporters. Additionally vitamin C may increase glomerular filtration rate by increasing blood flow to the afferent arterioles. Or put another way, vitamin C insufficiency may decrease these effects. As uric acid is quantitatively the most abundant antioxidant in human plasma, it makes a significant contribution to the total antioxidant defences of humans. Vitamin C is also a water soluble antioxidant, and so it has been theorised that high vitamin C intakes decrease the necessity for the production of high concentrations of uric acid. Therefore do humans produce more and excrete less uric acid, a situation that can lead to gout, when they have a borderline intake of vitamin C?
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