Uric acid is an essential compound in the body which in normal physiological ranges has potent anti-oxidant capacity while in excess leads to hyperuricemia, a clinical indicator of pro-oxidant and pro-inflammatory state. Uric acid is acquired through purine catabolism and dietary factors (alcohol or fructose-rich drinks) and its physiological balance is maintained by its secretion through the liver and kidney. Any imbalance in either process leads to either the accumulation (hyperuricemia) or reduction (hypouricemia) in uric acid serum levels. Both conditions are associated with disease states, though whether uric acid levels are causative or result of disease remains unclear.
Hyperuricemia has become more common in the modern population and causes uric acid to precipitate around joints resulting in gout. A number of pharmacological treatments are currently available for gout, but have many adverse side effects. Due to this shortcoming, new areas of research are exploring better therapies for hyperuricemia including the manipulation of the gut microbiome with probiotics and prebiotics. There is ample clinical and epidemiological evidence supporting the role of prebiotics and probiotics in reducing uric acid levels in serum, though the mechanisms remain elusive.
Probiotics can influence the bioavailability of the uric acid’s precursor, namely purine and it breakdown products inosine and guanosine, which could influence clinical uric acid profiles. Overall, there is a need for more sustainable treatment plans for hyperuricemia as uric acid dependent gout continues to rise and the use of the dietary factors probiotics and prebiotics is a strong candidate.
Continue reading full article PDF