Nonpharmacological Management of Gout and Hyperuricemia: Hints for Better Lifestyle

Abstract

We reviewed lifestyle factors that influence serum uric acid levels and risk of gout flare, and how to improve their deleterious effects. Since obesity increases uric acid and weight gain increases gout risk, weight reduction by daily exercise and limiting intake of excess calories is recommended. However, strenuous exercise, which causes adenine nucleotide degradation; starvation, which decreases uric acid excretion; and dehydration may raise the level of uric acid in serum and trigger gout. Increased intake of purine-rich foods, such as meat and seafood, raise the level of uric acid in serum and is associated with increased risk of gout, whereas dairy products, especially low-fat types, are associated with a lower risk of gout. Also, heavy alcohol drinking raises the uric acid level and increases the risk of gout through adenine nucleotide degradation and lactate production. Sweet fruits and soft drinks containing fructose should be moderated, since fructose may raise uric acid and increase gout risk through uric acid production and/or decreased excretion. On the other hand, the Mediterranean diet is recommended for gout patients, since it may also help prevent hyperuricemia. Furthermore, coffee and vitamin C supplementation could be considered as preventive measures, as those can lower serum uric acid levels as well as the risk of gout.

Keywords: exercise; lifestyle; nutrition; obesity; uric acid.

Figure 1.

Increased Uric Acid Influx Induced by Hyperinsulinemia. Insulin resistance/hyperinsulinemia increases reabsorption of sodium and monocarboxylic acid via SMCT1 with uric acid influx in exchange for monocarboxylic acid excretion via URAT1.

Figure 2.

Increased Adenosine Nucleotide Degradation by Fructose. Fructose is metabolized to fructose-1-phosphate by fructokinase in the liver, which then consumes ATP and phosphate. Depletion of phosphate induces decreased ATP recycling and activates AMP deaminase, which is suppressed by phosphate, then subsequently increases AMP degradation to IMP, inosine, hypoxanthine, xanthine, and finally uric acid.

Figure 3.

Mechanism of Increased Uric Acid by Alcoholic Beverage Consumption. Ethanol increases uric acid production resulting from acetate metabolism and enhanced adenosine nucleotide turnover,^, and increases lactic acid level in blood, leading to increased uric acid in serum.