The Effects of High Dietary Fructose Consumption on the Development of Gout

Abstract

Fructose is frequently used as a food ingredient due to its low production costs, its significant sweetening power and its easy incorporation into a broad variety of foods and beverages. In recent years, it has been observed that people on a Western diet high in fructose often have high levels of uric acid in their blood. It was recognized that the metabolism of fructose in the body might cause increased production of uric acid, which then may impact the intensity of lipogenesis and the development of metabolic syndrome (MetS), insulin resistance, gout, cardiovascular diseases, leptin resistance, non-alcoholic fatty liver disease, or some combination of the above. To date, the treatment of hyperuricemia has been the recommendation of a low-purine diet characterized by limiting protein-containing products and certain alcoholic beverages, in addition to consumption of tart cherry or the widely prescribed purine analog and xanthine oxidase inhibitor allopurinol in an attempt to decrease endogenous uric acid production. However, these recommendations often contribute to an increased intake of carbohydrate-rich foods that may contain fructose or high fructose corn syrup (HFCS) constituents. Increased fructose consumption may then enhance the secretion of uric acid and, consequently, attenuate or negate any potential therapeutic effects from the prescribed therapeutic regimen. A better option instead of a low-purine diet for some would be to follow a healthy meal plan such as DASH or the Mediterranean diet, which can also benefit metabolic parameters. This article provides an overview of this approach, focusing on MetS and hyperuricemia among high-fructose dieters.