Uric Acid Levels and Eating Disorders

Abstract

Uric acid (UA), the end product of purine metabolism, is actively reabsorbed and may modulate behaviors relevant to eating disorders (ED) and play a role in its pathophysiology. Previous evidence suggests higher UA levels among anorexia nervosa–binge eating/purging (AN-BP) subtypes and tophaceous gout as a potential complication in long-standing severe cases. Several factors may affect UA levels including fructose and purine dietary intake, hydration status, reproductive hormonal levels, and renal function, with chronic laxative and diuretic use and repeated vomiting associated with renal dysfunction and hyperuricemia. High UA levels have been proposed in turn to exert a central effect augmenting foraging-like, impulsive–addictive behavioral tendencies and may thus contribute to AN-BP pathophysiology. Larger case–control studies prospectively documenting UA among ED patients stratified according to restrictive and binge eating/purging subtypes are important to validate UA abnormalities in ED and establish its potential utility as an aid in clinical assessment and follow-up. UA and purinergic neurotransmission may constitute novel thitherto unexplored targets for the treatment of behavioral manifestations among AN-BP patients.