Arthritis News > Coffee Consumption and the Development of Gout
Coffee Consumption May Protect Against
the Development of Gout
Dietary risk factors, such as meat and alcohol consumption, are well recognized as contributing factors to gout flares in patients with established gout. These same factors have been shown to associate with elevated serum uric acid and an increased risk for the development of incident gout. Coffee consumption is a dietary risk factor that has been shown to be both harmful and beneficial in the development of a variety of health problems. Here, Choi et al (Arthritis Rheum 2007; 56(6): 2049) explore whether coffee consumption affects the risk of incident gout in men enrolled in the Health Professionals Follow-up Study.
The design of this study has previously been described on this site, development of incident of gout. For this analysis, the association of average self-reported consumption of caffeinated beverages (including coffee), categorized into quintiles of consumption, on the risk for incident gout was calculated, adjusting for potential confounders of incident gout (age; body mass index (BMI); meat, seafood, purine-rich vegetable, dairy, and alcohol consumption; hypertension; renal insufficiency; and diuretic use).
757 incident cases of gout were identified over 12 years of follow-up among 45,869 men at risk who had complete information on coffee consumption. Subjects in the highest quintiles of coffee consumption tended to consume more alcohol and meat, and were less likely to use diuretics or have a history of hypertension than those in lower quintiles of coffee consumption.
Increasing coffee consumption was associated with a decreased risk of incident gout, with those in the highest consumption group (6+ cups per day) demonstrating a significant 56% reduction in the risk of incident gout compared to those reporting no coffee consumption (RR 0.44 (95% CI 0.21-0.95) in analyses adjusted for age, BMI, and alcohol intake. Fully adjusting for potential confounding covariates and cigarette smoking did not alter substantial this observed protective effect of coffee consumption. Reported coffee consumption of 4 to 5 cups per day was also protective, with a 40% reduction in incident gout compared to those with no reported consumption in fully adjusted analyses.
Decaffeinated coffee showed a modest protective effect, but lacked a clear dose dependent effect compared to caffeinated coffee. Stratifying by tea intake or caffeine intake did not recreate the protective benefit of caffeinated coffee consumption.
Protective benefits of coffee consumption did not vary in analyses stratified by subgroup (BMI, alcohol intake, meat intake, and history of hypertension).
Increasing caffeinated coffee consumption was associated with a dose-dependent protective effect against the development of gout in men.
Coffee contains trimetyl xanthine which has the potential to inhibit xanthine oxidase, the enzyme responsible for the breakdown of purines to uric acid. These results suggest that a substance in coffee, such as trimethyl xanthine, may be responsible for the observed effect, since caffeine consumption did not recreate the effect and decaffeinated coffee demonstrated some, but not all, of the effect of caffeinated coffee. It is important to note that these effects are for incident gout, and do not necessarily implicate coffee as a treatment for gout in patients with established disease. Because of linked patterns of lifestyle behaviors in coffee drinkers (i.e. alcohol consumption, meat intake, cigarette smoking), it takes a large, well designed and carefully executed study such as this one to reliably parse out effects of individual exposures.