Interaction of Harmful Alcohol Use and Tea Consumption on Hyperuricemia Among Han Residents Aged 30–79 in Chongqing, China

Abstract

Objective The prevalence of hyperuricemia appears to be high worldwide. We aimed to explore the interaction between harmful alcohol use and tea consumption on hyperuricemia. Methods This study recruited 22,449 Han residents based on the data from the China Multi-Ethnic Cohort (CMEC) study, Chongqing province, to have a face-to-face electronic questionnaire, physical examination, and clinical laboratory tests. The difference in hyperuricemia between the different populations was compared by the Chi-square test. The interaction between harmful alcohol use and tea consumption was analyzed by the multivariate logistic regression model. Results Amongst 22,449 participants, the mean age was 51.5±11.8 years, and 46.83% of them were males. The proportion of harmful alcohol use, tea consumption, and harmful alcohol use and tea consumption were 14.01%, 21.01%, and 6.54%, respectively. Multivariate logistic regression showed that the odds ratio (OR) of harmful alcohol use and tea consumption (OR=2.21, 95% CI: 1.58–3.10) was greater than that of harmful alcohol use (OR=1.63, 95% CI:1.17–2.27) and tea consumption (OR=1.34, 95% CI:1.10–1.63). Among males, the results were similar (harmful alcohol use and tea consumption: OR=2.02, 95% CI: 1.43–2.84; harmful alcohol use: OR=1.61, 95% CI: 1.14–2.27; tea consumption: OR=1.28, 95% CI: 1.05–1.57). However, among females, the odds ratio of harmful alcohol use and tea consumption (OR=15.50, 95% CI: 1.36–176.50) was more than 10 times than that of only harmful alcohol use (OR=1.55, 95% CI: 0.42–5.69) or tea consumption (OR=1.22, 95% CI: 0.52–2.82). Conclusion The interaction of harmful alcohol use and tea consumption was a positive risk for hyperuricemia in Han residents aged 30–79 years in China.

Hyperuricemia: Current State and Prospects

“…Despite purine-rich foods potentially raising UA levels [8], especially in those with impaired UA clearance, excessive alcohol and fructose-rich beverages have also been linked to HU [10]. The associated factors such as ethanol catabolism, lactic acid inhibition of renal urate excretion, acute liver damage, and fructose consumption affect the production of UA metabolic enzymes and UA transporters [59] or intensifying adenosine triphosphate (ATP) degradation [60], contributing to elevated serum UA levels following alcohol or fructose intake. Encouraging moderation in alcohol consumption and ensuring adequate hydration are essential aspects of HU management.…”