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Objectives The association of tea or coffee consumption with gout is inconsistently reported. Few prospective studies have explored their dose-response relationship. Therefore, we aimed to quantitatively investigate the association between tea, coffee and the risk of developing gout. Methods The study included 447 658 participants in the UK Biobank who were initially free of gout. Tea and coffee consumption were assessed at baseline. We used Cox proportional hazards models to estimate the associations between tea/coffee consumption and incident gout, with restricted cubic spline added to the Cox models to evaluate the dose-response relationships. Results During a median follow-up period of 13.42 years, we recorded 3,053 gout cases. The associations between tea, coffee and gout were nonlinear, with a significant reduction in the risk by ∼6 cups/day of tea and 3 cups/day of coffee. Compared with those who were not tea and coffee drinkers, those who consumed >6 cups/day of tea or coffee were associated with 23% (HR 0.77, 95% CI, 0.66–0.91) and 40% (HR 0.60, 95% CI, 0.47–0.77) lower risks of gout, respectively, and both caffeinated and decaffeinated coffee consumption were associated with a decreased risk. Moreover, hyperuricemia may modify the association between coffee and gout. Compared with non-coffee consumers with hyperuricemia, those with ≥4 cups/day coffee intake without hyperuricemia had the lowest risk (HR 0.34, 95% CI, 0.28–0.41). Conclusion Consumption of tea or coffee had a strong nonlinear association in gout risk reduction. Hyperuricemia status had a potential effect modification on the association of coffee intake with gout.

We investigated whether lifestyle influences epigenetic aging in 143 monozygotic twin pairs discordant for the combined healthy lifestyle score. Twins were scored for four lifestyle factors as unhealthy or healthy; non-smoker, moderate drinker, adequate fruit and vegetable intake, and sufficient physical activity. The combined healthy lifestyle score was calculated for each participant by summing the binary score for each factor. Individual and co-twin analyses were used to assess the relationship between single or combined lifestyle scores, along with DNA methylation age acceleration (AA) calculated using Horvath’s and Li’s epigenetic clocks, focusing on AA and intrinsic epigenetic age acceleration (IEAA) measures. Compared with the twins that scored no or one healthy lifestyle point, those who scored four healthy lifestyle points had lower Li_IEAA with similar results observed in the co-twin analysis. No significant relationships were found in analyses based on Horvath’s clock, although the direction of correlations was consistent with that determined using Li’s clock. Smoking and drinking did not significantly affect DNA methylation AA; however, physical activity and intake of vegetables and fruits did, although the influence varied depending on the epigenetic clock. Our findings suggest that a healthy lifestyle may be an important way to delay aging and prevent age-related diseases.

Aim: Alcohol intake alters DNA methylation profiles and methylation might mediate the association between alcohol and disease, but limited number of positive CpG sites repeatedly replicated. Materials & methods: In total, 57 monozygotic (MZ) twin pairs discordant for alcohol drinking from the Chinese National Twin Registry and 158 MZ and dizygotic twin pairs in the Swedish Adoption/Twin Study of Aging were evaluated. DNA methylation was detected using the Infinium HumanMethylation450 BeadChip. Results: Among candidate CpG sites, cg07326074 was significantly correlated with drinking after adjusting for covariates in MZ twins in both datasets but not in the entire sample or dizygotic twins. Conclusion: The hypermethylation of cg07326074, located in the tumor-promoting gene C16orf59, was associated with alcohol consumption.