Abstract
BACKGROUND: The EAT-Lancet diet was developed to promote both human health and environmental sustainability. However, the association between the EAT-Lancet diet and kidney stone disease (KSD) risk remains unclear.</p>
OBJECTIVE: We aimed to investigate the association between adherence to the EAT-Lancet diet and KSD risk, evaluate the mediating role of body mass index (BMI), and explore whether genetic predisposition modifies these associations.</p>
METHODS: This prospective cohort study included 197,759 adults who completed at least one 24-hour dietary recall and were free of KSD from the UK Biobank. The EAT-Lancet Diet Index (ELD-I) was calculated using these recall data to assess the adherence to the EAT-Lancet diet. A polygenic risk score (PRS) was constructed using 20 single-nucleotide polymorphisms (SNPs) to evaluate genetic predisposition. Cox proportional hazards regression models were used to assess the associations between ELD-I, genetic predisposition, and KSD risk. The mediating role of body mass index (BMI) was also investigated.</p>
RESULTS: After 2,286,927 person-years of follow-up, 1,708 incident KSD cases were identified. In the multivariable-adjusted model, compared to participants with the lowest ELD-I, the hazard ratio (HR) and 95% confidence interval (CI) for participants with the highest ELD-I was 0.81 (0.69, 0.95). Mediation analysis indicated that BMI mediated 14.94% of the association between ELD-I and KSD risk. Moreover, no significant interaction between the genetic predisposition of KSD and ELD-I was observed. Joint analyses showed that compared to participants with the lowest ELD-I and higher genetic predisposition, the HR (95% CI) of those with the highest ELD-I and lower genetic predisposition was 0.61 (0.49, 0.76).</p>
CONCLUSION: Higher adherence to the EAT-Lancet diet was inversely associated with KSD among people with different genetic predispositions, and the association was partly mediated by BMI.</p>