Adherence to the EAT-Lancet diet, genetic predisposition, and risk of kidney stone disease: a population-based...

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.

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.

This prospective cohort study included 197,759 adults who completed at least one 24-h 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 was constructed using 20 single-nucleotide polymorphisms 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 BMI was also investigated.

After 2,286,927 person-years of follow-up, 1708 incident KSD cases were identified. In the multivariable-adjusted model, compared with participants with the lowest ELD-I, the hazard ratio (HR) for participants with the highest ELD-I was 0.81 [95% confidence interval (CI) 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 for KSD and ELD-I was observed. Joint analyses showed that, compared with participants with the lowest ELD-I and higher genetic predisposition, the HR of those with the highest ELD-I and lower genetic predisposition was 0.61 (95% CI: 0.49, 0.76).

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.