ArticleUrolithiasis2025
Dietary inflammatory index and phenotypic age mediate the association between the dietary index for gut microbiota and kidney stone disease among U.S. overweight/obese adults.
Article in Urolithiasis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Globally, kidney stone disease (KSD) constitutes one of the leading pathological conditions affecting the urinary system. Patients with KSD are characterized by imbalanced gut microbiota, which may be more pronounced in overweight/obese populations. The dietary index for gut microbiota (DI-GM) was developed to assess the effect of dietary patterns on gut microbial diversity. However, in overweight/obese populations, its association with KSD, along with the mechanisms, has not been fully elucidated. Data from National Health and Nutrition Examination Survey were analyzed. This cross-sectional study explored the association between DI-GM and KSD through weighted multivariable logistic regression, restricted cubic spline (RCS), multiple imputation, and subgroup analysis. Mediation analysis was subsequently conducted to examine whether the dietary inflammatory index (DII) and phenotypic age contributed to this association. Our study included 11,280 overweight/obese participants, with a weighted prevalence of KSD of 11.62%. After full adjustment, an inverse association was observed between DI-GM and KSD (OR = 0.93, 95%CI: 0.89 to 0.98). When DI-GM was treated categorically, individuals with DI-GM score ≥ 6 had 22% lower odds of KSD in comparison with the reference group (OR = 0.78, 95%CI: 0.64 to 0.96). Linear relationship was demonstrated between DI-GM and KSD through RCS. DII and phenotypic age exhibited significant mediating effects in the relationship between DI-GM and KSD, accounting for 26.77% and 8.43% of the total effect. In conclusion, the protective effect of DI-GM against KSD in overweight/obese populations appeared to be partially mediated by reductions of DII and phenotypic age. Given the observational design, longitudinal cohort studies are warranted to validate these results.
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