Association between the dietary index for gut microbiota and post-stroke depression: a cross-sectional study.

Abstract

Background: Gut microbiota dysbiosis plays a critical role in the pathogenesis of post-stroke depression (PSD). The role of microbiota-targeted dietary patterns in PSD remains uncharacterized. This population-based study evaluated the Dietary Index for Gut Microbiota (DI-GM) and PSD prevalence relationship in U.S. adults.

Methods: This cross-sectional study analyzed data from seven consecutive cycles (2005-2018) of the National Health and Nutrition Examination Survey (NHANES). Multivariable logistic regression assessed DI-GM-PSD associations, with restricted cubic splines (RCS) evaluating nonlinear trends. Stratified analyses assessed effect modification by demographic/clinical characteristics. Mediation analysis quantified the indirect effects of DI-GM on PSD through the mediator, body mass index (BMI).

Results: Adjusted analyses showed a negative association between DI-GM scores and PSD, with higher scores concurrently linked to lower PSD prevalence. The DI-GM scores ranged from 0 to 14. In Q4 DI-GM (7-14), PSD risk was 60% lower vs. Q1 (0-4) (OR = 0.40, 95% CI 0.23-0.71, p = 0.002). RCS regression depicted a curvilinear pattern between DI-GM scores and PSD risk (nonlinearity p = 0.015). Stratified analyses showed that higher DI-GM scores were associated with significantly lower rates of PSD in females (OR = 0.83, 95% CI 0.74-0.94; p-interaction = 0.026), but not in males. Mediation analysis suggested BMI partially mediated the association between DI-GM and PSD risk (proportion mediated: 19.2%, p = 0.018).

Conclusions: This study identified a negative association between DI-GM scores and the prevalence of PSD. Our findings suggest that dietary patterns beneficial to gut microbiota are associated with lower rates of PSD, and that this relationship is inter-related with BMI. These results highlight the potential clinical relevance of integrated dietary and weight management strategies, though longitudinal studies are needed to confirm any causal pathways.