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Tiffany L. Weir

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Open access Jul 2026

Gut microbiome dynamics and cardiometabolic disease progression: evidence from a secondary data analysis of pooled clinical datasets

Purpose Individuals with cardiometabolic disease (CMD) often exhibit decreased microbial alpha diversity and/or differences in beta diversity indices than those without CMD. However, it is unclear if these compositional changes in the gut microbiome are a cause or a consequence of CMD. Research suggests individual bacterial species act as drivers of disease, inducing shifts in microbial community and host metabolism. During this process, large-scale compositional changes can develop secondarily, obscuring the original microbial drivers. This study aimed to characterize the gut microbiota of healthy individuals compared to those with early risk factors for CMD to determine whether specific microbial taxa and community associations exist with early stages of hypertension, vascular dysfunction, dyslipidemia, and overweight/obesity. Procedure Baseline anthropometric, physiological, and gut microbiome data from three clinical studies previously conducted by our research groups were compiled and re-analyzed. Results No differences in alpha and/or beta diversity were observed across CMD parameters. Through a consensus-based differential abundance analysis, we observed that several health-related taxa decreased as CMD levels increased, including Akkermansia, Bacteroides, Bifidobacterium, Blautia, Eubacterium, Lachnospiraceae, Oscillospiraceae, Prevotella, Roseburia, and Ruminococcus. Furthermore, co-occurrence networks of individuals with elevated cardiometabolic parameters showed lower clustering coefficients, higher path lengths, lower degrees, higher modularity, and higher negative cohesion than those with normal parameters. Implications The loss of health-associated gut microbiota, along with decreased network connectivity and increased network fragmentation, may play a role in the progression of CMD.

Scott D Wrigley, Sarah A. Johnson, C. Gentile et al. · 0 citations

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