Alterations in gut microbial ecology have been linked to obesity, type 2 diabetes (T2D), and hypertension, but their biological significance remains difficult to separate from diet, medication use, adiposity, and other host factors. We synthesize evidence on intestinal barrier dysfunction, microbial translocation, low-grade inflammation, and microbiota-derived metabolites as interconnected mechanisms across these disorders. SCFAs, bile acids, trimethylamine N-oxide, tryptophan derivatives, branched-chain amino acid metabolites, and phenylacetylglutamine influence epithelial function, immune activation, insulin signaling, lipid handling, vascular tone, and renal physiology. Cross-cohort comparisons identify the greatest taxonomic overlap between obesity and T2D, whereas hypertension is characterized more consistently by shifts in community structure than by reproducible disease-specific taxa. Dietary modification, prebiotics, probiotics, synbiotics, postbiotics, and fecal microbiota transplantation produce modest and variable benefits, often shaped by baseline microbial features and clinical phenotype. The mechanistic and comparative data position the microbiome as a context-dependent contributor rather than an independent cause of cardiometabolic dysfunction. Progress requires longitudinal cohorts, repeated sampling, integrated multi-omics, standardized protocols, diverse populations, and prospective validation of functional biomarkers and treatment-response signatures before translation into clinical practice.