Abstract
The gut microbiota comprises approximately 100 trillion microorganisms, with beneficial bacteria accounting for 85% and harmful bacteria 15%, forming a crucial symbiotic relationship with the human body through functions including vitamin synthesis, short-chain fatty acid (SCFA) production, central nervous system regulation, immune system development, and pathogen defense. When gut dysbiosis occurs—characterized by decreased beneficial Akkermansia muciniphila and Bacteroidetes, along with an increased Firmicutes/Bacteroidetes ratio—it contributes significantly to the pathogenesis of classic cardiovascular risk factors. For hypertension, gut dysbiosis reduces SCFAs and indole, impairing regulation of the renin-angiotensin system and sympathetic activity, while increased Clostridium ramosum and Gram-negative bacteria raise serotonin and lipopolysaccharide (LPS) levels, causing vasoconstriction and inflammation. High-sodium diets act both directly on classic hypertensive mechanisms and indirectly by inducing gut dysbiosis, creating a pathological feedback loop. For diabetes mellitus, in type 1, dysbiosis reduces SCFA production, impairs immune self-tolerance, and increases intestinal permeability leading to LPS translocation and TLR4 activation, damaging beta cells. In type 2, similar mechanisms combine with altered bile acid pools and elevated branched-chain amino acids (BCAAs) to drive insulin resistance. For dyslipidemia, gut microbiota influences lipid metabolism through SCFA pathways (reduced lipogenesis, increased beta-oxidation), the TMA/TMAO axis (promoting foam cell formation and atherosclerosis), and bile acid metabolism. Regarding adjunctive therapeutic approaches, multiple meta-analyses demonstrate that probiotics/synbiotics significantly improve systolic/diastolic blood pressure, fasting glucose, HbA1C, and HOMA-IR in patients with hypertension, prediabetes, and diabetes. Mediterranean diet, intermittent fasting, fiber/polyphenol-rich diets, and appropriate physical exercise also show beneficial effects by modulating the gut microbiota.
