TMAO is a low‑molecular‑weight organic oxide formed when gut bacteria metabolize dietary compounds containing trimethylamine groups (for example, choline, carnitine, and certain phospholipids) and the host liver enzyme flavin‑containing monooxygenase 3 (FMO3) oxidizes trimethylamine to TMAO. Biochemically it is classified as a microbiome‑host co‑metabolite and behaves as an osmolyte in some tissues. Historically, interest in TMAO grew from biochemical studies of nitrogenous metabolites and later from clinical research linking circulating levels to patterns of vascular and metabolic physiology. Functionally, TMAO has been observed to interact with pathways involved in lipid handling, platelet activity, and endothelial signaling; these effects are reported as associations that help researchers and clinicians interpret broader cardiometabolic profiles.

Higher circulating TMAO levels are generally associated with greater microbial production from dietary precursors, altered hepatic conversion, or reduced renal excretion; in clinical studies elevated TMAO often parallels patterns of metabolic strain, altered lipid processing, platelet reactivity, and markers of vascular stress. Lower TMAO levels may reflect lower intake of precursors, a different gut microbial composition, efficient hepatic and renal clearance, or normal laboratory variation. Any single TMAO result gains meaning only when interpreted alongside other Cardio Zoomer markers (lipids, inflammation, endothelial function, renal markers and genetics) and the clinical picture.

Cardio Zoomer includes TMAO to assess the gut–liver–kidney axis and its contribution to cardiometabolic and vascular patterns. TMAO complements lipid, inflammatory, endothelial, oxidative stress, and genetic markers to help clinicians distinguish microbial or metabolic drivers of risk and to create a more personalized assessment of cardiovascular physiology.