The deep-sea secret that might be harming your heart

Health · Published 18 October 2026 Swipe more like this →

In short: In the crushing depths of the Mariana Trench, a small molecule allows fish to survive where proteins would normally collapse. But in humans, this same marine life-saver is being linked to increased risks of cardiovascular disease and mortality.

Trimethylamine N-oxide (TMAO) is a colorless amine oxide that serves as a vital 'piezolyte' for marine organisms. In deep-sea creatures like the fish Pseudoliparis swirei, TMAO accumulates in high concentrations to counteract the destabilizing effects of hydrostatic pressure and urea on proteins. By stabilizing these macromolecular structures, TMAO allows enzymes to maintain their native shape and function under extreme conditions.

In humans, however, TMAO is produced through a different biological pathway. Gut microbiota metabolize dietary choline and L-carnitine—found abundantly in red meat, eggs, dairy, and salt-water fish—into trimethylamine (TMA). The host's liver enzymes (FMO1 and FMO3) then oxygenate TMA into TMAO. While it is typically cleared by the kidneys, elevated plasma levels have been positively correlated with major adverse cardiovascular events and mortality, particularly in patients with chronic kidney disease.

By triggering inflammatory pathways, fostering foam cell creation, and modifying bile acid and cholesterol metabolism, this substance produces its atherogenic impact. Interestingly, while TMAO is a known risk marker, researchers are still debating whether it is a primary mediator of disease or merely a bystander. Current evidence suggests that genes play only a marginal role in determining human TMAO levels; instead, factors like diet, gut flora, and kidney function are the primary drivers.

Therapeutic strategies to lower TMAO include using broad-spectrum antibiotics to suppress TMA-producing bacteria (such as Deferribacteraceae or Proteobacteria) and promoting bacteria that utilize TMAO as a substrate. Despite these insights, clinical translation remains complex because many studies show that TMAO's prognostic value is attenuated when adjusted for renal function, highlighting a bidirectional relationship between the metabolite and kidney injury.

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