Abstract
ABSTRACTProduction of trimethylamine-N-oxide (TMAO) via the gut microbiota has recently been proposed as an important pathophysiological mechanism linking ingestion of ‘unhealthy foods’, such as beef (containing carnitine) and eggs (containing choline), and the development of atherosclerosis. Hence, TMAO has gained attention as a novel biomarker for cardiovascular disease. However, fish and seafood contain considerable amounts of TMAO and are generally accepted as cardioprotective: a puzzling paradox that seems to have been neglected. We suspect that the TMAO story may be a red herring.
Highlights
Production of trimethylamine-N-oxide (TMAO) via the gut microbiota has recently been proposed as an important pathophysiological mechanism linking ingestion of ‘unhealthy foods’, such as beef and eggs, and the development of atherosclerosis
Published works suggest a causal link between increased plasma levels of trimethylamineN-oxide (TMAO) and increased risk of cardiovascular disease [1,2,3]
Free TMAO in seafood is quantitatively significantly higher than the amount of TMAO that can be generated by the gut microbiota from choline and carnitine in red meat and eggs
Summary
Production of trimethylamine-N-oxide (TMAO) via the gut microbiota has recently been proposed as an important pathophysiological mechanism linking ingestion of ‘unhealthy foods’, such as beef (containing carnitine) and eggs (containing choline), and the development of atherosclerosis. KEYWORDS Carnitine; choline; gut microbiota; seafood; TMA; TMAO Published works suggest a causal link between increased plasma levels of trimethylamineN-oxide (TMAO) and increased risk of cardiovascular disease [1,2,3].
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