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Population studies of TMAO and its precursors may help elucidate mechanisms.

Over the past decade, a growing body of literature has implicated the metabolite trimethylamine N-oxide (TMAO) in cardiovascular disease (CVD) risk (1). These findings spurred research into TMAO, and investigations have expanded beyond CVD into metabolic, renal, and other outcomes. Much of this work has focused on patient-based or high-risk samples and there has been a relative lack of study in population-based samples. In this issue of the Journal, Fu et al. (2) report their findings on TMAO, microbiome, and cardiometabolic risk measures. Their work is a significant contribution to the field, as it addresses several important gaps in the existing literature.