Abstract
Plasma concentrations of trimethylamine N-oxide (TMAO) have been linked to cardiovascular disease (CVD) risk and mortality. TMAO is formed through the bacterial conversion of trimethylamine which is obtained either directly from food, generated from dietary precursors (e.g. choline) or derived from endogenous trimethyllysine (TML) production. In a previous article, we reported an increased risk of acute myocardial infarction with increased total choline intake in patients with stable angina pectoris. Due to the close link between TMAO, TML, choline metabolism and possibly CVD, we investigated whether plasma TMAO and TML modified the effect of total choline intake on acute myocardial infarction (AMI) risk in a post-hoc analysis. We found plasma TMAO and TML do not modify the association between higher dietary choline intake and increased AMI risk. Additionally, this association is not mediated via TMAO. • No effect modification by trimethylamine-N-oxide on the association between choline intake and acute myocardial infarction. • No effect modification by trimethyllysine on the association between choline intake and acute myocardial infarction. • No indirect effect of trimethylamine-N-oxide on the association between choline intake and acute myocardial infarction.
Highlights
Trimethylamine N-oxide (TMAO) is formed through bacterial conversion of trimethylamine (TMA) by flavin-monooxygenases in the liver
We recently reported that higher dietary choline intake is associated with increased risk of incident acute myocardial infarction (AMI) in patients with stable angina pectoris (SAP) [5]
We did not observe any effect modification according to baseline plasma TMAO and TML concentrations (Fig. 2)
Summary
Trimethylamine N-oxide (TMAO) is formed through bacterial conversion of trimethylamine (TMA) by flavin-monooxygenases in the liver. TMA is obtained directly from food (e.g. fish, which is rich in TMAO) or generated from dietary precursors such as choline, cholinecontaining compounds, betaine and L-carnitine or generated from the Lcarnitine metabolite gamma-butyrobetaine (γ-BB) [1,2]. TMAO and its precursors are mainly found in food items of animal origin such as fish, meat, eggs, poultry and milk [1]. In 2011, a link was reported between plasma TMAO and cardiovascular disease (CVD) risk [4]. TMAO seems to be proatherogenic [4]; in humans, increased plasma concentrations are associated with elevated risk of CVD and other diseases [1,2]. Inconsistencies remain and whether or not increased plasma TMAO is causally related to CVD remains unclear [1,2]
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