Determining Whether or Not Egg Ingestion Increases Concentrations of Trimethylamine N-oxide (TMAO) in Plasma and Urine and Activates LDL Oxidation in Humans

Diets low in choline have adverse health consequences, while observations in humans and experiments in mouse models suggest that a diet containing too much choline or phosphatidylcholine may activate inflammatory pathways and increase cardiovascular disease risk through bacterial conversion of choline to trimethylamine (TMA) and its subsequent oxidation to trimethylamine N-oxide (TMAO) in the liver. What is unclear is whether choline and phosphatidylcholine in eggs is a source of TMAO formation, and if so how many eggs must be eaten before enough TMAO is generated to cause increased oxidized LDL (a biomarker for atherosclerosis mechanisms). We hypothesize that TMAO will only be formed from eggs when very large quantities are ingested and that TMAO formation will vary greatly between individuals for any given dietary exposure. This variability will be determined by 1) the dose at which dietary choline or phosphatidylcholine exceeds the absorptive capacity of the volunteer's small intestine and therefore spills into large intestine where gut bacteria have access to it and 2) the bacterial populations that constitute the volunteer's microbiome.