Dietary choline undergoes anaerobic metabolism by gut microbes to form trimethylamine (TMA) which is then oxidized by liver enzymes to form trimethylamine N-oxide (TMAO), a newly recognized risk marker for cardiovascular disease.[1]
However, several dietary sources of choline (e.g., eggs) actually contain phosphatidylcholine, which may not have the same TMAO-elevating effects as choline (as choline bitartrate or other forms). For example, multiple studies have shown that eating up to 3 eggs per day (about 400 mg of choline) elevates plasma choline levels but does not increase TMAO.[2][3][4][5][6][7] On the other hand, TMAO levels increase up to 3-fold following the intake of 600 mg of choline bitartrate.[8] Adding choline to the diet from beef (3–6 ounces as part of a Dietary Approaches to Stop Hypertension diet) increases plasma choline by 10% and TMAO levels by 27% in older adults with obesity.[9]
Differences in gut microbiota may explain individual differences in TMAO production following choline intake. For example, high TMAO producers had more abundant lineages of Clostridium and Ruminococcaceae and Lachnospiraceae compared to low TMAO producers.[8]
Overall, because phosphatidylcholine is the major form of choline in food and phosphatidylcholine doesn’t appear to elevate TMAO levels, there’s no reason to avoid phosphatidylcholine over fears of its TMAO-elevating effects. Furthermore, meta-analyses have found no association between dietary choline/betaine intake and the risk of cardiovascular disease outcomes (e.g., coronary artery disease or stroke).[10]