We previously covered the study linking dietary meat carnitine and TMAO production. A new study is making the rounds with a similar conclusion, this time about a different molecule.
This study investigated the molecule phosphatidylcholine. Participants had to eat two eggs, each containing 500 mg of choline, alongside 250 mg of phosphatidylcholine (PC), which was radiolabeled. PC is a phospholipid (“lecithin” is a term sometimes used to refer to all dietary phospholipids, and will be used in this blog post for simplicity) that contains choline. By using labeled PC, the study’s authors were able to confirm that oral choline acutely increased serum TMAO, and that this was dependent on intestinal microflora (similar to what occurred with carnitine). It should also be noted that both choline and carnitine are trimethylamine compounds.
A gelatin capsule containing radiolabeled phosphatidylcholine (PC) was consumed alongside two (non-radiolabeled) eggs. The PC did increase serum TMAO dependent on intestinal bacteria. Although it is likely that eggs can also increase TMAO due to their choline content, this hasn’t been confirmed by this study.
Similarly to the carnitine study, this experiment confirmed a correlation between higher TMAO and cardiovascular risk with a cohort study design (4,007 people undergoing coronary angiography) with an adjusted hazard ratio of 1.30 (95% CI: 1.20–1.41): a weak correlation, but a positive one nonetheless.
There was a higher hazard ratio when looking only at the subset of “death from cardiovascular disease”: 3.37 (95% CI: 2.39–4.75); this is somewhat notable.
This study also confirmed a correlation between TMAO and cardiovascular disease risk, so it appears that TMAO (whether it is increased by dietary factors or other factors) may be a useful biomarker in the future.
That was basically the study. It can be used to support a correlation between TMAO and cardiovascular disease (CVD), and as with the carnitine study, this was confirmed at least acutely in humans. This new study can also be used to further support the link between CVD and a microbial conversion of choline to TMAO, so identifying this microbe might help treat or prevent CVD in the future (via modulating the increase of TMAO from the diet).
However, this study is not sufficient evidence to blame eggs for causing CVD. This is especially true when we factor in a variety of studies that explicitly found that egg consumption was not associated with an increase in cardiovascular disease. It can lend credence to the theory that choline increases atherosclerosis (as there is a plausible mechanism in humans), but is not proof of it; a few factors (having a mixed diet, not having the microbe, other negative regulators of atherosclerosis, such as exercise) could make the observations made here in a clinical setting irrelevant in a practical setting.
It is more likely that a microbe uses the trimethylamine structure of both choline and carnitine to make TMAO. This microbe, currently unidentified, is the causative agent here, and merely uses sources of trimethylamines to do its job.
Eggs should not be blamed for an increase in TMAO (which is correlated with an increased risk of cardiovascular disease). Any blame should rather be directed toward the intestinal microbe that helps convert trimethylamines to TMAO.
Related: are eggs healthy?