We previously covered the study that discussed the link between dietary carnitine from meat and TMAO production, which was associated with a higher risk of atherosclerosis. A new study is making the rounds with a similar conclusion, this time about a different molecule.
This study investigates the molecule Phosphatidylcholine. The study was conducted by having subjects eat two eggs, each containing 500mg Choline, alongside 250mg of phosphatidylcholine, which was radiolabeled. Phosphatidylcholine (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) which contains choline. By using labeled PC, the study’s authors were able to confirm that dietary 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.
Contrary to media reports, there is no molecular link between egg consumption and TMAO in this study. The radiolabeled phosphatidylcholine was consumed via a gelatin capsule alongside two (nonlabeled) eggs, which contained free choline. However, the PC increased serum TMAO dependent on intestinal bacteria, and it is definitely plausible (and likely) that eggs can increase TMAO via the choline content; this cannot be concluded right now though.
Similarly to the carnitine study, this experiment confirmed a correlation between higher TMAO and cardiovascular risk with a cohort study design (4007 persons undergoing coronary angiography) with an adjusted hazard ratio of 1.30 and 95% CI of 1.20 to 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,” which was an RR of 3.37 with a 95% CI, 2.39 to 4.75; this is somewhat notable.
This study also confirmed a correlation between TMAO and cardiovascular disease risk, so it appears that TMAO may be a useful biomarker in the future for cardiovascular disease risk. Whether TMAO is increased by dietary factors or other factors, it appears to be associated with an increased risk for heart disease.
That was basically the study. This study can be used to support the correlation between TMAO and cardiovascular disease, and similar to the previous carnitine study, this was confirmed at least acutely in humans. This study can also be used to further support the link between the microbe capable of choline -> TMAO conversion as a possibly causative link in the pathology of CVD, so identifying this microbe might be therapeutic or preventative in regards to 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 seen here in a clinical setting irrelevant in a practical setting.
More likely, the bacteria that helps convert to TMAO uses the trimethylamine structure (which both choline and carnitine are) to make TMAO. This bacteria (currently unidentified) is the causative agent here, and merely uses sources of trimethylamines (eggs being a source of choline via PC) to do its job.
While one can directly blame eggs for the increase in TMAO, it would be improper to blame egg consumption for increased TMAO (which is correlated with an increased risk for cardiovascular disease). Any blame would better be directed towards the intestinal metabolism and the bacteria that helps convert to TMAO.
Related: are eggs healthy?
Published By Kamal Patel on 2013-04-25 10:23:36