We can't find evidence that holds up here. Proponents are reasoning from mechanism or analogy rather than direct human data, and the most credible skeptics raise objections we can't dismiss.
for people that don't know TMAO is trimethylamine oxide and it has been widely I think incorrectly suggested to be associated with heart disease and as I was talking about with Tommy before the podcast it's mostly been epidemiologic it's been observational epidemiology not experimental epidemiology neither Tommy Ori is aware of any mechanistic studies or any interventional studies showing the TMAO causes cardiovascular disease
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I think that at this point we can put the TMAO thing to bed and I mean there's been a number of articles that have been published saying TMAO is a red herring you know kind of this tongue-in-cheek pun regarding the fact that fish have these preformed levels of TMAO
tmao is a co is a total red herring it's never been shown to be causally problematic for humans
where is the data in humans that tmao is mechanistically linked with problems
the basic takeaway from this paper they say our mendelian randomization finding support that type 2 diabetes and kidney disease increase tmao levels we know that because when the kidneys don't work due to diabetes or intrinsic kidney disease tmao is retained in the human body and observational evidence for cardiovascular diseases may be due to confounding or reverse causality
in fact i think there's very little evidence that tmao is in any way shape or form negatively contributing to cardiovascular disease