The article:
Basically, gut bacteria produce a molecule (imidazole propionate) that causes atherosclerosis.
They used humans, but the actual "causation’ comes from mouse studies, of which I’m not that big of a fan. That is, until there are human studies showing reduction of this molecule reduce or prevent atherosclerosis, I’m not going to believe this necessarily.
But it would help to describe why many people, including people on keto, get atherosclerosis.
Of course, they make all the statements I’ve come to hate (atherosclerosis is not “caused” by “fat”):
“The new results demonstrate that atherosclerosis is not only a disease caused by fat, but that it also has an inflammatory and autoimmune component, according to Sancho.”
And I think this is potentially misleading:
“The new study shows that blood levels of imidazole propionate are lower in people with diets rich in vegetables, fruits, whole grains, fish, tea, and low-fat dairy products.”
According to the article: “Sancho and his colleagues acknowledge that further research will be needed to identify the specific strains of bacteria capable of producing the molecule”. In other words, they have no idea what bacteria cause this, so there’s no way to say that a high(er) fat keto diet wold not be beneficial.
But even in the LMHR (lean mass hyper-responder) study, where people who go on keto diets who are lean and get very high LDL levels (the supposedly “bad” “cholesterol” that “causes” atherosclerosis), many of them had little to no atherosclerotic progression (some even had lowering of the atherosclerosis), yet some had atherosclerotic progression if they already had atherosclerosis at the start of the test. If these high-LDL folks are having progression, regression, or no progression, that means to me that LDL itself is probably not causative. Something else must be causing atherosclerosis. Maybe it’s gut bacteria?