Paul Saladino· MD
we cannot say that correlation is causation and we do not have interventional studies in humans to show
The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
we cannot say that correlation is causation and we do not have interventional studies in humans to show
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the majority of researchers i would say now are beginning to come around to the fact that that correlation is probably reverse causality and as i talked about with ivor that increased levels of tma and tmao are found in people who are diabetic and have kidney disease and we know that diabetic and kidney disease patients can have higher rates of cardiovascular disease too
there are men our mendelian randomization findings support that type 2 diabetes and kidney disease increase tmao levels in evidence for cardiovascular diseases may be due to confounding or reverse causality
there was an interesting paper that came out a few years ago and it really showed pretty strong reverse causality like between tmao and um things like heart disease or diabetes or kidney disease specifically and this is just this complex well overly esoteric statistical term that when you have kidney disease if your kidneys don't work well then you're going to accumulate more tmao so higher levels of tmao May associate with kidney disease but that doesn't mean that tmao causes kidney disease right if you have insulin resistance you're going to have higher levels of tmao doesn't mean insulin resistance it doesn't mean that insulin resistance is caused by tmao it's probably the reverse that insulin resistance causes TMA to go up and kidney disease causes tmao to go up