But if they have lower cholesterol and still have a heart attack, then certainly the causal link is not quite there. It seems you’re suggesting it’s a good proxy measurement if untampered by statins though
P1: exposure X is not causally linked to outcome Y if some individuals with lower exposure to X have outcome Y. P2: some individuals with lower exposure to serum cholesterol have heart attacks. C: serum cholesterol is not causally linked to heart attacks.
Because this has some wacky implications:
P1: exposure X is not causally linked to outcome Y if some individuals with lower exposure to X have outcome Y. P2: some individuals with lower exposure to cigarettes have lung cancer. C: smoking is not causally linked to lung cancer.
For example, smokers likely purchase more lighters than non-smokers so there should be some correlation between lighter purchase frequency and lung cancer. But we all know you can't get lung cancer merely from buying lighters.
I’m talking specifically about the claim that because individuals with a low exposure to something don’t necessarily have a given outcome, there is no causal pathway between the exposure and the outcome. It’s not clear to me how what you’ve written speaks to anything regarding that claim.
Not trying to be snarky, I just want to be really clear about the point I’m trying to make here.
Decades of plaque accumulation doesn't just go away when you lower your cholesterol.
The question is if people who keep their cholesterol/ApoB low (e.g. Mendellian randomization) have better health outcomes, and the evidence is clear. Lifelong exposure to cholesterol/ApoB mediates atherosclerosis.
I would normally interpret that to mean, lifelong elevated levels of cholesterol/ApoB _decreases_ atherosclerosis.
Is that what you meant?