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Thanks for the summary! I haven’t read tfa yet, so my apologies if this is answered in there, but: does this mean that we’ve already reduced the contribution from cholesterol to events? Or that cholesterol was simply associated and not causative? I imagine the truth is somewhere in between, perhaps we can guess that’s it’s 70% due to one and 30% due to the other?


It's more the former -- we've gotten so good at detecting high cholesterol and reducing it, that the majority of residual risk is now in the other factors.

(There are some people who dispute whether cholesterol is causative, but most cardiologists believe LDL cholesterol, or ApoB, causes heart attacks and strokes --based on both mechanistic evidence and randomized control trials.)


1. Thanks for the reply!

2. Having now read the article, i see that my question was indeed already addressed in the article — sorry for asking silly questions

3. Your good-natured, approachable response is great marketing for your company! I’m not the target audience, but I did click through your marketing material, and probably trust it more because of your response.


I'm interested in this subject. Can you cite some of the RCTs and mechanistic evidence?




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