I actually don't think your response is the exact opposite, but you touch on some of the skeptic stuff, so I'll respond to here:

First of all, I agree with your points that you should consider the individual. My long term interest in this is also from being a very fit, low blood pressure, metabolically healthy person who always had at least somewhat elevated LDL (sometimes very elevated) that doctors would flag.

PCSK9 people are as close to a natural experiment on the effects of life time low LDL as you will get and they get near total protection, even when they have no other risk factors. People like smokers, hypertensives and diabetes have ~90% less than other high risk people, but people without any of those factors also have significantly less heart disease. People with two broken PCSK9 genes have close to zero LDL and have noticeably completely plaque free arteries as adults. I do think this does pretty fatal damage to the theory that you must have some other health issue for LDL to be bad.

It's very likely that "LDL-C" the lab measurement isn't as good as measuring ApoB, but for most people, they are concordant. And ApoB is a different way of looking at low density lipids, by particle count instead of weight. Dietary stuff like the fats in the article that lowers LDL measurements typically also lowers ApoB in most people.

So, in part, I agree that more precise biomarkers can help adjust individual risk. But most people are concordant. And the evidence that the underlying "low density lipids", no matter how you measure them, are causally part of the disease process is very strong.