That was fast. This is why I love you and the rest of the community.

Before I say anything else, let me remind everyone of something. Atherosclerosis is a systemic disease. When we're talking about arterial disease, mortality is not the only endpoint we're interested in. Most of the time a cardiovascular event will not kill you, it will leave you disabled. It's also a hell of a painful way to die. A stroke very rarely kills you, but most of the time leaves you less functional. Microinfarctions in the brain will cause dementia, but you might not die of it. Atherosclerosis in the leg will first make you lose sensation and function in the leg, and later you might lose the whole leg. That will probably not be lethal either. It would of course be intellectually dishonest to say that these events are not correlated with mortality, however.

Since only citing things from Framingham or Cochrane is a hard constraint to keep I am forced to commit the minor sin of citing a work not published in a peer-reviewed journal and refer you to the Framingham Diet Study, a subpart of the Framingham Heart Study whose methodology was published appropriately but whose results for some reason weren't. A guy who tracked down the results reports on them here and finds that....

I'm sorry. I'm not trying to be extra difficult, but where is the original source? Is it authentic? (Edit: Here, unfortunately not accessible, thank you Yvain)

If you'll allow me to step out of Framingham and Cochrane for a moment I can also link to a review on egg consumption and LDL which found that in most of the population there's no relationship.

Permission granted ;) I accept that the effect of dietary intake varies between individuals. Even this review recognizes that there are "hyperresponders" to dietary cholesterol. I also think that for a motivated individual measuring their response to diet would be optimal compared to just blindly switching. Measuring lipid profiles and other risk factors is cheap. I'm not sure how to measure subtypes of LDL, however, and to be honest I know nothing about their clinical relevance.

You may also be interested in a Cochrane review that finds no effect reducing dietary fat consumption on cardiovascular events, cardiovascular mortality or total mortality, and finds that changing the type of fat slightly decreases cardiovascular events (look how close that confidence interval gets to 1!), but not cardiovascular mortality or total mortality.

As I said, mortality is not the only interesting endpoint. Also the CI upper bound for CVD is not over 1, not matter how hard we want to push it. The other review does support your conclusions. It doesn't however support increasing dietary saturated fat or changing nutritional guidelines in any other way.

The only lipid-lowering drugs that seem to be consistently awesome are, of course, the statins, but they seem to work equally well in high and low cholesterol populations leading some to think they also have non-cholesterol-related effects.

That statins work equally well in high and low cholesterol populations is to me the most interesting claim that you make. Can you provide a source for it? It is commonly accepted that they have benefits on top of them affecting lipids, but that the effect is completely isolated is contrary to my knowledge. The reason for the bonus effect is also a mystery. The other drugs you mention have common annoying side effects that mostly reduce compliance, and I wouldn't be surprised if some of the side effects increased mortality. In Finland they are also usually prescribed by a specialist and are never a first line treatment.

I also just think LDL is a lousy biomarker. A majority of heart attack patients have LDL levels considered normal; this is especially impressive considering the high results of high cholesterol even in the general population.

We have guidelines to measure lipid profiles after 48 hours of an ischemic vascular event. Within this time period, the LDL levels plummet, but then they rise again. Since this is a very recent guideline, it might explain the finding you present. Then again, it also might not. If I skimmed correctly there was no mention of the timing of the measurements. Look below for Edit2 for a better explanation.

Framingham found that mortality increased with increasing cholesterol in people younger than 50. In people older than 50 (ie 90% of heart attack victims) it found no relationship (other sources say low cholesterol led to higher mortality in these age groups, but I can't access the paper to check.)

Atherosclerosis is mostly a nonreversible progressive disease that can start as early as in late adolescence, so it makes sense that hypercholesterolemia before age 50 is most important for its development. All it takes for a plague to rupture after tens of years of accumulation is that the endothelium covering it fails, it doesn't necessarily have to grow anymore. (Edit: see additional explanations in the next comment) I'm definately more critical about these issues in older age groups and probably should read more about them. We're taught that statins are useful even in people over 75, but maybe this has nothing to do with cholesterol. If you can tell me what the other source is, I can look it up. I might have access ;) Edit: Apparently neither of us do.

Only standard labs are readily available to me in clinical practice. We have a mostly public health care system, and nonstandard labs are usually ridiculously pricey. Of course LDL is hardly the only measurement we take, and is combined with all the other risk factors when assessing total arterial disease risk.

I hope I have provided a POV of how background knowledge can change the way we interpret study findings, and how much easier it makes sceptiscism about them. I apologize that I don't have english sources ready at hand for the claims I make, and I know that you will not take them on authority. It is impossible to me to keep record of most of my sources, and most of them are in finnish language.

I will check out the book you recommend, I'm chillin' after all. I think there are far too few rationalists in medicine. The education methods are authoritative and many times frustratingly ineffective. Unfortunately I don't know how to change it (yet), and will do my best with what I have.