I'm sorry. I'm not trying to be extra difficult, but where is the original source? Is it authentic?

If I understand correctly, the original source is this. I can't find any way to access it online, but everyone who talks about it says the results mentioned in that blog post and no one says otherwise, so I'm assuming they didn't just make it up.

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.

I see where you're coming from. On the other hand, there is a $40 billion diet industry telling people to eat less fat and causing a spectacular amount of mental anguish around this idea (I don't know if this is true in Finland; it's definitely a big deal in America). That eating less fat has literally zero effect on any outcome seems like something we should be trying to make more widely known, whether or not the small effect of changing fat types on events but not mortality holds up.

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?

Apparently not; I know I've heard this but my attempts to Google a study in humans failed. I did find something in rabbits showing effects regardless of cholesterol, but even that wasn't a direct comparison.

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.

Right, but the studies on niacin and ezetimibe showed that they decreased cholesterol (ie were being used successfully and correctly) but failed to decrease cardiovascular endpoints.

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. This might be caused by a ruptured atherosclerotic plague releasing its contents in the blood stream. 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.

You're right that the measurements were taken within 24 hours, but I've heard this isn't such a big deal, and according to the full-text version of the Fonarow study (sorry, didn't find it until this morning) they agree with me. Also, if I'm reading their table right patients having acute coronary events had higher, not lower, cholesterol than those coming in with chronic complaints, and if the effect were really only 5-15% it wouldn't significantly affect the main finding of the paper by much.

If you can tell me what the other source is, I can look it up. I might have access ;)

It's the same Framingham paper. I can only reach the abstract (my medical school doesn't give me electronic access that far back) and I'm relying on reviews and comments to tell me what's inside.

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.

Right, this makes sense, I'm just saying it's the opposite of what Framingham shows. Framingham says that "there is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels"

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

Yes, I agree with this. But the thesis of Good Calories, Bad Calories is that this allows enough degrees of freedom to be able to back up infinite amounts of confirmation bias. That is, if you see a study that supports your hypothesis, you say "Great, studies have proven we're right!" And if you see a study that opposes your hypothesis, you say "in light of my background knowledge that my hypothesis is right, we can't take this study at face value", then seize on the first flaw you find in the study and use it to throw it all out. Kind of the "one person's modus ponens is the other person's modus tollens" thing people here keep talking about.

My new favorite study ever is the Biblically-named Lee, Lord, and Lepper, which asked people to evaluate the methodology of a study on the death penalty. They found that regardless of its actual methodology, if the experimenters wrote the conclusion such that it supported the opinions of the evaluators, the evaluators said it had good methodology. If the experimenters changed the conclusion so that it disagreed with the opinions of the evaluators, the evaluators were - surprise! - able to find a bunch of problems with the methodology and reasons why the study didn't apply to anything.

I have no idea to what degree that's happening in medicine these days; I'm really only beginning to seriously engage with the literature beyond a boring student level. I read Good Calories, Bad Calories on the advice of a bunch of other Less Wrongers, it was a really interesting book and has gotten me worried enough that I wanted to vent - as you pointed out, this wasn't the best place for it and I apologize.

But I do think that further investigation beyond the level of just agreeing we can use background knowledge to interpret away findings is necessary at this point. At the very least, you have to admit the Cochrane review showing restricting dietary fat had no effect on anything means that something has gone atrociously wrong somewhere between what doctors say to their patients and reality (actually, I don't know how that works in Finland; in the US dietary fat is a pretty big deal).