Is saturated fat bad for you?

Statins lower LDL cholesterol, yet only have marginal effectiveness in decreasing heart disease risk and mortality. Surely if LDL cholesterol was such a big factor in heart disease as you make it out to be, statins would completely eradicate it.

Lifetime LDL cholesterol is a big (the most important) factor in the development of heart disease. The best evidence to date is that atherosclerosis is literally starting at age 0, in utero. Why on earth would you expect drugs which lower LDL (doing nothing for all the other risk factors which obviously has an effect) for a few years to undo DECADES of damage that people are doing? The fact that it has an appreciable impact (see again my references) is certainly evidence for what I'm proposing. You suggesting that it should "eradicate" it is absolutely preposterous - nobody scientists involved in the development of these drugs ever thought this would be the case.

Even that marginal effectiveness could be the result of some mechanism other than lowering LDL cholesterol, such as antioxidant activity: Ezetimibe also lowers LDL cholesterol, yet has insignificant, or no effects on atherosclerosis, heart attack risk, and mortality.

I am going to go ahead and quote the thing you already allegedly read:

Statins have a significant impact on cardiovascular disease risk and mortality and this is primarily mediated by their reduction in LDL.

See in particular this quote:

However, long-term risk reduction is very similar among statin and nonstatin approaches to lowering plasma LDL concentration. Therefore, the LDL-lowering action of statins is clearly the most important mechanism by which they decrease the long-term risk of cardiovascular disease(24,25).

Processed sources of omega 6 fatty acids increase risk of atherosclerosis despite lowering LDL. Potentially by making it prone to oxidation, driving it into artery walls, thus removing it from circulation. Nuts however have plenty of vitamin E and other antioxidants to prevent their omega 6 content from being a problem.

All this really indicates is that there are modifying factors, which was never a point of contention. Yes, high processed omega 6 intake is pro-inflammatory and may do more harm than help, and nuts appear protective.

Coconut oil is 80% palmitic, myristic, and lauric acid, increases LDL, yet is not associated with heart disease, and in fact could be protective.

You wrote this non-sarcastically right after detailing how nuts, despite their high omega 6, might confer protective effects. Coconut oil has a high polyphenol content that may well modify its atherogenicity. No argument.

The conditions with higher levels of Lps correspond to a greater probability of oxidation. On the other hand, high plasma levels of unoxidized LDL have low or even zero affinity to macrophages. Thus, high amounts of LDL are not dangerous, but reducing its level is a clinically proven way to prevent its oxidation and to influence vascular homeostasis. Of course, it should be noted that oxidized lipoproteins are a common but not the sole initiator of an inflammation cascade in the vascular wall. [5]

Already replied to this in previous post, but all this indicates is that oxidation of LDL is a fundamental part of the atherosclerotic proccess, which has been known for decades. This does not speak to the fact that, all else constant, higher blood levels of LDL make it significantly more likely that more LDL winds up oxidized, or that very elevated levels of LDL, in and of itself, is inflammatory.

We hypothesize that small dense LDL might be more atherogenic than normal size LDL due to decreased hepatic clearance by the LDL receptor, and enhanced anchoring to LDL receptor-independent binding sites in extrahepatic tissues (e.g., the arterial wall), a process mediated, in part, by cell surface proteoglycans. [6]

Please read this again.

The level of ox-LDL and the ratio of ox-LDL/TC, ox-LDL/LDL-C, ox-LDL/HDL-C and ox-LDL/ALB are better biomarkers than TC, TG, HDL-C and LDL-C for discriminating between patients with coronary artery disease and healthy subjects. And patients who have a high ratio of ox-LDL /TC may have a higher risk for CAD [7]

I'm still baffled how this makes you skeptical since, as I said, all else constant, the higher the LDL the higher the likelihood of having elevated oxidized LDL.

The fact that even LDL-P (or LDL size/density/pattern) is a better predictor than LDL-C.

LDL-P might well be a better predictor, but that would only seem to support the model I'm proposing. LDL size very clearly isn't outside of its ability to roundaboutly predict LDL-p.

High lifetime LDL cholesterol could be the result of genetic disorders (such as familial hypercholesterolemia) or lifestyle factors (such as smoking) that cause damage through other mechanisms than simply increasing LDL cholesterol.

You're conflating Familial Hypercholesterolemia, a disorder with the net effect of having higher than normal circulating LDL, with smoking cigarettes, inhaling ~100+ harmful chemicals habitually in the lungs which has system-wide pro-inflammatory effects which roundaboutly (though significantly) increases atherosclerosis. Seriously?

As for the Brown and Golstein article, I have a few issues with it:

They only describe one piece of LDL regulation in a very complex system. There are several other pieces to the puzzle.

It was written in 1985. We've learned more since then.

Familial hypercholesterolemia is not a very good model of saturated fat consumption.

FH is a disease in which LDL receptor defects result in higher than normal circulating levels of LDL. Saturated fat can impair LDL receptor function such that the result is higher than normal circulating levels of LDL (see: metabolic ward trials). This seems like a reasonable analogy, and the people who awarded the nobel prize to Brown and Goldstein apparently agreed.

Animal studies. Humans metabolism is significantly different even from primates, let alone from vegetarian animals such as rabbits. We had 2 millions of years to get used to meat, after all. Why not try to induce atherosclerosis in cats instead? Oh, because they only develop atherosclerosis when fed starchy plants?

I don't disagree that it's "different", but you're arguing the somewhat absurd point that animal research would somehow be fundamentally meaningless. It's also worth noting that there are induced atherosclerosis models that use carnivores, though given our primate status, I'd think you'd take primate research more seriously since it's very obviously the best posible non-human animal model that exists.

The section where they talk about the connection of animal fat, blood cholesterol, and heart attacks, and mention Ancel Keys, is quite literally titled "speculations".

The fact that you're so comfortable brushing off the work of nobel prize winning scientists is a little disconcerting to me.

/r/nutrition Thread Parent