I know you're just laying the arguments out there and establishing a basis for hypothesis and discussion, and that's good of you, it's well presented.

But this isn't hard deductive reasoning but soft inductive reasoning and is only suitable for a hypothesis, some people would consider these arguments, but they are a warrant to go look for real evidence.

The reasoning goes: If saturated fat causes atherosclerosis we should expect to find the Inuit mummy, who ate a lot saturated fat, to have atherosclerosis. We do, therefore saturated fat causes atherosclerosis. This is the fallacy of affirming the consequent. Anybody who doesn't know it should look it up. That we observe them together doesn't mean that they are causal, of course. It could be that the oxidized PUFAs from cooking with seal oil were enough to produce atheroclerosis. They would have had a ton of oxidized PUFAs. Yikes. Like Jeff already pointed out, Chris Masterjohn's work argues well for oxidized PUFAs being a problem. We can't know which one it was. Same goes for the Koreans and American GIs. It's an elementary fallacy if employed as anything but a hypothesis.

And of course simply because Pritikin didn't have atherosclerosis it can't be inferred that it was the lack of saturated fat that was responsible. It could be the lack of polyunsaturated fat on a low fat diet. He might have had a very low level of inflammation, good intake of various antioxidants, low blood pressure, etc. I wonder if he was taking B12. Indian vegetarians who don't supplement tend to have a bad problem with atherosclerosis from elevated homocysteine, so I'm guessing that he did take supplements and thus had low homocysteine. His diet would have been rich in copper, which is needed to protect the arteries. I'm certainly not an advocate of a vegetarian diet for optimal health, but it doesn't necessarily cause atherosclerosis. I think I understand most of the mechanisms so it makes more sense to me than, say, the annoying finger-waging PETA chick waving a copy of The China Study.

I really haven't looked into the whole literature. I did find a study on the site Healthy Diets And Science, which is very biased and pushing one side of the story, but the data speaks for itself.

http://www.ncbi.nlm.nih.gov/pubmed/15531663

Saturated fat was associated with the least progression out of all macronutrients and at the highest quartile was inversely associated with progression, the only instance of an inverse association in these chronically unhealthy women. The quartile with the least total fat had the most progression compared with the other quartiles. The second quartile of total fat intake had the least progression, although the 4th had less than the 3rd, so that doesn't seem to be indicative of fat being inherently atherogenic.

Polyunsaturated fat was consistently associated with progression of atherosclerosis.

Granted these women had an average fat intake about half of what paleohackers tend to have, and it might become atherogenic at higher intakes, although we can't tell that from this study. So the exhortation to eat chicken breast or be vegan isn't supported by this study. Stearic acid, mostly from meat, was a little better than lauric, myristic, or palmitic acid, but all were inversely associated. Women are probably distinct from men in some respects, and this was also a hormone replacement trial, so I can't say for sure that this applies to everyone, but it is one of the best designed studies I have seen.

This one is an intervention study where oleic acid and stearic acid are inversely associated, although dietary cholesterol is associated with progression. It doesn't have anything in there about the other ones. Sounds like a prescription for some grass fed beef to me.

These people who have been indoctrinated to believe that saturated fat is going to kill them dead do seem to have a little more atherosclerosis depending upon saturated fat intake http://www.ncbi.nlm.nih.gov/pubmed/18175752 As always I'm going to pat my paleo halo and say that this doesn't apply to me and is indicative of many differences in risk factors that haven't been controlled for. The health-consciousness effect more or less renders North American epidemiology inert.

I don't like animal studies for this sort of thing because the environment in the body is always atherogenic and that is a lot different than what people will experience on the paleo diet. Animal studies are mixed and hard to extrapolate to humans. Oxidative stress, micronutrition, and inflammation are all important factors in the progression of atherosclerosis so it makes sense to view evidence that is reflective of one's own biological situation. I'm not sure that exists, and I'm not even sure of a great quality study in humans that controls for all important risk factors and just isolates serum LDL or dietary saturated fat irrespective of everything else that is going on. Only a statin company could afford to do that kind of study! Of course most of the literature has to do with myocardial infarction since that is where Occam's razor strikes. I care if I'm going to have a heart attack, and I care if I am going to die from anything at all. Lower LDL cholesterol is not associated with a longer life, and it is only associated with more mortality at higher concentrations than most of us have at 1 year of eating this way.

Anyway I do think you have a point that we can't just dismiss saturated fat as a potential risk in some people for atherosclerosis, but I don't think the evidence is there. I am more focused on what we do know is a big deal, which is a lot of things that have a profound effect on the progression of atherosclerosis.

I'll throw some ideas into the ring here.... Saturated fat seems to raise LDL and HDL, so it's generally not thought of as problematic. But if someone's LDL is hanging out in the blood for too long then excessive oxidation could occur and plaque can be built up. I've been reading a lot of Chris Masterjohn's work lately and the way I understand it is that you need hypercholesterolemia to induce atherosclerosis but it's not the direct cause. Here are some excerpts from various blogs he's written:

Atherosclerosis is largely driven by the degeneration of lipids which infiltrate the blood vessel and thereby cause inflammation. Inflammation from other sources may accelerate the process or further the degeneration of the atherosclerotic plaques once they are formed, but the initiating factor for fatty plaques appears to be the degeneration of lipids — especially the degeneration of PUFAs...

We need to distinguish between the infiltrating idea that it’s just too much lipid, and the degenerative idea that it’s about those lipids breaking down. Once we realize that it’s about the degeneration of these lipids, we can start to understand what the metabolic factors are that effect the degeneration of lipids, and how we move beyond our understanding of the amount of cholesterol in the blood to how do we protect these lipoproteins from degeneration....

What happens in the lipoprotein particle in order to cause atherosclerosis is the polyunsaturated fatty acids in the membrane of the lipoprotein particle are oxidized, which basically means the molecules are falling apart. Once they oxidize they become toxic and in order to protect the blood vessels from these toxic degenerated lipids,the immune system forms an atherosclerotic plaque. This is basically a protective mechanism but over time if these toxic lipids accumulate you get inflammation, the plaques fall apart and this is what ultimately leads to a clot in the blood and then a heart attack....

Likewise, the single man with a PCSK9 nonsense mutation in the study I cited above who developed heart disease died of a heart attack at the age of 68, but had an LDL-cholesterol level of only 53 mg/dl, well below the supposed "no risk" level. He was obese, smoked, and had high blood pressure. This supports Anitschkov's "combination theory" but flatly contradicts his "infiltration theory," in which it is the amount of cholesterol rather than the oxidation of lipoproteins that matters.

Perhaps this link will help us all to understand this issue.

This seem a deadly strategy to always live in the hope of avoiding inflammation since it comes from diet but also things like virus that you cannot always forsee and protect against. If you have too much sat. fat and sat. fat lead to plaques then you can have inflammation from unexpected source and then you get into heart trouble.

Because, as you know, in inflammation white blood cells invade the artery wall to promote the buildup of fatty deposits or plaques, and the sending of chemical danger signals to the body. These signals or “pro-inflammatory cytokines” make the liver release other molecules into the blood.

One of these markers of inflammation produced by the liver is C-reactive protein (CRP), which has been studied for several years, as CRP when measured with the high-sensitivity CRP (hs-CRP) blood test can indicate for example, which patients are at higher risk for having a future heart attack or stroke.

This are my opinions. How about you?

From what I can tell, Dr. Michael Eades points decidedly towards #2 on that list. But then again he rejects the lipid hypothesis, so I don't know if you'd find his work useful in answering your question.

Personally, I don't know, but I think a lot of studies trying to figure this out have failed to take micronutrient levels like chromium and magnesium into account , as well as the addition of medicinal herbs to the diet like garlic.

The story about the Korean and US soldiers atherosclerosis raises a number of questions for me. If I have my food history correct, margarine really caught on in popularity in the US around WWII, and by the time the Korean War rolled around I'm wagering most US soldiers had been eating it for a long time, so I'm not surprised by the degree of atherosclerosis the young soldiers would have had. If teenage boys had the same penchant for soda and candy then that they do now I think that could also have contributed to it. And lastly, there is the difference in the grain of choice between wheat and rice.

I'm also curious about the Inuit, I was under they impression that in general they lived long healthy lives before things like Cheerios were introduced into their diet. I apologize for being a bit off the question here, but if Cordain is correct on this one, would that be an argument for atherosclerosis being a non-issue in the absence of inflammation.

Dr. K also mentioned in passing the other day that he got rid of his atherosclerosis on a diet with plenty of saturated fat, so I'm also curious to know how he went about that. I'm guessing he's going to mention avoiding PUFA's, but if there are other variables I'm all ears.

I think there's a big genetic component at work as well, which complicates things. If you have certain genes (those that code for Lp(a) and ApoE4, etc.) that's going to change the whole picture regarding the relationship between diet and risk of developing plaque.

Good discussion. Kudos to everyone.

Dr. Ayers writes: “Saturated fats appear to be problematical primarily if chronic inflammation is established. Saturated fats are healthy in the absence of inflammation.”

This is why many of the studies on the health effects of saturated fats are flawed. They analyze the impact on coronary health, etc… of a typical diet(containing copious grains and other refined carbohydrates) versus a typical diet PLUS saturated fats.

This is a very good post, im going to reread it but I think it should be pointed out(not sure if the author still frequents here.) that CVD resulting in death doesn't necessarily need to be the end point to deem a quality unfavorable. In other words, having athlerosclerosis is bad news in terms of a myriad of conditions

And this is a great discussion so I'm gladly bumping it