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 is necessary 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.

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 is necessary to induce atherosclerosis but 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.