Lots of stuff in there to have trouble understanding.

I do have to say, I never really understood why there being a reason for increased ldl cholesterol--if it's due to increase in a subclass of fat trafficking due to increased reliance on body fat, that's fine--but why that particular cause of increased ldl cholesterol would mean that increased ldl cholesterol wouldn't have an impact on heart disease is a bit beyond me. If it's true that the pattern is harmless for most people on a ketogenic diet--you might have to go to reduced inflammation/reduced oxidation of ldl cholesterol, reduction in insulin etc. for an explanation. Or it might be that in some situations of increased cholesterol, say starvation, there are preserved pathways that prevent it from having an atherosclerotic burden. There is at least one model where starvation does increase atherosclerosis, the apoE-deficient mouse.

The question of whether ldl cholesterol and particle count is increased for the transport of fat for energy or as a result is interesting. Decreased clearance is a possible consequence of low insulin;



https://academic.oup.com/jn/article/129/11/2005/4721856

Giving a subtype of insulin resistance that might be problematic. If insulin is high, but LDL is also high, maybe a weird situation to try to avoid.

Peter's suggestion that the main purpose of ldl particles is reverse transport of cholesterol--dietary cholesterol, we tend to not absorb much of it into circulation. The cholesterol we store in our fat tissue might be a different story, perhaps there is an increased need for clearance of cholesterol as a result of increased lipolysis. A housekeeping role secondary to a fuel-source role.