The thing about lipoproteins is that it's still all based on a flawed premise - saturated fat, cholesterol, heart disease. So even if we get very precise measurements from experiments, it's still meaningless. There are far more meaningful things to measure such as insulin for example.
Here's a hypothesis derived from another. Insulin resistance is a risk factor for heart disease. Insulin resistance is in fact not what it appears to be just from the name, but the point is that insulin remains higher than normal. For insulin resistance, there's all kinds of wild ideas thrown around to explain the correlation, but it's all BS. Instead, it's simple - insulin itself causes heart disease directly.
There's an obscure experiment done by some obscure scientist on dogs decades ago. Barely anybody knows about it. So, he dripped insulin in the dog's leg, observed atherosclerosis. Clear-cut conclusion, right?
Hehe, I just found that paper. Full name: " Effect of intra-arterial insulin on tissue cholesterol and fatty acids in alloxan-diabetic dogs. "
Well then, don't need to fool around with hypotheses, just draw a straightforward conclusion from experiment - insulin causes heart disease. There's an interesting twist. Cholesterol shifts much less than fatty acids, so why are we looking at cholesterol as if it was the bad guy? Never mind, cholesterol isn't a bad anything, he's being pushed around by insulin, so are fatty acids. This means insulin has a much greater effect on fatty acids than it does on cholesterol, and neither cholesterol nor fatty acids are responsible for heart disease.
But it gets better. The normal dogs didn't show such a big effect. The difference is likely due to a functional pancreas which means the liver is involved. If the liver gets insulin from the pancreas as it should, there's a bunch of stuff happening there that somehow mitigates what happens everywhere else with insulin, cholesterol and fatty acids. What this means for insulin resistance, it confirms what I've been thinking about for a while (confirms my paradigm as well). It's not insulin resistance in the sense that all cells become resistant, instead it's just the liver, which is the same as if the liver was not receiving insulin from the pancreas, just like the alloxan-diabetic dogs in that experiment.
Anyways, basically this means that if we still only look at lipoproteins in the blood, we're missing a very large part of the big picture, can't conclude anything anyhow. We gotta look at insulin, arterial plaque content, liver function, etc. Now maybe it's not feasible to do all that, but there's an easy alternative, based on my paradigm. Look at 3 things - insulin, ketones, blood glucose - as a relationship to each other, as indicators of liver function, and ultimately as indicators of heart disease risk (well, it's not risk, it's actual on-going creation of it).
OK, so here's how it works. Two simple graphs to illustrate.
Insulin = +++
Ketones = -
BG = +++
= Impaired liver function, specifically impaired insulin-degrading enzyme, and/or impaired glycogenolysis, and or impaired ketogenesis, typical effect of high-carb diet, typical situation with diabetes type 2 as well but moreso, some on-going creation of heart disease
Insulin = +
Ketones = ++
BG = +
= Normal liver function, specifically normal insulin-degrading enzyme, and normal glycogenolysis, and normal ketogenesism typical effect of low-carb diet, typical effect of fasting, no on-going creation of heart disease or only a tiny amount
A third graph as bonus.
Insulin = 0
Ketones = +++
BG = +++
= Diabetes type 1, impaired liver function, specifically no insulin to regulate its various functions, hence hyperketonemia and hyperglycemia, no on-going creation of heart disease at all noway nohow never - no insulin
In this last graph, today we use exogenous insulin, which means we're basically causing heart disease unless we do it in a way that simulates normal insulin, i.e. an insulin pump hooked up to the same arteries that connect the pancreas to the liver. I'm sure there's a specific name for that vein, so that's the one.
For the rest of us, excess insulin still causes heart disease, but much less than if we were diabetic type 1 and injecting insulin, and much less than if our livers were pretty much broken. This is why it takes decades for the disease to kill us with arterial blockage and things like that. Another thing is that insulin is a growth agent, it causes growth of arteries (in a process I would describe as caused by long-term chronic hyperinsulinemia, similar to insulin-induced lipohypertrophy), they get thicker independently of the atherosclerotic plaques that form, yet it's a common cause anyways.
Huh, right, big text.