Very low-density lipoprotein

And the lipoprotein that is basically designed to carry triglycerides out of the liver are very low-density lipoproteins, VLDLs.

So if there's too many triglycerides, they get incorporated as the, uh, hepatocyte is constructing a VLDL particle.

So there's two ways, I guess, to get rid of triglycerides if you're the liver.

Shove off a lot of more extra VLDL particles, or don't do that.

Just make the VLDL humongous- Just a slight increase in the diameter of a lipoprotein, the volume of a sphere is the third power of the radius.

So even a half a millimeter increase or nanometer increase in VLDL size, you could carry a heck of a lot more triglycerides.

So what gets shot out of the liver very early in an insulin resistant person is too many large VLDL particles.

Total VLDL particle doesn't change that much, but large VLDL particles do.

And that's a whole other conversation, but see my other videos and other conversations elsewhere, like my blog, williamdavesmd.com, thousands of conversations, as well as my books, Super Gut, Super Body, Wheat Belly, Undoctored, where I show you why this is so important.

Because wheat grains and sugars, when ingested, cause the liver to engage in a process called liver de novo lipogenesis that causes the liver to produce VLDL particles, very low-density lipoproteins, that are converted to the small, dense LDL particles.

So it's wheat grain and sugar elimination also has a huge and powerful effect.

We also introduce nutrients lacking because of the way we conduct our lives.

They don't live on the ocean where all the iodine is located.

Now put those four nutrients together, vitamin D, omega-3 fatty acids, magnesium, iodine, and they act synergistically to reduce insulin resistance and inflammation.

That's important because that drives expansion and rupture of coronary atherosclerotic plaque, and it amps up, it amplifies liver de novo lipogenesis, their production of VLDL and small dense LDL particles.

Lastly, we address the microbiome, because if you have coronary disease, it's virtually certain you have SIBO, small intestinal bacterial overgrowth.

And we think the mechanism actually traces back to estrogen's role in the liver.

Estrogen upregulates the hepatic LDL receptor, increases VLDL, so these are specific, uh, lipoproteins, improves hepatic insulin sensitivity, and acts as a negative regulator of the LPA gene itself, meaning it normally suppresses Lp(a) production to some degree.

So as estrogen is declining, this is why we are seeing higher and higher levels.

Some of the LDL rise after menopause may also be mediated by an increase in PCSK9.

So because of this reason, you, again, you need to do further analysis to kind of untangle the different parameters, the different confounders.

so when you do multivariate analysis on the observational data what you see is that when you adjust for the content of the particles and for the number of the particles the effect of the particle size generally tends to go away most of the analysis show that and then you can confirm that with the genetics, same thing, you can look at which metric tracks best is it genetically determined lower size or genetically determined content or genetically determined particle number and again you find that the risk tracks best with particle number, with apob and in fact one thing that's come out recently in the last couple of years out of these genetic studies that's really tantalizing is that even VLDLs, which are by definition much larger than the largest LDLs, right? even VLDLs are atherogenic and it's now thought that they're equally atherogenic to LDLs so all of these apob carrying lipoproteins, they represent roughly the same risk.

now i'm not saying i'm not saying total LDLs versus total VLDLs because the number as we said previously is very different but particle by particle they're equally atherogenic, so each VLDL to each LDL And there's some speculation on why that would be and the mechanisms behind that.

We can touch on that if you want.

If this is coming out of the genetics that even VLDLs that are much larger are equally heterogenic, to posit that larger LDLs, which are kind of intermediate, you'd have to wrap around.

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So when we look at your standard test, most people know LDL.

They kind of know VLDL, but there are other particles, atherogenic particles that can contribute to plaque formation.

So your ApoB, there's only one ApoB protein.

on each particle that's out delivering cholesterol.