Here’s a video from my YouTube channel. (Oh, you didn’t know I had a YouTube channel? You can find almost 300 additional videos there.)

VLDL particles, NOT LDL cholesterol, determine whether heart disease is in your future or not, as VLDL is a pivotal lipoprotein particle that influences the composition of virtually all other lipoprotein particles in the bloodstream.

Statin cholesterol drugs therefore focus on the wrong measure. Good news: You have profound control over VLDL particles and their consequences using nutrition and selected nutritional supplements to reduce VLDL and the triglycerides they contain. That is one of the reasons the Wheat Belly lifestyle is so effective for addressing factors that lead to heart disease.


Meet VLDL:
The REAL Cause of Heart Disease
(Not LDL Cholesterol)

Let’s talk about Very Low Density Lipoproteins: VLDL. These are particles in the blood stream, like LDL particles, HDL particles and other things, that are the by-products of both digestion and liver metabolism.

It’s called VLDL (very low density lipoprotein) because it’s very rich in triglycerides, that is, fats. Fats are lighter than water — they’re lighter than an aqueous solution. So that’s why, when you have Italian dressing, for instance, the olive oil floats.

The VLDL particle is very light — very fluffy and light, because it’s filled with triglycerides or oils. I also call the VLDL particles “the life of the lipoprotein party”. The reason for that is VLDL particles like to interact with other particles.

Screen text: VLDL particles enrich LDL and HDL particle with triglycerides

When it interacts with LDL particles, it contributes a lot of triglycerides to the LDL particles. Likewise, when VLDL interacts with HDL particles, it contributes triglycerides. When LDL particles and HDL particles become triglyceride enriched, after meeting VLDL, they go through a series or reactions that make them much worse, and harmful to you.

LDL particles loaded with triglycerides become transformed into small LDL particles. Small LDL particles (not “LDL cholesterol”, that ridiculous kindergarten version of how heart disease is caused, that suits the statin drug industry very well) — small LDL particles, the products of VLDL interacting with LDL particles, are very adherent to the arterial wall, thereby much more likely to cause atherosclerotic plaque.

Once they actually get into the wall, they’re very adherent; they’re much more likely to provoke inflammatory reactions; they’re much more oxidation- and glycation-prone. They’re also much longer lasting, because the liver can’t recognize the abnormal LDL particle. It sticks around for 5-7 days, compared to the 24 hours of a large benign LDL particle. That’s what happens to LDL particles.

HDL, now that it’s triglyceride-enriched from meeting VLDL, also goes through a similar series of reactions. It makes the HDL particle small and relatively ineffective. Recall that HDL is protective for coronary disease — atherosclerotic heart disease. The HDL particle is now small, and dysfunctional.

So the VLDL particles, when abundant, and when enriched in triglycerides is a vigorous contributor of triglycerides to the LDL particles and to the HDL particles, making them much worse. So where do these VLDL particles come from? They come from the liver, when the liver is given lots of carbohydrates, such as the amylopectin A of wheat and grains, sucrose (table sugar), fructose (that’s rich in such things as agave nectar, high fructose corn syrup, sucrose table sugar, honey, and maple syrup). Anything rich in fructose, will cause this reaction.

Screen text: de novo lipogenesis: liver converts carbs to triglycerides

The reaction’s called de novo lipogenesis. All that means is that when you give your liver carbohydrates, sugars, it converts it to triglycerides, and the triglyceride’s released into the blood stream as VLDL.

So, the VLDL particle is pivotal. It’s the one that leads to small LDL particles, and to dysfunctional and non-protective HDL particles. Anything that causes an increase in VLDL particles, leads to heart disease — leads to all these problems. Carbohydrates do that, of course.

And, when your liver performs de novo lipogenesis, some of the triglycerides manufactured by the liver don’t get out into the blood stream. They stay in the liver. That’s how fatty liver develops. The key to not having VLDL particles is therefore to not consume foods that yield triglycerides and thereby VLDL particles: grains and sugars. You can track what your VLDL particles are doing.

Screen text: Triglycerides track with VLDL articles

You can do a lipoprotein analysis — that’s best way, but you can also look at a conventional cholesterol panel, and look at the triglycerides. You probably know I’m a vocal critic of cholesterol panels, because most of the numbers on that panel are silly. The total cholesterol’s completely worthless. LDL cholesterol is horribly inaccurate (it’s a calculated number, with the equation used to calculate it invalidated by any reduction in carbohydrates in your diet). Those numbers are useless. But there’s a triglyceride value, and triglycerides track very well with VLDL particles. Even if you don’t have a VLDL measure, you have a triglyceride measure of how much VLDL particles you have, and whether you’re contributing to fatty liver.

Screen text: Triglycerides 60 mg/dL or less

We try to keep our triglycerides 60 milligrams per deciliter or less. That’s about 47 millimoles per liter (47 mmol/L). How do you do that? Do my basic program.

Eliminate all wheat, grains and sugars. We restore factors that allow insulin sensitivity to be restored, like Vitamin D, magnesium, fish oil. And we cultivate healthy bowel flora. All those factors make a contribution to not having excess VLDL; not having high triglycerides, and you’re thereby spared from heart disease. I hope you appreciate how silly talking about the cholesterol and the LDL fraction is. We’re really concerned about what VLDL is doing, and how we create it, and how we eliminate it.