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.
Transcript:
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 live
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.