So, you've got your cholesterol tests in front of you - how do you interpret them?
What do you do with them? By the end of this video, you'll begin to
see that one of the most important things that you can get from your
cholesterol or lipid test is really something that doesn't have so much to
do with lipids itself. It has, again, to do with carbohydrate metabolism but we'll
get there in due time. Well, first of all, what is lipid? It's the medical term
meaning fats or oils and here's a quick list of the items that you see here. But
let's jump over that. That's - that can drive you crazy if you're not - not used
to it. First of all, let's talk about oils and let's talk about why we have the
cholesterol tests and what lipoproteins are. Again, we've heard what "lipo" means,
- or "lipid" - it means fats or oils and here's the thing; even if you're
Mediterranean, even if you're vegan, you clearly get fats and oils in your diet.
Olive oil, avocado - I think any of the diets would say - you know - those are both
healthy for you. A lot of people don't like salmon because of various reasons.
Most folks considered nuts and flaxes as healthy - but here's the thing,
think about those oils and then let's think about the very clear fact - you've
heard it a million times - oil and water don't mix. So, when you take these foods
how do you keep from having a fat embolus? Now, what's a fat embolus? First
of all, what's an embolus? It's - it's a glob or particle big enough to stop
blood flow in an artery. It's floating in the blood, it comes to an area, it lodges
and it stops the flow of blood. That's what happens with a heart attack or
stroke. In that case, the embolus is made from a blood clot - fibrinogen, the other
- and fiber, and the other - it's of a blood clot, plus platelets; and
that stops the blood flow to the heart or the brain - whatever tissue is distal
to where it - it happens. Now, fat embolus or fat embolism - fat emboli in plural
happen as well; and they've killed people, they do routinely - not as often as heart
attacks and strokes - but they happen a lot.
Pardon the ugly violent image here, but when we have a car wreck or a fall
from a long height and you get these massive fractures, the fat inside the
bone marrow tends to get out and fat embolism in multiple trauma is a big, big
deal for orthopedist to have to deal with in the ICU. It also happens after
surgery and that's what killed this lady. She was having some cosmetic surgery - had
fat emboli and that killed her. So, now, having heard about fat emboli and how
dangerous they can be - just as dangerous as a heart attack and stroke - let's go
back to the - what we had for lunch. How do we - how does our body keep the oils? We
clearly get more than a teaspoon of oil with a meal and a teaspoon is enough to
kill you if it were formed in one globule as an embolus. Well, here's where
proteins come in. There are proteins that the body makes. They form little balls
and the way that they form the ball - the inside of the ball is what we call
lipophilic. It likes - and it's - it creates an environment for fats and oils. The
outside of that ball is what we call hydrophilic it likes and fits well with
water. So we get back to this point about how do we keep from - how does the body
solve the problem that oil and water don't mix, yet we have to eat and we have
to get calories from fats and oils. We have protein.
They form little balls and those are called lipoproteins. Now, you may also
hear the term - and you will at some point - ApoA, ApoB - Apo means without - so in
- that's short term. A short language for Apolipoprotein. So an Apolipoprotein
is the protein alone in the particle. A lipoprotein is the part of the full
particle with the protein and the fat inside it. Now, as we're looking at
different lipoproteins just mentioned - let me just mention that there that LP(a)
as you see here is very similar to LDL. It's one of the low-density
lipoprotein families. It's a - it's a variation. You see these little hooks
that come off of LP(a) on the protein itself? Those are called repeat
kringles, and there are tiny little repeat sections when you look at - it
looks - it looks sort of like a hook and it hasn't really been proven but one of
the major thoughts behind the increased inflammatory process is associated with
LP(a) is this little hook. There's the thought - that this hook makes it
easier for LP(a) to latch on to damaged arterial wall. Now, as I said,
there are many, many populations of lipoproteins. They range in size and
density. Density meaning how well they float. So, for example, LDL is low density
lipoprotein - that's what you remember or you may hear. All this bad cholesterol; it
tends to float better than HDL (high density lipoprotein) but it doesn't. It
doesn't float as well as vLDL which is very low density lipoproteins. One of the
differences in all of these families is what drives both size and density is the
amount of cholesterol inside that particle. So the lighter and the larger,
the more fat it has. Fat floats more than protein - it's lower density. So, now, you're
beginning to get an idea. Now, it's these - the LDL family that you tend to see in
artery walls. You know there's a perception that the plaque is lining the
artery walls inside the artery in the lumen where the blood flows. It isn't.
Plaque happens when we get burning of that slick intima and then LDL goes
through that in the damaged intima or endothelium and lodges in the artery
wall. So maybe the vLDLs are too big to get through those cracks; HDL for one
reason or another doesn't go through and lodge. It probably goes through, helps
actually clean some of that cholesterol out and comes back out;
LDL goes into the artery wall when the intima is damaged and gets stuck there.
It also gets oxidized and that's where you get the term OX-LDL which you may
sometimes see on your cholesterol test. Now, speaking of cholesterol test, let's
go back up here and go through some of these actual items. Now that we've listed
some of them, you have your total numbers - you have triglycerides. Triglycerides are
a little bit different from cholesterol in that we've talked about these in
other videos ("Tri" means three fatty acids and "glycerin" - so there's a glycerine
- glycerine molecule that holds three fatty acids together)
What does triglycerides? it's fat. It's the fat that you find in love handles
and subcutaneous fat. By the way, something you'll remember down and you
will talk about it at the very end - triglyceride burning is shut down by
insulin. Insulin wants us to be able to decrease our blood sugar level so it
opens up the the blood sugar channels in the cell wall and it stops triglyceride
burning. We'll talk about that again at the end of this video.
HDL, remember, is the high density lipoprotein. It's got more protein and
less - less fat inside of it. Actually, the HDL is what pulls cholesterol out of the
body and brings it back to the liver. LDL is what gets deposited and causes the
problem with plaque. So that covers triglycerides, HDL, LDL. We've already
talked about LP(a) - it's just a form - a genetic variations of LDL which
has the kringle repeats sections on it; the little hook then makes it a little
bit more inflammatory. Now, we're gonna skip over the total cholesterol HDL
ratio and talk about the triglyceride over HDL ratio. I've done a couple of
videos on that and here's the thing - because cardiovascular inflammation
causes heart attack and stroke more so than LDL, we look at triglyceride/HDL
ratio and here's why: If you have insulin resistance, as you let me just back up -
remember, I said that at the end of it, we're going to talk about a carbohydrate
metabolism problem not so much a lipid problem. So here's what happens as I
mentioned insulin - if it's going along too high, it shuts off triglyceride
burning. So, when you have insulin resistance, your blood sugar tends to
creep up. As your blood sugar creeps up, your body has to put out more and more
insulin. As it continues to put out more and more insulin, you
get it into a chronic state of not burning triglycerides. Your triglyceride level
goes up. Meanwhile, as that happens, your body burns more HDL in order to try to
metabolize and burn up the LDL - the bad cholesterol, the bad fats. So you get in a
state with insulin resistance where you have too high triglycerides because
you're not burning them, too low HDL because you're burning them up, trying to
metabolize bad cholesterol particles. So that may sound a lot like a lot. In fact,
it probably is - but I've got several videos on LDL, HDL, triglyceride over HDL
ratios and what those mean. This was just a short video to help describe more of a
summary of all those and how to interpret your cholesterol test. if you
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