And if you’re one of those less than one
in 50 people that does have plaque but it didn’t show in the neck, there ways to
find that out too. You can ask that after the event, just contact me, I’ll show you
some ways to contact me at the end of the presentation. But let’s go on and talk a little bit
more about plaque and what it looks like. This is a cross-section from Cleveland
Heart Labs. They are one of the forward-thinking labs that has actually
provided this type of information. This is an image of a usually young, very
clean artery without any of this plaque and inflammation process. As the artery
gets older, more disease process going through it. More plaque, more
inflammation. You begin to see these things. You see F2 isoprostase which
are we call them the “lifestyle lie-detector.” Oxidized LDL… these are all
things that we can get through Cleveland Lab by the way. The thing that we focus
on is microalbumin creatinine ratio, the HS-CRP (c-reactive protein), MPO, and PLAC2.
MPO and PLAC2 are actually enzymes that are released by the cells
that we talked about a few minutes ago. I will look, jump over, and show you again
oxidized LDL and LDL. You know you keep hearing about LDL and cholesterol. Why do
you keep hearing about it? The vast majority of plaque is actually made up
of LDL and mostly oxidized LDL. That’s why we went down that bunny hole as a
medical for the past hundred years thinking it’s all cholesterol. I’m not
going to go into the rest of that story. You know that half of people that have a
heart attack have a normal cholesterol. It’s injury to the glycocalyx, an
inflammation that allows that cholesterol to pass through the
glycocalyx. It’s not LDL. I’m getting a little bit complicated. I’m gonna back up
to 30,000 feet. And let’s take a look at my own inflammation panel. I mentioned to
you myeloperoxidase, PLAC2, c-reactive protein, and microalbumin
creatinine ratio. Those are all tests that you see on
Cleveland Heart Lab that we can we can provide for you. If you’d like, I’m gonna
go a little bit deeper into detail on each of these very quickly.
Microalbumin, it’s maybe the most important. It has… it actually tests that
filter, that lining, the intima layer that we talked about several times. You see
that each kidney has about a million microscopic filters called glomerulus
and it filters nothing but a filter membrane that fluid passes through. Well
this is a glomerulus and the fluid passing through it is your blood. The
filter membrane is your intima, the lining of that artery, that’s what that
is. So here’s the thing. If you’re passing a
lot of albumin (the most common protein in the blood), that means you have injury
to that filter, right? Maybe holes in it, not so much holes but injury to it. And
that also means that you have injury to the intima lining of your artery.
Now again everything gets a little bit more complicated than this does too but
let me just make a couple of comments. If you start looking at this test on your
own, you’ll see, “Oh, a lab limit of 30 milligrams per gram.” That’s not what you
want, that’s not what we’re looking at. That’s a limit for kidney disease. For
heart attack and stroke and inflammation, for men, we look at the cut point of six,
and for women, a cut point of 16. And the microalbumin test strips that you could
get on Amazon, those don’t work. They’re not… they don’t
get deep enough and discreet enough. They don’t get a low enough level to be
helpful to us. I mentioned these different enzymes again if you want to
go just a little bit deeper in terms of a microscopic view. I mentioned PLAC2.
The technical name is lipoprotein- associated phospholipase A2.
But frankly who cares what that is. What that name is here. Here’s what it is.
It’s released by enzymes… it’s enzymes that are released by the
white cells the monocytes. These are all cells that are part of the
large family of immune cells and those are cells that as I mentioned before
digest that plaque. Here’s another image of monocytes from which turn into foam
cells. These images by the way are the muscle cells, the media
layer. This is the intima layer. This is the blood stream. Again getting very
microscopic, won’t spend a whole lot of detail going there. This is the blood
stream, the intima layer, a media layer, and plaque. And those were the monocytes
squeezing through and forming foam cells. MPO, myeloperoxidase, it’s the same
process. It’s just a different enzyme coming from a different type of immune
cell in the same immune cell family. Here’s a microscopic picture of it. So
again, we’ve got all of the science. We’ve got all the evidence showing what’s
going on here. And sooner or later this looking at and looking for
cardiovascular information will become part of the standards. But until it does,
I think there we go through some challenges in terms of getting it done.
So there’s some challenges in terms of getting it through routine through your
standard doc. Some docs are looking at it. The docs, they do look at… excuse me…
inflammation, usually just look at c-reactive protein.
The problem is c-reactive protein is that it’s there’s too many false
positives. If I gave a hundred if we get… excuse me… if we gave a hundred people a
flu shot today, the c-reactive protein for 60 of 66 of them would be positive two
days from now. So that’s why we look at a couple of other tests other than just
c-reactive. And here’s that image again of the
CANTOS study. I’m gonna skip over these questions. And now we’re going to
get into what’s by far the most common cause of plaque and inflammation, and its
insulin resistance, prediabetes. Here’s the thing. Just to go back and review a
slide we’ve already seen. This is that healthy glycocalyx and that keeps the
LDL no matter what level of LDL. And I’ve got plenty of patients that have
familial hypercholesterolemia with levels up around 250 on their LDL and
much higher for their total cholesterol. They still tend to not have problems
until they start getting maybe obesity, with insulin resistance, or smoking. If
you have any question about that, take a look at FH (familial hypercholesterolemia)
and my name on YouTube. You’ll see several videos where I’ve actually
interviewed actual patients that described this process. So what’s the
problem with insulin resistance. Well, if your blood sugar hangs around 180 for a
few hours or over 140 day after day, it only takes a few hours to destroy the
huge portions of this glycocalyx. When those portions of the glycocalyx are
destroyed, the LDL just goes right through there, no matter what level of
LDL you have. Now here’s the issue and we’re gonna talk the next few slides
about how prevalent prediabetes is. I’m just gonna go ahead and go off the
slides for a second and just make a comment.
UCLA has said well let me say this I’ll go back to the slides. The CDC has said,
look, there are 84 million Americans adults. One out of three with
prediabetes and the vast majority as in 90% do not know it we’re having this
problem. It’s burning our glycocalyx. It’s setting us up for heart attack, stroke,
dementia, blindness, kidney disease, and yes man, erectile dysfunction. And we
don’t know it. According to the CDC again, 84 million people, 9 out of 10, have
no clue. Here’s a breakdown in terms of age. I’m not gonna spend time on that.
Here’s where I’m gonna go next. We’re in many of a certain state of
California and guess what the UCLA University of California and Los Angeles
Public Health School did a study and they showed not a one in three adults
like you saw with the CDC. One in three young adults, when you add the young
adults in the higher prevalence in older adults, more than half of California
adults aged 30 and above have either prediabetes or diabetes. And for those
of us who are not in California where a good thing for us, right? No, come on think
about it. Prediabetes is far more prevalent than
we’ve ever recognized. I’ll tuck up for a minute a little bit later about CGM
(continuous glucose monitoring) as that’s now becoming very inexpensive and
available with the freestyle Libre. We’re finding more and more of this problem.
Now here’s some points about this. Let’s take a deeper look. There are
a lot of ways to find out about it and again like with the CIMT, there are
things available that we’re just not looking at. I’ve tuned I see patients for
this is what I still do. I’m supposed to be retired but this is my
passion. When patients come to me, most of them still have a triglyceride HDL
ratio because most of them have a cholesterol panel quite often that’s
elevated anytime that’s over one. Go home and look at yours. If it’s over one, you
need to be concerned about this and you need to be thinking about it.
Occasionally, I’ll see it… I’ll see people with a problem that don’t have an
elevated triglyceride over HDL ratio, but not very often, that’s a key point to
look at in your own studies there. Unfortunately, most docs rely on fasting
glucose and hemoglobin A1c. Those can be twenty one twenty percent off routinely
are twenty percent off so therefore I get patients and you’ll see them on our
channel every week or two saying, “I have full-blown diabetes. I did your testing. I
have full-blown diabetes, and my doc didn’t even know.” Or more commonly, “my doc
told me I had a touch of sugar but I didn’t know I’ve got significant
prediabetes.” So again, more and more discoveries of this process. Once we
discover it, then there are things we can do. And once there are things that we
once we start managing our blood sugars once we make sure that we’re not
spending hours and hours every day at 140, 160, 180, 200, we’d get it healthy
glycocalyx back. We get healthy arteries and we decrease our heart attack
and stroke risk and dementia risk and kidney disease risk and all of those
other bad things. There are other ways of looking at it. I’m getting a lot of
interest recently in HOMA-IR because again it’s an immediate easy test.
Take a minute, click the link below, you’ll find our membership page. All of
our digital products are there. Lots of free stuff too. Thanks.