Here's the thing. I felt like if I heard one more time or read one more sentence
about Weston Price or we need to to be eating animals that have been raised on
grass instead of corn, that my eyes were gonna cross.
So what's all this buzz about K2? Sometimes, it feels like there's a lot
more heat than light around this subject. I recently read that book "Vitamin K2 and
the Calcium Paradox" by the lady from Canada who's got a doctorate in
nutrition. And here's the thing. I felt like if I heard one more time or read
one more sentence about Weston Price or we need to to be eating animals that
have been raised on grass instead of corn that my eyes were gonna cross. Let's
not throw the baby out with the bathwater. When you start actually
digging into the science behind some of these issues, there's some very
interesting science there, and we're gonna cover just the beginning of an
early side story around the science in this video. It's gonna start with
a discussion about an article from a standard American medicine
cardiology journal, the Journal of the American College of Cardiology, JACC. This
article was in 2015 in June. I'll show you that in a minute. But here's the
title and it's intriguing given the topic we're talking about. "Vascular
Calcification, Arterial Damage, and Decline in Renal Function May Be
Triggered by the Inhibition of the Vitamin K-Dependent Protein Matrix Gamma-
carboxyglutamic acid (Gla/MGP) by vitamin K antagonists." Maybe we can simplify that
just a minute. Basically the story is this. We have known for a long time that
people on K1 inhibitors (specifically warfarin) tend to get a significant a lot
of increase in calcification of their arteries. Now what's that got to do with
K2? I'll leave that for a little bit later. But it does, and I'll tell you this,
it's some of that connection has to do with GLA the matrix protein. But
let's don't get too far ahead of ourselves again. Where was that article?
Journal of the American College of Cardiology, June 16, 2015.
Basically what they're saying is MGP, this protein, has a significant impact on
deposition of calcium. It is also impacted by an enzyme.
That matrix gla protein is impacted by vitamin K. In fact,
it's dependent on vitamin K. So guess what? In addition to blocking things like
warfarin... when they block vitamin K1, they block the K1's ability to change this
gla protein. In other words, this calcification depends on a protein
called MGP (matrix gla protein). That protein, in turn, is activated by vitamin
K. Vitamin K, in turn, if it's deactivated by warfarin, then takes you back to where
you're starting to get a lot of calcification. That's the basic point.
Warfarin inhibits the function of MGP which, in turn, antagonizes or stops the
the inhibitory role of MGP in the process of vascular calcification,
therefore, resulting in arterial damage and decline in renal function. If that
still sounds a little bit confusing, maybe this next couple of images will
help. Here's the matrix gla protein. It's non-carboxylated, so it's not active.
There's a process called "gamma- carboxylation" that activates this matrix
gla protein. However, vitamin K antagonists (like warfarin) stop that
gamma-carboxylation. If warfarin stops that gamma-carboxylation, then the matrix
gla protein cannot be activated. If it's not activated, it can't participate in
helping pull calcium out of the arteries. So that's the connection and
it has to do with basically inhibition of an activator. That's where
a little bit confusing. To show this on the cake and if you're thinking
about, "Well, wait a minute. This is all K1, Brewer. We're talking about K2. They're
very different." I understand that but as I said earlier, there is a connection in
this metabolism, and it has to do with the carboxylation. So if you look at
warfarin metabolism, it comes in and blocks vitamin K reductase and oxidation
of vitamin K and therefore it blocks the development of gamma of the
MGP development. Basically now, here's another way of looking at it
and it starts to get back to the vitamin K2 than the menaquinone. The matrix gla
protein... remember that... and if you're thinking, "Brewer, those are very that's an
ugly image." I understand that. Nope, no apologies. That matrix gla protein you
see means uncarbonated. So if you want to activate the matrix gla protein,
you need to carboxylate it. The matrix gla protein decreases calcium and
therefore inhibits vascular calcification. We're going to study in
other videos... we're going to look at osteocalcin which is a different enzyme.
It does exactly the opposite of matrix gla protein. When it is functioning, it
increases calcification and actually promotes bone minerals mineralization. So
matrix gla protein pulls it out of the vascular area, and osteocalcin puts it in
the bone. Now this has probably been a little bit much in terms of trying to
get the connections. I will cover it... will do several other videos in this area. I
just wanted to show the sciences. Again, it's also pretty clear on these actual
enzymes. This, for example, is the actual amino acid series involved with
the protein so that is the protein itself, gla protein,
matrix gla protein, in amino acid format. So again, maybe this is a little bit
confusing. I hope not. It's just the first in a series that I'm going to be doing
on K2. Actually, it's not the first. I'm doing another series on K2. If you've
made it through all this stuttering and stammering, and you're still there, I
appreciate your interest.
My name is Ford Brewer. I started off as an ER doc. Then I became very
frustrated with the fact that most things that bring people into the ER
were preventable like heart attack and stroke. I went to John Hopkins to get
training and ended up running the program there in prevention. There I
trained dozens of docs and again that was three decades ago. Since then, I've
trained thousands of docs and even more importantly supervised those docs and
even most importantly helped thousands of patients prevent things like heart
attack and stroke. Waiting for it for the disease and hoping for a cure for this
kind of devastation doesn't work. Come to Louisville on November 8 and 9. We have
a boot camp type of environment for two days where you learn all the things that
you didn't learn from your doc in terms of heart attack stroke prevention things
like cardiovascular inflammation, how to detect it, how to measure things like
insulin resistance (the number one cause of inflammation), how to detect it, how to
measure it, how to stop it, how to manage it. You also get... you can get the labs
there for that event if you'd like to get a complete evaluation in addition
you get an arterial scan called a CIMT. To get the right one of those is fairly