I've shared with you a couple of times. I I used to ignore vitamin K2. I
totally ignored it for a long time. Then some viewers asked me to look into
it. So I did I went straight to the clinical trials and there's just not
much on clinical trials on K2 yet. You know, maybe there will be, maybe there
won't be. But recently, I got interested yet again in vitamin K2 and I'm gonna
drop that discussion for just a second and pick up an entirely different thread
and see if you start to make the connection here. And again, this... there may
be a significant connection, maybe not.
Let me just read some titles. "Reduced serum concentrations of carboxylated and
undercarboxylated osteocalcin are associated with the risk of developing
type 2 diabetes." The next one, "Osteocalcin is related to enhanced insulin secretion
in gestational diabetes." The third one, "Association between serum
osteocalcin and markers of metabolic phenotypes." And when you get deeper into
the article, the metabolic phenotypes, they're talking about are for a look for
mostly insulin resistance, diabetes. So there's osteocalcin. Ring any bells?
Let's talk about that in just a minute. But first... but before we do I mean
there's article after article "Low osteocalcin level is a risk factor for
impaired glucose metabolism in a Chinese population." And it just over and over and
over again, this is... these are not two or three articles that I've just cherry
picked out of the science. There's clearly an implication for glucose
metabolism linked to osteocalcin. Now wait a minute.
I just... osteocalcin ring any bells yet for you? And to link it back to that
first topic i brought up about vitamin K2, remember we were talking about the
mechanism how can vitamin K2 impact both both soft tissue like artery walls and
hard tissue bones. Well it has to do with carboxylation.
That's undercarboxylated MGP and undercarboxylated osteocalcin with MGP matrix
gla protein (MGP). That once you carboxylate MGP, you can inhibit vascular
calcification with the bone. You actually you can increase calcification of the
bone by carboxylating osteocalcin, activating it.
You can. Also, what most people don't don't get into even the K2
Bureaus is that you can do... you can go both ways in terms of calcium and bone.
It helps to activate both osteoblasts (which build or deposit bone calcium and
bone) and osteoclasts (which cut calcium or and/or protein out of the bone). But
again, K2 is very involved in activation of the enzymes which are involved, in
turn, with managing calcium. So let's go one step further. As I mentioned, they
just gives you the topic that I covered just now. Osteoblasts, "B,"
build. And osteoclast, "C," cut. Both of them have to do very much to do with
bone mass. That's how our body continues to customize our bone mass to our
current needs and again it's MK7 is suppresses on the osteoclast side and it
stimulates on the osteoblasts side. So very interesting, right? But wait a minute.
Was this about K2 or was this about insulin resistance? So in humans,
osteocalcin levels are inversely correlated with multiple various
variables of type 2 diabetes such as glucose intolerance and insulin
resistance. Decreased levels of osteocalcin have also been correlated
with premature or myocardial infarction and coronary heart disease. So here is a
graph, looks kind of scatter shot at first, but as you begin to notice, you
don't have a lot of dots down here and a lot of dots up there. There is a fairly
reasonable correlation. What is it? Hemoglobin A1c on the vertical axis and
osteocalcin on the horizontal axis so it's interesting I haven't heard a lot
of discussion about K2 and whether there's any at the end of the day
whether there's any K2 relationship with insulin resistance and that's one of the
things that's just really intriguing to me right now.
But as I said, there's no question that I'll say that
K2 is related to osteocalcin, and osteocalcin is in turn related to
insulin resistance. Here's a visual on it. Osteocalcin increases both adiponectin,
adipocytes, fat cells, and proliferation of beta cells, and increased insulin, and
increased insulin sensitivity, leading to improve glucose handling and lower fat
mass. So what's going on here? Uh heck if I know
but it's a very interesting set of relationships, isn't it? If you've made it