If the terms “rapamycin,” “mTOR,” and “autophagy” aren’t familiar to you already, hang on this before you tune us out.
This has got some practical implications if you want to live a long healthy life.
In fact, what I’m doing. This is part 3 in a series on the book “Lifespan”
by David Sinclair. I had several requests from viewers like
Jon Touch Oh who asked me to review this and I’ve had a blast. It’s a long book. It
covers… it’s encyclopedic in length in terms of covering the major topics in
longevity. One of the reasons I’m enjoying it so much is I’ve done videos
on most of these topics. For example, rapamycin. Rapamycin was discovered on
the island of Rapa Nui. Most of us don’t remember Rapa Nui, but you do remember
Easter Island. It’s the islands that have the hundreds of statues of stone faces.
Rapamycin is also known as sirolimus. The biochemists classified it as a
macrolide. You may not remember that but if you’ve had involvement with medicine,
you know that they are a macrolide antibiotics. It’s already being used as
an immunosuppressant. It’s used in stent coatings as well as kidney transplants.
It comes from a bug that was… in fact, a bacteria that were found on the island of
Rapa Nui and hasn’t been found, it wasn’t found anywhere else.
Streptomyces hygroscopicus. That’s Streptomycin hygroscopicus. Don’t
get too wrapped up in that. It inhibits mTOR. Remember what mTOR stands for?
Mammalian target of rapamycin. And you may or may not remember, I’ve done
several videos on this fellow. His name is David Sabatini. He’s right
next door to David Sinclair at Harvard. He’s over at MIT. He’s the one
that discovered mTOR. And there’s been a huge amount of research growing out of
that now. Why is that mTOR has a lot to do with controlling catabolism versus
anabolism and catabolism, autophagy? Anabolism is building up, growing, and you
see things like anabolic steroids involved with that. So does that help you
maybe connect the dots on why men tend to have inflammation and cardiovascular
disease and positive calcium scores earlier than women? So there’s
a lot of work in that area. I also did a separate video on autophagy. This was
from a recent New England Journal article which was just going into the
depth of the mechanisms around autophagy. You may remember autophagy is where
the cell is doing recycling. So let’s get deep in that for just a second. First, you
have initiation using a sequence for which we look autophagy just means to eat.
We’re going to hold off on that for a second and look at how this phagophore is
growing around this dead organelle and that organelle is it’s like an organ in
the body except it’s within the cell. So it’s a very tiny component. If you look
more deeply, you can recognize this is the dead mitochondria that this vesicle
is wrapping around. As it continues to wrap around it, it closes up. And now then
it’s called autophagosome. Autophagosome, “auto” meaning self; “phago” meaning
eating. And some meaning by it’s a recycling body that’s within the cell,
the cytoplasm of the cell, which is basically the suit within the cell wall
and that’s a material out of phases own those then combined with what’s called a
lysosome. “Lyso” means to split, and again “some” means body. So you’ve got these
enzymes within the lysosomes. They combine with the autophagosome to form
an autolysosome. A lot of Greek words or Latin words you really don’t
need to know about. But the process itself I think is very very helpful. And
then what happened? What happens is that these enzymes from the lysosome dissolve
the old dead tissue, in this case, an old dead mitochondria. Mitochondrion then use
that for energy and building blocks for the future, for other new cell parts. Now
when we’ve got things like insulin, too much insulin, or insulin-like growth
factor as you see here up at the top, you get too much those tend to stop this
autophagy process. So if you look at this slide, this slide is basically to help us
connect the dots with other things that you may have
heard of, like insulin-like IGF, insulin like growth factor, AMPK. You may remember AMPK helps drive some of these processes autophagy vs.
anabolic processes. AMPK, by the way, you may remember and
Sinclair mentions in the book. AMPK is stimulated by metformin. Sinclair by the
way thinks that that is the total longevity mechanism for metformin. We’ll
talk about metformin and longevity as he did but we’ll do that in another
video on this series. Remember concepts of energy depletion
and starvation are fasting. Again those help drive this autophagy process.
Remember rapamycin? Rapamycin again helps direct this process. So again, hopefully
this helps you connect some dots that you may have heard in some other
videos and thank you for your interest. So I’m very excited to announce we now
have a membership page. Now, what is that? That’s the one place where you can go
and access all of our digital products. It starts off with a few free things,
like a lot of infographics which help you understand the basics of insulin
resistance, cardiovascular inflammation, and other key concepts on how to prevent
heart attack and stroke. The next free item is the intro and first chapter of
the book that we’re writing on plaque and the standards of medicine just aren’t
doing very well right now in terms of the number one killer and disabler.
Plaque, we don’t do a good job of measuring it, we don’t do a good job of
monitoring it, and there are better ways. So that’s what this book is all about.
Again, go in, and get a free look at the intro and in the first chapter. And if
you’ve purchased the cardiovascular inflammation and IR courses, thank you so
much for doing that. You purchased those at a time before we had them totally
cleaned up and we’ve cleaned them up now and they’re available for you right
there on the membership page. Hit the link below, register and go in, and take
look. Look forward to seeing you there. Thank you.