Why We Age – Dr Bill Andrews Talk Part Two

Remember I said that I was looking for
something that made more sense than just environmental effects on our aging, there
had to be some kind of clock. Well here it is. When I, when I heard
somebody describe this in 1992, I, I was in, was in an audience just like
this. I was instantly up at the front to talk this guy and I was working for the
guy two weeks later to try to figure out a way to prevent this. So the best example that I can give you
that telomeres effect aging is that there are people on this planet that are
born with telomeres already short. And these kids suffer from every age-related
ailment that normal old people do. They get osteoporosis, they get clogging in the arteries, they get Alzheimer’s, they get
everything. They die of old age at 20 years old. And if we could find a way to, to
prevent telomere shortening or even reverse telomere shortening, this would
be a cure for this disease. Because even though these kids have another mutation
called Lamin A that causes the telomere shortening, their only problem is they
have short telomeres. We could lengthen them, they’d be normal, living normal,
totally normal lives. And believe me, that’s something that scientists in my company
would really like to do even though there’s only 250 kids at any one time on
this planet that have this disease. Now they’re not the only ones, we all suffer
from short telomeres diseases. Fact, now, every single disease you ever heard of
has now been published in scientifically peer-reviewed journal articles showing
that the length of your telomere affects those diseases. I mean if you, anybody sees any
particular disease up there that they’d like to talk to me about later, feel free because
I can refer you to papers, publications, everything that’s, that’s associated with
telomeres here. But what I like to do is I’d like to focus on the first two on
the top, cardiovascular disease and cancer just for a minute because they
are the number one and two causes of death in the, in
our world. What is done is that there’s been now so many papers
published on cardiovascular disease and cancer that scientists have now
summarized all these papers and published what’s called a meta-analysis,
which means this is a summary of all the other papers as to what they’re all
saying. This meta-analysis is saying that short telomeres increases your risk of
cardiovascular disease. The same is done for cancer. Even more papers have been
published showing that when telomeres get short, you have an increased risk of getting cancer and a decreased risk of fighting your
cancer. I’d like to spend a little more time on this one because this one is really
important. Think about your chromosomes now as the
shoelace again. And when the shoelaces get really short you start
having chromosome breakage, joining the chromosome start fall apart. You can see this
in the microscope when you, when you take cells from a cancer person. You can see
these physical changes in the chromosomes because there are big
changes. Now what happens is these mutations caused the cancers, ok. Every
time somebody gets cancer is due to mutations in their chromosomes, but
what’s causing mutations? Well short telomeres is now known to be some
major cause of the mutations that lead to cancer. And what’s even a bigger, is
just as big a problem, is when you do something like chemotherapy to try to
treat that cancer, you can kill 99.9 percent of those cancer cells, but
because of the high mutation rate some of those cells, .01% of those cells are
going to survive. They’re going to mutate to be able to
survive whatever you, you treat them with and as a result those are going to grow
back. So the bottom line is we got to keep our telomeres long. We gotta keep
our telomeres long to keep from getting cancer. We got to keep our
telomeres long to increase the chances that therapies like chemotherapy will kill our cancer. And we got to keep
telomeres long to help keep our immune system to continue to fight the cancer
cause our immune systems our best defense against cancer. So it’s not just aging
we’re talking about today, but cancer is an aging related disease given the fact that it’s more prevalent
in the elderly than any other age. The take-home message today is bad things
happen when telomeres get short. This is something I go around saying. I
want everybody to just think of bad, short telomeres as bad. Long telomeres,
there’s nothing wrong with long telomeres. Nobody has ever found anything in the
petri dish, or in different tissue samples. No one has ever found anybody
that was suffering from anything because their telomeres were too long. So we
can get our telomeres long, it’s really good. The only thing that telomeres,
long telomeres do is make you younger. And as I mentioned before I’m going to show
you some stuff where people have actually demonstrated that in mice. If
you want to learn more because, because this is really like when I’m speaking at a
medical conference, I will go into a lot of details, show a lot of data. But instead
here, what I’d like to do is I’d like to anybody wants to learn more about how
telomeres affect every kind of disease or thing in your life that you can
imagine, go to something called pub med, P-U-B-M-E-D. That’s a brief, it’s short for
publications in medicine You don’t need to write down the website
because you can just google it and find, find the website. But just type in
telomere and then all capitals A-N-D and whatever like you wanted to, cancer,
multiple sclerosis, macular degeneration, any kind of thing, just find and you’ll
find all the scientifically peer-reviewed journal articles on that
subject. So what I want to say is quit reading the
press releases and newspapers, quit reading, listening to doctors that get on
talk shows because they’re all there. They’re, they’re all supported by
special interest groups that want to tell you something that’s not really
true. And so here’s where you can find the truth because this is, so if you
want to know is coffee good for you, this is where to find it. Is ibuprofen
bad for you, is aspartame bad for you, find out the facts here this is where to do it. But also learn all
about you, everything you can about telomeres. Ok, so I, I’ve just spent a lot of time
telling you about the problem. We have telomere shortening that’s causing us to
get sick and old. Every kind of disease you ever heard of is, is affected by the
length of your telomeres. We want to keep them long. Well how are we gonna do that? Well one of
the first things we gotta do is we gotta figure out why do they get shorter. And
so what I want to do describe how they get shorter and why they get shorter. Cause I
want you, I want to come up with an analogy. The analogy would be to think of
your chromosome, your DNA as the top row of bricks on a brick wall. Now think about it, every time you have a
set so you have made of a hundred trillion cells, every time one of those
cells want to divide to make two new daughter cells everything in that parent
cell has to be duplicated. So that when you get the two daughter cells the
contents inside those cells are identical to what that parent cell was.
So everything has to be duplicated and that includes that DNA molecule that I
told you that’s a hundred million bases long. It’s, it is duplicated through a
process called DNA replication. So think of the chromosome analysis top row brick
on a brick wall and when the DNA wants to, when the cell wants to divide it’s
going to make a new row of bricks on the brick wall. And 1, 1 row is going to go into 1
cell, 1 row is going to go into the other cell. So let’s get rid of the other bricks
and get rid of the cat and now cell’s getting ready to divide, the bricklayer
comes along and starts laying the bricks. Now this is a long arduous process.
Remember the chromosome’s about a hundred million bases in length and so it’s got,
it takes awhile to do and also it, it’s got to be done accurately because any
misplaced bricks are going to lead to mutations. Now the, the problem that we
want to really focus on the here is not really what’s happening here but what’s
happening way over at the telomere, the very end of the chromosome. Now we are
smart enough to know not to stand top of the brick wall when we’re making a
brick wall or making a row of bricks and you’ll see why. Because when this bricklayer
gets to the end, he can’t put a brick in the last place that he was standing. Ok so what’s the, what was the point of
all this? The point is is that this new chromosome
is shorter than the first chromosome. The reason why the chromosomes get shorter
every time a cell divides isn’t because something shoos him away. It’s because we
ourselves lack the ability to be able to duplicate the old chromosome into a new
one, lose, lacks the ability to replicate all
the way to the very tip. As a result the new chromosome is shorter. And so the
cells, cell divides and now so, it gets ready for another division. Again the
bricklayer come along and again the bricklayer’s going to fall off the end.
But the, now the chromosomes even going to be shorter and shorter and shorter
with every cell division. And I said before, there’s absolutely nothing we can
do about this. No matter how will we eat or exercise or do everything our doctors
tell us to do, we can’t stop this shortening. I call this basal level
telomere shortening. Meaning this is the slowest that we can get our telomeres to
shorten. As I mentioned before there’s nothing we can do to stop this, but we
can accelerate this. If anybody wants to live their age faster than they are right
now, this is how to do it. And that’s anything related to an unhealthy
lifestyle. So obesity, lack of exercise, psychological stress, smoking, all these
things cause the production of free radicals or inflammation that will
actually accelerate the rate. It will cleave the telomeres, and make them shorten at a
faster rate, so I call this accelerated telomere shortening. Now there are things
we can do to stop this and that includes like, exercise, quit smoking, lose weight,
meditation. Also you can do things like, omega-3 fatty acids, vitamin D, anti oxidants. And you’ll hear about a lot of
products on the market today that are saying that they protect your telomeres
and stuff, and that’s what they’re doing they’re providing you with things like
vitamin D, Omega threes, and antioxidants that will help reduce the rate of this
accelerated telomere shortening. But they don’t lengthen your telomeres and that’s
what we really got to do. We gotta because it, cause it’s only going to,
it’s only going to decrease the accelerated telomere shortening. We’re
still going to have that basal level telomere shortening as a result. Nothing can stop it. We gotta figure out
a way to stop it and lengthen it and that’s what I’m working on, the solution.
Let’s see, there was something I wanted to say, okay, yeah, that, that’s what
I want to say. The solution is that there are cells in our body that already
don’t age, okay. We’ve known this for a long, long time. I was going to give away one
of my books with this question but I thought, shoot there was reason I
wasn’t going to, it’s because I don’t have enough books. Okay, so, so there we have aging occurring
that doesn’t occur in our reproductive cells, and this has been known for a long
time because our children are born younger than we are and they come from
our old cells. So something in our reproduction process is preventing our
cells from getting, all those cells from getting older. That’s why our children are born young.
Well what we discovered was that telomeres don’t shorten in our
reproductive cells either. They’re the only cell in our whole body where we
don’t have telomere shortening. I said before, every time a cell divides the
telomeres get a little shorter. That’s true in every single cell of our body
except our reproductive cells. So I got into this business by trying to find
out why these cells don’t have telomere shortening. Because we’re understanding
that, that, as I already said, we pretty much understand why they shorten. What do these
cells do to keep them from shortening? And as a result I discovered this enzyme
called human telomerase. Screen bars here is showing the double helix, the DNA is a
double helix. Telomeres is shown as a factory. The factory is adding bases, these beads on a string, they’re adding
bases at the very end of the chromosome making it longer. And so this is how, how
the reproductive cells do it. I’ll think of it like a clock. When a regular cell
divides, telomeres get shorter, it’s like clock ticks once. Cell divides again,
telomere gets shorter, ticks again. But in our reproductive cells, the cell divides,
telomeres still get shorter, but then telomerase pushes it back a tick by relengthening telomere. Divides again, it gets shorter, telomerase pushes it back so
the clock doesn’t tick. It’s like a tug-of-war, shorten, lengthen, shorten, lengthen,
shorten, lengthen. That’s why in our reproductive cells, we don’t have any
telomere shortening.

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