THE BIG MIG SHOW
NOVEMBER 06, 2024
EPISODE 411– 7PM
Dr. Aubrey de Grey is a biomedical gerontologist based in Silicon Valley, California, USA, and is the founder, President and Chief Science Officer of LEV Foundation, a biomedical research and advocacy charity focused on repairing the molecular and cellular damage of aging. He received his BA in computer science and Ph.D. in biology from the University of Cambridge. His research interests encompass the characterization of all the types of damage that constitute mammalian aging and the design of interventions to repair and/or obviate that damage. https://www.levf.org
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All men are created equal, that they are endowed by their
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Creator with certain unalienable Rights, by liberty.
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If liberty means anything at all, it means right to tell
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people what they do not want to hear.
00:00:54
Hey, welcome back to the big big Show.
00:00:55
I'm your host Lance Miliaccio, of course with my Co host George
00:00:58
Ballantine. Rise and grind doing what we do.
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Of course on this show it's the tip of the spear because if
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liberty means anything at all, it means the right to tell
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We always try to bring you the right guess, the evidence, the
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They were $22.00 an ounce back then.
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So I think right now we're sitting at 34, aren't we,
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George? Somewhere like that.
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I haven't checked today, Lance. Yeah, interesting.
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Well, everything's up. Obviously since the election,
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people seem to be feeling like the financial markets are going
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to calm down and we'll be seeing good activity.
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Crypto's up, the meme coins are up, the stable coins are up
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even. Obviously Bitcoin hit a new high
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$75 or and it might even be higher than that now.
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That was earlier today. Listen, tonight we got a great
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show. Really, really interesting guy.
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You know, I read his book years ago.
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I'm now in about 3/4 of the way through his new book, maybe half
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right in there. Doctor Aubrey the Grey.
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Obviously, you've seen the show before.
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We try to bring people on that we feel like can add to your
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life and educate you in a way maybe that you're not used to
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being educated. And it's interesting that he
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said his real intent is to end aging.
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He believes in the 1000 year lifespan, forever young.
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He's not sure that we haven't already actually accomplished
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that. Of course, he is a biomedical
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gerontologist. He's based in a Silicon Valley,
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California, USA and is the founder and President Chief
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Science Officer at Lev Foundation, which is a
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biomedical research and advocacy charity focused on repairing the
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molecular and cellular damage of aging.
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He received ABA in computer Science and APHD in Biology from
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the University of Cambridge. His research interest
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encompassed the character characterizations of the all
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types of damage that constitute mammalian aging and the design
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of intervention to repair and or obviate that damage.
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Doctor de Grey is a fellow both the Gerontological Society of
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America and the American Aging Association.
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That's a tongue twister. I caught myself you when I was
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reading it backstage a couple of times, slipping on it.
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And of course, he sits on the editorial and scientific
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advisory boards of numerous journals and organizations.
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He's a highly sought after speaker who gives frequent
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invited talks at scientific conferences, including Ted
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talks, which I caught that over on YouTube.
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You might want to check that one out yourself.
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Universities campaigns in areas ranging from farmer to life
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insurance to the public. He's got I've got millions of
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views on on YouTube. I really feel blessed.
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If you have him here tonight, let's bring him in, George.
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No reason to leave him backstage, man.
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You don't even ask how it's doing today, right after the
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election. Let's forget it.
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All right? Welcome to the big, big show,
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Doc. See how he changed me, Doc, Do
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you see how I see how it goes? We don't need him.
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I listen. He gave you.
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He was given the introduction, your bio about you and a lot of
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the words he said. I couldn't even understand what
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he said. He was going fast.
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But we should have brought a dictionary Lance.
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Well, you know, I think for the audience, I'm going to start off
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with bio gerontology and I focus on the biological reasons behind
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aging. I think, you know, studies that
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influence the genetics on aging and I think it's environment,
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lifestyle, and the effects of the aging process happens to
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you. You know, we've had some people
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on the show, they've talked about GMO foods, we've talked
00:06:13
about heavy metals, we've talked about vaccines.
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We don't do a lot of that because obviously YouTube hates
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when we go down the vaccine route.
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You can get a quick suspension over that.
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You know, Doc, obviously your background might was math
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really. But tell me, how did you head
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down the road you had when you decided that aging was something
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you really wanted to tackle? And it's, it's a lifelong career
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and it really seems like you've really done some serious work
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over the years. Yeah, that was actually not
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until my late 20s. I had previously worked in
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computer science, as you just mentioned, my undergraduate
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degree in computer science, and I worked on artificial
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intelligence research for several years.
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And, you know, that was because I wanted to solve the problem of
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work. I felt that it was, you know,
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rather a pity that so many people have to spend so much of
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their time doing stuff that they would not do unless they were
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being paid for it. And so I thought, I'll fix that.
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I'll, you know, help computers to do things and I'll increase
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automation. And, you know, the reason I make
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that made that choice was because when I was a teenager, I
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started programming fund. I was good at it.
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So I thought, you know, that's my talent.
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But I always knew, even from a very young age, that even though
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that was a bad problem, the problem of aging was a far worse
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problem, and it was a problem that should be solvable.
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So I then the big mistake I made was I never actually took the
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trouble to talk about it to anybody.
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I never actually found out until my late 20s that most people
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don't think that way about aging.
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It was only when I met and married a biologist, a biologist
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who was quite a lot older than me.
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She was already a full professor at UC San Diego.
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Then I started to discover all of this.
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And eventually I just, I came to terms with it and decided that I
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had to switch fields because, you know, the people who were,
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you know, exceptionally suited to be working on the world's
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most important problem were just not doing so.
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And I, you know, by that time I had kind of come to the
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conclusion that I was pretty good at working on hard
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problems. So I thought, you know, maybe
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I've got a chance of making a contribution.
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You know, it's interesting. We talk about Big Pharma off and
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on on the show. Obviously we've had lots of
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people from both sides of the aisle because our show is
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unspecific when it comes to politics.
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We believe that what's going on in DC when you take Big pharma
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lobbying and you look at what a powerful institution that is,
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and of course their focus is never really about treating the
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diseases. It's about treating the
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symptoms. So obviously you address aging
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as it's a disease, which is an interesting perspective.
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Most people, including myself, feel like it's the natural
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progression of life that we assume that, but it but it's not
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based on the information you're providing.
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You really, truly have done some work that you believe you can
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stop or in fact slow down the aging process dramatically.
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Not that aging doesn't continue, but the side effects of aging
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and controlling what the free radical damage is.
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It's really an interesting perspective.
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I got to ask you about something that when I was researching you,
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I thought this was interesting and I, I was familiar with this
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problem. I, I had actually heard of it
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years ago, but the had, and I don't know if I'm pronouncing
00:09:30
this, but the Hadwiger Nelson problem.
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So, you know, a lot of guys have interesting hobbies.
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That problem sat around I think for more than 60 years before it
00:09:40
made any forward movement. And it looks like you've been
00:09:43
focused on trying to solve it for people out there.
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It's I think it's got to do and I'm going to just I'm not an
00:09:49
expert so I don't want to say this, but it's got to do with
00:09:50
the colors needed to a color plane so that no two points at a
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unit distance. I think Matt or meet, they're
00:09:58
signed by the same color. I don't know.
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I'm probably given very remedial version of that.
00:10:02
But that's kind of an interesting hobby and you made
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some huge headway the first time in 2018.
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Sixty or seventy years that problem sat with nobody getting
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any further along. So let me answer everything you
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just said. So first of all, I want to push
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back on the idea that, you know, I'm saying aging is not natural.
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Aging is perfectly natural. The thing is that tuberculosis
00:10:25
is also natural. And you know, we feel pretty
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good that we have brought tuberculosis under pretty
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comprehensive control. So, you know, that's how we
00:10:34
ought to think about it. Not to think that, you know,
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some things are unnatural and we should fix those and some things
00:10:39
are natural and we should leave them alone, but rather that lots
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of things are natural but undesirable.
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And what is natural about human nature is to fix the undesirable
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thing, to manipulate nature to make what's natural but
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undesirable go away. And that's what I'm doing.
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I just do medical research, nothing special.
00:11:00
It's just, you know, the particular target that I have
00:11:03
happens to be the thing that kills most people these days,
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that's all. Then I also want to mention
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something about the FDA and you know, about regulatory proposals
00:11:14
and the but big Pharma wanting to keep sick people alive rather
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than wanting to stop people from getting sick.
00:11:20
This is all true. It's very true, but it's not
00:11:23
really their fault. It's really the fault of the
00:11:26
public because the, The thing is that first of all, the FDA,
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well, if you look at that side of it, the first, they're just
00:11:36
implementing the law. They're just doing what our
00:11:40
elected representatives tell them to do.
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And our elected representatives, as we all know, have one goal in
00:11:47
life, which is to get reelected. So at the end of the day, they
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do what they think there are votes in.
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But ultimately, the main reason why there is so little
00:11:55
preventative medicine out there, whether it's preventative
00:11:58
medicine for the for the health problems of late life or indeed
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early life, is that the public don't believe in it.
00:12:05
The public are inherently hesitant to embrace medicines
00:12:09
that are new and thus experimental, and that they
00:12:13
perceive might just make them sick rather than postpone the
00:12:17
time at which they get sick. Now, of course, doctors and
00:12:21
researchers are constantly, you know, generating evidence that
00:12:26
that's not that's probably not going to happen.
00:12:29
In fact, overwhelmingly probably.
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But the public are just not very good at probabilities, and so
00:12:34
they focus on the worst case scenario, however outlandishly
00:12:38
unlikely it is, and that puts them off preventative medicine,
00:12:42
prevention in general, of course, preventative lifestyles
00:12:44
and so on, different matter. But when it comes to medicine,
00:12:47
that's the problem. And that's a good thing, because
00:12:50
I believe that we have a chance of educating the public about
00:12:55
this, of going to the point where the public does actually
00:12:57
understand that preventative medicine is something they want.
00:13:01
And as soon as that happens, the industry will follow the money.
00:13:04
The it's not as if different skills are required, different
00:13:07
technology to develop preventative medicine versus
00:13:10
sick care medicine that we have today.
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So it's all about educating the public.
00:13:15
That's why I spend so much of my time trying to do that.
00:13:17
Doctor, I'll talk about that Havoc and Nelson problem.
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You've got it pretty much right, actually.
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Yeah. Something that we've put forward
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in 1950 and no progress has ever been made.
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And I made a bit of progress in 2017.
00:13:31
Well, I, if I, if I heard you correctly, and I think I did, I
00:13:34
want to respectfully disagree with something because there's a
00:13:37
lot of holistic cures out there that the FDA will fight against.
00:13:41
Why? Because Big Pharma doesn't want
00:13:44
it. And for instance, like cures for
00:13:46
cancer, we'll say there's things out there that can help with
00:13:50
cancer that has been known to cure cancer, but the FDA and Big
00:13:53
Pharma want nothing to do with it because you won't have no
00:13:55
more cancer drugs, no more chemo, radiation.
00:13:59
So the FDA does play a big role. OK.
00:14:02
So you're not actually disagreeing with me that because
00:14:04
that's true, but it's a separate question.
00:14:06
These medicines that you're talking about are not, not
00:14:09
preventative medicines. They are medicines to treat
00:14:12
things just the same as the medicines that the FDA does
00:14:15
approve and does favour. You're quite right that this is
00:14:19
a problem, but it's a different problem.
00:14:21
It's a problem that is driven by the economics of the system, by
00:14:24
the fact that these holistic medicines typically don't have,
00:14:27
you know, they don't have intellectual property that is
00:14:29
owned by large companies. And plus, yes, absolutely, this
00:14:33
is a function of capitalism. It's, you know, it's, it's a
00:14:37
problem, but it's a different problem from what I was talking
00:14:39
about. Like if, if you I know I forget
00:14:41
the that was a doctor, I believe maybe doctor, but I don't know
00:14:45
something to do with apricot teas or something where he he
00:14:48
actually put out on his site that he had a cure for cancer
00:14:51
and because he put cure for cancer, they came after him.
00:14:54
They actually locked him up. So even though it did cure
00:14:57
cancer, but. Well.
00:15:00
You got to remember cancer is a tricky 1 because cancers differ
00:15:04
so much from one person to the next.
00:15:06
Every cancer is genetically different.
00:15:08
And that means that there is a wide, a large number of, you
00:15:14
know, exceptional, you know, miracle moments, you know,
00:15:18
people who can report that they've had they've been cured
00:15:20
of this or that. But if you actually look at the
00:15:22
proportion of people who have taken the intervention, whatever
00:15:25
it may be, whether it's apricots or whether it's some drug that
00:15:28
Big Pharma own, but only a minority of those people
00:15:31
actually benefit. Yeah, it's complicated,
00:15:35
obviously, because we're on social media, we see lots of
00:15:38
people talking about alternative remedies.
00:15:40
Obviously, there was lots of hoopla about ivermectin and
00:15:44
parasites and being some of those being the cause of
00:15:46
people's cancers. There's some recent studies that
00:15:49
are coming out about high doses of inositol and that's supposed
00:15:51
to have an impact. We've heard the stories about
00:15:53
the apricot seeds. Obviously there's lots of, you
00:15:56
know, material and it's confusing for the public.
00:15:58
They get confused and of course, their doctor tells them none of
00:16:01
that's going to work. You have to take this pill.
00:16:03
You got to get chemo. And again, maybe that puts you
00:16:05
into remission. Of course, chemo is a poison in
00:16:07
itself. So the body's reaction to that
00:16:09
is different for every individual.
00:16:11
It's much more complicated. I want to bring up a term you,
00:16:14
and this is interesting because Methuselah, obviously, according
00:16:17
to the Bible, he was the grandfather of Noah.
00:16:19
I think he lived 900 and some odd years, maybe 960 or
00:16:22
something. And of course that's, I think
00:16:25
that's, you know, a well known story to a lot of people.
00:16:27
You coined a term Methuselarity, I believe.
00:16:31
Am I right? Methuselarity.
00:16:34
That's not completely correct. That was coined by a friend of
00:16:37
mine and then going to pull neck the but I coined a very related
00:16:42
term, the term longevity escape velocity.
00:16:45
So I can explain to you what longevity escape velocity is
00:16:48
basically, but basically the methuselarity is the point at
00:16:54
which we reach longevity escape velocity.
00:16:56
So shall I explain? I explain both of those terms.
00:16:59
Please, yes, please do. To the audience, of course.
00:17:01
OK. So the concept of longevity
00:17:03
escape velocity, which I first started talking about about
00:17:07
2004, so 20 years ago, is as a consequence of the ideas I had a
00:17:15
few years before that about how we're going to actually bring
00:17:19
aging under comprehensive medical control.
00:17:22
And the key, you know, underpinning of that, that work
00:17:26
back then was that we're going to do it by reversing aging by
00:17:31
bonafide and rejuvenation. Whereas historically people in
00:17:35
the field had been focusing entirely on the idea of slowing
00:17:38
aging down rather than reversing it.
00:17:41
Now, slowing aging down is better than nothing, but
00:17:44
obviously for people who are already your age or mine, you
00:17:47
know, with the same age, right? Yeah.
00:17:49
Correct. I'm younger.
00:17:51
I'm. George, he had to throw that in.
00:17:54
I'm younger. For people, for people our age,
00:17:57
you know, we have already accumulated a lot of, you know,
00:18:00
molecular and cellular damage in the body.
00:18:02
We are already biologically old as well as being chronologically
00:18:05
old. And therefore, you know, even if
00:18:08
we were to, let's say, half the rate at which more damage would
00:18:11
accumulate in the future, still we're going to get to the point
00:18:14
of having enough damage that we get sick.
00:18:17
Whereas if we take people like you and me and we repair that
00:18:21
damage, which is what I've been working on ever since that time,
00:18:27
then we actually do benefit a lot.
00:18:29
We can take we can, we can take people backwards in biological
00:18:32
age. Now, the key thing about that is
00:18:35
it buys time for people like me. It means that if we take someone
00:18:39
who's, let's say, 61 and we take them back to being biologically
00:18:42
41, which we would be able to do with a panel of damage repair
00:18:47
rejuvenation treatments that was not completely comprehensive.
00:18:52
If it was completely comprehensive, then we'd get
00:18:54
back to, you know, 0, right? But if we get back to, you know,
00:18:58
middle, early middle age rather than late middle age, then it's
00:19:01
going to be 20 more years before those people are going to be
00:19:05
back to being biologically the age they were before we began,
00:19:09
right? And in all that time, people
00:19:12
like me are going to be able to improve the comprehensiveness of
00:19:15
the therapies. So if we're not able to improve
00:19:18
them, then people would get back to being biologically 60 or
00:19:21
whatever and they'd carry on getting biologically older as
00:19:23
they got chronologically older. And they'd get sick and die same
00:19:27
as now, exhausted, do so a bit later.
00:19:30
But if we are improving the therapies fast enough, then we
00:19:37
won't have that problem. We can re rejuvenate the same
00:19:39
people when they're 80 but biologically 60 for the second
00:19:43
time. So they won't be biologically
00:19:45
sexy for the third time until they're let's say 100 or 110 and
00:19:49
so on. So basically longevity escape
00:19:52
velocity is defined as the minimum rate at which scientists
00:19:58
will need to. Improve the comprehensiveness of
00:20:02
these damage repair therapies over time in the people who are
00:20:06
getting the state-of-the-art therapies at any point will stay
00:20:10
one of one step ahead of the aging problem and never get sick
00:20:13
as they get old. And I believe that we can hit
00:20:16
that point when we when we get the 1st 20 years, if we take
00:20:20
people who are let's say 60 and we give them 20 initial healthy
00:20:24
life, then that'll be enough for us to be with very high
00:20:29
probability, you know, improving things faster than time is
00:20:33
Percy. So that 20 year point is what my
00:20:36
friend called the particularity. Interesting.
00:20:41
You know, I, I want to, I want to back up here a little bit
00:20:43
because obviously that's to where you, I don't think a lot.
00:20:45
Some of that is where you are now.
00:20:46
Obviously that's what led you here, George.
00:20:48
Let's throw up the cover of his book, your first book, this.
00:20:50
I actually read this in 2010, you know, the mitochondrial free
00:20:54
radical theory of aging, which I guess was your thesis.
00:20:57
A bunch of your thesis papers combined, obviously very
00:21:00
scientific. I had to keep a dictionary and
00:21:03
a, a lot of other information sitting side by so I could look
00:21:07
up the information in it, you know, and let me give the
00:21:10
synopsis for the audience. So this is a, it's a, the, the
00:21:13
book is proposes a biological explanation for aging based on
00:21:16
mitochondrial activity and free radical damage.
00:21:20
You know, we always hear about free radicals.
00:21:22
That term has been obviously, obviously well used in the
00:21:24
media. And George, Oh, no, not that
00:21:26
book, George. It's the other cover.
00:21:28
It's the Gray and blue one. That's the next book.
00:21:30
That's the only book. No, you got to look further up,
00:21:33
buddy. Yeah, is what there's a blue and
00:21:35
Gray. Oh, I see that now.
00:21:36
Stuck that in there, Lance maybe?
00:21:41
Maybe I did. You know, sometimes I do that.
00:21:43
I'll throw a media in the last half hour when I'm getting
00:21:45
ready. While that's happening, let me
00:21:49
just interrupt and say a couple of things.
00:21:51
So first of all, the whole idea that mitochondrial damage might
00:21:55
be relevant to aging was by no means original with me.
00:21:59
It was first put forward in the 19 in the early 1970s, so nearly
00:22:03
30 years before I did. However, what I, what I did was
00:22:07
I refined it a lot. You know, I had various, various
00:22:11
hypotheses. That's the one.
00:22:12
Yeah, various hypotheses for the, the specific mechanistic
00:22:17
detail that the molecular level, the cellular level for how the
00:22:20
thing actually works. And that was all new, and it was
00:22:23
enough to get me my PhD, as you say.
00:22:26
You know, so obviously people hear about, you know, outside
00:22:29
influences in flat influences of what causes that kind of damage.
00:22:34
And obviously the mitochondria are kind of the engine in the
00:22:36
body for the cells. But the theory in this is that
00:22:39
the accumulation of damage is caused by those free radicals
00:22:42
that are produced. Why the mitochondria are
00:22:44
producing energy. So maybe you can explain that to
00:22:47
the audience and kind of how that happens because I think a
00:22:49
lot of them would not because again, I think this is a term
00:22:51
they probably haven't heard that reactive oxygen species, they
00:22:54
don't really know that term, I don't believe.
00:22:56
So if you could share that with them, that would be great.
00:22:58
Sure, yes. So first of all, the term
00:22:59
reactive oxygen species sounds a little bit, you know, technical,
00:23:03
but really it's just a slightly more general term than the term
00:23:06
free radical, which is is quite a lot.
00:23:09
So, yes, so the general idea is that we've got these little
00:23:14
machines in the cell called mitochondria, which are
00:23:18
responsible for extracting energy from the stuff that we
00:23:22
eat, especially from carbohydrates and fats that in a
00:23:28
way that can be used by the rest of the body.
00:23:32
So there's a, there's a molecule called ATP that the, that the
00:23:37
cells that cells use all the time to do pretty much
00:23:39
everything, everything that takes energy is, is driven by
00:23:44
extracting, but by, by essentially grabbing a, grabbing
00:23:49
a molecule or two of ATP and doing something with it and, you
00:23:53
know, expending that energy and lots and lots of things that the
00:23:56
cell needs to do take energy, you know, DNA replication,
00:23:59
synthesis of proteins, things like that.
00:24:02
So ATP is what's often called the currency of the cell.
00:24:05
And, and most of the ATP in the cell is generated by
00:24:07
mitochondria. Now, the particular way it's
00:24:10
generated is really complicated. It turns out that because of the
00:24:15
way chemistry works, just getting energy out of a sugar
00:24:18
molecule, for example, and into, you know, the creation of ATP is
00:24:23
not a simple thing. And the way in which cells do
00:24:28
it, the way which mitochondria do it only evolved once a couple
00:24:31
of billion years ago, and it's been used ever since.
00:24:36
And it works. It worked well, but it doesn't
00:24:38
work perfectly. Essentially, it has, you know,
00:24:41
right effects in the same way that, you know, your engine and
00:24:44
your car may, you know, accumulate contaminants in the
00:24:47
oil or whatever. Similarly, there are, sorry, you
00:24:51
know, toxic byproducts of the way in which the mitochondria
00:24:55
does what I just described. And those byproducts are called
00:24:59
free radicals. And free radicals are toxic.
00:25:02
They can do an awful lot of damage to many different things.
00:25:05
They can cause mutations in the DNA.
00:25:07
They can, they can damage proteins, for example, and make
00:25:11
them make, make them not only non functional but also
00:25:15
indigestible so that they'll can't get rid of them and
00:25:18
they're just waste products that accumulate things like that.
00:25:22
So yeah, so basically I was interested in figuring out what
00:25:27
to do about that. And first of all, I had to
00:25:29
figure out a bit more than people had figured out before
00:25:32
about, about the mechanistic details of all of this.
00:25:35
Why do, why does this kind of damage accumulate over time?
00:25:42
It turns out that's not a trivial question to answer.
00:25:45
And then what? How is this damage actually
00:25:47
toxic? How does 1 cell poison another
00:25:50
cell, for example, when the first cell is, you know, has has
00:25:54
been, you know, damaged too much by this kind of mechanism?
00:25:59
So I did all that, but I also proposed a way in which we might
00:26:03
fix it that involve genetic engineering.
00:26:07
And it turns out this was also not original with me.
00:26:09
It was first proposed back in the 1980s, in fact, by Albert,
00:26:13
other people. It turns out to be quite a
00:26:15
simple idea and people had tried this thing.
00:26:18
It was basically a case of copying the genetic material
00:26:21
from the mitochondrion into a normal chromosome in the nucleus
00:26:25
of cells. And, you know, people had tried
00:26:28
this and they'd made a little bit of progress, and then they'd
00:26:31
hit a bunch of roadblocks and they'd given up, largely because
00:26:34
academia forces people to be very short termists and they
00:26:37
couldn't work on hard stuff. And I said that won't do, let's
00:26:41
have another gut. So I've been working on this
00:26:43
with my research teams over the years and we've made a lot more
00:26:46
progress. Still we're not there.
00:26:49
And also some other alternatives have turned out that may
00:26:52
actually achieve the same thing by very different mechanisms.
00:26:56
So I'm pursuing a lot of avenues in all of this, but yeah, that's
00:27:00
the basis of it. You know, it's interesting and,
00:27:03
and George, you and I have seen this.
00:27:04
We've seen lots of individuals online that are talking about
00:27:06
biohacking their age. They're using Cryogenifix,
00:27:09
hyperbaric chambers, stem cell research, you know, KRP, all
00:27:14
kinds of other things that they allege works.
00:27:16
And of course, the, the nutritional world has obviously
00:27:20
told us that we have to take an, you know, obviously
00:27:22
antioxidants. Now, I don't know how successful
00:27:25
those are because you're talking about something that's amplified
00:27:28
cellular dysfunction when this happens for these age-related
00:27:31
diseases, correct? Do do antioxidants, for example,
00:27:35
any of this stuff that you see and you see these individuals
00:27:37
now online that look pretty young in the pictures.
00:27:40
I don't know if they've been photoshopped and they're and
00:27:42
they're, they're going in these crazy regimens.
00:27:44
Some of them are spending over $1 a year on these
00:27:47
thorough regimens. Do do you feel like there's any
00:27:49
of that stuff that's been effective at all or that you
00:27:51
found that works in your investigation?
00:27:55
Well, let me divide what you'd have to ask into two parts,
00:27:58
because the person you're talking about in the second part
00:28:01
of your question is undoubtedly Brian Johnson.
00:28:03
He's a good friend of mine and does spend $4 million on
00:28:06
everything. So I'll come back to that in a
00:28:08
moment. First of all, antioxidants.
00:28:10
This is a really important point because when a guy named Danim
00:28:16
Harmon thought of the idea that free radicals might be
00:28:19
instrumental in ageing, that was in the 1950s.
00:28:23
And it was the very first time that anyone had come up with a
00:28:25
bona fide mechanistic theory of ageing, an actual, actual
00:28:29
hypothesis that said, OK, the reason we accumulate damage over
00:28:32
time is because of this particular type of of chemical
00:28:36
reaction that's going on in the body.
00:28:38
And he tried a whole bunch of tricks and gave a lot of
00:28:42
antioxidants to a bunch of mice and rats in his lab for a while,
00:28:46
and they didn't really work. They were kind of protective,
00:28:51
but only for only against early death, basically, you know, like
00:28:55
any animal, especially back then when we didn't know as much as
00:28:58
we know now about how to keep mice happy and healthy in the
00:29:00
laboratory. You know, some of them died
00:29:03
early. And these antioxidants were
00:29:05
protective against that. They made the mice more kind of
00:29:08
resilient, but a lot of them, you know, the ones that were
00:29:11
dying late, you know, the, the kind of what's called the
00:29:14
maximum lifespan of the mice, that maximum was not increased
00:29:18
by antioxidants. And it was actually because of
00:29:21
that that, you know, Harman carried on thinking, this
00:29:23
unbelievably smart guy, I'm afraid he he died a few years
00:29:27
ago, but he got to the age of 98.
00:29:29
He didn't do too badly. Pretty good, fantastic guy, real
00:29:33
role model for me. He figured out in the 1970s one
00:29:39
way in which this could be 111 potential explanation for this,
00:29:43
which was to do with mitochondria, and he was the
00:29:46
first person to start talking about mitochondrial damage as
00:29:50
the Nexus of all of this. And basically it all came down
00:29:54
to localization. The antioxidants are chemicals,
00:29:59
chemical molecules. They have to get around.
00:30:01
They have to be in the right place at the right time to
00:30:05
essentially sacrifice themselves to a free radical as a way of
00:30:10
stopping the free radical from reacting in a toxic manner with
00:30:15
molecule that matters, like DNA. And essentially he figured out
00:30:22
ways in which it might be that antioxidants just can't get to
00:30:25
the right place at the right time and the and the free
00:30:28
radicals do their damage regardless of how many
00:30:33
antioxidants are being consumed. And that seems to be pretty much
00:30:36
true. Antioxidants are not very, are
00:30:38
not very beneficial indeed. If you get wrong, if you take
00:30:41
the wrong combination of antioxidants, they could be
00:30:43
actively detrimental. They could become pro oxidants,
00:30:47
however. Anyway, the point is that's not
00:30:49
the whole story because there are various other ways in which
00:30:51
you can manipulate this whole system to, you know, to to do
00:30:57
less damage or to do damage more slowly.
00:31:00
One way is people have been looking at ways to slow down the
00:31:04
rate at which mitochondria create free radicals in the 1st
00:31:07
place to make make mitochondria run more cleanly, to put it to
00:31:11
an engine analogy. And there are various tricks to
00:31:14
do that which work to some extent.
00:31:17
There's another trick which is to make the molecules around the
00:31:21
mitochondria, the the rest of the molecules in the cell less
00:31:24
susceptible to being oxidized by free to being damaged by free
00:31:29
radicals in the 1st place. And that also has some
00:31:31
interesting ideas around it, including one involving
00:31:34
deuterium, heavy hydrogen that we're actually pursuing in our
00:31:38
in our next experiment. Interesting.
00:31:41
You know, a lot of people, obviously it's their lifestyles.
00:31:44
We always talk about stress causing it.
00:31:46
We talk about smoking and alcohol.
00:31:49
Do you feel like you know of some of those?
00:31:51
Because I've seen some reports on nicotine that it maybe isn't
00:31:54
the enemy that people have described it as the other
00:31:56
chemicals that are in cigarettes.
00:31:58
What's out there right now? What do you think's accurate
00:32:01
when people hear about, oh, well, if you do that, it causes
00:32:04
inflammation. If you do this, you're causing
00:32:06
free radicals. And if you get too much sun,
00:32:08
this isn't good for you. What do you think the biggest
00:32:10
enemies are right now in people's lifestyles for aging?
00:32:14
There are really 2 mantras that answer that question in the most
00:32:18
general way that I can. 1 is different people are different.
00:32:23
Different people have somewhat different, you know, details of
00:32:27
their metabolism, different weak links in their metabolism.
00:32:31
And that that translates into those people needing different
00:32:37
supplements, different lifestyles, different.
00:32:39
Now, some people are just more prone to putting on weight than
00:32:41
others, for example. Yeah, I'm one of those
00:32:43
repulsively lucky people. I can eat and drink exactly what
00:32:46
I like and nothing happens, and I don't even need to do any
00:32:48
exercise. And we hate you for that.
00:32:49
Yeah, I hate you, doc. Yeah, quite right.
00:32:52
Wait a minute, Italian. We look at food and we gain
00:32:55
weight. Wait a minute.
00:32:56
So since you made that glorious statement.
00:32:59
I do want to finish. I do want to finish.
00:33:02
The other critical thing to remember is that even if you
00:33:05
figure out what's right for you, what's best for you, the amount
00:33:10
of benefit you're going to get relative to simply living the
00:33:13
way your mother told you to and just, you know, not smoking and
00:33:16
not getting seriously overweight and eating a reasonably varied
00:33:18
diet, you know, is very short, very small indeed.
00:33:22
You know, you'll get a year if you're lucky, really.
00:33:24
So, yeah. So we just can't do it yet.
00:33:27
That's why that's what drives my research.
00:33:30
My research is all about, you know, breaking that glass
00:33:33
ceiling earned using more high tech things, cell therapies and
00:33:37
gene therapies and so on to get far more than what we can do
00:33:42
with anything that we have today.
00:33:45
Hold up Lance, I got to ask a question since we're not so
00:33:49
blessed like you and we, you know, if we pasta, Lance might
00:33:53
put on a few pounds. What can what can we do?
00:33:55
Is there any you got any secrets?
00:33:58
Well, no, like I said, I mean, first of all, for myself, I
00:34:01
don't need to do anything. Secondly, for anyone who does
00:34:04
have trouble controlling their weight, you know, I'm, I'm, I'm
00:34:07
sorry, but I mean, things are better now, you know, Of course,
00:34:09
the GOP one, agonists like Zenpeg that have come along
00:34:12
recently are an absolute godsend, but they're not a
00:34:15
godsend for everybody. Some people have really pretty
00:34:17
bad negative reactions to them. They just can't take them, but a
00:34:21
lot of people can. A lot of people are benefiting a
00:34:24
lot from these things and that's a huge thing.
00:34:27
It actually comes back to what I was saying earlier about
00:34:29
medicines and the big Pharma and so on.
00:34:32
This is a real godsend because Ozempic is a preventative
00:34:37
medicine. It postpones the age at which
00:34:39
you're going to get diabetes, and that's really important.
00:34:42
But that's not why people take it.
00:34:44
The public are skeptical about preventative medicines, but this
00:34:48
one got in by the side door because in addition to being
00:34:52
preventative for diabetes, it's also a treatment for something
00:34:56
that's not called a disease, but that people really don't like to
00:34:59
have, namely obesity, right? So, so it's, so it's, it's a,
00:35:05
it's a huge godsend, but for, you know, a rather complicated
00:35:09
reason. Yeah, it's interesting.
00:35:12
Obviously, Ozempic's kind of been a big thing in the news the
00:35:14
last couple of years. Lots of it out there.
00:35:17
Of course, hormone replacements, another topic that comes up a
00:35:19
lot. Let's go into your book.
00:35:21
Before I talk about that, though, let's talk about ending
00:35:23
aging. Well, you had one before that
00:35:25
you had advancing conversations. I did not read this one,
00:35:28
Advocate for an indefinite human lifespan, which I think is
00:35:31
interesting. You had lots of artists and
00:35:33
authors and philosophers and economists, scientists and
00:35:35
activists who work was aimed at the future of progress.
00:35:38
It's pretty interesting. And this is where you really
00:35:40
start to talk about the Cens Research Foundation at that time
00:35:43
that you were involved with. Maybe give us a little detail on
00:35:45
that and kind of why you took that project kind of because it
00:35:48
looks like you wanted some, you really wanted to bring in a
00:35:50
diverse group to kind of look over everything that you guys
00:35:53
have been working on it seemed like.
00:35:55
That one book Advancing Conversation, I think I just had
00:35:58
one chapter in there right there definitely wasn't something that
00:36:00
I wrote. But coming back to the rest of
00:36:04
your question, yeah, I mean, basically as soon as I
00:36:09
established, you know, with good confidence that I was onto
00:36:12
something with this whole damage repair approach, I knew that it
00:36:16
was up to me to bring people together to actually do the
00:36:20
right research. And that involved getting the
00:36:22
scientists interested. And it also involves getting the
00:36:24
money for the scientists to do what they're what I've got them
00:36:27
interested in. Turned out the first of those
00:36:29
was really easy scientists. I used to actually have a slide
00:36:33
in my talks that would be entitled Scientists will do
00:36:36
anything interesting for food I. Didn't see that one.
00:36:41
It's it's more or less true. So I never had any trouble
00:36:44
persuading people that they would do what I wanted them to
00:36:49
do, just as long as I could pay them.
00:36:51
So my job was to bring in the money.
00:36:54
And after I spoke at Ted in 2006 and started speaking at other
00:36:58
high profile places, you know, I decided to meet, you know, with
00:37:02
people who were willing to fund the philanthropic venture.
00:37:05
Philanthropy is an enormously important part of all of this
00:37:09
because there all I've got to do is get wealthy people to trust
00:37:12
me, OK? I don't have to do anything
00:37:15
else. Whereas the other sources of
00:37:17
money that are available, you've basically got industry or you've
00:37:20
got academia in the industry. They don't.
00:37:24
The people who are actually writing the checks don't give a
00:37:26
flying fuck about whether I'm right.
00:37:29
They just care whether going to make money and no.
00:37:32
Surprise there. And in particular, anyone who
00:37:34
wants to make money wants to make it tomorrow.
00:37:37
So there is an enormous pressure towards short termism, towards
00:37:41
the low hanging fruit at the expense of, you know, things
00:37:45
that are just as vital for this divide and conquer damage repair
00:37:48
approach. But just in whatever even
00:37:52
harder. Now it turns out that academia
00:37:54
is every bit as short term as industry or a bit for a
00:37:57
completely different reason there.
00:37:59
The issue is there's never enough money being provided by
00:38:02
the government or, you know, or institute or whatever to, to,
00:38:09
to, to support the research. So the researchers are competing
00:38:12
against each other. And the way that that
00:38:15
competition is always decided is by this horrible repulsive
00:38:19
mechanism called peer review, where essentially some of the
00:38:22
experts in a given field are sequestered, you know, are are
00:38:27
basically brought together to evaluate the relative quality
00:38:32
of, you know, ideas for research that are being put forward by
00:38:36
the others. Why is that so repulsive?
00:38:39
Because there's never enough money.
00:38:41
And so the best one in the world, these people are coming
00:38:44
in and they have to, they're just looking for reasons to say
00:38:47
no. They're looking for stupid
00:38:50
reasons to choose one particular grant application over another.
00:38:56
For example, they're saying, OK, you know, this person's got more
00:38:59
track record or whatever. It's completely in fact, it's
00:39:05
not even that. It's not like the track record
00:39:07
is defined in a stupid way. It's defined by how many times
00:39:11
papers that the person has published have been referenced
00:39:15
by other scientists. And and worse than that, it's
00:39:20
quick, you know, like it doesn't matter how important somebody's
00:39:23
work was that they did 10 years ago.
00:39:25
It only matters what they did like two years ago.
00:39:28
You know, it's like it's. Yeah, it's really, it sounds
00:39:31
really arbitrary and it's tough for somebody that's obviously
00:39:33
being innovative, assuming that there is no track record and
00:39:37
it's obviously a a, a a topic. Well, listen, we're going to
00:39:40
hold you there for a minute. And when we come back, we're
00:39:41
going to be talking about his ground breaking book that
00:39:44
represents obviously a road map for ending the aging process.
00:39:48
You know, obviously through radical life extension
00:39:50
techniques. You're going to want to hear
00:39:52
this when we come back. Doctor Aubrey de Grey, The Big
00:39:55
Ming Show, George Ballantine, Lance Miliacho.
00:39:57
Stay tuned. There's a chance for your Lance.
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Thank you all. So Dak when, when when it comes
00:45:10
to like anti aging. So I get the part like you can
00:45:14
look on the outside, you know, the ageing, you know, you look
00:45:18
whatever younger. Does it also on the inside of
00:45:20
your organs too? Or reverse that in a sense?
00:45:23
Oh for sure, for sure. The outside, you know how you
00:45:26
look is overwhelmingly a side effect of the inside.
00:45:30
You know the the skin is a constantly regenerating tissue.
00:45:34
Remember, we lose skin, we have stem cells at the base of the
00:45:37
skin that are constantly making new skin cells.
00:45:40
And that means that the health of the skin, how it looks is
00:45:45
substantially determined by what's going on in the
00:45:49
bloodstream that is feeding those those stem cells.
00:45:53
And of course, the bloodstream is also feeding everything else.
00:45:56
It's a kind of, you know, information highway between
00:45:59
everything. But the more below that level of
00:46:02
the skin, there's another level called the dermis, which is
00:46:06
largely responsible for the elasticity of the skin.
00:46:09
So when we get wrinkles, which is obviously one aspect of the
00:46:13
superficial ageing of the skin, that's because the dermis is
00:46:17
suffering damage to the lattice of proteins called the
00:46:21
extracellular matrix that holds those cells together and which
00:46:25
is supposed to be elastic and becomes less elastic as a result
00:46:28
of oxidative damage. So I'm feeling pretty good right
00:46:33
now 'cause I'm looking at my skin, I got good skin, so the
00:46:35
insides work. Why?
00:46:37
What are you laughing? I'm being serious.
00:46:38
It's good genetics. So, you know, at the end of the
00:46:40
day, I think that's part of it. But yeah, you live pretty well.
00:46:42
You haven't had a drink and you don't smoke.
00:46:44
I mean, really. Take care to smoke, I Take care
00:46:46
of myself, I. Had a drink in about 11 years
00:46:48
Doc He's been clean and sober for about 11.
00:46:50
I I myself don't drink very much and I don't smoke and.
00:46:53
Everything why you look so bad bro what's up?
00:46:55
Hey, you know this was miles in the sun here if I'm looking at
00:46:57
aged. I always been in the sun a lot
00:46:59
more than you probably, but it's OK.
00:47:02
I don't know, maybe. I still love you, answer my
00:47:04
brother from another mother, but the same father, so it's all
00:47:06
good. All right, so Doc, you made a,
00:47:09
you had a quote that says there is no ticking time bomb.
00:47:11
I mentioned it backstage, just the accumulation of damage.
00:47:16
And I want you to go and maybe share with the audience, kind of
00:47:18
take us through the process of, you know, what are the, the big
00:47:21
ones, You know, where's the big damage and how's it caused?
00:47:25
Yeah, sure. OK.
00:47:25
So first of all, let me amplify on that quite a little bit
00:47:30
because here's what I'm trying to disabuse people of.
00:47:36
We see that through, you know, 20 or 30 years of adulthood,
00:47:42
nothing goes wrong. I mean, yes, a 50 year old can't
00:47:45
run as fast as a 20 year old necessarily.
00:47:48
Not usually right, but nearly as fast.
00:47:50
You know, you know, in terms of normal day-to-day activities,
00:47:54
whether mental or physical, there's not a lot of difference
00:47:57
between a 20 year old and a 50 year old.
00:48:01
And then after that, things start to go wrong.
00:48:03
And when they do start to go wrong, they go wrong at a
00:48:05
progressive, you know, an accelerating rate.
00:48:07
So on the face of it, it looks like, you know, the body's got
00:48:12
some, you know, timer in there, you know, that says, you know,
00:48:16
that the body can just get on and do what it likes for a
00:48:18
while. And then eventually, you know,
00:48:22
there's something that times up, so to speak, and, and the body
00:48:25
kind of, you know, a whistle gets blown and, and everything
00:48:28
starts to go to hell in a handbasket.
00:48:31
And I want to make sure that people understand that that's
00:48:34
not the case. That's why I often use analogies
00:48:38
where simple man made machines like cars or aeroplanes or
00:48:41
whatever. You know, a car doesn't have one
00:48:44
of them either, right? It's just got a warranty period
00:48:47
that arises from how it was built, from the quality of the
00:48:52
components, from the, you know, the which, what type of metal
00:48:54
they saw that thing was made out of themselves.
00:48:57
And it's exactly the same for the human body.
00:48:59
The quality of how how we're built, how well we are capable
00:49:04
of holding ourselves together is something that's built into our
00:49:09
genetics. But there's nothing built in
00:49:12
that says, OK, now stop trying, so to speak.
00:49:16
Now you know, you know, just go downhill on purpose.
00:49:19
That's something that people really need to understand.
00:49:21
And it's helpful because it's what underpins the whole idea
00:49:25
that all we need to do in order to keep ourselves healthy for a
00:49:29
lot longer, maybe indefinitely longer, is preventative
00:49:33
maintenance. Just as long as the preventative
00:49:35
maintenance is comprehensive enough.
00:49:38
Because all of us do preventative maintenance on our
00:49:40
cars, but nearly all of us only do the minimum amount of
00:49:44
preventative maintenance that the law requires.
00:49:46
Because we're perfectly happy with the idea that eventually
00:49:48
the car will fall apart and we'll get a new one.
00:49:50
Right. You can't do that with the with
00:49:52
your own body. You know, you can't get a new
00:49:54
one, not yet anyway. So we've got to do proper
00:49:58
preventative maintenance. And that of course is inspired
00:50:01
by what we can do with cars, with vintage cars.
00:50:04
There are cars around right now that are, that were built 100
00:50:08
years ago or more. And if you ask how come, how,
00:50:12
how did they get that way? The answer is not because they
00:50:16
were built for the last 100 years.
00:50:17
They were built for the last 10 or 15 years at the outside, but
00:50:21
just by periodic, comprehensive preventative maintenance, here
00:50:25
they are. And of course, they'll be here
00:50:27
in another 100 years. Yeah, it's, it's interesting and
00:50:31
I think people are always wondering what does that, you
00:50:33
know, to prevent aging. They're obviously looking for
00:50:35
that fix. And you're right, people
00:50:37
obviously want the quick fix. They don't want to do what's
00:50:40
necessary. You, you mentioned that
00:50:42
preventing aging is a really complex issue when it comes to
00:50:45
maintenance. I guess the regimen of that is
00:50:48
what's, how far along are you with that?
00:50:50
Because you talk about something that I knew nothing about AG, ES
00:50:54
and zombie cells and that accumulation of waste that
00:50:58
builds up. Have you, Have you.
00:51:00
So let's, let's make sure the audience understands that first
00:51:02
'cause you and I are talking straight out of the book.
00:51:04
So they may not even understand unless they've read the book.
00:51:06
So let's talk about that first. But then have you found
00:51:09
processes to help clear that out of your system to shut down the
00:51:12
zombie cells and actually at the same time get rid of that
00:51:14
intracellular an extracellular waste?
00:51:17
So, sure. I mean, everything that I've
00:51:19
been working on over all these years has been precisely to
00:51:22
develop ways to eliminate these various types of damage that I
00:51:26
enumerated back in the year 2000.
00:51:30
Now I want to start one thing. First of all, that the number of
00:51:34
types of damage that we need to repair in a machine that's so
00:51:37
insanely complicated as a human body is very large.
00:51:41
And So what I did in the year 2000 was simply to classify
00:51:45
those many types of damage into 7 categories.
00:51:49
The first question that I need to explain that for is why is
00:51:53
that classification useful? You know, how did that change
00:51:55
anything? The answer is because for each
00:51:57
of those seven categories, I can actually describe a generic
00:52:02
approach to fixing it, something that says, OK, you know,
00:52:07
different examples within a category may need slightly
00:52:10
different approaches, but they'll all have a lot in
00:52:12
common. And so as we get one or two of
00:52:14
them working, it will be much quicker to get the next one
00:52:16
working and the one after that. That was the real, the real
00:52:20
inspiration. All right, so let's look at what
00:52:23
the the examples that you just mentioned.
00:52:26
Zombie cells I wouldn't call senescent cells in the technical
00:52:29
community. So actually I haven't done much
00:52:32
work on them. I've done some, but basically
00:52:35
that's one that I've been able to leave to other people simply
00:52:38
because it got going, you know, pretty quickly.
00:52:41
Maybe 2025 years ago, people figured out good, good ideas for
00:52:45
how to move it forward. But yeah, it had moved forward
00:52:48
very well. We now have ways to eliminate
00:52:51
such cells pretty selectively, you know, to give drugs to
00:52:55
animals that will make those cells die without making too
00:53:00
many other cells die. And and that's extremely
00:53:04
helpful. In fact, it's been shown in
00:53:05
various experiments to actually extend life.
00:53:08
So we're very, we're very much focused on that as one of the
00:53:11
things we want to do the elimination of waste products
00:53:15
and especially the elimination of these things called AG ES
00:53:18
that you mentioned, which is a convenient acronym for something
00:53:21
extremely complicated and. Can you share with the audience
00:53:23
talk? I don't want to step on you
00:53:24
there, but can you share with them?
00:53:25
Because I hate to say this, I've eaten browned and blackened meat
00:53:28
many times, not realizing that I was probably doing myself some
00:53:31
real harm in eating meat like that.
00:53:33
But go ahead. All right.
00:53:36
So remember you're talking about 3 of my categories
00:53:39
simultaneously there. So let me just focus on the one
00:53:41
you're focusing on, which is 80. The the thing there that gives
00:53:45
the problem is something called stiffening, lots of elasticity.
00:53:50
And this happens because of chemical reactions that that
00:53:53
occurred between proteins in the outside of the cell, what's
00:53:57
called the extracellular matrix and sugar that's in the
00:54:01
circulation, just that's wandering around.
00:54:04
Sometimes those reactions cause new chemical bonds to form
00:54:07
between proteins that are not supposed to be joined together.
00:54:10
And that that causes the, the stiffening I'm talking about.
00:54:14
So we want to break those things.
00:54:17
Now. Don't worry too much about
00:54:19
eating stuff with that's brown. You're, you're quite right that
00:54:23
at the chemical level, what you're eating has a bunch of
00:54:25
those, those cross links in it, those, those links between
00:54:29
protein. But those cross-linked proteins
00:54:32
don't get into cells. They don't get into the, well,
00:54:35
they probably don't get into the body at all really.
00:54:37
Maybe it's to the extent that they get into the bloodstream
00:54:39
even a little bit. It doesn't matter because they
00:54:42
won't get into cells hardly at all.
00:54:44
And if they do get into cells, they won't be incorporated into
00:54:47
new proteins. So one way or another, my view,
00:54:52
and you know, I've been looking at this for a while because
00:54:54
people have been espousing the contrary view, my view, my sperm
00:55:01
view is that this is the red herring.
00:55:03
But we don't need to worry about any kind of toxicity around.
00:55:10
Yeah. So.
00:55:13
So yeah, basically, you know, each of these types of damage
00:55:15
needs it's own approach. So look, if we look at that
00:55:19
particular one, we do need to get rid of these cross links,
00:55:22
just not the ones in the diet. We just need to get rid of the
00:55:24
ones that spontaneously arise in the body.
00:55:27
And I was able to support a project, one of my, my previous
00:55:32
foundation was able to support for several years, an important
00:55:35
project at Yale University, which led to some real
00:55:38
breakthroughs publishing science magazine.
00:55:41
And that led to the spinning out of a company which is now
00:55:43
pushing that forward quite effectively.
00:55:46
It's, you know, but it's really tough research.
00:55:48
Now there's just this one company.
00:55:49
I don't know of any other company looking at this problem
00:55:52
as you know, thoroughly as this one is.
00:55:55
And you know, we definitely need a dozen such companies.
00:55:57
They don't exist because there's not enough money in buying this
00:56:00
this field at this point. Yeah, it's and I and I get that,
00:56:06
you know, when I, when I look at research, obviously this is,
00:56:09
this seems to be on the cutting edge.
00:56:10
Of course they spend, there are companies that spend exorbitant
00:56:14
amounts of money on researching the possibility of creating a
00:56:17
cream that will make you look younger.
00:56:20
But of course that's from the outside and not the inside out.
00:56:23
And I don't know that that solves anything, you know.
00:56:26
So we talked about, you've got 7 topics here and you talk about
00:56:29
cell loss and atrophy, which obviously I don't know what the
00:56:33
solution. One of the things for atrophy,
00:56:35
we hear a lot of people talking about hormone replacement.
00:56:37
Has that had any positive effect in those areas?
00:56:39
Growth hormone? Testosterone.
00:56:42
So there are various ways to address cell loss in accuracy.
00:56:46
The one that I talked about the most back 20 odd years ago was
00:56:50
stem cell therapy. And that's definitely the way to
00:56:53
go in certain cases. So one very important case of
00:56:57
this is Parkinson's disease, which is caused by the loss of a
00:57:01
particular type of brain cells, the particular neuron called a
00:57:04
dopaminergic neuron. Dopaminergic neurons are really
00:57:09
hard work horses. They, they, they, they, they do
00:57:13
stuff that's that's energetically very demanding.
00:57:17
Basically they make the chemical called dopamine, of course, and
00:57:22
that result, the result is they die a lot more frequently than
00:57:25
your average neuron does, and they're not replaced.
00:57:29
So all of us by our age have lost maybe 2 thirds, 3/4 of
00:57:33
that's right, about one third, one quarter of the of the
00:57:38
dopaminergic neurons that we had in young adulthood.
00:57:42
That's fine though. We don't have Parkinson's
00:57:44
disease because the system is set up to tolerate that amount
00:57:46
of loss. Well, it's not set up to
00:57:48
tolerate losing 2/3 or three courses.
00:57:50
And some people lose them faster and they're by the time they're
00:57:54
in their old age, they have lost that number.
00:57:56
And those are the people who get Parkinson's.
00:57:59
All right. So what you do to fix this is
00:58:00
very straightforward. You just put stem cells back
00:58:02
into the relevant part of the brain that have been programmed
00:58:07
in the right way to divide and create the replacements for the
00:58:13
cells that the body's not replacing on it's own.
00:58:15
And it works. It works spectacularly well.
00:58:18
Now can I stop? You does that work for dementia,
00:58:21
Alzheimer's also or just Parkinson's?
00:58:23
Not exactly, but I'll come to that in a moment.
00:58:25
Oh, great. OK.
00:58:26
Parkinson's. This was tried 30 years ago, but
00:58:30
then it only occasionally worked because people didn't really
00:58:32
know what to do with preparing the stem cells into the right
00:58:36
state before they injected them. Now we know all about that, and
00:58:41
there's half a dozen clinical trials going on right now doing
00:58:44
this, and everyone's very optimistic this will be a real
00:58:46
cure for Parkinson's. Because back then, 30 years ago,
00:58:49
when it did work, on those rare occasions when it did work, it
00:58:52
worked spectacularly well. People were completely cured for
00:58:55
like 10 or 15 years, all right? And that was just one injection.
00:59:01
All right, So you asked an excellent question, whether the
00:59:05
same kind of thing could work for Alzheimer's disease.
00:59:08
It's a lot harder for Alzheimer's disease because the
00:59:13
cells that die in Alzheimer's disease are spread across most
00:59:17
of the brain. There are certain places that
00:59:19
are more affected than others, but a lot of places that are
00:59:22
affected. Whereas in Parkinson's, it's
00:59:23
just one teeny tiny part of the brain called the substantial
00:59:26
nigra. And that matters because when
00:59:29
you inject cells into the brain, they don't move around.
00:59:33
If you inject cells into the bloodstream, they of course move
00:59:36
all over the all over body, but the, the, the equivalent of the
00:59:40
bloodstream in the brain is called the cerebrospinal fluid
00:59:44
and it's sticky, it's viscous, and so things don't move around.
00:59:49
But we founded a group, I founded a group for several
00:59:52
years looking at a really elegant and ingenious solution
00:59:56
to that that essentially involves genetically engineering
00:59:58
these dopaminergic precursors, as they're called, so they know
01:00:02
how to swim, so they know how to actually distribute themselves
01:00:06
around the body. You don't use, but for
01:00:09
Alzheimer's, you don't use dopaminergic precursors, you use
01:00:12
cholinergic or Gabaergic or whatever.
01:00:14
But the point is you, you can make them swim so you can
01:00:17
overcome this problem. And that's still very much a
01:00:20
research area, but it's, it's promising then.
01:00:23
So you were asking more generally about about cell loss
01:00:27
and cell atrophy and you were asking about growth hormones and
01:00:30
such like. So they're, so there's been some
01:00:34
very exciting work on one really one other really important area
01:00:38
of cell loss in ageing, which is called thymic involution, where
01:00:42
this organ called the thymus loses cells and the result is
01:00:46
eventually the immune system doesn't work so well.
01:00:49
It's been found that you can use growth hormone along with a
01:00:53
couple of other things that effectively address the side
01:00:56
effects of growth hormone and you can get a rejuvenation of
01:01:00
this thing called the thymus, this organ near the heart.
01:01:04
And it looks like it does actually restore immune function
01:01:06
to some significant extent early stage, but at least it's being
01:01:10
done. It's being done in human beings.
01:01:11
You know, it's not just in in, in mice or anything.
01:01:14
So it's very exciting. And then the third thing that I
01:01:17
want to mention, the last thing in this area is partial
01:01:21
reprogramming. So what the hell is that?
01:01:23
Well, about 18 years ago, a group in Japan figured out a way
01:01:29
to make normal cells from you and me into the most primitive
01:01:34
cells we know about, cells called embryonic stem cells,
01:01:37
like into into things that behave almost exactly like
01:01:40
embryonic stem cells. And this was, this is very
01:01:42
useful because if you've got those cells, you can make other
01:01:45
cells from them really well. Now thing is though, you don't
01:01:50
want to put those cells into the body because they won't know
01:01:53
what to do. They're too primitive.
01:01:55
They know what to do in the early embryo.
01:01:57
They don't want to know what to do in you and me.
01:01:59
So what you do is you want to make them into other cells
01:02:02
before you do that. Now, why is that interesting?
01:02:05
Because you might be able to use the same factors, the same
01:02:08
things that are used in a Petri dish to create those cells.
01:02:12
You might be able to use them in the body, but you use them in a
01:02:16
very delicate way. You only just, you know, you
01:02:18
know, do it transiently for a day or two or something like
01:02:22
that. And that might slightly push
01:02:26
cells back into that direction, but only slightly.
01:02:28
And that might be useful. It might make them more
01:02:31
regenerative. People have been trying that,
01:02:33
and they've got very promising results.
01:02:35
So that's a very live topic that Jeff Bezos put $3 billion into a
01:02:38
company that was mostly focused on that.
01:02:40
Yeah, it's interesting. Obviously one of the side
01:02:42
effects of growth hormone is acromeglia, so I don't know if
01:02:45
that's one of the side effects you were talking about.
01:02:47
People talk about Neanderthalism when you use too much.
01:02:50
And of course hormone replacement for the anti aging
01:02:53
clinics, that's part of the obviously the regimen that they
01:02:57
put you on. They do a bunch of blood screens
01:02:59
and the rest of it. And then some people think it's
01:03:01
because of inflammation that obviously your hormone levels
01:03:04
and of course aging in your body determines that you don't need
01:03:07
as many hormones and fight or flight response is different as
01:03:10
you get older. So it's a lot more complicated
01:03:12
than that. So first of all, both hormone
01:03:15
itself, it's pretty clear that you don't want to have high
01:03:19
levels of growth hormone when you're growing during
01:03:22
development. It's good to have low levels
01:03:24
when you're growing, either low levels of growth hormone itself
01:03:27
or of other molecules that are important for the activity of
01:03:31
growth hormone. However, after you're growing,
01:03:34
when you're when, when you're an adult, the situation is very
01:03:38
different. Secondly, it's very important to
01:03:41
recognise that we're not talking about the normal use of growth
01:03:46
hormone that made growth hormone famous, namely improving muscle,
01:03:51
because it turns out it's not very good with muscle.
01:03:54
There are other things you can do.
01:03:55
For example, there's a very interesting project called
01:03:57
follistatin which is good and muscle, but growth horn yes, you
01:04:02
get more let. Me ask, you tell me filostatin
01:04:04
was used for myostatin inhibition, wasn't wasn't that
01:04:07
kind of the idea? That you actually statin is yes,
01:04:09
yeah for myostatin, for myo is Greek for muscle.
01:04:14
Again, statin is Greek for inhibition.
01:04:16
So basically the more myostatin you have, the less muscle you
01:04:19
have. Folostatin antagonizers inhibits
01:04:22
myostatin. So you're acting kind of one
01:04:24
step removed, but you're actually causing more muscle to
01:04:27
happen. If you have more folostatin, and
01:04:29
it often works in biology, that being one step removed is more
01:04:34
is a good way of avoiding side effects a better way than if you
01:04:37
do things in the more route one approach for various reasons.
01:04:42
Hold it there for a second Doc. Hey George, look up myostatin
01:04:44
inhibition on the the Google. You'll find some dogs, some
01:04:49
greyhound looking dogs. You'll also find some bulls that
01:04:52
are missing the actual gene that is out there.
01:04:55
Now, some people have said they can use CRISPR technology and
01:04:58
that obviously that would allow you to develop muscle really
01:05:01
with absolutely no action, not even going to the gym.
01:05:04
Is there any truth in that that some people are using CRISPR
01:05:06
technology to modify their genome?
01:05:09
Yes, it's certainly, well, actually not CRISPR per SE.
01:05:12
You don't use CRISPR to insert a new gene, not these days anyway.
01:05:16
You do CRISPR to modify genes that are already there.
01:05:19
But you can certainly use gene therapy to insert a new copy of
01:05:24
an extra copy of forestatin. And various people, including my
01:05:28
great friend Liz Parrish have done that.
01:05:32
So, you know, it's it's an exciting possibility.
01:05:35
And as I say, it seems to work better for muscle with growth
01:05:37
hormone. But when we come back to the
01:05:39
thymus, which is what I was talking about earlier, the
01:05:42
immune system there, it seems that growth hormone itself has
01:05:45
genuine benefits and as I say, side effects.
01:05:50
So the people who were working on this and giving this to
01:05:52
people were not just giving growth hormone itself, they were
01:05:56
also giving a couple of other things, DHEA and metformin to to
01:06:01
to limit those side effects. You know, there's been a lot of
01:06:05
discussions about different peptides and peptide
01:06:07
technologies changed. What do you see?
01:06:10
Do you see anything on the horizon on that that seems to be
01:06:12
maybe working on some of the things that you because you
01:06:15
always talk about engineering solutions versus versus medical
01:06:19
solutions. So I don't know if that falls
01:06:21
into that when you start using peptides or is that really a
01:06:23
medical solution? First of all, let me correct
01:06:29
your terminology there. And I don't really say that
01:06:32
engineering solutions are not medical solutions.
01:06:35
You know, your, your audience may, may get the impression that
01:06:40
I'm thinking there's medicine and then there's like
01:06:41
cybernetics. I'm not talking about that kind
01:06:43
of. So there's definitely, I think
01:06:47
engineering means just thinking like an engineer.
01:06:49
You know, I came up with this whole idea of damage repair,
01:06:52
this divide and conquer approach and it was, it took me 6 or 8
01:06:57
years really to get my colleagues in the community who
01:07:01
are very, very knowledgeable, of course, to understand that what
01:07:05
I was saying with even scientific, let alone plausible.
01:07:08
You know, it was, it was tough because it was such a paradigm
01:07:11
share just because I was thinking like an engineer.
01:07:14
So it's definitely medical. But yeah, I mean peptides, OK,
01:07:20
peptides have that. They're a controversial area and
01:07:24
they're controversial for a good reason, namely that the main
01:07:28
groups that were promoting and, you know, reporting really
01:07:33
promising results with with these peptides were from Russia
01:07:38
and were, well, the Soviet Union as it was back then, and were
01:07:43
not reporting things in what Westerners would consider
01:07:47
rigorous ways. And there was a a conspicuous
01:07:53
lack of corroboration of their results by other scientists from
01:07:57
other labs. So there is still a lot of
01:08:01
skepticism around the efficacy of peptides.
01:08:06
Interesting. Hey George, I threw one of the
01:08:08
dogs in Notion. I just wanted the audience to
01:08:10
see because obviously what happens when you inhibit
01:08:13
myostatin, you actually end up, it seems like with almost double
01:08:16
muscle. There's bulls that actually are
01:08:19
missing that gene and others. I don't know if it's been
01:08:21
scientifically, you know, if that's what they did, if it was
01:08:24
science, or if the animals were born that way.
01:08:26
It seems like most of the stuff I've read, the animals were born
01:08:28
that way. Have people successfully removed
01:08:30
the myostatin inhibition from their body?
01:08:33
So first of all, you're right, the the gene was a spontaneous
01:08:37
mutation that knocks out myostatic.
01:08:40
As far as I'm aware, nobody has tried doing that or even, you
01:08:45
know, reducing the expression of myostatin simply because
01:08:49
increasing the expression of filostatin is appears to be a
01:08:53
safer way to go about things. Essentially what you're doing
01:08:57
with these, you know, interventions that are one step
01:09:02
removed. If you're giving the body more
01:09:05
of a chance to figure out how to minimize side effects, even side
01:09:09
effects that you don't know about yet, You're essentially,
01:09:12
you know, you're, you're, you're giving, you're, you're letting
01:09:16
the body's inherent self protection machinery be more
01:09:20
influential in, you know, optimizing the situation.
01:09:24
That's the way I look at it. I got you.
01:09:27
Well, obviously we've seen lots of crazy sports technology
01:09:30
coming out of the Eastern Bloc nations that everybody's always
01:09:33
trying to obviously improve their life performance, trying
01:09:36
to find something that can't be tested for.
01:09:38
So and and some of that falls over into anti aging because
01:09:40
they're obviously trying to extend their longevity in
01:09:43
sports. It's a lot of it.
01:09:45
You know, you, we mentioned a little while ago we were talking
01:09:48
about that maybe the, there's, there's an issue on one side of
01:09:51
this where people, you know, may have a moral issue with it or
01:09:55
may have a, you know, obviously population issue.
01:09:59
You know, do you feel like you've dealt with a lot of that
01:10:02
where obviously some people don't want to extend the
01:10:05
lifespan? Because obviously there's a lot
01:10:06
of discussions about all these different, you know, World
01:10:11
Economic Forum type agencies are obviously globalists, that a lot
01:10:15
of people have this belief that they want to reduce the global
01:10:17
population, they want to increase.
01:10:19
And of course, if you were successful in in increasing
01:10:22
people's lifespan three to four, 5-6 hundred years, that
01:10:25
obviously goes against what it seems like people just right
01:10:28
now, people think that the plan is overpopulated.
01:10:31
What are your thoughts on that? Have you had a lot of
01:10:32
interaction with people that have said that to you?
01:10:35
So I haven't had it when people are asking me questions of
01:10:38
counting the number of times that they say the word
01:10:40
obviously, and you say it five times.
01:10:42
That's not counting the time that you said, of course.
01:10:43
And the reason I, the reason I do that is because it's a, it's
01:10:49
a pretty, it's a pretty reliable red flag for things that are
01:10:53
remotely obvious. So first of all, the the idea
01:11:01
that there would be some kind of overpopulation consequence of
01:11:05
aging under control is probably the single most common concern
01:11:10
that people raise. But it is one of many concerns
01:11:14
that people just like, you know, it's just an embarrassment that
01:11:19
people raise them because they are so trivial to rebut.
01:11:23
And, yeah, people don't want to listen to the rebuttal.
01:11:27
They want to believe that aging is some kind of blessing in
01:11:30
disguise. You know, in particular for
01:11:32
overpopulation. You just have to do the numbers.
01:11:34
You just have to say, well, OK, look, how many people do we
01:11:37
have? We have 8 billion people, right?
01:11:39
How many acres do we have on the planet of land?
01:11:41
Do we have on the planet? It's well over 8 billion, You
01:11:44
know, even if you don't count the places that are unpleasant
01:11:47
to live. So, so, you know, there's not a
01:11:50
shortage of space. The only problem is pollution.
01:11:53
Obviously we are making far too much carbon.
01:11:54
We're making far too much, you know, plastics that don't
01:11:58
degrade and so on. But hello, in case anybody had
01:12:01
forgotten, we are working on on technologies to fix that, which
01:12:04
will be completely out there way before there's any demographic
01:12:08
consequence of dealing with aging.
01:12:10
Even if we take a completely worst case scenario in terms of
01:12:16
women continue to have kids as the same rate as they are today,
01:12:19
which obviously we know from past history is not going to
01:12:21
happen anyway. So.
01:12:23
So that's nonsense. But yeah, I mean, you know,
01:12:27
there's all many of other things here that are nonsense.
01:12:31
The first one is this whole idea that the powers that be want us
01:12:35
to have fewer people on the planet.
01:12:36
Why would they want that? You know, I mean, perhaps
01:12:39
because they haven't realized, they've forgotten that we are
01:12:42
getting rid of, you know, there's a carbon capture
01:12:45
technology coming and so on. You know, the fact is at the
01:12:50
moment the issue is the global economy.
01:12:52
That's the actual issue. The people who are actually in
01:12:54
charge are, you know, the people who governments and heads of
01:12:59
state of the major economies and what they want is prosperity.
01:13:03
How are they going to get prosperity by no longer spending
01:13:07
all this an unbelievable amount of money keeping sick people
01:13:10
alive? How we do that we stop them
01:13:13
getting sick in the 1st place. Even in the early stages when
01:13:18
these first generation interventions are going to be
01:13:23
probably fairly expensive to administer.
01:13:26
So what? Because they'll still pay for
01:13:28
themselves. Why many made times over really
01:13:31
quickly right now I want to also point out since obviously from
01:13:36
my accent, everybody can tell that I am from that far off
01:13:38
place called the rest of the world where we don't, where we
01:13:41
pay for our health care in a different way.
01:13:44
You know, you know, it doesn't matter how you pay for it.
01:13:48
It doesn't matter. The point is, you know, whether
01:13:51
it's through subsidies or taxation or whatever, it's
01:13:54
trivial to distribute the increased prosperity prosperity
01:13:59
equitably, right? So that everybody who's old
01:14:01
enough to need such therapies gets them.
01:14:04
Everybody who's entitled to make money out of the therapies
01:14:06
because they've got the intellectual property gets it.
01:14:08
You know, it's just like it's, it's like it's completely
01:14:13
obvious. And, you know, so the question
01:14:16
we have to ask ourselves is why do people cling to the idea that
01:14:20
there are all these problems and that, you know, that aging is
01:14:23
some kind of blessing in disguise?
01:14:25
And the answer is very, very, very obvious.
01:14:28
It's simply that people are terrified of getting their hopes
01:14:30
up. People have been doing what I'm
01:14:32
doing today since the beginning of civilization.
01:14:35
They've been saying we are, we have the way to bring aging
01:14:38
under control, to have the fountain of you, right?
01:14:42
I'm not saying we have it yet. I'm saying, but I am saying
01:14:44
we're going to have it fairly soon with high probability,
01:14:46
right? So the point is, everyone before
01:14:51
me has been wrong, right? So why should people, you know,
01:14:55
not? I mean, I think it's justifiable
01:14:56
to hesitate to be, to be a little skeptical until there's
01:14:59
more evidence that I'm actually not wrong, right?
01:15:02
Yeah. I don't have a problem with
01:15:04
that. But the point is it does
01:15:06
underpin this unbelievably deep seated irrationality which comes
01:15:10
out everywhere. Look at the look at the science
01:15:13
fiction that's written. Look at all the movies.
01:15:14
This. Yeah, it's.
01:15:15
Incredible. This, this, this constant stream
01:15:17
of movies about a post aging world, right?
01:15:20
And that's all dystopic. They're all dystopic in one way
01:15:23
or another. And the reason is that sells.
01:15:26
And the reason it sells is because people want their, what
01:15:29
I often call the pro aging trance, to be entrenched.
01:15:35
Yeah, I get you. Well, let me ask you this.
01:15:37
What do you think? What scientific advancements do
01:15:39
you believe are the most urgent that they were going to be
01:15:42
prioritized? Is there a list of them that you
01:15:43
would say to achieve that meaningful life extension in the
01:15:47
next few decades? What has to happen now for that
01:15:49
to move forward? Though I have a rather perhaps
01:15:53
counterintuitive answer to that, I don't think that we need big
01:15:59
progress in human beings. We do need it, of course, as
01:16:02
soon as possible, but I don't think that's what we could be
01:16:05
looking at as our priority. Well, I think we should be
01:16:07
looking at rather counter intuitively, is big progress in
01:16:11
mice. Why the hell would I say that?
01:16:14
The answer is that that's what acknowledged experts care about.
01:16:20
So I'm an acknowledged expert, but I'm only one, OK?
01:16:24
And I am the only one who has the luxury of being able to to
01:16:27
tell it like it is because I lead a nonprofit that's funded
01:16:31
independently by philanthropy. Everybody else, either they work
01:16:34
in industry or they work in academia and they have to, you
01:16:37
know, kiss us all the time. So they can't say things that
01:16:44
can be characterized by others as irresponsible, right, However
01:16:50
much they're not irresponsible. So therefore, what has to happen
01:16:54
is enough progress in the laboratories around the world,
01:16:57
whether it's my laboratory or somebody else's, that the rest
01:17:02
of the expert community feel they have permission to say
01:17:06
publicly the kind of thing that I've been saying for 20 years,
01:17:09
That we're in striking distance of bringing aging under true
01:17:12
medical control. And thus that the time is now
01:17:16
when the world should be putting proper money, proper effort into
01:17:21
hastening that point and saving the most astronomical number of
01:17:25
lives. Literally, we're talking about
01:17:26
40 million lives a year, right? And of course, all the attendant
01:17:32
suffering that's that's associated with, you know,
01:17:35
getting old before you die. Now, how is that going to
01:17:39
happen? Answer is what at the moment we,
01:17:43
if we take mice of the thought that I was talking about
01:17:45
earlier, mice are in middle age, right?
01:17:48
What we do at Mice Foundation and we try to extend their
01:17:52
lives, which is extended by about 30 or 40%.
01:17:58
All right. Now, what does that mean?
01:18:00
What does that mean in actual numbers?
01:18:02
These mice on average live about 2 1/2 years.
01:18:05
And so we start when they're 1 1/2 years old, and the amount
01:18:09
that we can add to that is about four months, All right?
01:18:14
Now, if you ask what could we do 100 years ago, the answer was we
01:18:20
could already get four months. Is that fucking crazy or what
01:18:25
You know? Yeah, that is kind of crazy
01:18:27
actually. You could do it back then.
01:18:29
Right. And that underpins why we, my
01:18:34
colleagues are so hesitant to say, yeah, in the relatively
01:18:38
near future we're going to be able to do a lot better.
01:18:41
I believe we can do a lot better where the divide and conquer,
01:18:44
you know, combinatorial approach, throwing lots of
01:18:46
different damage repair treatments at Meister already
01:18:50
middle-aged before we do anything right.
01:18:52
And that's what we're doing at my foundation.
01:18:55
And I believe that when we get it right, which which I believe
01:18:58
won't take more than another couple of attempts, we will get
01:19:03
a full year of life extension. Now, that means three times the
01:19:08
effect size of what we can do so well, what we can do today,
01:19:12
right? That is the kind of dramatic
01:19:15
transcending of what people have done in the past that will give
01:19:19
my colleagues permission to stand alongside me and say,
01:19:23
listen, Mr. Trump, listen, all the.
01:19:26
Yeah, Mr. Mr. She and everyone around the world, you know, get
01:19:31
the fuck on with it. And it won't be just us saying
01:19:34
that. So the following day Oprah
01:19:36
Winfrey's going to be saying it, and then DeGeneres and all those
01:19:38
people, and the day after that, it will be impossible to get
01:19:42
elected, whoever you are, without having a manifesto
01:19:45
commitment to do it. So that is my focus.
01:19:50
So do you think, I mean, how close do you think you are to
01:19:52
reaching longevity escape velocity for a human that's a
01:19:55
mouse? When do you think it'll actually
01:19:57
be a reality for the human race? Are we on a 10 year timeline?
01:20:00
A 20 year timeline? What do you think?
01:20:02
So that is across the right question, but it comes down to
01:20:05
what I said about MICE. I think we have a 5050 chance of
01:20:09
going to that threshold of one year extension in mice within
01:20:12
three to four years from now, maybe even a couple of years if
01:20:15
we're lucky right now. The question then is assuming
01:20:20
that I'm right about the societal reaction to that, which
01:20:24
is these steps, you know, first of all, the experts start saying
01:20:27
different things, then Oprah Winfrey starts saying different
01:20:29
things, then the government start doing different things,
01:20:31
right? If that's all true, if that's
01:20:34
all true, which I think it's with, I think it's nailed on,
01:20:37
that's nailed on. Then I think we are looking at
01:20:43
about a decade from that point. So in other words, three or four
01:20:46
years from now to get to the mass and then another 10 years
01:20:49
to get to the humans. Now, of course, again, I'm, I'm
01:20:52
emphasizing as I always have to do, but this is all
01:20:54
probabilistic. There's all manner of unforeseen
01:20:56
obstacles that we might encounter because this is
01:20:58
pioneering technology. But who the hell cares?
01:21:01
I mean, I certainly think there's at least a 5% chance
01:21:03
that we won't get to any to, to, to, to, you know, longevity to
01:21:07
the theatre larity for 100 years.
01:21:10
But who the hell cares about that?
01:21:12
A 50% chance is quite enough to be worth fighting for.
01:21:16
No doubt and I'm sure the market obviously would would be would
01:21:20
be obviously their appetite would be voracious.
01:21:23
They would obviously be super excited about the possibility
01:21:25
that what do you think? Obviously AI is on everybody's
01:21:28
mind. Every time I turn around
01:21:29
somebody's asking about the impact of AI and this business
01:21:31
that business or otherwise. What do you think a is role is
01:21:35
in playing to achieve life extension?
01:21:36
I mean, do you think it's in regards to the research and
01:21:39
development and obviously potential therapies, do you
01:21:41
think it's going to be a tool that maybe in the next two or
01:21:44
three years actually can improve those numbers you just gave me
01:21:47
as far as timelines? Yeah, so you always said
01:21:49
obviously twice then. And sure enough, what, what what
01:21:52
you said was much less nonsense. The roadway I is very, very
01:21:59
large indeed. It already is.
01:22:01
You know, I mean, it's no accident that the Nobel Prizes
01:22:03
for physics and chemistry both got awarded to breakthroughs in
01:22:07
AI this year. The breakthrough in chemistry,
01:22:11
the the price in chemistry was given mainly to well, one part
01:22:15
of it was given to Dennis Hassabis, the seminar that we've
01:22:18
been friends with since he was an undergrad.
01:22:19
You know, one of the, you know, probably the single smartest
01:22:22
person I've ever met. And that's a huge statement
01:22:24
because I've met an awful lot of very smart people.
01:22:29
The main thing it was given for was the creation of a program
01:22:33
called Alpha Fold, which is all about predicting the
01:22:39
three-dimensional shape of a protein by from its amino acid
01:22:44
sequence. It's the sequence of these
01:22:48
little units called amino acids that it's built from.
01:22:51
This is a classic problem in biology and nobody had got
01:22:56
anywhere with it for decades and now it's more or less completely
01:23:00
solved. Now, the reason that's so
01:23:02
important is because it means that you can, you can skip a
01:23:08
huge, big step in the development of drugs.
01:23:11
For example, if you want to know how to develop a drug, you want
01:23:13
to know that it fits correctly against a protein.
01:23:16
You know when it interacts with the protein in a particular way.
01:23:20
And the way to do that is to figure out what the shape of the
01:23:22
protein is first and then, you know, design your drug
01:23:27
appropriately. Now you can do that without
01:23:29
figuring out the type of the protein in the test tube.
01:23:32
You can just do it in silica, that it makes an enormous
01:23:36
difference to how rapidly you can develop drugs.
01:23:39
So, you know, you think about when the human genome was
01:23:42
sequenced 20 years ago, what was the utility of that same deal?
01:23:46
Anyone could sequence things before that, but they had to.
01:23:50
It was a very, very laborious process.
01:23:52
Suddenly they didn't need to because they already had the
01:23:54
sequence before they started. And so it's speed up a whole
01:23:58
bunch of biology all over the place.
01:24:00
So this applies to the whole of medical research, not just to
01:24:04
aging. That's fine.
01:24:05
It applies to aging. So, so the rest of medical
01:24:09
research can have it. And we're going to get more and
01:24:11
more of this AI is applicable to many other areas of medical
01:24:17
research. And if it gets better and
01:24:20
better, which it's doing obviously at an insane rate
01:24:22
right now, you know, we will see that over and over again very
01:24:25
quickly. Here's my last question for you,
01:24:28
doc. I'm just wondering, you know,
01:24:29
what are your thoughts on aging as far as an evolutionary
01:24:31
process? Do you think there's a chance
01:24:33
that by extending life we might disrupt biological balances that
01:24:37
we don't necessarily understand as of yet?
01:24:39
Is there anything like that that might have an impact?
01:24:43
So I I think I explained earlier that the reason we age is
01:24:46
because, well, I didn't really explain this properly, so let me
01:24:48
do it from scratch. The reason we age is because
01:24:52
evolution doesn't care enough about old individual.
01:24:56
Evolution cares about the perpetuation of genetic
01:24:58
information. So that means that after an
01:25:02
individual has reached the delta and sexual maturity and has has
01:25:05
had offspring, then evolution doesn't care anymore.
01:25:08
Evolution let's suck individuals age.
01:25:11
This has been known for, you know, many many decades.
01:25:14
It's not controversial at all. This is not me saying this is
01:25:17
just known, right? OK, so then the question is
01:25:22
supposedly we suddenly didn't have aging in humans.
01:25:25
What difference would that make? You can ask that at 2 levels.
01:25:28
You can say, well, OK, what difference would it make to the
01:25:32
global ecology? Well, honestly, we're making
01:25:36
enough impact on the global ecology already.
01:25:38
I don't think that's kind of a thing.
01:25:40
You know it. Might be a quality of life
01:25:42
question right where you might be worried about their quality
01:25:44
of life physically and mentally. So that's what I was going to
01:25:47
come to next. The question is, is evolution in
01:25:49
any sense going to fight back? Is the body going to try and
01:25:52
make us be miserable because we were born a long time ago?
01:25:56
And the answer is absolutely no, because the body is a machine,
01:26:00
just like the car. It's a machine that is
01:26:02
functioned both mental and physical, is determined by its
01:26:07
structure. And what we're doing here is
01:26:09
we're restoring the structure, we're eliminating damage.
01:26:13
Damage is changes to the structure and composition right
01:26:16
at the molecular and cellular level.
01:26:17
So we're restoring the structure and thus we are restoring the
01:26:21
function as well. That's all it's about.
01:26:25
But, you know, it's, it's, it's really important to understand
01:26:27
this. And of course, one can see
01:26:29
things where we have had, you know, complicated interactions
01:26:35
between technology and evolution.
01:26:37
Probably the best one is the immune system.
01:26:39
People have a weaker immune system now than what they did
01:26:41
100 years ago or 200 years ago now.
01:26:44
Why? Because we can, because we've
01:26:47
got medicine now. And so people who had a weak
01:26:51
immune system genetically, you know, used to die before they
01:26:55
could reproduce. Now they don't, so they can
01:26:58
reproduce. And so on average, we have
01:27:01
people with a weaker immune system.
01:27:02
Actually, it's even stronger than that because it turns out
01:27:04
that women with a weaker immune system are more fertile on
01:27:07
account of like, basically they have less risk of rejecting the
01:27:10
fetus. So it's been insanely rapid over
01:27:12
half a dozen generations. We've got a big reduction in
01:27:15
the, but who cares because we do have modern medicine that's not
01:27:18
going to just randomly disappear.
01:27:19
If it did, then we'd be screwed, but it's not going to.
01:27:23
Got you. That's a great answer.
01:27:24
It actually makes a lot of sense.
01:27:26
All right, for the audience. Listen, Doctor Aubrey de Grey,
01:27:28
we really appreciate you joining the show tonight.
01:27:30
Thank you for the information. It's great.
01:27:32
We'll obviously stay on top of it.
01:27:33
Why don't you share with the audience if they would like to
01:27:35
get involved with the Longevity Escape Velocity Project, your
01:27:39
social media or anything else you've got upcoming books or
01:27:41
maybe appearances around the country.
01:27:43
Sure, totally. So first of all, you have kindly
01:27:45
put my foundation's website under my name.
01:27:50
I I assume that the audience can see that the same icon.
01:27:52
Absolutely. In the chat also.
01:27:54
Right, so that's the place to go.
01:27:55
Of course we have links to all our social media on there.
01:27:59
I'm on all the obvious places, LinkedIn, Twitter and so on.
01:28:02
So it's easy to find me. I do a lot of public speaking.
01:28:07
I don't know whether we have yet got a calendar up on on our
01:28:13
website of where in the world Aubrey Degray is going to be.
01:28:16
But honestly, you know, seeing me in podcasts like this, it's
01:28:20
just as good as seeing me in person.
01:28:22
And if for most people, so, you know, looking me up on YouTube
01:28:26
works as well. And I, you know, I thank you for
01:28:30
having me on the show and for giving me exposure to a new
01:28:34
audience that I hope has learnt a bit about where we are in all
01:28:39
of this, why it's so important and how you can help, namely by
01:28:44
supporting this work. I do want to talk a little bit
01:28:46
about support. It's just in my last comment,
01:28:49
please, because you know, a lot of people will say to
01:28:52
themselves, okay, I can't do this.
01:28:53
I'm not well, okay, some of you are biologists.
01:28:56
Hello, you know, choose the right field to go into.
01:28:59
Then there's of course, people are in the media, people like
01:29:01
you. You know, you've done a good,
01:29:02
you've done a good thing here. You've saved a bunch of lives in
01:29:05
the future by just interviewing me a bunch of lives, you know,
01:29:10
Because every day that we bring forward the defeat of aging is
01:29:13
110 lives. I mean, that's 30 fucking World
01:29:16
Trade Centres, right? Yeah, there was no doubt, right?
01:29:21
I think our plan always and George and I try to do that as
01:29:23
much as possible as educate and unify the country.
01:29:25
Division and chaos is obviously a tool on the left.
01:29:28
We try to keep it that everybody wants to unify and this
01:29:31
information you're providing when it comes to health, and of
01:29:33
course all of us are aging, it's a big concern.
01:29:36
You know, my wife is actually a competitor.
01:29:37
She's competes in the IFBB Pro. So that aging topic, skin
01:29:41
elasticity, you know, loss of muscle atrophy, those are
01:29:45
discussions that she's regularly engaged in.
01:29:47
She's obviously much more knowledgeable than I am.
01:29:49
But I think the audience is really because we've had a
01:29:52
reaction to the other shows that were like this, that were health
01:29:54
oriented and the reaction's always been over the top, lots
01:29:57
of details. They wanted to get more
01:29:58
information, they wanted to understand more about it.
01:30:00
So I think it's always great. George, you got anything in the
01:30:02
chat? Anything else you want to share
01:30:04
or you good? No, we're good and.
01:30:06
While George is looking, let me just say, you know, it's all
01:30:09
about money. At the end of the day, these
01:30:11
experiments are expensive. Every single experiment that we
01:30:13
do cost 3 or $3 or more because the the 1000 mice giving
01:30:18
them a lot of different interventions.
01:30:21
So you know, anyone who feels able to contribute, even, you
01:30:24
know, every dollar counts. It's like it's, it makes all the
01:30:28
difference. It really, you know, it's, it's
01:30:30
essential to get these experiments done to figure out
01:30:33
what's going to work and kick off what the, the, the, the
01:30:36
cascade of events that I mentioned earlier, you know, at
01:30:39
the end of the year, people who want to get a tax write off,
01:30:41
obviously we're A5O1C3. So that's an issue.
01:30:45
And we actually currently have a matching campaign going.
01:30:50
One of our donors has given a few $100 which will with
01:30:55
which he will double anything that people give so.
01:31:00
That's great. What I'll do Doctor, We'll share
01:31:03
that with our audience. I'll put I'll post it up for
01:31:05
you. I actually saw that matching,
01:31:07
you know, endowment. I didn't know if it was still
01:31:09
going on, but I'll make sure I put that up on my social media.
01:31:11
I want to thank you again, Sir, for joining us.
01:31:12
We really appreciate it. Now tomorrow night we have Josie
01:31:14
Glavich, the red headed Libertarian coming on you guys
01:31:17
like that. She's got a lot to say.
01:31:19
You've seen her over on Tim Poole's show.
01:31:20
She'll be great at the end of the week.
01:31:22
That's it for interviews for this week.
01:31:23
So of course we've got, we've got the Global Finance Forum on
01:31:26
Friday and we should, George, you think 2 weeks away on the
01:31:29
Crypto Power Hour, you think that show will be up?
01:31:31
No 3 weeks. Probably more you.
01:31:35
Think so. OK.
01:31:36
All right, well, I appreciate listening.
01:31:37
Doctor Aubrey. Great.
01:31:38
We really appreciate you joining us tonight.
01:31:40
Thank you so very much for being here and keep up the good work.
01:31:43
God country family, we're out of here.
01:31:45
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01:31:47
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01:31:53
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They would run up to the bamboo fence and they would be shooting
01:33:58
between the bamboo at the buildings, you know, just
01:34:01
shooting inside. The Wanted man is Joseph Kony,
01:34:05
charged with abducting huge numbers of children, forcing
01:34:08
them to kill and mutilate innocent victims.
01:34:12
Somebody had to pay the price. Sam did that.
01:34:15
Sam Childers never stopped, because the bad things never
01:34:18
stop. There is only one Sam Childer.
01:34:20
There is no one else like him in the world.
01:34:23
And I said to him, I said. Would you go?
01:34:26
Now to get Kony in the Congo, he says, without a doubt in a
01:34:29
second. Now it's the DRC.
01:34:31
Tell us what's happening to children in the DRC.
01:34:33
Do you have ISIS there? You have Islamic State and you
01:34:37
have ADF? Hey, Sandy.
01:34:38
Joseph Kony's still alive. He's in the Congo, and now God
01:34:41
has me in the Congo, you know, So hopefully we'll meet up one
01:34:45
day, but maybe I can lead him to the Lord or send him there.
01:34:50
One or the other, huh?